Pubmed	Chromosome	Start_position	End_position	Enhancer_related_genes	Description	Species	Tissue_class	Experiment_class	Title	SNP_related	SNP_id	Disease	Cell_class	Enhancer_id	Enhancer_experiment	Enhancer_tar_ex_De	Enhancer_type	target_gene_strong_experiment	target_gene_weak_experiment	target_gene_experiment_description	target_gene_other_name	Enhancer_function	Enhancer_function_experiment	En_function_ex_de	TF_name	TF_other_name	Experiment	TF_experiment_de	SNP_position	SNP_experiment	Target_gene
29364907	chr2	28389994	28391994	FOSL2	FOSL2 levels were only minimally reduced, indicating that 20861 cell proliferation is completely dependent on expression of the E6 and E7 oncogenes.	human	Cervix	High+Lowthroughput	HPV integration hijacks and multimerizes a cellular enhancer to generate a viral-cellular super-enhancer that drives high viral oncogene expression	否		HPV positive tumors	cervical-derived cell line 20861	E_01_0001	Southern blot,ChIP-seq,Immunofluorescence,ChIP-qPCR,RNA-seq,FISH	FOSL2 levels were only minimally reduced, indicating that 20861 cell proliferation is completely dependent on expression of the E6 and E7 oncogenes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FOSL2 levels were only minimally reduced, indicating that 20861 cell proliferation is completely dependent on expression of the E6 and E7 oncogenes.	Immunohistochemical staining	FOSL2 levels were only minimally reduced, indicating that 20861 cell proliferation is completely dependent on expression of the E6 and E7 oncogenes.	FOSL2		Southern blot,ChIP-seq,Immunofluorescence,ChIP-qPCR,RNA-seq,FISH	FOSL2 levels were only minimally reduced, indicating that 20861 cell proliferation is completely dependent on expression of the E6 and E7 oncogenes.			
29364907	chr17	32412637	32414637	Brd4	ChIP-seq analysis showed two strong peaks of enrichment of the super-enhancer markers Brd4 and H3K27ac at both the viral URR and adjacent cellular sequence at the integration locus, the latter of which was not observed in the same region of cellular DNA in the W12 20863 sub-clone that harbors extrachromosomal viral DNA	mouse	Cervix	High+Lowthroughput	HPV integration hijacks and multimerizes a cellular enhancer to generate a viral-cellular super-enhancer that drives high viral oncogene expression	否		HPV positive tumors	cervical-derived cell line 20861	E_01_0001	Southern blot,ChIP-seq,Immunofluorescence,ChIP-qPCR,RNA-seq,FISH	ChIP-seq analysis showed two strong peaks of enrichment of the super-enhancer markers Brd4 and H3K27ac at both the viral URR and adjacent cellular sequence at the integration locus, the latter of which was not observed in the same region of cellular DNA in the W12 20863 sub-clone that harbors extrachromosomal viral DNA	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ChIP-seq analysis showed two strong peaks of enrichment of the super-enhancer markers Brd4 and H3K27ac at both the viral URR and adjacent cellular sequence at the integration locus, the latter of which was not observed in the same region of cellular DNA in the W12 20863 sub-clone that harbors extrachromosomal viral DNA		ChIP-seq analysis showed two strong peaks of enrichment of the super-enhancer markers Brd4 and H3K27ac at both the viral URR and adjacent cellular sequence at the integration locus, the latter of which was not observed in the same region of cellular DNA in the W12 20863 sub-clone that harbors extrachromosomal viral DNA	Immunohistochemical staining	ChIP-seq analysis showed two strong peaks of enrichment of the super-enhancer markers Brd4 and H3K27ac at both the viral URR and adjacent cellular sequence at the integration locus, the latter of which was not observed in the same region of cellular DNA in the W12 20863 sub-clone that harbors extrachromosomal viral DNA			Southern blot,ChIP-seq,Immunofluorescence,ChIP-qPCR,RNA-seq,FISH				Brd4
29363938	chr2	207527779	207529779	CREB1	The addition of AuNP-p(T)DNA to HeLa lysate containing GFP, GCN5, CREB1, and XBP-1S mRNA increased protein synthesis by 1.80, 1.99, 1.95 and 2.20-fold respectively.	human	Cervix	High+Lowthroughput	Universal mRNA Translation Enhancement with Gold Nanoparticles Conjugated to Oligonucleotides with a Poly(T) Sequence	否		cervical cancer	HeLa cell	E_01_0002	Western blot,RT-PCR,PCR	The addition of AuNP-p(T)DNA to HeLa lysate containing GFP, GCN5, CREB1, and XBP-1S mRNA increased protein synthesis by 1.80, 1.99, 1.95 and 2.20-fold respectively.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The addition of AuNP-p(T)DNA to HeLa lysate containing GFP, GCN5, CREB1, and XBP-1S mRNA increased protein synthesis by 1.80, 1.99, 1.95 and 2.20-fold respectively.	Immunohistochemical staining	The addition of AuNP-p(T)DNA to HeLa lysate containing GFP, GCN5, CREB1, and XBP-1S mRNA increased protein synthesis by 1.80, 1.99, 1.95 and 2.20-fold respectively.	CREB1		Western blot,RT-PCR,PCR	The addition of AuNP-p(T)DNA to HeLa lysate containing GFP, GCN5, CREB1, and XBP-1S mRNA increased protein synthesis by 1.80, 1.99, 1.95 and 2.20-fold respectively.			
29363553	chr6	47503992	47505992	Ezh2	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.	mouse	Bone marrow	High+Lowthroughput	Hematopoietic stem/progenitor cell senescence is associated with altered expression profiles of cellular memory-involved gene	否	Enhancer_experiment	senescence associated disease	progenitor cell	E_02_0001	qRT-PCR	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.		Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.	Immunohistochemical staining	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.			qRT-PCR				Ezh2
29358714	chr15	58585627	58587627	ADAM10	ADAM10 is a metalloproteinase acting on the amyloid precursor protein (APP) as an alpha-secretase in neurons.	human,mouse	Nerve	High+Lowthroughput	Identification of disulfiram as a secretase-modulating compound with beneficial effects on Alzheimer's disease hallmarks	否		Alzheimer’s disease	SH-SY5Y human neuronal cell	E_02_0002	Western blot,RT-PCR	ADAM10 is a metalloproteinase acting on the amyloid precursor protein (APP) as an alpha-secretase in neurons.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ADAM10 is a metalloproteinase acting on the amyloid precursor protein (APP) as an alpha-secretase in neurons.		ADAM10 is a metalloproteinase acting on the amyloid precursor protein (APP) as an alpha-secretase in neurons.	Immunohistochemical staining	ADAM10 is a metalloproteinase acting on the amyloid precursor protein (APP) as an alpha-secretase in neurons.			Western blot,RT-PCR				ADAM10
29358650	chr4	139461205	139463205	Pax7	Pax7 binds its targeted enhancers rapidly, but chromatin remodeling and gene activation are slower.	mouse	Hypophysoma	High+Lowthroughput	Pioneer factor Pax7 deploys a stable enhancer repertoire for specification of cell fate	否		Hypophysoma	AtT-20 cell	E_02_0003	ChIP–seq,ATAC–seq,RNA-seq	Pax7 binds its targeted enhancers rapidly, but chromatin remodeling and gene activation are slower.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Pax7 binds its targeted enhancers rapidly, but chromatin remodeling and gene activation are slower.		Pax7 binds its targeted enhancers rapidly, but chromatin remodeling and gene activation are slower.	Immunohistochemical staining	Pax7 binds its targeted enhancers rapidly, but chromatin remodeling and gene activation are slower.			ChIP–seq,ATAC–seq,RNA-seq				Pax7
29357419	chr7	148804764	148806764	EZH2	Polycomb group proteins,EZH2, and menin binds at PAX2 gene and has been demonstrated to decrease transcription of PAX2	human	Kidney	High+Lowthroughput	Modulation of apolipoprotein L1-microRNA-193a axis prevents podocyte dedifferentiation in high-glucose milieu	否		kidney disease	epithelial cell	E_01_0003	Western blot,Immunofluorescence,Transfection	Polycomb group proteins,EZH2, and menin binds at PAX2 gene and has been demonstrated to decrease transcription of PAX2	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Polycomb group proteins,EZH2, and menin binds at PAX2 gene and has been demonstrated to decrease transcription of PAX2	Immunohistochemical staining	Polycomb group proteins,EZH2, and menin binds at PAX2 gene and has been demonstrated to decrease transcription of PAX2	EZH2		Western blot,Immunofluorescence,Transfection	Polycomb group proteins,EZH2, and menin binds at PAX2 gene and has been demonstrated to decrease transcription of PAX2			
29344674	chr7	148805135	148807135	EZH2	In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR‑138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells.	human	Oral cavity	High+Lowthroughput	Long non-coding RNA H1 promotes cell proliferation and invasion by acting as a ceRNA of miR?138 and releasing EZH2 in oral squamous cell carcinoma	否		oral squamous cell carcinoma	oral squamous cell carcinoma cell	E_01_0004	RT-qPCR,transfection,Western blot	In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR‑138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR‑138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells.	Immunohistochemical staining	In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR‑138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells.	EZH2		RT-qPCR,transfection,Western blot	In addition, H19 was found to regulate the expression of oncogene enhancer of zeste homolog 2 (EZH2) by competing with miR‑138; the inhibition of miR-138 attenuated the inhibitory effects of H19 knockdown on OSCC cells.			
29344090	chr12	102954386	102956386	ASCL1	As a consequence of the rearrangement ASCL1 was brought into proximity of the IGHJ-Cμ enhancer and was highly overexpressed in the aberrant B-cells of the patient, as shown by qPCR and immunohistochemistry.	human	Bone marrow and lymphatic tissue	High+Lowthroughput	Overexpression of the proneural transcription factor ASCL1 in chronic lymphocytic leukemia with a t(12;14)(q23.2;q32.3)	否		chronic lymphocytic leukemia	chronic lymphocytic leukemia cell	E_01_0005	qPCR,FISH	As a consequence of the rearrangement ASCL1 was brought into proximity of the IGHJ-Cμ enhancer and was highly overexpressed in the aberrant B-cells of the patient, as shown by qPCR and immunohistochemistry.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			As a consequence of the rearrangement ASCL1 was brought into proximity of the IGHJ-Cμ enhancer and was highly overexpressed in the aberrant B-cells of the patient, as shown by qPCR and immunohistochemistry.	Immunohistochemical staining	As a consequence of the rearrangement ASCL1 was brought into proximity of the IGHJ-Cμ enhancer and was highly overexpressed in the aberrant B-cells of the patient, as shown by qPCR and immunohistochemistry.	ASCL1		qPCR,FISH	As a consequence of the rearrangement ASCL1 was brought into proximity of the IGHJ-Cμ enhancer and was highly overexpressed in the aberrant B-cells of the patient, as shown by qPCR and immunohistochemistry.			
29344006	chr6	113930322	113932322	HDAC2	HDAC2 can attenuate lipopolysaccharide-induced inflammation by regulating c-Jun and PAI-1 expression in macrophages.	human	Connective tissue	High+Lowthroughput	Histone deacetylase 2 (HDAC2) attenuates lipopolysaccharide (LPS)-induced inflammation by regulating PAI-1 expression	否		Sepsis	macrophage	E_01_0006	ChIP,qRT-PCR,Western blot	HDAC2 can attenuate lipopolysaccharide-induced inflammation by regulating c-Jun and PAI-1 expression in macrophages.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HDAC2 can attenuate lipopolysaccharide-induced inflammation by regulating c-Jun and PAI-1 expression in macrophages.		HDAC2 can attenuate lipopolysaccharide-induced inflammation by regulating c-Jun and PAI-1 expression in macrophages.	Immunohistochemical staining	HDAC2 can attenuate lipopolysaccharide-induced inflammation by regulating c-Jun and PAI-1 expression in macrophages.			ChIP,qRT-PCR,Western blot				HDAC2
29344006	chr6	31572978	31574978	TNF	Results revealed that PAI-1, TNF, and MIP-2 expression were inhibited by theophylline, an HDAC2 enhancer, in a RAW macrophage cell line, following LPS-induced inflammation.	human	Connective tissue	High+Lowthroughput	Histone deacetylase 2 (HDAC2) attenuates lipopolysaccharide (LPS)-induced inflammation by regulating PAI-1 expression	否		Sepsis	macrophage	E_01_0006	ChIP,qRT-PCR,Western blot	Results revealed that PAI-1, TNF, and MIP-2 expression were inhibited by theophylline, an HDAC2 enhancer, in a RAW macrophage cell line, following LPS-induced inflammation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Results revealed that PAI-1, TNF, and MIP-2 expression were inhibited by theophylline, an HDAC2 enhancer, in a RAW macrophage cell line, following LPS-induced inflammation.	Immunohistochemical staining	Results revealed that PAI-1, TNF, and MIP-2 expression were inhibited by theophylline, an HDAC2 enhancer, in a RAW macrophage cell line, following LPS-induced inflammation.	TNF		ChIP,qRT-PCR,Western blot	Results revealed that PAI-1, TNF, and MIP-2 expression were inhibited by theophylline, an HDAC2 enhancer, in a RAW macrophage cell line, following LPS-induced inflammation.			
29343853	chr7	78700257	78702257	Acan	Thus, the Acan enhancers orchestrate the precise spatiotemporal expression of this gene in cartilage types at different stages of development and adulthood	mouse	Cartilage tissue	High+Lowthroughput	Differential tissue specific, temporal and spatial expression patterns of the Aggrecan gene is modulated by independent enhancer elements	否		In debilitating diseases such as osteoarthritis, where increased mechanical stress on chondrocytes.	chondroblast	E_02_0004	Western blot	Thus, the Acan enhancers orchestrate the precise spatiotemporal expression of this gene in cartilage types at different stages of development and adulthood	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, the Acan enhancers orchestrate the precise spatiotemporal expression of this gene in cartilage types at different stages of development and adulthood		Thus, the Acan enhancers orchestrate the precise spatiotemporal expression of this gene in cartilage types at different stages of development and adulthood	Immunohistochemical staining	Thus, the Acan enhancers orchestrate the precise spatiotemporal expression of this gene in cartilage types at different stages of development and adulthood			Western blot				Acan
29343853	chr17	72118279	72120279	SOX9	The transcription factor SOX9 interacted with all the enhancers in vitro and mutation of SOX9 binding sites in one of the enhancers (−30) resulted in a loss of its chondrocyte specificity and ectopic enhancer reporter activity.	human	Cartilage tissue	High+Lowthroughput	Differential tissue specific, temporal and spatial expression patterns of the Aggrecan gene is modulated by independent enhancer elements	否		In debilitating diseases such as osteoarthritis, where increased mechanical stress on chondrocytes.	chondroblast	E_02_0004	Western blot	The transcription factor SOX9 interacted with all the enhancers in vitro and mutation of SOX9 binding sites in one of the enhancers (−30) resulted in a loss of its chondrocyte specificity and ectopic enhancer reporter activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The transcription factor SOX9 interacted with all the enhancers in vitro and mutation of SOX9 binding sites in one of the enhancers (−30) resulted in a loss of its chondrocyte specificity and ectopic enhancer reporter activity.	Immunohistochemical staining	The transcription factor SOX9 interacted with all the enhancers in vitro and mutation of SOX9 binding sites in one of the enhancers (−30) resulted in a loss of its chondrocyte specificity and ectopic enhancer reporter activity.	SOX9		Western blot	The transcription factor SOX9 interacted with all the enhancers in vitro and mutation of SOX9 binding sites in one of the enhancers (−30) resulted in a loss of its chondrocyte specificity and ectopic enhancer reporter activity.			
29343500	chr9	123505056	123507056	Ccr9	Furthermore, cbfβ2 endows extrathymic progenitors with thymus-homing capacity by inducing expression of the principal thymus-homing receptor, ccr9.	mouse	Thymus	High+Lowthroughput	Cbfβ2 controls differentiation of and confers homing capacity to prethymic progenitors	否		thymus homing	thymocyte	E_02_0005	Western blot,ChIP-seq,RNA-seq	Furthermore, cbfβ2 endows extrathymic progenitors with thymus-homing capacity by inducing expression of the principal thymus-homing receptor, ccr9.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, cbfβ2 endows extrathymic progenitors with thymus-homing capacity by inducing expression of the principal thymus-homing receptor, ccr9.		Furthermore, cbfβ2 endows extrathymic progenitors with thymus-homing capacity by inducing expression of the principal thymus-homing receptor, ccr9.	Immunohistochemical staining	Furthermore, cbfβ2 endows extrathymic progenitors with thymus-homing capacity by inducing expression of the principal thymus-homing receptor, ccr9.			Western blot,ChIP-seq,RNA-seq				Ccr9
29343500	chr8	105894833	105896833	Cbfb	Cbfβ forms transcription factor complexes with runx proteins, and here we show that cbfβ2, encoded by an rnA splice variant of the cbfb gene, is essential for extrathymic differentiation of t cell progenitors.	mouse	Thymus	High+Lowthroughput	Cbfβ2 controls differentiation of and confers homing capacity to prethymic progenitors	否		thymus homing	thymocyte	E_02_0005	Western blot,ChIP-seq,RNA-seq	Cbfβ forms transcription factor complexes with runx proteins, and here we show that cbfβ2, encoded by an rnA splice variant of the cbfb gene, is essential for extrathymic differentiation of t cell progenitors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cbfβ forms transcription factor complexes with runx proteins, and here we show that cbfβ2, encoded by an rnA splice variant of the cbfb gene, is essential for extrathymic differentiation of t cell progenitors.		Cbfβ forms transcription factor complexes with runx proteins, and here we show that cbfβ2, encoded by an rnA splice variant of the cbfb gene, is essential for extrathymic differentiation of t cell progenitors.	Immunohistochemical staining	Cbfβ forms transcription factor complexes with runx proteins, and here we show that cbfβ2, encoded by an rnA splice variant of the cbfb gene, is essential for extrathymic differentiation of t cell progenitors.			Western blot,ChIP-seq,RNA-seq				Cbfb
29343483	chr7	34815932	34817932	Cebpa	Mechanistically, we demonstrate that NR4A1/3 restrict HSC proliferation in part through activation of a C/EBPα-driven anti-proliferative network by directly binding to a hematopoietic-specific Cebpa enhancer and activating Cebpa transcription.	mouse	Bone marrow	High+Lowthroughput	NR4A1 and NR4A3 restrict HSC proliferation via reciprocal regulation of C/EBPα and inflammatory signaling	否		myelodysplastic disease	hematopoietic stem cell	E_02_0006	RT-qPCR	Mechanistically, we demonstrate that NR4A1/3 restrict HSC proliferation in part through activation of a C/EBPα-driven anti-proliferative network by directly binding to a hematopoietic-specific Cebpa enhancer and activating Cebpa transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mechanistically, we demonstrate that NR4A1/3 restrict HSC proliferation in part through activation of a C/EBPα-driven anti-proliferative network by directly binding to a hematopoietic-specific Cebpa enhancer and activating Cebpa transcription.		Mechanistically, we demonstrate that NR4A1/3 restrict HSC proliferation in part through activation of a C/EBPα-driven anti-proliferative network by directly binding to a hematopoietic-specific Cebpa enhancer and activating Cebpa transcription.	Immunohistochemical staining	Mechanistically, we demonstrate that NR4A1/3 restrict HSC proliferation in part through activation of a C/EBPα-driven anti-proliferative network by directly binding to a hematopoietic-specific Cebpa enhancer and activating Cebpa transcription.			RT-qPCR				Cebpa
29343483	chr12	52019947	52021947	NR4A1	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses	human,mouse	Bone marrow	High+Lowthroughput	NR4A1 and NR4A3 restrict HSC proliferation via reciprocal regulation of C/EBPα and inflammatory signaling	否		myelodysplastic disease	hematopoietic stem cell	E_02_0006	RT-qPCR	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses		Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses	Immunohistochemical staining	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses			RT-qPCR				NR4A1
29343483	chr9	99818517	99820517	NR4A3	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses	human,mouse	Bone marrow	High+Lowthroughput	NR4A1 and NR4A3 restrict HSC proliferation via reciprocal regulation of C/EBPα and inflammatory signaling	否		myelodysplastic disease	hematopoietic stem cell	E_02_0006	RT-qPCR	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses		Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses	Immunohistochemical staining	Taken together, our results reveal a novel coordinate control of HSC quiescence by NR4A1/3 through direct activation of C/EBPα and suppression of activation of NF-κB-driven proliferative inflammatory responses			RT-qPCR				NR4A3
29343442	chr12	57092345	57094345	STAT6	Thus, the IL-4-STAT6 signaling pathway establishes an alternative polarization-specific epigenenomic signature resulting in dampened macrophage responsiveness to inflammatory stimuli.	human,mouse	Bone marrow	High+Lowthroughput	The Transcription Factor STAT6 Mediates Direct Repression of Inflammatory Enhancers and Limits Activation of Alternatively Polarized Macrophages	否		inflammatory diseases	macrophage	E_02_0007	ATAC-seq, ChIP-seq,GRO-seq,RNA-seq,Western Blot,qPCR,ChIP-qPCR	Thus, the IL-4-STAT6 signaling pathway establishes an alternative polarization-specific epigenenomic signature resulting in dampened macrophage responsiveness to inflammatory stimuli.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, the IL-4-STAT6 signaling pathway establishes an alternative polarization-specific epigenenomic signature resulting in dampened macrophage responsiveness to inflammatory stimuli.		Thus, the IL-4-STAT6 signaling pathway establishes an alternative polarization-specific epigenenomic signature resulting in dampened macrophage responsiveness to inflammatory stimuli.	Immunohistochemical staining	Thus, the IL-4-STAT6 signaling pathway establishes an alternative polarization-specific epigenenomic signature resulting in dampened macrophage responsiveness to inflammatory stimuli.			ATAC-seq, ChIP-seq,GRO-seq,RNA-seq,Western Blot,qPCR,ChIP-qPCR				STAT6
29343442	chr5	141618696	141620696	HDAC3	The Presence of HDAC3 Is Required for IL-4-STAT6-Mediated Repression on a Subset of Genes	human,mouse	Bone marrow	High+Lowthroughput	The Transcription Factor STAT6 Mediates Direct Repression of Inflammatory Enhancers and Limits Activation of Alternatively Polarized Macrophages	否		ainflammatory diseases	macrophage	E_02_0007	ATAC-seq, ChIP-seq,GRO-seq,RNA-seq,Western Blot,qPCR,ChIP-qPCR	The Presence of HDAC3 Is Required for IL-4-STAT6-Mediated Repression on a Subset of Genes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The Presence of HDAC3 Is Required for IL-4-STAT6-Mediated Repression on a Subset of Genes		The Presence of HDAC3 Is Required for IL-4-STAT6-Mediated Repression on a Subset of Genes	Immunohistochemical staining	The Presence of HDAC3 Is Required for IL-4-STAT6-Mediated Repression on a Subset of Genes			ATAC-seq, ChIP-seq,GRO-seq,RNA-seq,Western Blot,qPCR,ChIP-qPCR				HDAC3
29342503	chr5	173229371	173231371	NKX2-5	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	human	Vascular tissue	High+Lowthroughput	Molecular Basis for Dysregulated Activation of NKX2-5 in the Vascular Remodeling of Systemic Sclerosis	是	rs3095870	scleroderma associated pulmonary hypertensio	smooth muscle cell of the pulmonary artery	E_01_0007	Western blot,qPCR	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	Immunohistochemical staining	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	NKX2-5		Western blot,qPCR	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.			
29342503	chr11	12671461	12673461	TEAD1	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	human	Vascular tissue	High+Lowthroughput	Molecular Basis for Dysregulated Activation of NKX2-5 in the Vascular Remodeling of Systemic Sclerosis	是	rs3095870	scleroderma associated pulmonary hypertensio	smooth muscle cell of the pulmonary artery	E_01_0007	Western blot,qPCR	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	Immunohistochemical staining	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	TEAD1		Western blot,qPCR	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease			
29342133	chr15	63714919	63952099	Myc	The transcription factor Myc is essential for the regulation of haematopoietic stem cells and progenitors and has a critical function in haematopoietic malignancies	mouse	Haematopoietic tissue	Low+High throughput	A Myc enhancer cluster regulates normal and leukaemic haematopoietic stem cell hierarchies	否	--	Leukaemia	hematopoietic stem cell	E_02_0008	ChIP-seq	Here we show that an evolutionarily conserved region located 1.7 megabases downstream of the Myc gene that has previously been labelled as a ‘super_x0002_enhancer’2 is essential for the regulation of Myc expression levels in both normal haematopoietic and leukaemic stem cell hierarchies in mice and humans. Deletion of this region in mice leads to a complete loss of Myc expression in haematopoietic stem cells and progenitors.	Super-Enhancer	--	ChIP-seq,ATAC-seq,RT-qPCR	In line with this hypothesis, chromatin conformation capture performedon mouse leukaemic cells2 as well as DNA proximity analysis using fluorescence in situ hybridization (DNA FISH) in LSK cells showed that the Myc promoter and BENC are in close physical proximity to each other, suggesting that cis-regulation is mediated by chromosomal looping in haematopoietic stem and progenitor cells.	AU0167572,Niard,Nird,bHLHe39,?Myc	Clusters of enhancers, such as BENC, form highly combinatorial systems that allow precise control of gene expression across normal cellular hierarchies and which also can be hijacked in malignancies.	ATAC-seq,RT-qPCR	Analysis of mice carrying deletions of individual Enhancer modules suggests that specific Myc expression levels throughout most of the haematopoietic hierarchy are controlled by the combinatorial and additive activity of individual Enhancer modules, which collectively function as a ‘blood Enhancer cluster’(BENC).	--	--	--	--	--	--	Myc
29339538	chr7	55016139	55018139	EGFR	Whole genome ChIP-seq and RNA-seq results revealed that CaSki cells contained super-enhancers in the proto-oncogenes EGFR and c-MET.	human	Cervix	High+Lowthroughput	E6 Protein Expressed by High-Risk HPV Activates Super-Enhancers of the EGFR and c-MET Oncogenes by Destabilizing the Histone Demethylase KDM5C	否		human papillomaviruses	CaSki cell(human cervical cancer cell line)	E_01_0008	ChIP-seq,RNA-seq	Whole genome ChIP-seq and RNA-seq results revealed that CaSki cells contained super-enhancers in the proto-oncogenes EGFR and c-MET.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Whole genome ChIP-seq and RNA-seq results revealed that CaSki cells contained super-enhancers in the proto-oncogenes EGFR and c-MET.	Immunohistochemical staining	Whole genome ChIP-seq and RNA-seq results revealed that CaSki cells contained super-enhancers in the proto-oncogenes EGFR and c-MET.	EGFR		ChIP-seq,RNA-seq	Whole genome ChIP-seq and RNA-seq results revealed that CaSki cells contained super-enhancers in the proto-oncogenes EGFR and c-MET.			
29339538	chrX	53173366	53175366	KDM5C	Restoration of KDM5C significantly suppressed the tumorigenicity of CaSki cells, an HPV16-positive cervical cancer cell line.	human	Cervix	High+Lowthroughput	E6 Protein Expressed by High-Risk HPV Activates Super-Enhancers of the EGFR and c-MET Oncogenes by Destabilizing the Histone Demethylase KDM5C	否		human papillomaviruses	CaSki cell(human cervical cancer cell line)	E_01_0008	ChIP-seq,RNA-seq	Restoration of KDM5C significantly suppressed the tumorigenicity of CaSki cells, an HPV16-positive cervical cancer cell line.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Restoration of KDM5C significantly suppressed the tumorigenicity of CaSki cells, an HPV16-positive cervical cancer cell line.	Immunohistochemical staining	Restoration of KDM5C significantly suppressed the tumorigenicity of CaSki cells, an HPV16-positive cervical cancer cell line.	KDM5C		ChIP-seq,RNA-seq	Restoration of KDM5C significantly suppressed the tumorigenicity of CaSki cells, an HPV16-positive cervical cancer cell line.			
29339121	chr8	144288666	144290666	HSF1	HSF1 was found to promote proliferation, migration and invasion of gastric cancer cells.	human	Gastric cancer tissues	High+Lowthroughput	HSF1, in association with MORC2, downregulates ArgBP2 via the PRC2 family in gastric cancer cells	否		gastric cancer	gastric cancer cell	E_01_0009	ChIP,Real-time PCR,Western blot	HSF1 was found to promote proliferation, migration and invasion of gastric cancer cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			HSF1 was found to promote proliferation, migration and invasion of gastric cancer cells.	Immunohistochemical staining	HSF1 was found to promote proliferation, migration and invasion of gastric cancer cells.	HSF1		ChIP,Real-time PCR,Western blot	HSF1 was found to promote proliferation, migration and invasion of gastric cancer cells.			
29339121	chr7	148804519	148806519	EZH2	EZH2, as the core and contributing catalytic subunit of PRC2, which is composed of EED	human	Gastric cancer tissues	High+Lowthroughput	HSF1, in association with MORC2, downregulates ArgBP2 via the PRC2 family in gastric cancer cells	否		gastric cancer	gastric cancer cell	E_01_0009	ChIP,Real-time PCR,Western blot	EZH2, as the core and contributing catalytic subunit of PRC2, which is composed of EED	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2, as the core and contributing catalytic subunit of PRC2, which is composed of EED	Immunohistochemical staining	EZH2, as the core and contributing catalytic subunit of PRC2, which is composed of EED	EZH2		ChIP,Real-time PCR,Western blot	EZH2, as the core and contributing catalytic subunit of PRC2, which is composed of EED			
29339121	chr22	30922434	30924434	MORC2	In view of this, we speculated that HSF1 may regulate ArgBP2 as well as associate with MORC2	human	Gastric cancer tissues	High+Lowthroughput	HSF1, in association with MORC2, downregulates ArgBP2 via the PRC2 family in gastric cancer cells	否		gastric cancer	gastric cancer cell	E_01_0009	ChIP,Real-time PCR,Western blot	In view of this, we speculated that HSF1 may regulate ArgBP2 as well as associate with MORC2	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In view of this, we speculated that HSF1 may regulate ArgBP2 as well as associate with MORC2		In view of this, we speculated that HSF1 may regulate ArgBP2 as well as associate with MORC2	Immunohistochemical staining	In view of this, we speculated that HSF1 may regulate ArgBP2 as well as associate with MORC2			ChIP,Real-time PCR,Western blot				MORC2
29337370	chr16	28929378	28931378	CD19	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	human	Lymphoid tissue bone marrow	High+Lowthroughput	Modulating Gene Expression in Epstein-Barr Virus (EBV)-Positive B Cell Lines with CRISPRa and CRISPRi	否		Epstein-Barr virus	B cell	E_01_0010	ChIP-seq,ChIA-PET,RT-PCR	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).		GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	Immunohistochemical staining	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).			ChIP-seq,ChIA-PET,RT-PCR				CD19
29337370	chr3	122052540	122054540	CD86	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	human	Lymphoid tissue bone marrow	High+Lowthroughput	Modulating Gene Expression in Epstein-Barr Virus (EBV)-Positive B Cell Lines with CRISPRa and CRISPRi	否		Epstein-Barr virus	B cell	E_01_0010	ChIP-seq,ChIA-PET,RT-PCR	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	Immunohistochemical staining	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).	CD86		ChIP-seq,ChIA-PET,RT-PCR	GM12878 LCL and P3HR-1 Burkitt lymphoma cells stably expressing activating dCas9-VP64 were transduced with either control sgRNA or sgRNAs targeting the indicated genes(CD19 or CD86).			
29334376	chr1	94526560	94528560	F3	We further show that genetic deletion of a single Met-VEL at the F3 locus blocks metastatic cell outgrowth in the lung.	human	Osteosarcoma	High+Lowthroughput	Positively selected enhancer elements endow osteosarcoma cells with metastatic competence	否		Osteosarcoma	osteosarcoma cell	E_01_0011	RNA-seq,ChIP–seq	We further show that genetic deletion of a single Met-VEL at the F3 locus blocks metastatic cell outgrowth in the lung.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We further show that genetic deletion of a single Met-VEL at the F3 locus blocks metastatic cell outgrowth in the lung.		We further show that genetic deletion of a single Met-VEL at the F3 locus blocks metastatic cell outgrowth in the lung.	Immunohistochemical staining	We further show that genetic deletion of a single Met-VEL at the F3 locus blocks metastatic cell outgrowth in the lung.			RNA-seq,ChIP–seq				F3
29331299	chr16	29880720	29882720	Hes1	During the transition from osteoblasts to osteocytes, Hes1 is upregulated rather than Hes3 and Hes5, and Hes3 and Hes5 null mice display no skeletal phenotype, indicating that Hes1 is a major target of Notch signaling conduction in the skeleton	human,mouse	Bone	High+Lowthroughput	The regulatory roles of Notch in osteocyte differentiation via the crosstalk with canonical Wnt pathways during the transition of osteoblasts to osteocytes	否			osteocyte	E_02_0009	RT-qPCR,Western blot, transfection, Immunofluorescence	During the transition from osteoblasts to osteocytes, Hes1 is upregulated rather than Hes3 and Hes5, and Hes3 and Hes5 null mice display no skeletal phenotype, indicating that Hes1 is a major target of Notch signaling conduction in the skeleton	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	During the transition from osteoblasts to osteocytes, Hes1 is upregulated rather than Hes3 and Hes5, and Hes3 and Hes5 null mice display no skeletal phenotype, indicating that Hes1 is a major target of Notch signaling conduction in the skeleton		During the transition from osteoblasts to osteocytes, Hes1 is upregulated rather than Hes3 and Hes5, and Hes3 and Hes5 null mice display no skeletal phenotype, indicating that Hes1 is a major target of Notch signaling conduction in the skeleton	Immunohistochemical staining	During the transition from osteoblasts to osteocytes, Hes1 is upregulated rather than Hes3 and Hes5, and Hes3 and Hes5 null mice display no skeletal phenotype, indicating that Hes1 is a major target of Notch signaling conduction in the skeleton			RT-qPCR,Western blot, transfection, Immunofluorescence				Hes1
29331016	chr10	112947442	112949442	TCF7L2	The SNP rs7903146 at the transcription factor 7-like 2 (TCF7L2) locus is established as the strongest known genetic marker for type 2 diabetes via genome-wide association studies.	human	Liver	High+Lowthroughput	A candidate functional SNP rs7074440 in TCF7L2 alters gene expression through C-FOS in hepatocytes	是	rs7903146	type 2 diabetes	hepatocyte	E_01_0012	qRT-PCR,ChIP,Transfection	The SNP rs7903146 at the transcription factor 7-like 2 (TCF7L2) locus is established as the strongest known genetic marker for type 2 diabetes via genome-wide association studies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The SNP rs7903146 at the transcription factor 7-like 2 (TCF7L2) locus is established as the strongest known genetic marker for type 2 diabetes via genome-wide association studies.	Immunohistochemical staining	The SNP rs7903146 at the transcription factor 7-like 2 (TCF7L2) locus is established as the strongest known genetic marker for type 2 diabetes via genome-wide association studies.	TCF7L2		qRT-PCR,ChIP,Transfection	The SNP rs7903146 at the transcription factor 7-like 2 (TCF7L2) locus is established as the strongest known genetic marker for type 2 diabetes via genome-wide association studies.			
29327713	chr7	148804434	148806434	EZH2	EZH2 is an important enzymatic subunit of the epigenetic regulator polycomb repressive complex 2 (PRC2), which controls gene silencing through post-translational modification, and is overexpressed in various carcinomas and hematopoietic neoplasms.	human	Lymphoid tissue	High+Lowthroughput	Expression of enhancer of zeste homolog 2 (EZH2) protein in histiocytic and dendritic cell neoplasms with evidence for p-ERK1/2-related, but not MYC- or p-STAT3-related cell signaling	否		histiocytic and dendritic cell neoplasms	histiocytic and dendritic cell neoplasm cell	E_01_0013	Immunohistochemical staining	EZH2 is an important enzymatic subunit of the epigenetic regulator polycomb repressive complex 2 (PRC2), which controls gene silencing through post-translational modification, and is overexpressed in various carcinomas and hematopoietic neoplasms.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2 is an important enzymatic subunit of the epigenetic regulator polycomb repressive complex 2 (PRC2), which controls gene silencing through post-translational modification, and is overexpressed in various carcinomas and hematopoietic neoplasms.	Immunohistochemical staining	EZH2 is an important enzymatic subunit of the epigenetic regulator polycomb repressive complex 2 (PRC2), which controls gene silencing through post-translational modification, and is overexpressed in various carcinomas and hematopoietic neoplasms.	EZH2		Immunohistochemical staining	EZH2 is an important enzymatic subunit of the epigenetic regulator polycomb repressive complex 2 (PRC2), which controls gene silencing through post-translational modification, and is overexpressed in various carcinomas and hematopoietic neoplasms.			
29325110	chr5	56096484	56098484	ANKRD55	As an example, we found that rs71624119, shared with three other autoimmune diseases and located in a primed enhancer (H3K4me1) with potential binding for STAT transcription factors, significantly associates with ANKRD55 expression.	human	Lymphoid tissue	High+Lowthroughput	Impact of genetic risk loci for multiple sclerosis on expression of proximal genes in patients	是	rs71624119	multiple sclerosis	peripheral blood mononuclear cell	E_01_0014	RNA-Seq	As an example, we found that rs71624119, shared with three other autoimmune diseases and located in a primed enhancer (H3K4me1) with potential binding for STAT transcription factors, significantly associates with ANKRD55 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	As an example, we found that rs71624119, shared with three other autoimmune diseases and located in a primed enhancer (H3K4me1) with potential binding for STAT transcription factors, significantly associates with ANKRD55 expression.		As an example, we found that rs71624119, shared with three other autoimmune diseases and located in a primed enhancer (H3K4me1) with potential binding for STAT transcription factors, significantly associates with ANKRD55 expression.	Immunohistochemical staining	As an example, we found that rs71624119, shared with three other autoimmune diseases and located in a primed enhancer (H3K4me1) with potential binding for STAT transcription factors, significantly associates with ANKRD55 expression.			RNA-Seq				ANKRD55
29323272	chr19	10958350	10960350	SMARCA4	Mutation of SMARCA4 (BRG1), the ATPase of BAF (mSWI/SNF) and PBAF complexes, contributes to a range of malignancies and neurologic disorders.	human	Tumor	High+Lowthroughput	Dominant-negative SMARCA4 mutants alter the accessibility landscape of tissue-unrestricted enhancers	否		Tumor	embryonic stem cell	E_01_0015	Western blot,ATAC-seq,ChIP-seq,RNA-seq	Mutation of SMARCA4 (BRG1), the ATPase of BAF (mSWI/SNF) and PBAF complexes, contributes to a range of malignancies and neurologic disorders.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mutation of SMARCA4 (BRG1), the ATPase of BAF (mSWI/SNF) and PBAF complexes, contributes to a range of malignancies and neurologic disorders.	Immunohistochemical staining	Mutation of SMARCA4 (BRG1), the ATPase of BAF (mSWI/SNF) and PBAF complexes, contributes to a range of malignancies and neurologic disorders.	SMARCA4		Western blot,ATAC-seq,ChIP-seq,RNA-seq	Mutation of SMARCA4 (BRG1), the ATPase of BAF (mSWI/SNF) and PBAF complexes, contributes to a range of malignancies and neurologic disorders.			
29321660	chr3	186043535	186045535	ETV5	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.	human,mouse	Neuroblastoma	High+Lowthroughput	Activated ALK signals through the ERK-ETV5-RET pathway to drive neuroblastoma oncogenesis	否		neuroblastoma	neuroblastoma cell lines	E_02_0010	ChIP-seq,RT-qPCR	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.		Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.	Immunohistochemical staining	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.			ChIP-seq,RT-qPCR				ETV5
29321660	chr10	43074431	43076431	RET	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.	human,mouse	Neuroblastoma	High+Lowthroughput	Activated ALK signals through the ERK-ETV5-RET pathway to drive neuroblastoma oncogenesis	否		neuroblastoma	neuroblastoma cell lines	E_02_0010	ChIP-seq,RT-qPCR	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.		Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.	Immunohistochemical staining	Altogether, these results define the ERK–ETV5–RET pathway as a critical axis driving neuroblastoma oncogenesis downstream of activated ALK.			ChIP-seq,RT-qPCR				RET
29321583	chr3	34155732	34157732	Sox2ot	Our study indicates that, in addition to previously reported in trans mechanisms, Sox2ot can regulate Sox2 by an allele-specific mechanism, in particular during development.	mouse	Embryo	High+Lowthroughput	Allele-specific repression of Sox2 through the long non-coding RNA Sox2ot	否			embryonic stem cell	E_02_0011	qRT-PCR,qPCR,ChIP,3C	Our study indicates that, in addition to previously reported in trans mechanisms, Sox2ot can regulate Sox2 by an allele-specific mechanism, in particular during development.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our study indicates that, in addition to previously reported in trans mechanisms, Sox2ot can regulate Sox2 by an allele-specific mechanism, in particular during development.		Our study indicates that, in addition to previously reported in trans mechanisms, Sox2ot can regulate Sox2 by an allele-specific mechanism, in particular during development.	Immunohistochemical staining	Our study indicates that, in addition to previously reported in trans mechanisms, Sox2ot can regulate Sox2 by an allele-specific mechanism, in particular during development.			qRT-PCR,qPCR,ChIP,3C				Sox2ot
29321583	chr3	34702062	34704062	Sox2	The transcription factor Sox2 controls the fate of pluripotent stem cells and neural stem cells.	mouse	Embryo	High+Lowthroughput	Allele-specific repression of Sox2 through the long non-coding RNA Sox2ot	否			embryonic stem cell	E_02_0011	qRT-PCR,qPCR,ChIP,3C	The transcription factor Sox2 controls the fate of pluripotent stem cells and neural stem cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcription factor Sox2 controls the fate of pluripotent stem cells and neural stem cells.		The transcription factor Sox2 controls the fate of pluripotent stem cells and neural stem cells.	Immunohistochemical staining	The transcription factor Sox2 controls the fate of pluripotent stem cells and neural stem cells.			qRT-PCR,qPCR,ChIP,3C				Sox2
29320736	chr15	41514637	41516637	RPAP1	We conclude that Mediator/RPAP1/RNA Pol II is an ancient module, conserved from plants to mammals, critical for establishing and maintaining cell identity.	human,mouse	Connective tissue	High+Lowthroughput	The RNA Polymerase II Factor RPAP1 Is Critical for Mediator-Driven Transcription and Cell Identity	否		maintaining cell identity	stem cell	E_02_0012	ChIP-qPCR,ChIP-Seq,RNA-Seq,qRT-PCR	We conclude that Mediator/RPAP1/RNA Pol II is an ancient module, conserved from plants to mammals, critical for establishing and maintaining cell identity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We conclude that Mediator/RPAP1/RNA Pol II is an ancient module, conserved from plants to mammals, critical for establishing and maintaining cell identity.		We conclude that Mediator/RPAP1/RNA Pol II is an ancient module, conserved from plants to mammals, critical for establishing and maintaining cell identity.	Immunohistochemical staining	We conclude that Mediator/RPAP1/RNA Pol II is an ancient module, conserved from plants to mammals, critical for establishing and maintaining cell identity.			ChIP-qPCR,ChIP-Seq,RNA-Seq,qRT-PCR				RPAP1
29320702	chr1	3066690	3068690	PRDM16	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	human,mouse	Adipose Tissue	High+Lowthroughput	Repression of Adipose Tissue Fibrosis through a PRDM16-GTF2IRD1 Complex Improves Systemic Glucose Homeostasis	否		obesity or type 2 diabetes	fat cell	E_02_0013	RNA-Seq,ChIP	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.		These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	Immunohistochemical staining	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.			RNA-Seq,ChIP				PRDM16
29320702	chr7	74450980	74452980	GTF2IRD1	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	human,mouse	Adipose Tissue	High+Lowthroughput	Repression of Adipose Tissue Fibrosis through a PRDM16-GTF2IRD1 Complex Improves Systemic Glucose Homeostasis	否		obesity or type 2 diabetes	fat cell	E_02_0013	RNA-Seq,ChIP	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.		These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	Immunohistochemical staining	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.			RNA-Seq,ChIP				GTF2IRD1
29320702	chr9	137616279	137618279	EHMT1	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	human,mouse	Adipose Tissue	High+Lowthroughput	Repression of Adipose Tissue Fibrosis through a PRDM16-GTF2IRD1 Complex Improves Systemic Glucose Homeostasis	否		obesity or type 2 diabetes	fat cell	E_02_0013	RNA-Seq,ChIP	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.		These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.	Immunohistochemical staining	These results suggest a mechanism by which repression of obesity-associated adipose tissue fibrosis through the PRDM16 complex leads to an improvement in systemic glucose homeostasis.			RNA-Seq,ChIP				EHMT1
29316219	chr9	81580914	81582914	TLE1	These studies identify 150 direct FOXG1 targets, several of which are also TLE1 targets, involved in cell proliferation, differentiation, survival,chemotaxis and angiogenesis.	human	Brain	High+Lowthroughput	Characterization of a FOXG1:TLE1 transcriptional network in glioblastoma-initiating cells	否		Glioblastoma	glioblastoma-initiating cells	E_01_0016	ChIP-Seq,RNA-Seq,RT-qPCR	These studies identify 150 direct FOXG1 targets, several of which are also TLE1 targets, involved in cell proliferation, differentiation, survival,chemotaxis and angiogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These studies identify 150 direct FOXG1 targets, several of which are also TLE1 targets, involved in cell proliferation, differentiation, survival,chemotaxis and angiogenesis.	Immunohistochemical staining	These studies identify 150 direct FOXG1 targets, several of which are also TLE1 targets, involved in cell proliferation, differentiation, survival,chemotaxis and angiogenesis.	TLE1		ChIP-Seq,RNA-Seq,RT-qPCR	These studies identify 150 direct FOXG1 targets, several of which are also TLE1 targets, involved in cell proliferation, differentiation, survival,chemotaxis and angiogenesis.			
29311615	chr12	54030827	54032827	HOXC5	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	human	Somatic tissue	High+Lowthroughput	HoxC5 and miR-615-3p target newly evolved genomic regions to repress hTERT and inhibit tumorigenesis	否		Tumor	somatic cell	E_01_0017	Luciferase reporter assay,Western blot,ChIP-Seq,qRT-PCR,3C-qPCR	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	Immunohistochemical staining	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	HOXC5		Luciferase reporter assay,Western blot,ChIP-Seq,qRT-PCR,3C-qPCR	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.			
29309299	chr19	19143072	19145072	MEF2B	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.	human	Lymphoid tissue	High+Lowthroughput	Comparison of Myocyte Enhancer Factor 2B Versus Other Germinal Center-associated Antigens in the Differential Diagnosis of B-Cell Non-Hodgkin Lymphomas	否		Lymphomas	B cell	E_01_0018	Immunohistochemical Staining	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.		Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.	Immunohistochemical staining	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.			Immunohistochemical Staining				MEF2B
29307778	chr17	43750876	43752876	SOST	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	human	Bone	High+Lowthroughput	Computational and functional characterization of four SNPs in the SOST locus associated with osteoporosis	是	rs1230399, rs7220711, rs1107748, rs75901553	osteoporosis	Germinal center B-cells	E_01_0019	Luciferase reporter assay,ChIP,qPCR	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.		The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	Immunohistochemical staining	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.			Luciferase reporter assay,ChIP,qPCR				SOST
29307778	chr16	67559199	67561199	CTCF	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	human	Bone	High+Lowthroughput	Computational and functional characterization of four SNPs in the SOST locus associated with osteoporosis	是	rs1230399, rs7220711, rs1107748, rs75901553	osteoporosis	Germinal center B-cells	E_01_0019	Luciferase reporter assay,ChIP,qPCR	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	Immunohistochemical staining	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	CTCF		Luciferase reporter assay,ChIP,qPCR	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.			
29304378	chr6	151654024	151656024	ESR1	Only variants in ESR1 and close proximity to RANKL showed a clear effect dependency on age.	human	Bone	High+Lowthroughput	Life-Course Genome-wide Association Study Meta-analysis of Total Body BMD and Assessment of Age-Specific Effects	是	rs2982562-C	osteoporosis	osteocyte	E_01_0020	Knockout	Only variants in ESR1 and close proximity to RANKL showed a clear effect dependency on age.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Only variants in ESR1 and close proximity to RANKL showed a clear effect dependency on age.	Immunohistochemical staining	Only variants in ESR1 and close proximity to RANKL showed a clear effect dependency on age.	ESR1		Knockout	Only variants in ESR1 and close proximity to RANKL showed a clear effect dependency on age.			
29303507	chr11	68036369	68038369	TCIRG1	These findings suggest that TCIRG1 functions as a metastatic enhancer by modulating growth, death and EMT in HCC cells.	human	HCC tissue	High+Lowthroughput	T-cell immune regulator 1 enhances metastasis in hepatocellular carcinoma	否		hepatocellular carcinoma	HCC cell lines	E_01_0021	Western blot,transfection	These findings suggest that TCIRG1 functions as a metastatic enhancer by modulating growth, death and EMT in HCC cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggest that TCIRG1 functions as a metastatic enhancer by modulating growth, death and EMT in HCC cells.		These findings suggest that TCIRG1 functions as a metastatic enhancer by modulating growth, death and EMT in HCC cells.	Immunohistochemical staining	These findings suggest that TCIRG1 functions as a metastatic enhancer by modulating growth, death and EMT in HCC cells.			Western blot,transfection				TCIRG1
29302059	chr1	133246792	133248792	Kiss1	Polycomb group (PcG) proteins control the timing of puberty by repressing the Kiss1 gene in hypothalamic arcuate nucleus (ARC) neurons.	human,mouse	Hypothalamic tissue	High+Lowthroughput	Trithorax dependent changes in chromatin landscape at enhancer and promoter regions drive female puberty	否		female puberty	Automatic Recognition of Cells	E_02_0014	qPCR,RNA-seq,ChIP	Polycomb group (PcG) proteins control the timing of puberty by repressing the Kiss1 gene in hypothalamic arcuate nucleus (ARC) neurons.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Polycomb group (PcG) proteins control the timing of puberty by repressing the Kiss1 gene in hypothalamic arcuate nucleus (ARC) neurons.		Polycomb group (PcG) proteins control the timing of puberty by repressing the Kiss1 gene in hypothalamic arcuate nucleus (ARC) neurons.	Immunohistochemical staining	Polycomb group (PcG) proteins control the timing of puberty by repressing the Kiss1 gene in hypothalamic arcuate nucleus (ARC) neurons.			qPCR,RNA-seq,ChIP				Kiss1
29301908	chr6	6874986	6876986	Dlx5	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.	mouse	Inner ear	High+Lowthroughput	Deletion of a Long-Range Dlx5 Enhancer Disrupts Inner Ear Development in Mice	否		inner ear dysmorphologies	inner hair cells	E_02_0015	DNA-seq	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.		Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.	Immunohistochemical staining	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.			DNA-seq				Dlx5
29301908	chr6	6038754	6040754	Slc25a13	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.	mouse	Inner ear	High+Lowthroughput	Deletion of a Long-Range Dlx5 Enhancer Disrupts Inner Ear Development in Mice	否		inner ear dysmorphologies	inner hair cells	E_02_0015	DNA-seq	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.		Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.	Immunohistochemical staining	Slc25a13hspn/hspn mice provide a new animal 40 model for studying long-range enhancer effects on Dlx5 expression in the developing inner ear.			DNA-seq				Slc25a13
29300379	chr15	67061032	67063032	SMAD3	These variants regulate SMAD3 transcription in an allele-specific manner through enhancer elements in introns of SMAD3.	human	Thyroid	High+Lowthroughput	The role of SMAD3 in the genetic predisposition to papillary thyroid carcinoma	是	rs17293632,rs4562997	papillary thyroid carcinoma	thyroid cancer cell lines	E_01_0022	ChIP,siRNA Knockdown,Luciferase reporter assay,Transfection,qPCR	These variants regulate SMAD3 transcription in an allele-specific manner through enhancer elements in introns of SMAD3.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These variants regulate SMAD3 transcription in an allele-specific manner through enhancer elements in introns of SMAD3.	Immunohistochemical staining	These variants regulate SMAD3 transcription in an allele-specific manner through enhancer elements in introns of SMAD3.	SMAD3		ChIP,siRNA Knockdown,Luciferase reporter assay,Transfection,qPCR	These variants regulate SMAD3 transcription in an allele-specific manner through enhancer elements in introns of SMAD3.			
29300379	chr5	142307853	142309853	SPRY4	The sprouty RTK signaling antagonist 4 (SPRY4)gene was found to be the second-most dysregulated candidate gene	human	Thyroid	High+Lowthroughput	The role of SMAD3 in the genetic predisposition to papillary thyroid carcinoma	是	rs17293632,rs4562997	papillary thyroid carcinoma	thyroid cancer cell lines	E_01_0022	ChIP,siRNA Knockdown,Luciferase reporter assay,Transfection,qPCR	The sprouty RTK signaling antagonist 4 (SPRY4)gene was found to be the second-most dysregulated candidate gene	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The sprouty RTK signaling antagonist 4 (SPRY4)gene was found to be the second-most dysregulated candidate gene		The sprouty RTK signaling antagonist 4 (SPRY4)gene was found to be the second-most dysregulated candidate gene	Immunohistochemical staining	The sprouty RTK signaling antagonist 4 (SPRY4)gene was found to be the second-most dysregulated candidate gene			ChIP,siRNA Knockdown,Luciferase reporter assay,Transfection,qPCR				SPRY4
29300302	chrX	129537551	129539551	OCRL	The OCRL1 protein contains several domains, including an N-terminal pleckstrin homology (PH) domain, a central 5-phosphatase catalytic domain, an ASH (ASPM, SPD-2, Hydin) domain,and a C-terminal noncatalytic Rho-GTPase activating protein (GAP) domain	human	Kidney	High+Lowthroughput	Splicing Analysis of Exonic OCRL Mutations Causing Lowe Syndrome or Dent-2 Disease	否		Lowe syndrome and Dent-2 disease	COS7 cells	E_01_0023	Transfection,RT-PCR	The OCRL1 protein contains several domains, including an N-terminal pleckstrin homology (PH) domain, a central 5-phosphatase catalytic domain, an ASH (ASPM, SPD-2, Hydin) domain,and a C-terminal noncatalytic Rho-GTPase activating protein (GAP) domain	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The OCRL1 protein contains several domains, including an N-terminal pleckstrin homology (PH) domain, a central 5-phosphatase catalytic domain, an ASH (ASPM, SPD-2, Hydin) domain,and a C-terminal noncatalytic Rho-GTPase activating protein (GAP) domain		The OCRL1 protein contains several domains, including an N-terminal pleckstrin homology (PH) domain, a central 5-phosphatase catalytic domain, an ASH (ASPM, SPD-2, Hydin) domain,and a C-terminal noncatalytic Rho-GTPase activating protein (GAP) domain	Immunohistochemical staining	The OCRL1 protein contains several domains, including an N-terminal pleckstrin homology (PH) domain, a central 5-phosphatase catalytic domain, an ASH (ASPM, SPD-2, Hydin) domain,and a C-terminal noncatalytic Rho-GTPase activating protein (GAP) domain			Transfection,RT-PCR				OCRL
29297498	chr16	29880412	29882412	Hes1	Thus, our results support that IEC-intrinsic Hes1 maintains gut homeostasis by preventing microbial dysbiosis partially through regulating mucosal microhabitats.	mouse	Small intestine	High+Lowthroughput	Epithelial Hes1 maintains gut homeostasis by preventing microbial dysbiosis	否		intestinal microbial dysbiosis and disturbed homeostasis	enterocyte	E_02_0016	qPCR,Western blot	Thus, our results support that IEC-intrinsic Hes1 maintains gut homeostasis by preventing microbial dysbiosis partially through regulating mucosal microhabitats.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, our results support that IEC-intrinsic Hes1 maintains gut homeostasis by preventing microbial dysbiosis partially through regulating mucosal microhabitats.		Thus, our results support that IEC-intrinsic Hes1 maintains gut homeostasis by preventing microbial dysbiosis partially through regulating mucosal microhabitats.	Immunohistochemical staining	Thus, our results support that IEC-intrinsic Hes1 maintains gut homeostasis by preventing microbial dysbiosis partially through regulating mucosal microhabitats.			qPCR,Western blot				Hes1
29294297	chr7	148804388	148806388	EZH2	We conclude that EZH2 plays a negative role during the odontogenic differentiation of hDPCs.	human	Dental pulp tissue	High+Lowthroughput	EZH2 Impairs Human Dental Pulp Cell Mineralization via the Wnt/β-Catenin Pathway	否		Oral Diseases	dental pulp cell	E_01_0024	ChIP	We conclude that EZH2 plays a negative role during the odontogenic differentiation of hDPCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We conclude that EZH2 plays a negative role during the odontogenic differentiation of hDPCs.	Immunohistochemical staining	We conclude that EZH2 plays a negative role during the odontogenic differentiation of hDPCs.	EZH2		ChIP	We conclude that EZH2 plays a negative role during the odontogenic differentiation of hDPCs.			
29294065	chr19	33297489	33299489	CEBPA	Therefore, CEBPA is likely to bind to the “c” region of the PCP4 promoter.	human	Adrenal tissues	High+Lowthroughput	Purkinje Cell Protein 4 Expression Is Associated With DNA Methylation Status in Aldosterone-Producing Adenoma	否		adrenocortical adenoma	cortical cell of adrenal gland	E_01_0025	qPCR,ChIP	Therefore, CEBPA is likely to bind to the “c” region of the PCP4 promoter.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Therefore, CEBPA is likely to bind to the “c” region of the PCP4 promoter.	Immunohistochemical staining	Therefore, CEBPA is likely to bind to the “c” region of the PCP4 promoter.	CEBPA		qPCR,ChIP	Therefore, CEBPA is likely to bind to the “c” region of the PCP4 promoter.			
29286144	chr7	148804229	148806229	EZH2	Overall, the present study demonstrated that the lncrna PVt1 may contribute to the tumorigenesis and metastasis of melanoma through binding to eZH2 and regulating the expression of mir-200c.	human	Melanoma tissue	High+Lowthroughput	Effect of long non-coding RNA PVT1 on cell proliferation and migration in melanoma	否		Melanoma	melanoma cells	E_01_0026	Western blot,ChIP	Overall, the present study demonstrated that the lncrna PVt1 may contribute to the tumorigenesis and metastasis of melanoma through binding to eZH2 and regulating the expression of mir-200c.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Overall, the present study demonstrated that the lncrna PVt1 may contribute to the tumorigenesis and metastasis of melanoma through binding to eZH2 and regulating the expression of mir-200c.	Immunohistochemical staining	Overall, the present study demonstrated that the lncrna PVt1 may contribute to the tumorigenesis and metastasis of melanoma through binding to eZH2 and regulating the expression of mir-200c.	EZH2		Western blot,ChIP	Overall, the present study demonstrated that the lncrna PVt1 may contribute to the tumorigenesis and metastasis of melanoma through binding to eZH2 and regulating the expression of mir-200c.			
29286132	chr7	148804179	148806179	EZH2	Its ability to facilitate invasion makes EZH2 a promising target for the management of advanced RCC	human	Kidney	High+Lowthroughput	EZH2 enhances the invasive capability of renal cell carcinoma cells via activation of STAT3	否		renal cell carcinoma	nephrocyte	E_01_0027	Western blot	Its ability to facilitate invasion makes EZH2 a promising target for the management of advanced RCC	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Its ability to facilitate invasion makes EZH2 a promising target for the management of advanced RCC	Immunohistochemical staining	Its ability to facilitate invasion makes EZH2 a promising target for the management of advanced RCC	EZH2		Western blot	Its ability to facilitate invasion makes EZH2 a promising target for the management of advanced RCC			
29259014	chr7	55016411	55018411	EGFR	We therefore performed a genome-wide CRISPR/Cas9 enhancer/suppressor screen in EGFR-dependent lung cancer PC9 cells treated with erlotinib þ THZ1 (CDK7/12 inhibitor) combination therapy, a combination previously shown to suppress drug-tolerant cells in this setting.	human	Lung	High+Lowthroughput	"ER Stress Signaling Promotes the Survival of Cancer ""Persister Cells"" Tolerant to EGFR Tyrosine Kinase Inhibitors"	否		Tumor	PC9 cells	E_01_0028	qRT-PCR,RNA-seq	We therefore performed a genome-wide CRISPR/Cas9 enhancer/suppressor screen in EGFR-dependent lung cancer PC9 cells treated with erlotinib þ THZ1 (CDK7/12 inhibitor) combination therapy, a combination previously shown to suppress drug-tolerant cells in this setting.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We therefore performed a genome-wide CRISPR/Cas9 enhancer/suppressor screen in EGFR-dependent lung cancer PC9 cells treated with erlotinib þ THZ1 (CDK7/12 inhibitor) combination therapy, a combination previously shown to suppress drug-tolerant cells in this setting.	Immunohistochemical staining	We therefore performed a genome-wide CRISPR/Cas9 enhancer/suppressor screen in EGFR-dependent lung cancer PC9 cells treated with erlotinib þ THZ1 (CDK7/12 inhibitor) combination therapy, a combination previously shown to suppress drug-tolerant cells in this setting.	EGFR		qRT-PCR,RNA-seq	We therefore performed a genome-wide CRISPR/Cas9 enhancer/suppressor screen in EGFR-dependent lung cancer PC9 cells treated with erlotinib þ THZ1 (CDK7/12 inhibitor) combination therapy, a combination previously shown to suppress drug-tolerant cells in this setting.			
29257325	chr5	88714072	88716072	MEF2C	The present study investigated whether cardiomyocytes from mouse fibroblasts may be reprogrammed in vitro with four cardiac transcription factors, including GATA binding protein 4, myocyte‑specific enhancer factor 2C, T-box transcription factor 5, and heartand neural crest derivatives-expressed protein 2 (GMTH)	human,mouse	Heart tissue	High+Lowthroughput	Optimization and enrichment of induced cardiomyocytes derived from mouse fibroblasts by reprogramming with cardiac transcription factors	否		Ischemic heart disease	cardiac muscle cell (sensu Arthopoda)	E_02_0017	RT-qPCR,qPCR,Immunostaining	The present study investigated whether cardiomyocytes from mouse fibroblasts may be reprogrammed in vitro with four cardiac transcription factors, including GATA binding protein 4, myocyte‑specific enhancer factor 2C, T-box transcription factor 5, and heartand neural crest derivatives-expressed protein 2 (GMTH)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present study investigated whether cardiomyocytes from mouse fibroblasts may be reprogrammed in vitro with four cardiac transcription factors, including GATA binding protein 4, myocyte‑specific enhancer factor 2C, T-box transcription factor 5, and heartand neural crest derivatives-expressed protein 2 (GMTH)		The present study investigated whether cardiomyocytes from mouse fibroblasts may be reprogrammed in vitro with four cardiac transcription factors, including GATA binding protein 4, myocyte‑specific enhancer factor 2C, T-box transcription factor 5, and heartand neural crest derivatives-expressed protein 2 (GMTH)	Immunohistochemical staining	The present study investigated whether cardiomyocytes from mouse fibroblasts may be reprogrammed in vitro with four cardiac transcription factors, including GATA binding protein 4, myocyte‑specific enhancer factor 2C, T-box transcription factor 5, and heartand neural crest derivatives-expressed protein 2 (GMTH)			RT-qPCR,qPCR,Immunostaining				MEF2C
29256825	chr4	108045000	108047000	LEF1	β-catenin nuclear translocation, T cell factor (TCF) and lymphoid enhancerbinding factor (LEF) up-regulation have been shown to be involved in canonical Wnt pathways [20], and in our studies, Western blot results showed that the amount of β- catenin protein in nuclei was increased in treated cells	human	Liver	High+Lowthroughput	Salvianolic Acid B Enhances Hepatic Differentiation of Human Embryonic Stem Cells Through Upregulation of WNT Pathway and Inhibition of Notch Pathway	否		Liver disease	Hepatocytes	E_01_0029	qRT-PCR,Immunofluorescence staining,PCR,Western blot	β-catenin nuclear translocation, T cell factor (TCF) and lymphoid enhancerbinding factor (LEF) up-regulation have been shown to be involved in canonical Wnt pathways [20], and in our studies, Western blot results showed that the amount of β- catenin protein in nuclei was increased in treated cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			β-catenin nuclear translocation, T cell factor (TCF) and lymphoid enhancerbinding factor (LEF) up-regulation have been shown to be involved in canonical Wnt pathways [20], and in our studies, Western blot results showed that the amount of β- catenin protein in nuclei was increased in treated cells	Immunohistochemical staining	β-catenin nuclear translocation, T cell factor (TCF) and lymphoid enhancerbinding factor (LEF) up-regulation have been shown to be involved in canonical Wnt pathways [20], and in our studies, Western blot results showed that the amount of β- catenin protein in nuclei was increased in treated cells	LEF1		qRT-PCR,Immunofluorescence staining,PCR,Western blot	β-catenin nuclear translocation, T cell factor (TCF) and lymphoid enhancerbinding factor (LEF) up-regulation have been shown to be involved in canonical Wnt pathways [20], and in our studies, Western blot results showed that the amount of β- catenin protein in nuclei was increased in treated cells			
29256171	chr10	24357349	24375452	CCN2	CCN2 is a critical matricellular protein that is expressed in several cells with major implications in physiology and different pathologies.	mouse	Connective tissue	Low+High throughput	Multiple enhancer regions govern the transcription of CCN2 during embryonic development	否	--	--	endothelial cell	E_02_0018	Transgenic mice,ChIP-seq,DNase I Hypersensitivity Assay	Four functional enhancers were identified, with each driving distinct, tissue-specific patterns of transgene expression. An enhancer located -100 kb from the CCN2 transcription start site facilitated expression within vascular tissue. An enhancer -135 kb upstream of CCN2 drove expression within the articular chondrocytes of synovial joints.The other two enhancers, located at -198 kb and -229 kb, mediated transgene expression within dermal fibroblasts, however the most prevalent activity was found within hypertrophic chondrocytes and periosteal tissue, respectively. 	Enhancer	--	PCR,Transgenic mice	Four functional enhancers were identified, with each driving distinct, tissue-specific patterns of transgene expression. An enhancer located -100 kb from the CCN2 transcription start site facilitated expression within vascular tissue. An enhancer -135 kb upstream of CCN2 drove expression within the articular chondrocytes of synovial joints.The other two enhancers, located at -198 kb and -229 kb, mediated transgene expression within dermal fibroblasts, however the most prevalent activity was found within hypertrophic chondrocytes and periosteal tissue, respectively. 	Ctgf,Fisp12,Hcs24,fisp-12	--	--	--	--	--	--	--	--	--	Ccn2
29255029	chr5	28659278	28661278	Shh	Transcriptome analysis indicates that ectopic expression of Shh up-regulates Chordin (Chrd) that antagonizes bone morphogenetic protein signaling in the interdigital region.	mouse	Toe	High+Lowthroughput	Enhancer adoption caused by genomic insertion elicits interdigital Shh expression and syndactyly in mouse	否		syndactyly	interdigital cell	E_02_0019	ATAC-seq,PCR	Transcriptome analysis indicates that ectopic expression of Shh up-regulates Chordin (Chrd) that antagonizes bone morphogenetic protein signaling in the interdigital region.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Transcriptome analysis indicates that ectopic expression of Shh up-regulates Chordin (Chrd) that antagonizes bone morphogenetic protein signaling in the interdigital region.		Transcriptome analysis indicates that ectopic expression of Shh up-regulates Chordin (Chrd) that antagonizes bone morphogenetic protein signaling in the interdigital region.	Immunohistochemical staining	Transcriptome analysis indicates that ectopic expression of Shh up-regulates Chordin (Chrd) that antagonizes bone morphogenetic protein signaling in the interdigital region.			ATAC-seq,PCR				Shh
29249800	chr18	27930050	27932050	CDH2	DBC1 functions as a coactivator for AR-V7 and is required for the expression of AR-V7 target genes including CDH2, a mesenchymal marker linked to CRPC progression.	human	CRPC tissues	High+Lowthroughput	DBC1 promotes castration-resistant prostate cancer by positively regulating DNA binding and stability of AR-V7	否		castration-resistant prostate cancer	castration-resistant prostate cancer cell	E_01_0030	qRT-PCR,ChIP,3C	DBC1 functions as a coactivator for AR-V7 and is required for the expression of AR-V7 target genes including CDH2, a mesenchymal marker linked to CRPC progression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			DBC1 functions as a coactivator for AR-V7 and is required for the expression of AR-V7 target genes including CDH2, a mesenchymal marker linked to CRPC progression.	Immunohistochemical staining	DBC1 functions as a coactivator for AR-V7 and is required for the expression of AR-V7 target genes including CDH2, a mesenchymal marker linked to CRPC progression.	CDH2		qRT-PCR,ChIP,3C	DBC1 functions as a coactivator for AR-V7 and is required for the expression of AR-V7 target genes including CDH2, a mesenchymal marker linked to CRPC progression.			
29248547	chr7	148804663	148806663	EZH2	Here we report that enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressive complex 2 (PRC2) which mediates histone H3 lysine 27 trimethylation(H3K27me3), is over-expressed in CD30+ anaplastic cells in PCALCL and large-cell transformed CTCL.	human	PCALCL tissue	High+Lowthroughput	Dual Role of EZH2 in Cutaneous Anaplastic Large Cell Lymphoma: Promoting Tumor Cell Survival and Regulating Tumor Microenvironment	否		cutaneous CD30+ lymphoproliferative disease	Primary cutaneous anaplastic T cell lymphoma cell	E_01_0031	ChIP,qRT-PCR,Western blot	Here we report that enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressive complex 2 (PRC2) which mediates histone H3 lysine 27 trimethylation(H3K27me3), is over-expressed in CD30+ anaplastic cells in PCALCL and large-cell transformed CTCL.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here we report that enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressive complex 2 (PRC2) which mediates histone H3 lysine 27 trimethylation(H3K27me3), is over-expressed in CD30+ anaplastic cells in PCALCL and large-cell transformed CTCL.	Immunohistochemical staining	Here we report that enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressive complex 2 (PRC2) which mediates histone H3 lysine 27 trimethylation(H3K27me3), is over-expressed in CD30+ anaplastic cells in PCALCL and large-cell transformed CTCL.	EZH2		ChIP,qRT-PCR,Western blot	Here we report that enhancer of zeste homolog 2 (EZH2), the catalytic subunit of polycomb repressive complex 2 (PRC2) which mediates histone H3 lysine 27 trimethylation(H3K27me3), is over-expressed in CD30+ anaplastic cells in PCALCL and large-cell transformed CTCL.			
29245050	chr13	83649881	83651881	Mef2c	Interestingly, senescence and NANOG had dramatic effect on the expression level of Mef2c, which regulates myoblast proliferation by exercising transcriptional control of cell cycle related genes	human,mouse	Skeletal muscle	High+Lowthroughput	NANOG restores the impaired myogenic differentiation potential of skeletal myoblasts after multiple population doublings	否		impaired myogenic differentiation potential	skeletal muscle myoblast	E_02_0020	Western blot,Immunohistochemical Staining,qPCR	Interestingly, senescence and NANOG had dramatic effect on the expression level of Mef2c, which regulates myoblast proliferation by exercising transcriptional control of cell cycle related genes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Interestingly, senescence and NANOG had dramatic effect on the expression level of Mef2c, which regulates myoblast proliferation by exercising transcriptional control of cell cycle related genes		Interestingly, senescence and NANOG had dramatic effect on the expression level of Mef2c, which regulates myoblast proliferation by exercising transcriptional control of cell cycle related genes	Immunohistochemical staining	Interestingly, senescence and NANOG had dramatic effect on the expression level of Mef2c, which regulates myoblast proliferation by exercising transcriptional control of cell cycle related genes			Western blot,Immunohistochemical Staining,qPCR				Mef2c
29244146	chr7	148804295	148806295	EZH2	It is caused by heterozygous mutations in enhancer of zeste homolog 2 (EZH2), a histone methyltransferase responsible for histone H3 at lysine 27 (H3K27) trimethylation.	human,mouse	Embryonic tissues	High+Lowthroughput	Ezh2 Mutations Found in the Weaver Overgrowth Syndrome Cause a Partial Loss of H3K27 Histone Methyltransferase Activity	否		Weaver syndrome	chondroblast	E_02_0021	Transfection,Immunostaining	It is caused by heterozygous mutations in enhancer of zeste homolog 2 (EZH2), a histone methyltransferase responsible for histone H3 at lysine 27 (H3K27) trimethylation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	It is caused by heterozygous mutations in enhancer of zeste homolog 2 (EZH2), a histone methyltransferase responsible for histone H3 at lysine 27 (H3K27) trimethylation.		It is caused by heterozygous mutations in enhancer of zeste homolog 2 (EZH2), a histone methyltransferase responsible for histone H3 at lysine 27 (H3K27) trimethylation.	Immunohistochemical staining	It is caused by heterozygous mutations in enhancer of zeste homolog 2 (EZH2), a histone methyltransferase responsible for histone H3 at lysine 27 (H3K27) trimethylation.			Transfection,Immunostaining				EZH2
29233846	chr6	47504530	47506530	Ezh2	Ezh2 is the catalytic subunit containing a SET domain, which harbors the active site for histone H3 trimethylation on lysine 27 (H3K27me3), although Suz12 and Eed association is needed for optimal enzymatic activity8.	human	Ovarian tissue	High+Lowthroughput	VE-Cadherin-Mediated Epigenetic Regulation of Endothelial Gene Expression	否		Ovarian carcinoma	endothelial cell	E_01_0032	Immunofluorescence,Western blot,RNA-seq ,qRT–PCR,ChIP	Ezh2 is the catalytic subunit containing a SET domain, which harbors the active site for histone H3 trimethylation on lysine 27 (H3K27me3), although Suz12 and Eed association is needed for optimal enzymatic activity8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ezh2 is the catalytic subunit containing a SET domain, which harbors the active site for histone H3 trimethylation on lysine 27 (H3K27me3), although Suz12 and Eed association is needed for optimal enzymatic activity8.		Ezh2 is the catalytic subunit containing a SET domain, which harbors the active site for histone H3 trimethylation on lysine 27 (H3K27me3), although Suz12 and Eed association is needed for optimal enzymatic activity8.	Immunohistochemical staining	Ezh2 is the catalytic subunit containing a SET domain, which harbors the active site for histone H3 trimethylation on lysine 27 (H3K27me3), although Suz12 and Eed association is needed for optimal enzymatic activity8.			Immunofluorescence,Western blot,RNA-seq ,qRT–PCR,ChIP				Ezh2
29231261	chr7	148804801	148806801	EZH2	LncRNA AWPPH can promote cell proliferation, autophagy and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.	human	Bladder tissue	High+Lowthroughput	LncRNA AWPPH inhibits SMAD4 via EZH2 to regulate bladder cancer progression	否		bladder cancer	human bladder epithelial cell line	E_01_0033	Transfection,qRT-PCR,Western blot,ChIP	LncRNA AWPPH can promote cell proliferation, autophagy and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			LncRNA AWPPH can promote cell proliferation, autophagy and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.	Immunohistochemical staining	LncRNA AWPPH can promote cell proliferation, autophagy and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.	EZH2		Transfection,qRT-PCR,Western blot,ChIP	LncRNA AWPPH can promote cell proliferation, autophagy and migration, as well as inhibit cell apoptosis in BC by inhibiting SMAD4 via EZH2.			
29227829	chr6	135178878	135180878	MYB	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.	human	Hematopoietic tissue	High+Lowthroughput	A long noncoding RNA from the HBS1L-MYB intergenic region on chr6q23 regulates human fetal hemoglobin expression	是	rs66650371	sickle cell disease and β-thalassemia	HUDEP-2 cell	E_01_0034	RT–PCR,qPCR,Western blot	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.		HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.	Immunohistochemical staining	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.			RT–PCR,qPCR,Western blot				MYB
29227829	chr6	134957756	134959756	HBS1L	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.	human	Hematopoietic tissue	High+Lowthroughput	A long noncoding RNA from the HBS1L-MYB intergenic region on chr6q23 regulates human fetal hemoglobin expression	否		sickle cell disease and β-thalassemia	HUDEP-2 cell	E_01_0034	RT–PCR,qPCR,Western blot	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.		HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.	Immunohistochemical staining	HMI-LNCRNA might be a potential therapeutic target for HbF induction treatment in sickle cell disease and β-thalassemia.			RT–PCR,qPCR,Western blot				HBS1L
29223978	chr7	148804763	148806763	EZH2	Our results indicate that EZH2 is not required to repress chondrogenesis in the CM downstream of Wnt/b-catenin signaling.	mouse	Cartilage	High+Lowthroughput	PRC2 Is Dispensable in Vivo for β-Catenin-Mediated Repression of Chondrogenesis in the Mouse Embryonic Cranial Mesenchyme	否			chondroblast	E_02_0022	Immunofluorescencet,RNA-seq ,RT–qPCR,ChIP-seq	Our results indicate that EZH2 is not required to repress chondrogenesis in the CM downstream of Wnt/b-catenin signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results indicate that EZH2 is not required to repress chondrogenesis in the CM downstream of Wnt/b-catenin signaling.		Our results indicate that EZH2 is not required to repress chondrogenesis in the CM downstream of Wnt/b-catenin signaling.	Immunohistochemical staining	Our results indicate that EZH2 is not required to repress chondrogenesis in the CM downstream of Wnt/b-catenin signaling.			Immunofluorescencet,RNA-seq ,RT–qPCR,ChIP-seq				EZH2
29220426	chr13	116431913	116433913	Isl1	Insulin enhancer binding protein-1 (Isl1), a member of the LIM-homeodomain family, is a well-known activator of the insulin gene (14,15) and is essential for the development of the pancreas (16).	mouse	Liver	High+Lowthroughput	Isl1β Overexpression With Key β Cell Transcription Factors Enhances Glucose-Responsive Hepatic Insulin Production and Secretion	否		diabete	b cell	E_02_0023	Western blot,Luciferase Reporter Assay,qRT-PCR	Insulin enhancer binding protein-1 (Isl1), a member of the LIM-homeodomain family, is a well-known activator of the insulin gene (14,15) and is essential for the development of the pancreas (16).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Insulin enhancer binding protein-1 (Isl1), a member of the LIM-homeodomain family, is a well-known activator of the insulin gene (14,15) and is essential for the development of the pancreas (16).		Insulin enhancer binding protein-1 (Isl1), a member of the LIM-homeodomain family, is a well-known activator of the insulin gene (14,15) and is essential for the development of the pancreas (16).	Immunohistochemical staining	Insulin enhancer binding protein-1 (Isl1), a member of the LIM-homeodomain family, is a well-known activator of the insulin gene (14,15) and is essential for the development of the pancreas (16).			Western blot,Luciferase Reporter Assay,qRT-PCR				Isl1
29207119	chr7	148804312	148806312	EZH2	Enhancer of zeste homologue 2 (EZH2), a catalytic subunit of polycomb repressive complex 2, is overexpressed in a number of different tumors including breast cancer, and serves important roles in cell cycle regulation, proliferation, apoptosis, tumorigenesis and drug resistance.	human	Breast	High+Lowthroughput	EZH2 inhibition sensitizes tamoxifen?resistant breast cancer cells through cell cycle regulation	否		breast cancer	breast cancer cell	E_01_0035	Transfection,RT-qPCR,Western blot	Enhancer of zeste homologue 2 (EZH2), a catalytic subunit of polycomb repressive complex 2, is overexpressed in a number of different tumors including breast cancer, and serves important roles in cell cycle regulation, proliferation, apoptosis, tumorigenesis and drug resistance.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homologue 2 (EZH2), a catalytic subunit of polycomb repressive complex 2, is overexpressed in a number of different tumors including breast cancer, and serves important roles in cell cycle regulation, proliferation, apoptosis, tumorigenesis and drug resistance.	Immunohistochemical staining	Enhancer of zeste homologue 2 (EZH2), a catalytic subunit of polycomb repressive complex 2, is overexpressed in a number of different tumors including breast cancer, and serves important roles in cell cycle regulation, proliferation, apoptosis, tumorigenesis and drug resistance.	EZH2		Transfection,RT-qPCR,Western blot	Enhancer of zeste homologue 2 (EZH2), a catalytic subunit of polycomb repressive complex 2, is overexpressed in a number of different tumors including breast cancer, and serves important roles in cell cycle regulation, proliferation, apoptosis, tumorigenesis and drug resistance.			
29207028	chr5	88714236	88716236	MEF2C	Within the four key cellular signaling pathways involved in muscle fiber regulation, there are five important signaling factors: p38 MAPK, ERK2, CBP, MEF2C and AMPKα1.	human,mouse	Muscle	High+Lowthroughput	Role of the cofilin 2 gene in regulating the myosin heavy chain genes in mouse myoblast C2C12 cells	否		myofibrillar formation.	C2C12 cells	E_02_0024	RT-qPCR,RT-PCR,Western blot	Within the four key cellular signaling pathways involved in muscle fiber regulation, there are five important signaling factors: p38 MAPK, ERK2, CBP, MEF2C and AMPKα1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Within the four key cellular signaling pathways involved in muscle fiber regulation, there are five important signaling factors: p38 MAPK, ERK2, CBP, MEF2C and AMPKα1.		Within the four key cellular signaling pathways involved in muscle fiber regulation, there are five important signaling factors: p38 MAPK, ERK2, CBP, MEF2C and AMPKα1.	Immunohistochemical staining	Within the four key cellular signaling pathways involved in muscle fiber regulation, there are five important signaling factors: p38 MAPK, ERK2, CBP, MEF2C and AMPKα1.			RT-qPCR,RT-PCR,Western blot				MEF2C
29203251	chrX	67541434	67543434	AR	Previous studies have shown that PCa development is closely-linked to the androgen receptor (AR)	human,mouse	Prostate	High+Lowthroughput	Androgen receptor (AR) degradation enhancer ASC-J9(?) in an FDA-approved formulated solution suppresses castration resistant prostate cancer cell growth	否		prostate cancer	prostate cancer cell	E_02_0025	Western blot,qPCR	Previous studies have shown that PCa development is closely-linked to the androgen receptor (AR)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Previous studies have shown that PCa development is closely-linked to the androgen receptor (AR)		Previous studies have shown that PCa development is closely-linked to the androgen receptor (AR)	Immunohistochemical staining	Previous studies have shown that PCa development is closely-linked to the androgen receptor (AR)			Western blot,qPCR				AR
29180489	chr12	114350941	114352941	TBX5	TBX5 deficiency-mediated downregulation of NFAT3 is crucial for the high cytokine-producing activity of T cells.	human	Lymphoid tissue	High+Lowthroughput	Downregulation of NFAT3 Due to Lack of T-Box Transcription Factor TBX5 Is Crucial for Cytokine Expression in T Cells	否			T cell	E_01_0036	Transfection	TBX5 deficiency-mediated downregulation of NFAT3 is crucial for the high cytokine-producing activity of T cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TBX5 deficiency-mediated downregulation of NFAT3 is crucial for the high cytokine-producing activity of T cells.	Immunohistochemical staining	TBX5 deficiency-mediated downregulation of NFAT3 is crucial for the high cytokine-producing activity of T cells.	TBX5		Transfection	TBX5 deficiency-mediated downregulation of NFAT3 is crucial for the high cytokine-producing activity of T cells.			
29180467	chr11	102107486	102109486	YAP1	In a mouse xenograft model of UCB, dual inhibition of COX2 and YAP1 elicited a long-lasting therapeutic response by limiting CSC expansion after chemotherapy and EGFR inhibition.	human,mouse	Bladder tissue	High+Lowthroughput	YAP1 and COX2 Coordinately Regulate Urothelial Cancer Stem-like Cells	否		urothelial carcinoma	urothelial cell	E_02_0026	Western blot,PCR	In a mouse xenograft model of UCB, dual inhibition of COX2 and YAP1 elicited a long-lasting therapeutic response by limiting CSC expansion after chemotherapy and EGFR inhibition.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In a mouse xenograft model of UCB, dual inhibition of COX2 and YAP1 elicited a long-lasting therapeutic response by limiting CSC expansion after chemotherapy and EGFR inhibition.		In a mouse xenograft model of UCB, dual inhibition of COX2 and YAP1 elicited a long-lasting therapeutic response by limiting CSC expansion after chemotherapy and EGFR inhibition.	Immunohistochemical staining	In a mouse xenograft model of UCB, dual inhibition of COX2 and YAP1 elicited a long-lasting therapeutic response by limiting CSC expansion after chemotherapy and EGFR inhibition.			Western blot,PCR				YAP1
29180467	chr3	181708705	181710705	SOX2	Here we report that the pro-inflammatory COX2/PGE2 pathway and the YAP1 growth regulatory pathway cooperate to recruit the stem cell factor SOX2 in expanding and sustaining the accumulation of urothelial CSC.	human,mouse	Bladder tissue	High+Lowthroughput	YAP1 and COX2 Coordinately Regulate Urothelial Cancer Stem-like Cells	否		urothelial carcinoma	urothelial cell	E_02_0026	Western blot,PCR	Here we report that the pro-inflammatory COX2/PGE2 pathway and the YAP1 growth regulatory pathway cooperate to recruit the stem cell factor SOX2 in expanding and sustaining the accumulation of urothelial CSC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we report that the pro-inflammatory COX2/PGE2 pathway and the YAP1 growth regulatory pathway cooperate to recruit the stem cell factor SOX2 in expanding and sustaining the accumulation of urothelial CSC.		Here we report that the pro-inflammatory COX2/PGE2 pathway and the YAP1 growth regulatory pathway cooperate to recruit the stem cell factor SOX2 in expanding and sustaining the accumulation of urothelial CSC.	Immunohistochemical staining	Here we report that the pro-inflammatory COX2/PGE2 pathway and the YAP1 growth regulatory pathway cooperate to recruit the stem cell factor SOX2 in expanding and sustaining the accumulation of urothelial CSC.			Western blot,PCR				SOX2
29180399	chr19	15232268	15234268	BRD4	We therefore describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in CTCL, and suggest targeting of these components as a potentially effective therapy for CTCL patients.	human,mouse	Skin tissue	High+Lowthroughput	Diminished microRNA-29b level is associated with BRD4-mediated activation of oncogenes in cutaneous T-cell lymphoma	否		cutaneous T-cell lymphoma	T cell	E_02_0027	RT-PCR,ChIP,Transfection	We therefore describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in CTCL, and suggest targeting of these components as a potentially effective therapy for CTCL patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We therefore describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in CTCL, and suggest targeting of these components as a potentially effective therapy for CTCL patients.		We therefore describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in CTCL, and suggest targeting of these components as a potentially effective therapy for CTCL patients.	Immunohistochemical staining	We therefore describe a novel oncogenic pathway featuring IL-15, miR-29b, and BRD4 in CTCL, and suggest targeting of these components as a potentially effective therapy for CTCL patients.			RT-PCR,ChIP,Transfection				BRD4
29177481	chr7	148804952	148806952	EZH2	The fact that EZH2 catalyzes the methylation of H3K27me3, a repressive mark known to be induced at DNA damage sites,prompted us to test whether the level of H3K27me3 at damage sites is affected by CDYL1.	human		High+Lowthroughput	CDYL1 fosters double-strand break-induced transcription silencing and promotes homology-directed repair	否				E_01_0037	Transfection,Immunofluorescence,Western blot,ChIP	The fact that EZH2 catalyzes the methylation of H3K27me3, a repressive mark known to be induced at DNA damage sites,prompted us to test whether the level of H3K27me3 at damage sites is affected by CDYL1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The fact that EZH2 catalyzes the methylation of H3K27me3, a repressive mark known to be induced at DNA damage sites,prompted us to test whether the level of H3K27me3 at damage sites is affected by CDYL1.	Immunohistochemical staining	The fact that EZH2 catalyzes the methylation of H3K27me3, a repressive mark known to be induced at DNA damage sites,prompted us to test whether the level of H3K27me3 at damage sites is affected by CDYL1.	EZH2		Transfection,Immunofluorescence,Western blot,ChIP	The fact that EZH2 catalyzes the methylation of H3K27me3, a repressive mark known to be induced at DNA damage sites,prompted us to test whether the level of H3K27me3 at damage sites is affected by CDYL1.			
29175454	chr10	68557509	68559509	TET1	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	human	Tumor	High+Lowthroughput	Selective inhibition of CTCF binding by iAs directs TET-mediated reprogramming of 5-hydroxymethylation patterns in iAs-transformed cells	否		iAs-mediated carcinogenesis	transformed cell	E_01_0038	qRT-PCR,ChIP	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	Immunohistochemical staining	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	TET1		qRT-PCR,ChIP	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.			
29175454	chr4	105143899	105145899	TET2	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	human	Tumor	High+Lowthroughput	Selective inhibition of CTCF binding by iAs directs TET-mediated reprogramming of 5-hydroxymethylation patterns in iAs-transformed cells	否		iAs-mediated carcinogenesis	transformed cell	E_01_0038	qRT-PCR,ChIP	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.		To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	Immunohistochemical staining	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.			qRT-PCR,ChIP				TET2
29175454	chr16	67559779	67561779	CTCF	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	human	Tumor	High+Lowthroughput	Selective inhibition of CTCF binding by iAs directs TET-mediated reprogramming of 5-hydroxymethylation patterns in iAs-transformed cells	否		iAs-mediated carcinogenesis	transformed cell	E_01_0038	qRT-PCR,ChIP	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	Immunohistochemical staining	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.	CTCF		qRT-PCR,ChIP	To gain an understanding into how iAs might impact TET expression, we found that iAs inhibits the binding of CTCF at the proximal, weak CTCF binding sites of the TET1 and TET2 gene promoters and enhances CTCF binding at the stronger distal binding site.			
29162563	chr16	86507790	86509790	FOXF1	We uncover that FOXF1 defi nes the core-regulatory circuitry in GIST through both direct transcriptional regulation and pioneer factor function.	human	Gastrointestinal tract	High+Lowthroughput	FOXF1 Defines the Core-Regulatory Circuitry in Gastrointestinal Stromal Tumor	否		gastrointestinal stromal tumor	gastrointestinal stromal tumor cell	E_01_0039	siRNA Transfection,qRT-PCR,ChIP,ChIP-qPCR,ATAC-seq,ChIP-seq	We uncover that FOXF1 defi nes the core-regulatory circuitry in GIST through both direct transcriptional regulation and pioneer factor function.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We uncover that FOXF1 defi nes the core-regulatory circuitry in GIST through both direct transcriptional regulation and pioneer factor function.	Immunohistochemical staining	We uncover that FOXF1 defi nes the core-regulatory circuitry in GIST through both direct transcriptional regulation and pioneer factor function.	FOXF1		siRNA Transfection,qRT-PCR,ChIP,ChIP-qPCR,ATAC-seq,ChIP-seq	We uncover that FOXF1 defi nes the core-regulatory circuitry in GIST through both direct transcriptional regulation and pioneer factor function.			
29162563	chr7	13888509	13890509	ETV1	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	human	Gastrointestinal tract	High+Lowthroughput	FOXF1 Defines the Core-Regulatory Circuitry in Gastrointestinal Stromal Tumor	否		gastrointestinal stromal tumor	gastrointestinal stromal tumor cell	E_01_0039	siRNA Transfection,qRT-PCR,ChIP,ChIP-qPCR,ATAC-seq,ChIP-seq	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	Immunohistochemical staining	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	ETV1		siRNA Transfection,qRT-PCR,ChIP,ChIP-qPCR,ATAC-seq,ChIP-seq	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis			
29162563	chr4	54654533	54656533	KIT	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	human	Gastrointestinal tract	High+Lowthroughput	FOXF1 Defines the Core-Regulatory Circuitry in Gastrointestinal Stromal Tumor	否		gastrointestinal stromal tumor	gastrointestinal stromal tumor cell	E_01_0039	siRNA Transfection,qRT-PCR,ChIP,ChIP-qPCR,ATAC-seq,ChIP-seq	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	Immunohistochemical staining	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis	KIT		siRNA Transfection,qRT-PCR,ChIP,ChIP-qPCR,ATAC-seq,ChIP-seq	Here, we uncover that in gastrointestinal stromal tumor (GIST), the forkhead family member FOXF1 directly controls the transcription of two master regulators, KIT and ETV1, both required for GIST precursor-interstitial cells of Cajal lineage specifi cation and GIST tumorigenesis			
29162511	chr1	11782707	11784707	MTHFR	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	human	Thymus	High+Lowthroughput	The thymidylate synthase enhancer region (TSER) polymorphism increases the risk of thymic lymphoid hyperplasia in patients with Myasthenia Gravis	是	rs1801133	thymic lymphoid hyperplasia	B cell	E_01_0040		Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis		Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	Immunohistochemical staining	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis							MTHFR
29162511	chr1	236792078	236794078	MTR	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	human	Thymus	High+Lowthroughput	The thymidylate synthase enhancer region (TSER) polymorphism increases the risk of thymic lymphoid hyperplasia in patients with Myasthenia Gravis	是	rs1805087	thymic lymphoid hyperplasia	B cell	E_01_0040		Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis		Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	Immunohistochemical staining	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis							MTR
29162511	chr18	654552	656552	TYMS	Therefore, the lack of association that we observed between the TYMS TSER polymorphism and thymoma risk might be due to different histological, molecular and pathological pathways leading to either thymoma or follicular hyperplasia in MG patients	human	Thymus	High+Lowthroughput	The thymidylate synthase enhancer region (TSER) polymorphism increases the risk of thymic lymphoid hyperplasia in patients with Myasthenia Gravis	是	rs45445694	thymic lymphoid hyperplasia	B cell	E_01_0040		Therefore, the lack of association that we observed between the TYMS TSER polymorphism and thymoma risk might be due to different histological, molecular and pathological pathways leading to either thymoma or follicular hyperplasia in MG patients	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, the lack of association that we observed between the TYMS TSER polymorphism and thymoma risk might be due to different histological, molecular and pathological pathways leading to either thymoma or follicular hyperplasia in MG patients		Therefore, the lack of association that we observed between the TYMS TSER polymorphism and thymoma risk might be due to different histological, molecular and pathological pathways leading to either thymoma or follicular hyperplasia in MG patients	Immunohistochemical staining	Therefore, the lack of association that we observed between the TYMS TSER polymorphism and thymoma risk might be due to different histological, molecular and pathological pathways leading to either thymoma or follicular hyperplasia in MG patients							TYMS
29162511	chr5	7849068	7851068	MTRR	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	human	Thymus	High+Lowthroughput	The thymidylate synthase enhancer region (TSER) polymorphism increases the risk of thymic lymphoid hyperplasia in patients with Myasthenia Gravis	是	rs1801394	thymic lymphoid hyperplasia	B cell	E_01_0040		Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis		Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis	Immunohistochemical staining	Little is still known about the contribution of MTHFR, MTR and MTRR polymorphisms in clinical subtypes of autoimmune diseases, except for some controversial studies suggesting a possible contribution of MTHFR polymorphisms to both risk and response to methotrexate treatment of rheumatoid arthritis							MTRR
29158184	chr11	112670256	112672256	Sox9	These findings link Sox9 to intrinsic mechanisms of TGF-β signaling in renal fibrosis and may have therapeutic potential for tissue fibrosis	mouse	Kidney	High+Lowthroughput	TGF-β-mediated upregulation of Sox9 in fibroblast promotes renal fibrosis	否		renal fibrosis	kidney fibroblast cell	E_02_0028	Transfection,qPCR,ChIP	These findings link Sox9 to intrinsic mechanisms of TGF-β signaling in renal fibrosis and may have therapeutic potential for tissue fibrosis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings link Sox9 to intrinsic mechanisms of TGF-β signaling in renal fibrosis and may have therapeutic potential for tissue fibrosis		These findings link Sox9 to intrinsic mechanisms of TGF-β signaling in renal fibrosis and may have therapeutic potential for tissue fibrosis	Immunohistochemical staining	These findings link Sox9 to intrinsic mechanisms of TGF-β signaling in renal fibrosis and may have therapeutic potential for tissue fibrosis			Transfection,qPCR,ChIP				Sox9
29155305	chr3	8725613	8727613	Hey1	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development	mouse	Tooth germ	High+Lowthroughput	Hey1 and Hey2 are differently expressed during mouse tooth development	否		tooth injury	dental mesenchymal cell	E_02_0029	qRT-PCR	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development		Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development	Immunohistochemical staining	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development			qRT-PCR				Hey1
29155305	chr10	30705725	30707725	Hey2	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development	mouse	Tooth germ	High+Lowthroughput	Hey1 and Hey2 are differently expressed during mouse tooth development	否		tooth injury	dental mesenchymal cell	E_02_0029	qRT-PCR	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development		Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development	Immunohistochemical staining	Our data implied that Hey2 function is restricted to transient amplifying cells of the ameloblast cell lineage and that Hey1 plays a role in the composition of the subodontoblastic layer, in addition to ameloblast differentiation. These findings provide novel clues for the better understanding of tooth development			qRT-PCR				Hey2
29154949	chr12	56115695	56117695	ESYT1	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	human	Lung CF tissue	High+Lowthroughput	A novel microscopy-based assay identifies extended synaptotagmin-1 (ESYT1) as a positive regulator of anoctamin 1 traffic	否		Cystic Fibrosis	bronchial epithelial cell	E_01_0041	siRNA transfection,Immunostaining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.		We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	Immunohistochemical staining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.			siRNA transfection,Immunostaining				ESYT1
29154949	chr11	69983331	69985331	ANO1	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	human	Lung CF tissue	High+Lowthroughput	A novel microscopy-based assay identifies extended synaptotagmin-1 (ESYT1) as a positive regulator of anoctamin 1 traffic	否		Cystic Fibrosis	bronchial epithelial cell	E_01_0041	siRNA transfection,Immunostaining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	Immunohistochemical staining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	ANO1		siRNA transfection,Immunostaining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.			
29154949	chr11	14440611	14442611	COPB1	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	human	Lung CF tissue	High+Lowthroughput	A novel microscopy-based assay identifies extended synaptotagmin-1 (ESYT1) as a positive regulator of anoctamin 1 traffic	否		Cystic Fibrosis	bronchial epithelial cell	E_01_0041	siRNA transfection,Immunostaining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.		We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.	Immunohistochemical staining	We demonstrate the robustness and specificity of this cell-based assay, by the identification of siRNAs acting both as ANO1 traffic enhancer and inhibitor, targeting respectively COPB1 and ESYT1 (extended synaptotagmin-1), the latter involved in coupling of the endoplasmic reticulum to the PM at specific microdomains.			siRNA transfection,Immunostaining				COPB1
29154784	chr16	29880401	29882401	Hes1	Sox9 and Hes1 are downstream targets of Jagged1–Notch signaling and are responsible for the timing of the maturation of primitive ductal structures	mouse	Liver	High+Lowthroughput	TGF-β1 signaling regulates mouse hepatic stellate cell differentiation via the Jagged1/Notch pathway	否		liver disease	hepatic stellate cell	E_02_0030	Western blot,ChIP,Transfection,qRT-PCR,Immunofluorescence	Sox9 and Hes1 are downstream targets of Jagged1–Notch signaling and are responsible for the timing of the maturation of primitive ductal structures	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Sox9 and Hes1 are downstream targets of Jagged1–Notch signaling and are responsible for the timing of the maturation of primitive ductal structures		Sox9 and Hes1 are downstream targets of Jagged1–Notch signaling and are responsible for the timing of the maturation of primitive ductal structures	Immunohistochemical staining	Sox9 and Hes1 are downstream targets of Jagged1–Notch signaling and are responsible for the timing of the maturation of primitive ductal structures			Western blot,ChIP,Transfection,qRT-PCR,Immunofluorescence				Hes1
29148101	chr3	130901584	130903584	Lef1	Considering that Bmp2, Bmp4, and Lef1 are essential for promoting odontoblast differentiation, our findings are consistent with previous studies.	mouse	Tooth-germ	High+Lowthroughput	Homeobox protein MSX-1 inhibits expression of bone morphogenetic protein 2, bone morphogenetic protein 4, and lymphoid enhancer-binding factor 1 via Wnt/β-catenin signaling to prevent differentiation of dental mesenchymal cells during the late bell stage	否		congenital tooth agenesis	dental mesenchymal cell	E_02_0031	Western blot,qPCR	Considering that Bmp2, Bmp4, and Lef1 are essential for promoting odontoblast differentiation, our findings are consistent with previous studies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Considering that Bmp2, Bmp4, and Lef1 are essential for promoting odontoblast differentiation, our findings are consistent with previous studies.		Considering that Bmp2, Bmp4, and Lef1 are essential for promoting odontoblast differentiation, our findings are consistent with previous studies.	Immunohistochemical staining	Considering that Bmp2, Bmp4, and Lef1 are essential for promoting odontoblast differentiation, our findings are consistent with previous studies.			Western blot,qPCR				Lef1
29142074	chr7	94002773	94005073	STAT3	Yet, a certain threshold level of STAT3 activity is essential to support activation of the COL1A2 enhancer and TGFβ signalling in fibroblasts.	human	Lung	Low throughput	STAT3 controls COL1A2 enhancer activation cooperatively with JunB, regulates type I collagen synthesis posttranscriptionally, and is essential for lung myofibroblast differentiation	否	--	--	Myofibroblast	E_02_0032	Luciferase Reporter Assay,ChIP	The structure of the COL1A2 far-upstream enhancer and the HS4 region is shown in Figure 1A.Enhancer activation was determined by measuring luciferase expression.	Enhancer	--	Luciferase Reporter Assay,ChIP	We created two different luciferase reporter gene constructs under the control of the COL1A2 enhancer and proximal promoter.When the enhancer is engaged, it contacts the RNA polymerase complex forming at the collagen promoter. Thus, an RNA polymerase ChIP signal is a direct measure of enhancer engagement. 	EDSARTH2,EDSCV,OI4	--	--	--	STAT3	ADMIO,ADMIO1,APRF,HIES	ChIP-qPCR	ChIP analysis using qPCR for the binding of STAT3, JunB, and RNA polymerase II, in the HS4 region of SSc fibroblasts after treatment with SD1029, STAT3 siRNA (siSTAT3), or nontargeting siRNA (siNT). * = p < 0.05.	--	--	COL1A2
29142074	chr7	94002773	94005073	COL1A2	Yet, a certain threshold level of STAT3 activity is essential to support activation of the COL1A2 enhancer and TGFβ signalling in fibroblasts.	human	Lung	Low throughput	STAT3 controls COL1A2 enhancer activation cooperatively with JunB, regulates type I collagen synthesis posttranscriptionally, and is essential for lung myofibroblast differentiation	否	--	--	Myofibroblast	E_02_0032	Luciferase Reporter Assay,ChIP	The structure of the COL1A2 far-upstream enhancer and the HS4 region is shown in Figure 1A.Enhancer activation was determined by measuring luciferase expression.	Enhancer	--	Luciferase Reporter Assay,ChIP	We created two different luciferase reporter gene constructs under the control of the COL1A2 enhancer and proximal promoter.When the enhancer is engaged, it contacts the RNA polymerase complex forming at the collagen promoter. Thus, an RNA polymerase ChIP signal is a direct measure of enhancer engagement. 	EDSARTH2,EDSCV,OI4	--	--	--	STAT3	ADMIO,ADMIO1,APRF,HIES	ChIP-qPCR	ChIP analysis using qPCR for the binding of STAT3, JunB, and RNA polymerase II, in the HS4 region of SSc fibroblasts after treatment with SD1029, STAT3 siRNA (siSTAT3), or nontargeting siRNA (siNT). * = p < 0.05.	--	--	COL1A2
29141987	chr2	103887795	103888195	Lmo2	T controls the expression of Lmo2, a master regulator of hematopoietic and endothelial development	mouse	Embryo	Low+High throughput	BRACHYURY directs histone acetylation to target loci during mesoderm development	否	--	--	hematopoietic and endothelial cell	E_02_0033	ChIP-seq	We overlapped TBS with genome‐wide H3K4me1 peaks from T WT mesodermal cells and found the same trend of decreased H3K27ac within ±1 kb of TBS/H3K4me1 sites (Fig EV4E), suggesting that T functions to coordinate H3K27ac at putative enhancer regions throughout the genome, and may regulate the switch between poised H3K4me1(+) enhancers and active H3K27ac/H3K4me1(+) enhancer regions.	Enhancer	--	RT-qPCR,ChIP-qPCR,ChIP-seq	Both the ?70 enhancer and the TSS of Lmo2 display a decrease in H3K27ac in T Y88A mutant mesodermal cells, in the ChIP‐Seq data and confirmed by ChIP‐qPCR (Figs ?(Figs5A5A and B, and EV5A). We reasoned that T binding to the ?70 enhancer of Lmo2 may recruit permissive chromatin marks to the TSS to regulate expression, and that this regulation is disrupted in T Y88A mutant mesodermal cells.	Rbtn-2,Rbtn2,Rhom-2,Ttg2	--	--	--	T	Bra,D17Mit170,Low,Lr1,Tbxt,Tl2,Tl3,cou,me75,T	ChIP-seq,ChIP-qPCR	We performed a co-immunoprecipitation analysis from in vitrodifferentiated mesodermal cells and found an interaction between endogenous T and p300.Strikingly, loss of H3K27ac was found at TBS upstream of the T genomic locus itself by ChIP-Seq . We validated this decrease in H3K27ac at the T genomic locus by ChIP-qPCR in TY88A and TWT mesodermal cells differentiated in vitro.	--	--	Lmo2
29141987	chr2	103887795	103888195	T	Here, we show that cooperative function of BRACHYURY (T) with histone-modifying enzymes is essential for mouse embryogenesis.	mouse	Embryo	Low+High throughput	BRACHYURY directs histone acetylation to target loci during mesoderm development	否	--	--	hematopoietic and endothelial cell	E_02_0033	ChIP-seq	We overlapped TBS with genome‐wide H3K4me1 peaks from T WT mesodermal cells and found the same trend of decreased H3K27ac within ±1 kb of TBS/H3K4me1 sites (Fig EV4E), suggesting that T functions to coordinate H3K27ac at putative enhancer regions throughout the genome, and may regulate the switch between poised H3K4me1(+) enhancers and active H3K27ac/H3K4me1(+) enhancer regions.	Enhancer	--	RT-qPCR,ChIP-qPCR,ChIP-seq	Both the ?70 enhancer and the TSS of Lmo2 display a decrease in H3K27ac in T Y88A mutant mesodermal cells, in the ChIP‐Seq data and confirmed by ChIP‐qPCR (Figs ?(Figs5A5A and B, and EV5A). We reasoned that T binding to the ?70 enhancer of Lmo2 may recruit permissive chromatin marks to the TSS to regulate expression, and that this regulation is disrupted in T Y88A mutant mesodermal cells.	Rbtn-2,Rbtn2,Rhom-2,Ttg2	--	--	--	T	Bra,D17Mit170,Low,Lr1,Tbxt,Tl2,Tl3,cou,me75,T	ChIP-seq,ChIP-qPCR	We performed a co-immunoprecipitation analysis from in vitrodifferentiated mesodermal cells and found an interaction between endogenous T and p300.Strikingly, loss of H3K27ac was found at TBS upstream of the T genomic locus itself by ChIP-Seq . We validated this decrease in H3K27ac at the T genomic locus by ChIP-qPCR in TY88A and TWT mesodermal cells differentiated in vitro.	--	--	Lmo2
29138985	chr4	108044731	108046731	LEF1	Lymphoid enhancer-binding factor-1 (LEF1) is one of the 48-kD nuclear proteins that is often expressed in the T and pre-B cells and is also a very significant member of the Wnt/β-catenin in embryonic stem cells	human,mouse	Skin tissue	High+Lowthroughput	Effects of microRNA-708 on Epithelial-Mesenchymal Transition, Cell Proliferation and Apoptosis in Melanoma Cells by Targeting LEF1 through the Wnt Signaling Pathway	否		Melanoma	Melanoma Cell Line	E_02_0034	RT-qPCR,Dual-Luciferase Reporter Assay	Lymphoid enhancer-binding factor-1 (LEF1) is one of the 48-kD nuclear proteins that is often expressed in the T and pre-B cells and is also a very significant member of the Wnt/β-catenin in embryonic stem cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Lymphoid enhancer-binding factor-1 (LEF1) is one of the 48-kD nuclear proteins that is often expressed in the T and pre-B cells and is also a very significant member of the Wnt/β-catenin in embryonic stem cells		Lymphoid enhancer-binding factor-1 (LEF1) is one of the 48-kD nuclear proteins that is often expressed in the T and pre-B cells and is also a very significant member of the Wnt/β-catenin in embryonic stem cells	Immunohistochemical staining	Lymphoid enhancer-binding factor-1 (LEF1) is one of the 48-kD nuclear proteins that is often expressed in the T and pre-B cells and is also a very significant member of the Wnt/β-catenin in embryonic stem cells			RT-qPCR,Dual-Luciferase Reporter Assay				LEF1
29138798	chr3	8725482	8727482	Hey1	Taken together, the findings indicate that Hey1 may be a positive regulator of odontoblastic differentiation.	mouse	Dental pulp tissue	High+Lowthroughput	Hey1 functions as a positive regulator of odontogenic differentiation in odontoblast?lineage cells	否		Oral Disease	odontoblast	E_02_0035	Western blot,ChIP,Transfection,RT‑qPCR,Immunofluorescence staining	Taken together, the findings indicate that Hey1 may be a positive regulator of odontoblastic differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, the findings indicate that Hey1 may be a positive regulator of odontoblastic differentiation.		Taken together, the findings indicate that Hey1 may be a positive regulator of odontoblastic differentiation.	Immunohistochemical staining	Taken together, the findings indicate that Hey1 may be a positive regulator of odontoblastic differentiation.			Western blot,ChIP,Transfection,RT‑qPCR,Immunofluorescence staining				Hey1
29129693	chr17	76133482	76135482	FOXJ1	FOXJ1 as a tumor inducer in bladder cancer and an enhancer in glycolysis.	human	Bladder cancer tissues	High+Lowthroughput	FOXJ1 promotes bladder cancer cell growth and regulates Warburg effect	否		bladder cancer	bladder cancer cell	E_01_0042	Western blot	FOXJ1 as a tumor inducer in bladder cancer and an enhancer in glycolysis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FOXJ1 as a tumor inducer in bladder cancer and an enhancer in glycolysis.	Immunohistochemical staining	FOXJ1 as a tumor inducer in bladder cancer and an enhancer in glycolysis.	FOXJ1		Western blot	FOXJ1 as a tumor inducer in bladder cancer and an enhancer in glycolysis.			
29127222	chr15	99562705	99564705	MEF2A	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	human	Placental tissue	High+Lowthroughput	MEF2 transcription factors in human placenta and involvement in cytotrophoblast invasion and differentiation	否		placenta-related pregnancy disorders	cytotrophoblast cell lines	E_01_0043	Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Immunohistochemical staining	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	MEF2A		Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.			
29127222	chr19	19143005	19145005	MEF2B	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	human	Placental tissue	High+Lowthroughput	MEF2 transcription factors in human placenta and involvement in cytotrophoblast invasion and differentiation	否		placenta-related pregnancy disorders	cytotrophoblast cell lines	E_01_0043	Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.		These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Immunohistochemical staining	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.			Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR				MEF2B
29127222	chr5	88714205	88716205	MEF2C	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	human	Placental tissue	High+Lowthroughput	MEF2 transcription factors in human placenta and involvement in cytotrophoblast invasion and differentiation	否		placenta-related pregnancy disorders	cytotrophoblast cell lines	E_01_0043	Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Immunohistochemical staining	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	MEF2C		Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.			
29127222	chr1	156460887	156462887	MEF2D	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	human	Placental tissue	High+Lowthroughput	MEF2 transcription factors in human placenta and involvement in cytotrophoblast invasion and differentiation	否		placenta-related pregnancy disorders	cytotrophoblast cell lines	E_01_0043	Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.		These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.	Immunohistochemical staining	These findings suggest individual members of MEF2 family distinctively regulate 40 cytotrophoblast proliferation, invasion, and differentiation.			Transfection,Immunofluorescence,Western blot,ChIP,RT-PCR				MEF2D
29113912	chr14	18175266	18186392	Ang2	Importantly, sorafenib treatment, which suppresses H3K27 acetylation and Ang2 expression, profoundly halts the progression of Arid1a-deficient HCCs	mouse	Liver	Low+High throughput	Arid1a regulates response to anti-angiogenic therapy in advanced hepatocellular carcinoma	否	--	Hepatocellular Carcinoma	HCC cell lines	E_02_0036	ChIP-seq	Notably, histone modification markers, including H3K4me1,H3K4me3, H3K27me3 and H3K27ac were presented at the Ang2 gene locus in liver tumor cells and were strongly colocal_x0002_ized with the two Arid1a-binding sites, suggesting an associa_x0002_tion between Arid1a binding and histone modification at the Ang2 gene locus (Fig. 4A). ChIP-qPCR analysis showed Arid1a knockdown increased the H3K27ac at the Ang2 proximal and distal regions.	Enhancer	--	ChIP-seq,ChIP-qPCR	Notably, histone modification markers, including H3K4me1,H3K4me3, H3K27me3 and H3K27ac were presented at the Ang2 gene locus in liver tumor cells and were strongly colocal_x0002_ized with the two Arid1a-binding sites, suggesting an associa_x0002_tion between Arid1a binding and histone modification at the Ang2 gene locus (Fig. 4A). ChIP-qPCR analysis showed Arid1a knockdown increased the H3K27ac at the Ang2 proximal and distal regions.	Angrp,Raa3,Rnase5b	--	--	--	Ep300	A430090G16,A730011L11,KAT3B,p300,p300 HAT	ChIP-seq,ChIP-PCR	Interestingly,published ChIP-seq data also showed that p300 bound to the Ang2 gene locus, as we validated by ChIP-PCR.	--	--	Ang2
29113912	chr14	18175266	18186392	Arid1a	Arid1a-deficiency promotes Ang2- dependent angiogenesis leading to hepatocellular carcinoma progression.	mouse	Liver	Low+High throughput	Arid1a regulates response to anti-angiogenic therapy in advanced hepatocellular carcinoma	否	--	Hepatocellular Carcinoma	HCC cell lines	E_02_0036	ChIP-seq	Notably, histone modification markers, including H3K4me1,H3K4me3, H3K27me3 and H3K27ac were presented at the Ang2 gene locus in liver tumor cells and were strongly colocal_x0002_ized with the two Arid1a-binding sites, suggesting an associa_x0002_tion between Arid1a binding and histone modification at the Ang2 gene locus (Fig. 4A). ChIP-qPCR analysis showed Arid1a knockdown increased the H3K27ac at the Ang2 proximal and distal regions.	Enhancer	--	ChIP-seq,ChIP-qPCR	Notably, histone modification markers, including H3K4me1,H3K4me3, H3K27me3 and H3K27ac were presented at the Ang2 gene locus in liver tumor cells and were strongly colocal_x0002_ized with the two Arid1a-binding sites, suggesting an associa_x0002_tion between Arid1a binding and histone modification at the Ang2 gene locus (Fig. 4A). ChIP-qPCR analysis showed Arid1a knockdown increased the H3K27ac at the Ang2 proximal and distal regions.	Angrp,Raa3,Rnase5b	--	--	--	Ep300	A430090G16,A730011L11,KAT3B,p300,p300 HAT	ChIP-seq,ChIP-PCR	Interestingly,published ChIP-seq data also showed that p300 bound to the Ang2 gene locus, as we validated by ChIP-PCR.	--	--	Ang2
29107694	chr7	148804477	148806477	EZH2	Notably, EZH2 can catalyze histone H3 lysine 27 tri-methylation (H3K27me3) to inhibit gene transcription	human,mouse	Pancreas	High+Lowthroughput	Chaetospirolactone reverses the apoptotic resistance towards TRAIL in pancreatic cancer	否		pancreatic cancer	pancreatic cancer cell	E_02_0037	Western blot,ChIP,qPCR	Notably, EZH2 can catalyze histone H3 lysine 27 tri-methylation (H3K27me3) to inhibit gene transcription	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Notably, EZH2 can catalyze histone H3 lysine 27 tri-methylation (H3K27me3) to inhibit gene transcription		Notably, EZH2 can catalyze histone H3 lysine 27 tri-methylation (H3K27me3) to inhibit gene transcription	Immunohistochemical staining	Notably, EZH2 can catalyze histone H3 lysine 27 tri-methylation (H3K27me3) to inhibit gene transcription			Western blot,ChIP,qPCR				EZH2
29106960	chr7	148804589	148806589	EZH2	Thus, SIRT1/EZH2 regulation could be used as a new therapeutic strategy for fibrogenesis.	human	Liver	High+Lowthroughput	Carnosol-mediated Sirtuin 1 activation inhibits Enhancer of Zeste Homolog 2 to attenuate liver fibrosis	否		hepatic fibrosis	Myofibroblast	E_01_0044	Western blot, RT-PCR,Immunofluorescence staining,Transfection	Thus, SIRT1/EZH2 regulation could be used as a new therapeutic strategy for fibrogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, SIRT1/EZH2 regulation could be used as a new therapeutic strategy for fibrogenesis.	Immunohistochemical staining	Thus, SIRT1/EZH2 regulation could be used as a new therapeutic strategy for fibrogenesis.	EZH2		Western blot, RT-PCR,Immunofluorescence staining,Transfection	Thus, SIRT1/EZH2 regulation could be used as a new therapeutic strategy for fibrogenesis.			
29089464	chr7	148804445	148806445	EZH2	Histone methylation is a member of the histone modifications with histone methyltransferase activity, wherein SET and MYND domain containing 3 (SMYD3) and Enhancer of Zeste Homolog 2 (EZH2) are reported to be involved in the development of multiple cancers and play important roles in transcriptional regulation	human	Breast cancer tissue	High+Lowthroughput	Correlations of EZH2 and SMYD3 gene polymorphisms with breast cancer susceptibility and prognosis	否		breast cancer	breast cancer cell	E_01_0045	RT-qPCR,Western blot	Histone methylation is a member of the histone modifications with histone methyltransferase activity, wherein SET and MYND domain containing 3 (SMYD3) and Enhancer of Zeste Homolog 2 (EZH2) are reported to be involved in the development of multiple cancers and play important roles in transcriptional regulation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Histone methylation is a member of the histone modifications with histone methyltransferase activity, wherein SET and MYND domain containing 3 (SMYD3) and Enhancer of Zeste Homolog 2 (EZH2) are reported to be involved in the development of multiple cancers and play important roles in transcriptional regulation	Immunohistochemical staining	Histone methylation is a member of the histone modifications with histone methyltransferase activity, wherein SET and MYND domain containing 3 (SMYD3) and Enhancer of Zeste Homolog 2 (EZH2) are reported to be involved in the development of multiple cancers and play important roles in transcriptional regulation	EZH2		RT-qPCR,Western blot	Histone methylation is a member of the histone modifications with histone methyltransferase activity, wherein SET and MYND domain containing 3 (SMYD3) and Enhancer of Zeste Homolog 2 (EZH2) are reported to be involved in the development of multiple cancers and play important roles in transcriptional regulation			
29070695	chr17	19492823	19494823	SLC47A1	These results suggest that the 5’ CpG island of SLC47A1 acts as an enhancer for SLC47A1, and DNA methylation in the CpG island plays an important role in inter-individual differences in hepatic MATE1 expression.	human	Liver	High+Lowthroughput	Relationship between DNA Methylation in the 5' CpG Island of the SLC47A1 (Multidrug and Toxin Extrusion Protein MATE1) Gene and Interindividual Variability in MATE1 Expression in the Human Liver	否			HepG2 cell	E_01_0046	qRT-PCR	These results suggest that the 5’ CpG island of SLC47A1 acts as an enhancer for SLC47A1, and DNA methylation in the CpG island plays an important role in inter-individual differences in hepatic MATE1 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that the 5’ CpG island of SLC47A1 acts as an enhancer for SLC47A1, and DNA methylation in the CpG island plays an important role in inter-individual differences in hepatic MATE1 expression.		These results suggest that the 5’ CpG island of SLC47A1 acts as an enhancer for SLC47A1, and DNA methylation in the CpG island plays an important role in inter-individual differences in hepatic MATE1 expression.	Immunohistochemical staining	These results suggest that the 5’ CpG island of SLC47A1 acts as an enhancer for SLC47A1, and DNA methylation in the CpG island plays an important role in inter-individual differences in hepatic MATE1 expression.			qRT-PCR				SLC47A1
29059175	chr16	67559364	67561364	CTCF	Because CTCF is a multifunctional TF that can function as either an activator or a repressor of transcription, we first confirmed the role of CTCF in regulation of MSMP expression using siRNA.	human	Tumor	High+Lowthroughput	Induction of anti-VEGF therapy resistance by upregulated expression of microseminoprotein (MSMP)	否		Tumor	cancer cell	E_01_0047	qRT–PCR,Immunostaining,Western blot	Because CTCF is a multifunctional TF that can function as either an activator or a repressor of transcription, we first confirmed the role of CTCF in regulation of MSMP expression using siRNA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Because CTCF is a multifunctional TF that can function as either an activator or a repressor of transcription, we first confirmed the role of CTCF in regulation of MSMP expression using siRNA.	Immunohistochemical staining	Because CTCF is a multifunctional TF that can function as either an activator or a repressor of transcription, we first confirmed the role of CTCF in regulation of MSMP expression using siRNA.	CTCF		qRT–PCR,Immunostaining,Western blot	Because CTCF is a multifunctional TF that can function as either an activator or a repressor of transcription, we first confirmed the role of CTCF in regulation of MSMP expression using siRNA.			
29059175	chr9	35749798	35751798	MSMP	These findings imply that MSMP inhibition combined with the use of antiangiogenesis drugs may be a new strategy to overcome resistance to antiangiogenesis therapy	human	Tumor	High+Lowthroughput	Induction of anti-VEGF therapy resistance by upregulated expression of microseminoprotein (MSMP)	否		Tumor	cancer cell	E_01_0047	qRT–PCR,Immunostaining,Western blot	These findings imply that MSMP inhibition combined with the use of antiangiogenesis drugs may be a new strategy to overcome resistance to antiangiogenesis therapy	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings imply that MSMP inhibition combined with the use of antiangiogenesis drugs may be a new strategy to overcome resistance to antiangiogenesis therapy		These findings imply that MSMP inhibition combined with the use of antiangiogenesis drugs may be a new strategy to overcome resistance to antiangiogenesis therapy	Immunohistochemical staining	These findings imply that MSMP inhibition combined with the use of antiangiogenesis drugs may be a new strategy to overcome resistance to antiangiogenesis therapy			qRT–PCR,Immunostaining,Western blot				MSMP
29059150	chr12	54572339	54574339	PPP1R1A	We found that PPP1R1A is one of the top ranked target genes of EWS/FLI, the master regulator of ES, and is upregulated by EWS/FLI via a GGAA microsatellite enhancer element	human,mouse	Tumor	High+Lowthroughput	Protein phosphatase 1 regulatory subunit 1A in ewing sarcoma tumorigenesis and metastasis	否		ewing sarcoma	ewing sarcoma cell	E_02_0038	qRT–PCR,ChIP-Seq,Luciferase reporter assay	We found that PPP1R1A is one of the top ranked target genes of EWS/FLI, the master regulator of ES, and is upregulated by EWS/FLI via a GGAA microsatellite enhancer element	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found that PPP1R1A is one of the top ranked target genes of EWS/FLI, the master regulator of ES, and is upregulated by EWS/FLI via a GGAA microsatellite enhancer element		We found that PPP1R1A is one of the top ranked target genes of EWS/FLI, the master regulator of ES, and is upregulated by EWS/FLI via a GGAA microsatellite enhancer element	Immunohistochemical staining	We found that PPP1R1A is one of the top ranked target genes of EWS/FLI, the master regulator of ES, and is upregulated by EWS/FLI via a GGAA microsatellite enhancer element			qRT–PCR,ChIP-Seq,Luciferase reporter assay				PPP1R1A
29054992	chr5	69231968	69233968	CDK7	CDK7 is a key regulator of the cell cycle	mouse	Tumor	High+Lowthroughput	Suppression of Adaptive Responses to Targeted Cancer Therapy by Transcriptional Repression	否		Tumor	cancer cell	E_02_0039	RNA-seq,ChIP-Seq,ChIP,RT-PCR	CDK7 is a key regulator of the cell cycle	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CDK7 is a key regulator of the cell cycle		CDK7 is a key regulator of the cell cycle	Immunohistochemical staining	CDK7 is a key regulator of the cell cycle			RNA-seq,ChIP-Seq,ChIP,RT-PCR				CDK7
29053336	chr7	148804334	148806334	EZH2	These findings suggest that a novel and functionally interdependent interplay between EZH2 and G9a regulates histone methylation-mediated epigenetic repression of the antifibrotic CXCL10 gene in IPF. This interdependent interplay may prove to be a target for epigenetic intervention to restore the expression of CXCL10 and other anti-fibrotic genes in IPF.	human	Lung	High+Lowthroughput	Interplay between EZH2 and G9a Regulates CXCL10 Gene Repression in Idiopathic Pulmonary Fibrosis	否		Pulmonary Fibrosis		E_01_0048	ChIP	These findings suggest that a novel and functionally interdependent interplay between EZH2 and G9a regulates histone methylation-mediated epigenetic repression of the antifibrotic CXCL10 gene in IPF. This interdependent interplay may prove to be a target for epigenetic intervention to restore the expression of CXCL10 and other anti-fibrotic genes in IPF.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These findings suggest that a novel and functionally interdependent interplay between EZH2 and G9a regulates histone methylation-mediated epigenetic repression of the antifibrotic CXCL10 gene in IPF. This interdependent interplay may prove to be a target for epigenetic intervention to restore the expression of CXCL10 and other anti-fibrotic genes in IPF.	Immunohistochemical staining	These findings suggest that a novel and functionally interdependent interplay between EZH2 and G9a regulates histone methylation-mediated epigenetic repression of the antifibrotic CXCL10 gene in IPF. This interdependent interplay may prove to be a target for epigenetic intervention to restore the expression of CXCL10 and other anti-fibrotic genes in IPF.	EZH2		ChIP	These findings suggest that a novel and functionally interdependent interplay between EZH2 and G9a regulates histone methylation-mediated epigenetic repression of the antifibrotic CXCL10 gene in IPF. This interdependent interplay may prove to be a target for epigenetic intervention to restore the expression of CXCL10 and other anti-fibrotic genes in IPF.			
29044515	chr12	32787839	32789839	PKP2	Moreover, our data suggest that Plakophilin-2 may act as an antagonist of β-catenin/TCF complexes on Wnt-activated promoters.	human	Colon tissue	High+Lowthroughput	The human PKP2/plakophilin-2 gene is induced by Wnt/β-catenin in normal and colon cancer-associated fibroblasts	否		colon cancer	colon cancer-associated fibroblast	E_01_0049	RNA-Seq,RT-qPCR,Western blot	Moreover, our data suggest that Plakophilin-2 may act as an antagonist of β-catenin/TCF complexes on Wnt-activated promoters.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, our data suggest that Plakophilin-2 may act as an antagonist of β-catenin/TCF complexes on Wnt-activated promoters.		Moreover, our data suggest that Plakophilin-2 may act as an antagonist of β-catenin/TCF complexes on Wnt-activated promoters.	Immunohistochemical staining	Moreover, our data suggest that Plakophilin-2 may act as an antagonist of β-catenin/TCF complexes on Wnt-activated promoters.			RNA-Seq,RT-qPCR,Western blot				PKP2
29024000	chr16	29880620	29882620	Hes1	In conclusion, we demonstrate that myeloid Notch1 deficiency promotes the JSAP1- mediated RhoA/ROCK signaling pathway and exacerbates liver damage by depressing its target gene Hes1 in IR-stressed livers.	mouse	Liver	High+Lowthroughput	Myeloid Notch1 deficiency activates the RhoA/ROCK pathway and aggravates hepatocellular damage in mouse ischemic livers	否		Liver Injury	hepatocyte	E_02_0040	Immunohistochemistry staining,qRT-PCR,Immunofluorescence staining	In conclusion, we demonstrate that myeloid Notch1 deficiency promotes the JSAP1- mediated RhoA/ROCK signaling pathway and exacerbates liver damage by depressing its target gene Hes1 in IR-stressed livers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, we demonstrate that myeloid Notch1 deficiency promotes the JSAP1- mediated RhoA/ROCK signaling pathway and exacerbates liver damage by depressing its target gene Hes1 in IR-stressed livers.		In conclusion, we demonstrate that myeloid Notch1 deficiency promotes the JSAP1- mediated RhoA/ROCK signaling pathway and exacerbates liver damage by depressing its target gene Hes1 in IR-stressed livers.	Immunohistochemical staining	In conclusion, we demonstrate that myeloid Notch1 deficiency promotes the JSAP1- mediated RhoA/ROCK signaling pathway and exacerbates liver damage by depressing its target gene Hes1 in IR-stressed livers.			Immunohistochemistry staining,qRT-PCR,Immunofluorescence staining				Hes1
28994199	chr1	47213269	47215269	TAL1	Here, addition of PD0325901 to the culture was associated with increased transcript levels of GATA1, LMO2, TAL1 and FOG which are known to be the key transcription factors for normal erythroid differentiation	human	Haematopoietic tissue	High+Lowthroughput	Inhibition of MEK/ERK signalling pathway promotes erythroid differentiation and reduces HSCs engraftment in ex?vivo expanded haematopoietic stem cells	否			hematopoietic stem cell	E_01_0050	qPCR,Immunohistochemical staining	Here, addition of PD0325901 to the culture was associated with increased transcript levels of GATA1, LMO2, TAL1 and FOG which are known to be the key transcription factors for normal erythroid differentiation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, addition of PD0325901 to the culture was associated with increased transcript levels of GATA1, LMO2, TAL1 and FOG which are known to be the key transcription factors for normal erythroid differentiation	Immunohistochemical staining	Here, addition of PD0325901 to the culture was associated with increased transcript levels of GATA1, LMO2, TAL1 and FOG which are known to be the key transcription factors for normal erythroid differentiation	TAL1		qPCR,Immunohistochemical staining	Here, addition of PD0325901 to the culture was associated with increased transcript levels of GATA1, LMO2, TAL1 and FOG which are known to be the key transcription factors for normal erythroid differentiation			
28974397	chr7	148804688	148806688	EZH2	A promising epigenetic target is EZH2 (enhancer of zeste homolog 2), the catalytic subunit of the polycomb repressive complex 2 that methylates the 27th H3K27.	human	Soft tissue	High+Lowthroughput	Comprehensive Genomic Sequencing of Urothelial Tumors Identifies Rare SMARCB1 (INI-1)-Deficient Carcinomas of the Urinary?System	否		urothelial carcinoma	tumor cell	E_01_0051	Immunohistochemical staining	A promising epigenetic target is EZH2 (enhancer of zeste homolog 2), the catalytic subunit of the polycomb repressive complex 2 that methylates the 27th H3K27.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			A promising epigenetic target is EZH2 (enhancer of zeste homolog 2), the catalytic subunit of the polycomb repressive complex 2 that methylates the 27th H3K27.	Immunohistochemical staining	A promising epigenetic target is EZH2 (enhancer of zeste homolog 2), the catalytic subunit of the polycomb repressive complex 2 that methylates the 27th H3K27.	EZH2		Immunohistochemical staining	A promising epigenetic target is EZH2 (enhancer of zeste homolog 2), the catalytic subunit of the polycomb repressive complex 2 that methylates the 27th H3K27.			
28974397	chr22	23784056	23786056	SMARCB1	Functioning as a tumor suppressor, biallelic loss of SMARCB1/INI1 through mutation or deletion results in tumor formation.	human	Soft tissue	High+Lowthroughput	Comprehensive Genomic Sequencing of Urothelial Tumors Identifies Rare SMARCB1 (INI-1)-Deficient Carcinomas of the Urinary?System	否		urothelial carcinoma	tumor cell	E_01_0051	Immunohistochemical staining	Functioning as a tumor suppressor, biallelic loss of SMARCB1/INI1 through mutation or deletion results in tumor formation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Functioning as a tumor suppressor, biallelic loss of SMARCB1/INI1 through mutation or deletion results in tumor formation.		Functioning as a tumor suppressor, biallelic loss of SMARCB1/INI1 through mutation or deletion results in tumor formation.	Immunohistochemical staining	Functioning as a tumor suppressor, biallelic loss of SMARCB1/INI1 through mutation or deletion results in tumor formation.			Immunohistochemical staining				SMARCB1
28971975	chr17	61449600	61451600	TBX4	Transcriptome analysis revealed that TBX4 could broadly regulate fibroblast-related pathways and partly contribute to super-enhancer-mediated transcriptional programs.	human		High+Lowthroughput	TBX4 is involved in the super-enhancer-driven transcriptional programs underlying features specific to lung fibroblasts	否		pathogenesis of respiratory diseases	lung fibroblasts cell	E_01_0052	RNA-seq,RT-PCR	Transcriptome analysis revealed that TBX4 could broadly regulate fibroblast-related pathways and partly contribute to super-enhancer-mediated transcriptional programs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Transcriptome analysis revealed that TBX4 could broadly regulate fibroblast-related pathways and partly contribute to super-enhancer-mediated transcriptional programs.	Immunohistochemical staining	Transcriptome analysis revealed that TBX4 could broadly regulate fibroblast-related pathways and partly contribute to super-enhancer-mediated transcriptional programs.	TBX4		RNA-seq,RT-PCR	Transcriptome analysis revealed that TBX4 could broadly regulate fibroblast-related pathways and partly contribute to super-enhancer-mediated transcriptional programs.			
28970250	chr7	148804484	148806484	EZH2	Finally, EZH2 inhibition or PPARg activation ameliorated fibrogenesis in cKO mice.	human,mouse	Liver	High+Lowthroughput	SIRT1 antagonizes liver fibrosis by blocking hepatic stellate cell activation in mice	否		liver fibrosis	hepatic stellate cell	E_02_0041	Western blot, qPCR,Transfection,ChIP	Finally, EZH2 inhibition or PPARg activation ameliorated fibrogenesis in cKO mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Finally, EZH2 inhibition or PPARg activation ameliorated fibrogenesis in cKO mice.		Finally, EZH2 inhibition or PPARg activation ameliorated fibrogenesis in cKO mice.	Immunohistochemical staining	Finally, EZH2 inhibition or PPARg activation ameliorated fibrogenesis in cKO mice.			Western blot, qPCR,Transfection,ChIP				EZH2
28951561	chr17	42697786	42699786	EZH1	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.	human,mouse	Bone marrow	High+Lowthroughput	Dual inhibition of EZH1/2 breaks the quiescence of leukemia stem cells in acute myeloid leukemia	否		Acute myeloid leukemia	leukemia stem cell	E_02_0042	Western blot	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.		Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.	Immunohistochemical staining	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.			Western blot				EZH1
28951561	chr7	148804920	148806920	EZH2	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.	human,mouse	Bone marrow	High+Lowthroughput	Dual inhibition of EZH1/2 breaks the quiescence of leukemia stem cells in acute myeloid leukemia	否		Acute myeloid leukemia	leukemia stem cell	E_02_0042	Western blot	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.		Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.	Immunohistochemical staining	Taken together, these results show that dual inhibition of EZH1/2 is an effective strategy for eliminating AML LSCs.			Western blot				EZH2
28939663	chr7	148804966	148806966	EZH2	As CCRK drives hepatocarcinogenesis through upregulation of EZH2,which can function as a transcriptional activator of NF-κB targets	human	Liver	High+Lowthroughput	Hepatoma-intrinsic CCRK inhibition diminishes myeloid-derived suppressor cell immunosuppression and enhances immune-checkpoint blockade efficacy	否		hepatocellular carcinoma	Myeloid-derived suppressor cell	E_01_0053	Transfection	As CCRK drives hepatocarcinogenesis through upregulation of EZH2,which can function as a transcriptional activator of NF-κB targets	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			As CCRK drives hepatocarcinogenesis through upregulation of EZH2,which can function as a transcriptional activator of NF-κB targets	Immunohistochemical staining	As CCRK drives hepatocarcinogenesis through upregulation of EZH2,which can function as a transcriptional activator of NF-κB targets	EZH2		Transfection	As CCRK drives hepatocarcinogenesis through upregulation of EZH2,which can function as a transcriptional activator of NF-κB targets			
28925507	chr7	148804490	148806490	EZH2	In accord with this, we confirmed that EGCG and GSK343 could both significantly arrest the G0/G1 phase in RKO cell cycle, suggesting EGCG and EZH2 inhibitor share a common mechanism of action in RKO cells.	human	CRC tissue	High+Lowthroughput	(-)-Epigallocatechin-3-gallate and EZH2 inhibitor GSK343 have similar inhibitory effects and mechanisms of action on colorectal cancer cells	否		colorectal cancer	colorectal cancer (CRC) cell line	E_01_0054	Western blot,Immunofluorescence	In accord with this, we confirmed that EGCG and GSK343 could both significantly arrest the G0/G1 phase in RKO cell cycle, suggesting EGCG and EZH2 inhibitor share a common mechanism of action in RKO cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In accord with this, we confirmed that EGCG and GSK343 could both significantly arrest the G0/G1 phase in RKO cell cycle, suggesting EGCG and EZH2 inhibitor share a common mechanism of action in RKO cells.	Immunohistochemical staining	In accord with this, we confirmed that EGCG and GSK343 could both significantly arrest the G0/G1 phase in RKO cell cycle, suggesting EGCG and EZH2 inhibitor share a common mechanism of action in RKO cells.	EZH2		Western blot,Immunofluorescence	In accord with this, we confirmed that EGCG and GSK343 could both significantly arrest the G0/G1 phase in RKO cell cycle, suggesting EGCG and EZH2 inhibitor share a common mechanism of action in RKO cells.			
28925391	chr7	148804797	148806797	EZH2	Here, we show enhancer of zeste homolog 2(EZH2), an enzyme that catalyzes H3 lysine trimethylation and associates with oncogenic function, contributes to PARPi sensitivity in breast cancer cells.	human	Tumor	High+Lowthroughput	EZH2 contributes to the response to PARP inhibitors through its PARP-mediated poly-ADP ribosylation in breast cancer	否		breast cancer	breast cancer cell	E_01_0055	ChIP,qPCR,RT-qPCR,Western blot	Here, we show enhancer of zeste homolog 2(EZH2), an enzyme that catalyzes H3 lysine trimethylation and associates with oncogenic function, contributes to PARPi sensitivity in breast cancer cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we show enhancer of zeste homolog 2(EZH2), an enzyme that catalyzes H3 lysine trimethylation and associates with oncogenic function, contributes to PARPi sensitivity in breast cancer cells.	Immunohistochemical staining	Here, we show enhancer of zeste homolog 2(EZH2), an enzyme that catalyzes H3 lysine trimethylation and associates with oncogenic function, contributes to PARPi sensitivity in breast cancer cells.	EZH2		ChIP,qPCR,RT-qPCR,Western blot	Here, we show enhancer of zeste homolog 2(EZH2), an enzyme that catalyzes H3 lysine trimethylation and associates with oncogenic function, contributes to PARPi sensitivity in breast cancer cells.			
28923345	chr10	67881952	67883952	SIRT1	Thus, SIRT1 is a novel transcriptional enhancer of GR-induced transcriptional activity possibly by functioning as a scaffold for the  transcriptional complex formed on GR.	human		High+Lowthroughput	SIRT1 is a transcriptional enhancer of the glucocorticoid receptor acting independently to its deacetylase activity	否			HeLa cell	E_01_0056	Transfection,Western blot,RNA-seq,PCR,ChIP	Thus, SIRT1 is a novel transcriptional enhancer of GR-induced transcriptional activity possibly by functioning as a scaffold for the  transcriptional complex formed on GR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, SIRT1 is a novel transcriptional enhancer of GR-induced transcriptional activity possibly by functioning as a scaffold for the  transcriptional complex formed on GR.	Immunohistochemical staining	Thus, SIRT1 is a novel transcriptional enhancer of GR-induced transcriptional activity possibly by functioning as a scaffold for the  transcriptional complex formed on GR.	SIRT1		Transfection,Western blot,RNA-seq,PCR,ChIP	Thus, SIRT1 is a novel transcriptional enhancer of GR-induced transcriptional activity possibly by functioning as a scaffold for the  transcriptional complex formed on GR.			
28922471	chr19	35742614	35744614	PSENEN	The co-existence of the two disorders was recently found to result from mutations in PSENEN, encoding protein presenilin enhancer gamma-secretase subunit.	human		High+Lowthroughput	A phenotype combining hidradenitis suppurativa with Dowling-Degos disease caused by a founder mutation in PSENEN	否		Dowling-Degos disease	keratinocyte cell	E_01_0057	qRT-PCR	The co-existence of the two disorders was recently found to result from mutations in PSENEN, encoding protein presenilin enhancer gamma-secretase subunit.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The co-existence of the two disorders was recently found to result from mutations in PSENEN, encoding protein presenilin enhancer gamma-secretase subunit.		The co-existence of the two disorders was recently found to result from mutations in PSENEN, encoding protein presenilin enhancer gamma-secretase subunit.	Immunohistochemical staining	The co-existence of the two disorders was recently found to result from mutations in PSENEN, encoding protein presenilin enhancer gamma-secretase subunit.			qRT-PCR				PSENEN
28902616	chr5	88714680	88716680	MEF2C	The MADS-box transcription factor myocyte enhancer factor 2C (MEF2C) is required for the cardiac development and postnatal adaptation and in mice-targeted disruption of the MEF2C gene results in dilated cardiomyopathy (DCM).	human	Heart	High+Lowthroughput	MEF2C loss-of-function mutation associated with familial dilated cardiomyopathy	否		dilated cardiomyopathy	HeLa cell	E_01_0058	Transfection,dual-luciferase reporter assay	The MADS-box transcription factor myocyte enhancer factor 2C (MEF2C) is required for the cardiac development and postnatal adaptation and in mice-targeted disruption of the MEF2C gene results in dilated cardiomyopathy (DCM).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The MADS-box transcription factor myocyte enhancer factor 2C (MEF2C) is required for the cardiac development and postnatal adaptation and in mice-targeted disruption of the MEF2C gene results in dilated cardiomyopathy (DCM).	Immunohistochemical staining	The MADS-box transcription factor myocyte enhancer factor 2C (MEF2C) is required for the cardiac development and postnatal adaptation and in mice-targeted disruption of the MEF2C gene results in dilated cardiomyopathy (DCM).	MEF2C		Transfection,dual-luciferase reporter assay	The MADS-box transcription factor myocyte enhancer factor 2C (MEF2C) is required for the cardiac development and postnatal adaptation and in mice-targeted disruption of the MEF2C gene results in dilated cardiomyopathy (DCM).			
28898113	chr1	209782978	209784978	IRF6	Interferon regulatory factor 6 (IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expression of target genes.	human,mouse	Salivary gland	High+Lowthroughput	Interferon Regulatory Factor 6 Is Necessary for Salivary Glands and Pancreas Development	否		xerostomia	acinar cell	E_02_0043	Immunofluorescent Staining,RNA-Seq	Interferon regulatory factor 6 (IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expression of target genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Interferon regulatory factor 6 (IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expression of target genes.		Interferon regulatory factor 6 (IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expression of target genes.	Immunohistochemical staining	Interferon regulatory factor 6 (IRF6) acts as a tumor suppressor and controls cell differentiation in ectodermal and craniofacial tissues by regulating expression of target genes.			Immunofluorescent Staining,RNA-Seq				IRF6
28862715	chr7	148804307	148806307	EZH2	EZH2 positivity was significantly correlated with WHO tumor grade and worse prognosis in gliomas.	human	Tumor	High+Lowthroughput	Prognostic role of EZH2 in gliomas: a meta-analysis	否		gliomas	tumor cell	E_01_0059	Meta-analysis	EZH2 positivity was significantly correlated with WHO tumor grade and worse prognosis in gliomas.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2 positivity was significantly correlated with WHO tumor grade and worse prognosis in gliomas.	Immunohistochemical staining	EZH2 positivity was significantly correlated with WHO tumor grade and worse prognosis in gliomas.	EZH2		Meta-analysis	EZH2 positivity was significantly correlated with WHO tumor grade and worse prognosis in gliomas.			
28858300	chr7	148804693	148806693	EZH2	Aberrant activity of enhancer of zeste homolog 2 (EZH2) is associated with a wide range of human cancers.	human	Tumor	High+Lowthroughput	Development of a high-throughput fluorescence polarization assay for the discovery of EZH2-EED interaction inhibitors	否		Tumor	cancer cell	E_01_0060	PCR	Aberrant activity of enhancer of zeste homolog 2 (EZH2) is associated with a wide range of human cancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Aberrant activity of enhancer of zeste homolog 2 (EZH2) is associated with a wide range of human cancers.	Immunohistochemical staining	Aberrant activity of enhancer of zeste homolog 2 (EZH2) is associated with a wide range of human cancers.	EZH2		PCR	Aberrant activity of enhancer of zeste homolog 2 (EZH2) is associated with a wide range of human cancers.			
28811072	chr16	81236	83236	NPRL3	One globin gene cluster, linked to the gene NPRL3, is preserved in all vertebrates, including a gene cluster encoding the highly divergent globins from jawless vertebrates.	human		High+Lowthroughput	Evolution of hemoglobin loci and their regulatory elements	否			erythroid cell	E_01_0061		One globin gene cluster, linked to the gene NPRL3, is preserved in all vertebrates, including a gene cluster encoding the highly divergent globins from jawless vertebrates.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	One globin gene cluster, linked to the gene NPRL3, is preserved in all vertebrates, including a gene cluster encoding the highly divergent globins from jawless vertebrates.		One globin gene cluster, linked to the gene NPRL3, is preserved in all vertebrates, including a gene cluster encoding the highly divergent globins from jawless vertebrates.	Immunohistochemical staining	One globin gene cluster, linked to the gene NPRL3, is preserved in all vertebrates, including a gene cluster encoding the highly divergent globins from jawless vertebrates.							NPRL3
28810932	chr7	148804688	148806688	EZH2	RIP and ChIP assays suggest that NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression. These findings indicate that NEAT1 exerts oncogenic effects in CCA.	human	CCA tissue	High+Lowthroughput	Long Noncoding RNA NEAT1 Promotes Growth and Metastasis of Cholangiocarcinoma Cells	否		cholangiocarcinoma	Cholangiocarcinoma Cell	E_01_0062	qRT-PCR,ChIP,Western blot	RIP and ChIP assays suggest that NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression. These findings indicate that NEAT1 exerts oncogenic effects in CCA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			RIP and ChIP assays suggest that NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression. These findings indicate that NEAT1 exerts oncogenic effects in CCA.	Immunohistochemical staining	RIP and ChIP assays suggest that NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression. These findings indicate that NEAT1 exerts oncogenic effects in CCA.	EZH2		qRT-PCR,ChIP,Western blot	RIP and ChIP assays suggest that NEAT1 is recruited to the E-cadherin promoter by EZH2 (enhancer of zeste homolog 2), where it represses E-cadherin expression. These findings indicate that NEAT1 exerts oncogenic effects in CCA.			
28796375	chr7	148804611	148806611	EZH2	Consequently, we find that EZH2 promotes LA cell invasion and metastasis by inhibiting SPRY4-IT1 expression. This article is protected by copyright.	human	LA tissue	High+Lowthroughput	Effects of long noncoding RNA SPRY4-IT1-mediated EZH2 on the invasion and migration of lung adenocarcinoma	否		lung adenocarcinoma	lung adenocarcinoma (LA) cell	E_01_0063	Western blot,RT-qPCR	Consequently, we find that EZH2 promotes LA cell invasion and metastasis by inhibiting SPRY4-IT1 expression. This article is protected by copyright.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Consequently, we find that EZH2 promotes LA cell invasion and metastasis by inhibiting SPRY4-IT1 expression. This article is protected by copyright.	Immunohistochemical staining	Consequently, we find that EZH2 promotes LA cell invasion and metastasis by inhibiting SPRY4-IT1 expression. This article is protected by copyright.	EZH2		Western blot,RT-qPCR	Consequently, we find that EZH2 promotes LA cell invasion and metastasis by inhibiting SPRY4-IT1 expression. This article is protected by copyright.			
28795320	chr7	148804483	148806483	EZH2	Taken together, our results suggest that EZH2 regulates cell proliferation potentially by targeting RUNX3 through the Wnt/b-catenin signaling pathway in laryngeal carcinoma.	human	Laryngeal carcinoma tissue	High+Lowthroughput	EZH2 promotes cell proliferation by regulating the expression of RUNX3 in laryngeal carcinoma	否		laryngeal carcinoma	laryngeal carcinoma cell	E_01_0064	Western blot,qRT-PCR	Taken together, our results suggest that EZH2 regulates cell proliferation potentially by targeting RUNX3 through the Wnt/b-catenin signaling pathway in laryngeal carcinoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Taken together, our results suggest that EZH2 regulates cell proliferation potentially by targeting RUNX3 through the Wnt/b-catenin signaling pathway in laryngeal carcinoma.	Immunohistochemical staining	Taken together, our results suggest that EZH2 regulates cell proliferation potentially by targeting RUNX3 through the Wnt/b-catenin signaling pathway in laryngeal carcinoma.	EZH2		Western blot,qRT-PCR	Taken together, our results suggest that EZH2 regulates cell proliferation potentially by targeting RUNX3 through the Wnt/b-catenin signaling pathway in laryngeal carcinoma.			
28774779	chr12	57092763	57094763	STAT6	Our results suggest that there is a novel, so far uncharacterized cistromic crosstalk between RXR and STAT6 that is likely to contribute to the formation of the active enhancer repertoire, transcriptome and differential signal-specific gene regulation of polarized macrophages.	human		High+Lowthroughput	Extensive and functional overlap of the STAT6 and RXR cistromes in the active enhancer repertoire of human CD14+ monocyte derived differentiating macrophages	否			macrophage	E_01_0065	ChIP,ChIP-seq,RNA-Seq,qPCR	Our results suggest that there is a novel, so far uncharacterized cistromic crosstalk between RXR and STAT6 that is likely to contribute to the formation of the active enhancer repertoire, transcriptome and differential signal-specific gene regulation of polarized macrophages.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our results suggest that there is a novel, so far uncharacterized cistromic crosstalk between RXR and STAT6 that is likely to contribute to the formation of the active enhancer repertoire, transcriptome and differential signal-specific gene regulation of polarized macrophages.	Immunohistochemical staining	Our results suggest that there is a novel, so far uncharacterized cistromic crosstalk between RXR and STAT6 that is likely to contribute to the formation of the active enhancer repertoire, transcriptome and differential signal-specific gene regulation of polarized macrophages.	STAT6		ChIP,ChIP-seq,RNA-Seq,qPCR	Our results suggest that there is a novel, so far uncharacterized cistromic crosstalk between RXR and STAT6 that is likely to contribute to the formation of the active enhancer repertoire, transcriptome and differential signal-specific gene regulation of polarized macrophages.			
28763207	chr7	148804454	148806454	EZH2		human		High+Lowthroughput	Inhibition of Human Enhancer of Zeste Homolog 2 with Tambjamine Analogs	否				E_01_0066	Immunofluorescence staining		Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq				Immunohistochemical staining		EZH2		Immunofluorescence staining				
28763207	chr9	128680837	128682837	SET		human		High+Lowthroughput	Inhibition of Human Enhancer of Zeste Homolog 2 with Tambjamine Analogs	否				E_01_0066	Immunofluorescence staining		Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq				Immunohistochemical staining				Immunofluorescence staining				SET
28763207	chr12	19401102	19403102	AEBP2		human		High+Lowthroughput	Inhibition of Human Enhancer of Zeste Homolog 2 with Tambjamine Analogs	否				E_01_0066	Immunofluorescence staining		Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq				Immunohistochemical staining				Immunofluorescence staining				AEBP2
28752422	chr16	15702106	15704106	Cebpd	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	mouse	Bone	High+Lowthroughput	Regulation of Clock Genes by Adrenergic Receptor Signaling in Osteoblasts	否			cementoblast	E_02_0044		These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.		These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	Immunohistochemical staining	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.							Cebpd
28752422	chr14	46618115	46620115	Bmp4	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	mouse	Bone	High+Lowthroughput	Regulation of Clock Genes by Adrenergic Receptor Signaling in Osteoblasts	否			cementoblast	E_02_0044		These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.		These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	Immunohistochemical staining	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.							Bmp4
28752422	chr13	53118269	53120269	Nfil3	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	mouse	Bone	High+Lowthroughput	Regulation of Clock Genes by Adrenergic Receptor Signaling in Osteoblasts	否			cementoblast	E_02_0044		These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.		These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.	Immunohistochemical staining	These findings suggest that the effects of Cebpd are due to the circadian regulation of Bmp4 expression, at least in part, by the up-regulated expression of the clock gene Nfil3 in response to α1B-AR signaling in osteoblasts.							Nfil3
28744818	chr9	81580972	81582972	TLE1	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice	mouse	Small intestine	High+Lowthroughput	Epigenetic modification of TLE1 induce abnormal differentiation in diabetic mice intestinal epithelium	否		diabetes mellitus	enterocyte	E_02_0045	Western Blot,RT-PCR,Dual-luciferase reporter assay	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice		Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice	Immunohistochemical staining	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice			Western Blot,RT-PCR,Dual-luciferase reporter assay				TLE1
28744818	chr16	29880216	29882216	Hes1	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice	mouse	Small intestine	High+Lowthroughput	Epigenetic modification of TLE1 induce abnormal differentiation in diabetic mice intestinal epithelium	否		diabetes mellitus	enterocyte	E_02_0045	Western Blot,RT-PCR,Dual-luciferase reporter assay	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice		Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice	Immunohistochemical staining	Subsequently, TLE1, through the transcriptional suppression on expression of Hes1, contributes to the aberrant differentiation of IECs in DM mice			Western Blot,RT-PCR,Dual-luciferase reporter assay				Hes1
28722764	chr7	148804258	148806258	EZH2	We previously demonstrated that Enhancer Zeste of Homolog 2 (EZH2), the catalytic subunits of PRC2 complex, contributes to inhibit muscle differentiation in eRMS and its down-regulation causes a partial recovery of myogenesis.	human		High+Lowthroughput	12-O-tetradecanoylphorbol-13-acetate and EZH2 inhibition: A novel approach for promoting myogenic differentiation in embryonal rhabdomyosarcoma cells	否		Rhabdomyosarcoma	myocyte	E_01_0067	Western blot,Real-Time PCR	We previously demonstrated that Enhancer Zeste of Homolog 2 (EZH2), the catalytic subunits of PRC2 complex, contributes to inhibit muscle differentiation in eRMS and its down-regulation causes a partial recovery of myogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We previously demonstrated that Enhancer Zeste of Homolog 2 (EZH2), the catalytic subunits of PRC2 complex, contributes to inhibit muscle differentiation in eRMS and its down-regulation causes a partial recovery of myogenesis.	Immunohistochemical staining	We previously demonstrated that Enhancer Zeste of Homolog 2 (EZH2), the catalytic subunits of PRC2 complex, contributes to inhibit muscle differentiation in eRMS and its down-regulation causes a partial recovery of myogenesis.	EZH2		Western blot,Real-Time PCR	We previously demonstrated that Enhancer Zeste of Homolog 2 (EZH2), the catalytic subunits of PRC2 complex, contributes to inhibit muscle differentiation in eRMS and its down-regulation causes a partial recovery of myogenesis.			
28720764	chr7	148804667	148806667	EZH2	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.	mouse	Bone marrow	High+Lowthroughput	High expression of ABCG2 induced by EZH2 disruption has pivotal roles in MDS pathogenesis	否		myelodysplastic syndromes	bone marrow cell	E_02_0046	SQ-RT-PCR,ChIP	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.		The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.	Immunohistochemical staining	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.			SQ-RT-PCR,ChIP				EZH2
28720764	chr6	58558640	58560640	Abcg2	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.	mouse	Bone marrow	High+Lowthroughput	High expression of ABCG2 induced by EZH2 disruption has pivotal roles in MDS pathogenesis	否		myelodysplastic syndromes	bone marrow cell	E_02_0046	SQ-RT-PCR,ChIP	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.		The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.	Immunohistochemical staining	The present results indicate that Abcg2 derepression induced by EZH2 mutations play crucial roles in MDS pathogenesis.			SQ-RT-PCR,ChIP				Abcg2
28718381	chr7	148804593	148806593	EZH2	Third, the involvement of EZH2 and epigenetic changes as shown in this study lends further support for the notion that endometriosis is an epigenetic disease79 and justifies the use of HDACIs as therapeutics for endometriosis.	human	Ectopic endometrial tissue	High+Lowthroughput	Histological and Immunohistochemical Characterization of the Similarity and Difference Between Ovarian Endometriomas and Deep Infiltrating Endometriosis	否		Ovarian endometrioma (OMA) and deep infiltrating endometriosis (DIE)	endothelial cell	E_01_0068	immunostaining	Third, the involvement of EZH2 and epigenetic changes as shown in this study lends further support for the notion that endometriosis is an epigenetic disease79 and justifies the use of HDACIs as therapeutics for endometriosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Third, the involvement of EZH2 and epigenetic changes as shown in this study lends further support for the notion that endometriosis is an epigenetic disease79 and justifies the use of HDACIs as therapeutics for endometriosis.	Immunohistochemical staining	Third, the involvement of EZH2 and epigenetic changes as shown in this study lends further support for the notion that endometriosis is an epigenetic disease79 and justifies the use of HDACIs as therapeutics for endometriosis.	EZH2		immunostaining	Third, the involvement of EZH2 and epigenetic changes as shown in this study lends further support for the notion that endometriosis is an epigenetic disease79 and justifies the use of HDACIs as therapeutics for endometriosis.			
28681918	chr7	148804320	148806320	EZH2	Human gene of enhancer of zeste homolog 2 (EZH2) was originally found to encode a histone methyltransferase forming the catalytic component of the polycomb repressive complex-2, thus exerting functional regulations on epigenetic silencing during the process of cell fate decisions	human	Cervical epithelial tissue	High+Lowthroughput	MicroRNA-137 is negatively associated with clinical outcome and regulates tumor development through EZH2 in cervical cancer	否		cervical cancer	CC cell line	E_01_0069	qPCR,Dual-luciferase reporter assay	Human gene of enhancer of zeste homolog 2 (EZH2) was originally found to encode a histone methyltransferase forming the catalytic component of the polycomb repressive complex-2, thus exerting functional regulations on epigenetic silencing during the process of cell fate decisions	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Human gene of enhancer of zeste homolog 2 (EZH2) was originally found to encode a histone methyltransferase forming the catalytic component of the polycomb repressive complex-2, thus exerting functional regulations on epigenetic silencing during the process of cell fate decisions	Immunohistochemical staining	Human gene of enhancer of zeste homolog 2 (EZH2) was originally found to encode a histone methyltransferase forming the catalytic component of the polycomb repressive complex-2, thus exerting functional regulations on epigenetic silencing during the process of cell fate decisions	EZH2		qPCR,Dual-luciferase reporter assay	Human gene of enhancer of zeste homolog 2 (EZH2) was originally found to encode a histone methyltransferase forming the catalytic component of the polycomb repressive complex-2, thus exerting functional regulations on epigenetic silencing during the process of cell fate decisions			
28681114	chr7	148804493	148806493	EZH2	Enhancer of zeste homolog 2 (EZH2), a stemness factor, plays roles in regulation of cell differentiation and embryonic development as well as cancer progression.	human	Tumor	High+Lowthroughput	Predicting the Correlation of EZH2 and Cancer Stem Cell Markers in Esophageal Squamous Cell Carcinoma	否		Esophageal Squamous Cell Carcinoma	Cancer Stem Cell	E_01_0070	qRT-PCR	Enhancer of zeste homolog 2 (EZH2), a stemness factor, plays roles in regulation of cell differentiation and embryonic development as well as cancer progression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2 (EZH2), a stemness factor, plays roles in regulation of cell differentiation and embryonic development as well as cancer progression.	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2), a stemness factor, plays roles in regulation of cell differentiation and embryonic development as well as cancer progression.	EZH2		qRT-PCR	Enhancer of zeste homolog 2 (EZH2), a stemness factor, plays roles in regulation of cell differentiation and embryonic development as well as cancer progression.			
28621459	chr1	39078887	39080887	MACF1	Microtubule actin crosslinking factor 1 (MACF1), a key cytoskeletal linker, has been shown to play key roles in signal transduction and in diverse cellular processes	human,mouse	Bone	High+Lowthroughput	Microtubule actin crosslinking factor 1 promotes osteoblast differentiation by promoting β-catenin/TCF1/Runx2 signaling axis	否		Osteoblast differentiation	cementoblast	E_02_0047	Western blot,Real time PCR	Microtubule actin crosslinking factor 1 (MACF1), a key cytoskeletal linker, has been shown to play key roles in signal transduction and in diverse cellular processes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Microtubule actin crosslinking factor 1 (MACF1), a key cytoskeletal linker, has been shown to play key roles in signal transduction and in diverse cellular processes		Microtubule actin crosslinking factor 1 (MACF1), a key cytoskeletal linker, has been shown to play key roles in signal transduction and in diverse cellular processes	Immunohistochemical staining	Microtubule actin crosslinking factor 1 (MACF1), a key cytoskeletal linker, has been shown to play key roles in signal transduction and in diverse cellular processes			Western blot,Real time PCR				MACF1
28621459	chr4	108044719	108046719	LEF1	It has been demonstrated that TCF1 but not LEF1 binds directly to Runx2 promoter in MC3T3-E1 cells and that Runx2 is a direct target of β-catenin/TCF1 for the stimulation of osteoblast differentiation	human,mouse	Bone	High+Lowthroughput	Microtubule actin crosslinking factor 1 promotes osteoblast differentiation by promoting β-catenin/TCF1/Runx2 signaling axis	否		Osteoblast differentiation	cementoblast	E_02_0047	Western blot,Real time PCR	It has been demonstrated that TCF1 but not LEF1 binds directly to Runx2 promoter in MC3T3-E1 cells and that Runx2 is a direct target of β-catenin/TCF1 for the stimulation of osteoblast differentiation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	It has been demonstrated that TCF1 but not LEF1 binds directly to Runx2 promoter in MC3T3-E1 cells and that Runx2 is a direct target of β-catenin/TCF1 for the stimulation of osteoblast differentiation		It has been demonstrated that TCF1 but not LEF1 binds directly to Runx2 promoter in MC3T3-E1 cells and that Runx2 is a direct target of β-catenin/TCF1 for the stimulation of osteoblast differentiation	Immunohistochemical staining	It has been demonstrated that TCF1 but not LEF1 binds directly to Runx2 promoter in MC3T3-E1 cells and that Runx2 is a direct target of β-catenin/TCF1 for the stimulation of osteoblast differentiation			Western blot,Real time PCR				LEF1
28462489	chr5	179729425	179731425	MAML1	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.	human	Tumor	High+Lowthroughput	Role of MAML1 and MEIS1 in Esophageal Squamous Cell Carcinoma Depth of Invasion	否		esophageal squamous cell carcinoma	tumor cell	E_01_0071	qRT-PCR	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.		In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.	Immunohistochemical staining	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.			qRT-PCR				MAML1
28462489	chr2	66430871	66432871	MEIS1	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.	human	Tumor	High+Lowthroughput	Role of MAML1 and MEIS1 in Esophageal Squamous Cell Carcinoma Depth of Invasion	否		esophageal squamous cell carcinoma	tumor cell	E_01_0071	qRT-PCR	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.		In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.	Immunohistochemical staining	In the present study, we analyzed cross talk between NOTCH pathway and HOX genes through assessment of probable correlation betweenMAML1 and MEIS1 as the main transcription factor of NOTCH pathway and enhancer of HOX transcriptional machinery, respectively in esophageal squamous cell carcinoma (ESCC) patients.			qRT-PCR				MEIS1
28442495	chr13	27958465	27960465	CDX2	CDX2, a transcription factor required to form intestinal epithelium, is a target of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, which can be inhibited by aspirin.	human		High+Lowthroughput	Aspirin prevents NF-κB activation and CDX2 expression stimulated by acid and bile salts in oesophageal squamous cells of patients with Barrett's oesophagus	否		Esophageal Diseases	oesophageal squamous cell	E_01_0072	Western blot	CDX2, a transcription factor required to form intestinal epithelium, is a target of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, which can be inhibited by aspirin.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			CDX2, a transcription factor required to form intestinal epithelium, is a target of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, which can be inhibited by aspirin.	Immunohistochemical staining	CDX2, a transcription factor required to form intestinal epithelium, is a target of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, which can be inhibited by aspirin.	CDX2		Western blot	CDX2, a transcription factor required to form intestinal epithelium, is a target of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signalling, which can be inhibited by aspirin.			
28115742	chr5	88714348	88716348	MEF2C	However, neurodevelopmental factors play an important role in schizophrenia,and alterations in MEF2C and other TF expression may have impacted diseased brains at earlier periods of pre- and postnatal life	human,mouse	Brain tissue	High+Lowthroughput	MEF2C transcription factor is associated with the genetic and epigenetic risk architecture of schizophrenia and improves cognition in mice	否		schizophrenia and related disorders	pluripotent stem cell	E_02_0048	ChIP-seq,ChIP-PCR	However, neurodevelopmental factors play an important role in schizophrenia,and alterations in MEF2C and other TF expression may have impacted diseased brains at earlier periods of pre- and postnatal life	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, neurodevelopmental factors play an important role in schizophrenia,and alterations in MEF2C and other TF expression may have impacted diseased brains at earlier periods of pre- and postnatal life		However, neurodevelopmental factors play an important role in schizophrenia,and alterations in MEF2C and other TF expression may have impacted diseased brains at earlier periods of pre- and postnatal life	Immunohistochemical staining	However, neurodevelopmental factors play an important role in schizophrenia,and alterations in MEF2C and other TF expression may have impacted diseased brains at earlier periods of pre- and postnatal life			ChIP-seq,ChIP-PCR				MEF2C
28027119	chr4	108044503	108046503	LEF1	Lymphoid enhancer-factor 1 (LEF1), a recently emerged marker, is part of the Wnt pathway with b-catenin but has not been studied in DTF	human	Soft tissue	High+Lowthroughput	Comparison of β-Catenin and LEF1 Immunohistochemical Stains in Desmoid-type Fibromatosis and its Selected Mimickers, With Unexpected Finding of LEF1 Positivity in Scars	否		desmoid-type fibromatosis		E_01_0073	Immunohistochemical staining	Lymphoid enhancer-factor 1 (LEF1), a recently emerged marker, is part of the Wnt pathway with b-catenin but has not been studied in DTF	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Lymphoid enhancer-factor 1 (LEF1), a recently emerged marker, is part of the Wnt pathway with b-catenin but has not been studied in DTF	Immunohistochemical staining	Lymphoid enhancer-factor 1 (LEF1), a recently emerged marker, is part of the Wnt pathway with b-catenin but has not been studied in DTF	LEF1		Immunohistochemical staining	Lymphoid enhancer-factor 1 (LEF1), a recently emerged marker, is part of the Wnt pathway with b-catenin but has not been studied in DTF			
27997051	chr7	44101517	44103517	AEBP1	Adipocyte enhancer binding protein 1 (AEBP1) activates inflammatory responses via the NF-κB pathway in macrophages and regulates adipogenesis in preadipocytes	human	Hippocampal tissue	High+Lowthroughput	Association of adipocyte enhancer-binding protein 1 with Alzheimer's disease pathology in human hippocampi	否		Alzheimer’s disease	smooth muscle cell line	E_01_0074	Western blot	Adipocyte enhancer binding protein 1 (AEBP1) activates inflammatory responses via the NF-κB pathway in macrophages and regulates adipogenesis in preadipocytes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Adipocyte enhancer binding protein 1 (AEBP1) activates inflammatory responses via the NF-κB pathway in macrophages and regulates adipogenesis in preadipocytes		Adipocyte enhancer binding protein 1 (AEBP1) activates inflammatory responses via the NF-κB pathway in macrophages and regulates adipogenesis in preadipocytes	Immunohistochemical staining	Adipocyte enhancer binding protein 1 (AEBP1) activates inflammatory responses via the NF-κB pathway in macrophages and regulates adipogenesis in preadipocytes			Western blot				AEBP1
27845419	chr7	87500277	87502277	ABCB1	These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.	human	Liver	High+Lowthroughput	ABC transporter polymorphisms are associated with irinotecan pharmacokinetics and neutropenia	是	rs12720066,rs6498588	Neutropenia	Hep G2 cell	E_01_0075	Enhancer Assay	These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.	Immunohistochemical staining	These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.	ABCB1		Enhancer Assay	These results suggest that genetic variation in ABCC1 and ABCB1 may contribute to irinotecan-induced neutropenia by altering expression of transporters involved in irinotecan metabolite disposition.			
26842780	chr22	39517640	39519640	ATF4	While suppressing general protein translation, eIF2α phosphorylation also promotes the selective translation of some mRNAs, such as ATF4 that induces CCAAT/enhancer binding homologous protein (CHOP), a pro-apoptotic transcription factor.	human,mouse	Spinal cord tissue	High+Lowthroughput	Activating Transcription Factor-6α Deletion Modulates the Endoplasmic Reticulum Stress Response after Spinal Cord Injury but Does Not Affect Locomotor Recovery	否		Spinal cord injury	Oligodendrocytes	E_02_0049	Western blot,RT-PCR	While suppressing general protein translation, eIF2α phosphorylation also promotes the selective translation of some mRNAs, such as ATF4 that induces CCAAT/enhancer binding homologous protein (CHOP), a pro-apoptotic transcription factor.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	While suppressing general protein translation, eIF2α phosphorylation also promotes the selective translation of some mRNAs, such as ATF4 that induces CCAAT/enhancer binding homologous protein (CHOP), a pro-apoptotic transcription factor.		While suppressing general protein translation, eIF2α phosphorylation also promotes the selective translation of some mRNAs, such as ATF4 that induces CCAAT/enhancer binding homologous protein (CHOP), a pro-apoptotic transcription factor.	Immunohistochemical staining	While suppressing general protein translation, eIF2α phosphorylation also promotes the selective translation of some mRNAs, such as ATF4 that induces CCAAT/enhancer binding homologous protein (CHOP), a pro-apoptotic transcription factor.			Western blot,RT-PCR				ATF4
28860350	chr2	43219398	43221398	ZFP36L2	Notably, ZFP36L2 is associated with super-enhancer in healthy oesophageal mucosa; Dna hypermethylation in its super-enhancer reduced active histone markers in squamous cancer cells, suggesting an epigenetic inactivation of a super-enhancerassociated Scc suppressor	human	Non-malignant oesophagus tissue	High+Lowthroughput	Identification of distinct mutational patterns and new driver genes in oesophageal squamous cell carcinomas and adenocarcinomas	否		Oesophageal squamous cell carcinoma (OScc) and adenocarcinoma (Oac)	squamous cell line	E_01_0076	ChIP-seq,WGBS	Notably, ZFP36L2 is associated with super-enhancer in healthy oesophageal mucosa; Dna hypermethylation in its super-enhancer reduced active histone markers in squamous cancer cells, suggesting an epigenetic inactivation of a super-enhancerassociated Scc suppressor	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Notably, ZFP36L2 is associated with super-enhancer in healthy oesophageal mucosa; Dna hypermethylation in its super-enhancer reduced active histone markers in squamous cancer cells, suggesting an epigenetic inactivation of a super-enhancerassociated Scc suppressor		Notably, ZFP36L2 is associated with super-enhancer in healthy oesophageal mucosa; Dna hypermethylation in its super-enhancer reduced active histone markers in squamous cancer cells, suggesting an epigenetic inactivation of a super-enhancerassociated Scc suppressor	Immunohistochemical staining	Notably, ZFP36L2 is associated with super-enhancer in healthy oesophageal mucosa; Dna hypermethylation in its super-enhancer reduced active histone markers in squamous cancer cells, suggesting an epigenetic inactivation of a super-enhancerassociated Scc suppressor			ChIP-seq,WGBS				ZFP36L2
29028630	chr7	148804878	148806878	EZH2	EZH2 plays an important role in this inflammatory process of dental pulp.	human,mouse	dental pulp tissue	High+Lowthroughput	EZH2 regulates dental pulp inflammation by direct effect on inflammatory factors	否		dental pulp inflammation	dental pulp cell	E_02_0050	qPCR,ChIP,Western blot	EZH2 plays an important role in this inflammatory process of dental pulp.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EZH2 plays an important role in this inflammatory process of dental pulp.		EZH2 plays an important role in this inflammatory process of dental pulp.	Immunohistochemical staining	EZH2 plays an important role in this inflammatory process of dental pulp.			qPCR,ChIP,Western blot				EZH2
31980609	chr1	47213215	47215215	TAL1	Allele-specific targeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer progression in xenotransplants.	mouse	lymph	High+Lowthroughput	Interrogation of enhancer function by enhancer_x0002_targeting CRISPR epigenetic editing	否	无		K562 cell，Jurkat cell	E_02_0051	Flow cytometry, cell viability detection, QRT PCR, Western blot, RNA SEQ, chip SEQ,	Allele-specific targeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer progression in xenotransplants.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Allele-specific targeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer progression in xenotransplants.		Allele-specific targeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer progression in xenotransplants.	Immunohistochemical staining	Allele-specific targeting of enCRISPRa to oncogenic TAL1 super-enhancer modulates TAL1 expression and cancer progression in xenotransplants.			流式细胞术，细胞活力检测， qRT-PCR ，Western blot，RNA-seq，ChIP-seq，				TAL1
31980500	chr2	233757381	233759381	UGT1A1	An LXR specific enhancer site on the UGT1A1 gene was identified, along with convincing evidence that LXRα is crucial in maintaining constitutive expression of UGT1A1 in adult hUGT1 mice.	mouse	Liver, kidney	High+Lowthroughput	Differential role of LXRα and LXRβ in the regulation of UDP-glucuronosyltransferase 1A1 in humanized UGT1 mice	否	无	hepatic fibrosis 	HepG2，HK293 cell	E_02_0052	QRT PCR, Western blot, glucuronidation assay, transfection, chromatin immunoprecipitation assay, agarose gel electrophoresis	An LXR specific enhancer site on the UGT1A1 gene was identified, along with convincing evidence that LXRα is crucial in maintaining constitutive expression of UGT1A1 in adult hUGT1 mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	An LXR specific enhancer site on the UGT1A1 gene was identified, along with convincing evidence that LXRα is crucial in maintaining constitutive expression of UGT1A1 in adult hUGT1 mice.		An LXR specific enhancer site on the UGT1A1 gene was identified, along with convincing evidence that LXRα is crucial in maintaining constitutive expression of UGT1A1 in adult hUGT1 mice.	Immunohistochemical staining	An LXR specific enhancer site on the UGT1A1 gene was identified, along with convincing evidence that LXRα is crucial in maintaining constitutive expression of UGT1A1 in adult hUGT1 mice.			qRT-PCR，Western Blot，葡萄糖醛酸化分析，转染，染色质免疫沉淀分析，琼脂糖凝胶电泳				UGT1A1
31975641	chr1	118880199	118882199	TBX15	Our findings from GWAS index, proxy, and imputed SNPs suggest that a few SNPs, including three in a 0.7-kb cluster, act as causal regulatory variants to fine-tune TBX15 expression and, thereby, affect both obesity and osteoporosis risk.	human	bone marrow	High+Lowthroughput	Osteoporosis- and obesity-risk interrelationships: an epigenetic analysis of GWAS-derived SNPs at the developmental gene TBX15	是	Rs10494217， rs61730011，rs984222，rs1106529，rs9659323，rs12742627，, rs961470，rs17023223	Osteoporosis	cementoblast	E_01_0077	RNA SEQ, GWAS derived SNPs and LD analysis	Our findings from GWAS index, proxy, and imputed SNPs suggest that a few SNPs, including three in a 0.7-kb cluster, act as causal regulatory variants to fine-tune TBX15 expression and, thereby, affect both obesity and osteoporosis risk.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our findings from GWAS index, proxy, and imputed SNPs suggest that a few SNPs, including three in a 0.7-kb cluster, act as causal regulatory variants to fine-tune TBX15 expression and, thereby, affect both obesity and osteoporosis risk.	Immunohistochemical staining	Our findings from GWAS index, proxy, and imputed SNPs suggest that a few SNPs, including three in a 0.7-kb cluster, act as causal regulatory variants to fine-tune TBX15 expression and, thereby, affect both obesity and osteoporosis risk.	TBX15		 RNA-seq，GWAS衍生的SNPs和LD分析	Our findings from GWAS index, proxy, and imputed SNPs suggest that a few SNPs, including three in a 0.7-kb cluster, act as causal regulatory variants to fine-tune TBX15 expression and, thereby, affect both obesity and osteoporosis risk.			
31969149	chr1	8001716	8003716	ERRFI1	 The minor allele rs72635708 (rs72635708-C) might affect the ERRFI1 promoter activity, which results in unstable expression of ERRFI1, enhancing the risk of psoriasis via disruption of lipid metabolism and skin cell proliferation. 	human	lung	High+Lowthroughput	An integrated analysis of public genomic data unveils a possible functional mechanism of psoriasis risk via a long-range ERRFI1 enhancer	是	rs72635708	psoriasis	IMR-90 cell	E_01_0078	ChIP-seq	 The minor allele rs72635708 (rs72635708-C) might affect the ERRFI1 promoter activity, which results in unstable expression of ERRFI1, enhancing the risk of psoriasis via disruption of lipid metabolism and skin cell proliferation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 The minor allele rs72635708 (rs72635708-C) might affect the ERRFI1 promoter activity, which results in unstable expression of ERRFI1, enhancing the risk of psoriasis via disruption of lipid metabolism and skin cell proliferation. 		 The minor allele rs72635708 (rs72635708-C) might affect the ERRFI1 promoter activity, which results in unstable expression of ERRFI1, enhancing the risk of psoriasis via disruption of lipid metabolism and skin cell proliferation. 	Immunohistochemical staining	 The minor allele rs72635708 (rs72635708-C) might affect the ERRFI1 promoter activity, which results in unstable expression of ERRFI1, enhancing the risk of psoriasis via disruption of lipid metabolism and skin cell proliferation. 			ChIP-seq				ERRFI1
31968281	chr16	88712787	88714787	PIEZO1	Our results first suggested that SNP rs62048221 might mediate the PIEZO1 expression level via modulating the activity of cis-regulatory elements and then further affect the BMD.	mouse	bone marrow	High+Lowthroughput	Identification of PIEZO1 polymorphisms for human bone mineral density	是	rs62048221	Osteoporotic fracture	mesenchymal stem cell	E_02_0053	Luciferase reporter assay, chip qPCR	Our results first suggested that SNP rs62048221 might mediate the PIEZO1 expression level via modulating the activity of cis-regulatory elements and then further affect the BMD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results first suggested that SNP rs62048221 might mediate the PIEZO1 expression level via modulating the activity of cis-regulatory elements and then further affect the BMD.		Our results first suggested that SNP rs62048221 might mediate the PIEZO1 expression level via modulating the activity of cis-regulatory elements and then further affect the BMD.	Immunohistochemical staining	Our results first suggested that SNP rs62048221 might mediate the PIEZO1 expression level via modulating the activity of cis-regulatory elements and then further affect the BMD.			荧光素酶报告分析，ChIP-qPCR 				PIEZO1
31967103	chr7	148804333	148806333	EZH2	We tested UNC1999, a small molecule inhibitor that blocks enhancer of zeste homolog 2, an enzyme that maintains closed polycomb chromatin. 	human	kidney	High+Lowthroughput	Site-directed targeting of transcriptional activation-associated proteins to repressed chromatin restores CRISPR activity	否	无		HEK293 cell	E_01_0079	Transfection, luciferase assay, flow cytometry, chip qPCR,	We tested UNC1999, a small molecule inhibitor that blocks enhancer of zeste homolog 2, an enzyme that maintains closed polycomb chromatin. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We tested UNC1999, a small molecule inhibitor that blocks enhancer of zeste homolog 2, an enzyme that maintains closed polycomb chromatin. 	Immunohistochemical staining	We tested UNC1999, a small molecule inhibitor that blocks enhancer of zeste homolog 2, an enzyme that maintains closed polycomb chromatin. 	EZH2		转染，荧光素酶分析，流式细胞术，ChIP-qPCR，	We tested UNC1999, a small molecule inhibitor that blocks enhancer of zeste homolog 2, an enzyme that maintains closed polycomb chromatin. 			
31963554	chr10	52311442	52313442	DKK1	Taken together, these observations suggest that 1,25D3 promotes the mineralization of osteoblasts through activation of DKK1 followed by an increase of C/EBPβ.	human	Bone, mesenchymal tissue	High+Lowthroughput	DKK1 Induced by 1,25D3 Is Required for the Mineralization of Osteoblasts	否	无	Osteoporosis	osteogenitorcell,cementoblast，SaOS2 cell	E_01_0080	QPCR, Western blot, immunofluorescence, luciferase assay, chromatin immunoprecipitation assay	Taken together, these observations suggest that 1,25D3 promotes the mineralization of osteoblasts through activation of DKK1 followed by an increase of C/EBPβ.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, these observations suggest that 1,25D3 promotes the mineralization of osteoblasts through activation of DKK1 followed by an increase of C/EBPβ.		Taken together, these observations suggest that 1,25D3 promotes the mineralization of osteoblasts through activation of DKK1 followed by an increase of C/EBPβ.	Immunohistochemical staining	Taken together, these observations suggest that 1,25D3 promotes the mineralization of osteoblasts through activation of DKK1 followed by an increase of C/EBPβ.			qPCR，Western Blot，免疫荧光，荧光素酶分析，染色质免疫沉淀分析				DKK1
31961892	chr11	55334650	55336650	Atox1	Nuclear translocation of Atox1 potentiates activin A-induced cell migration and colony formation in colon cancer	human	colon	High+Lowthroughput	Nuclear translocation of Atox1 potentiates activin A-induced cell migration and colony formation in colon cancer	否	无	Colon cancer	SW480 cell	E_01_0081	Immunofluorescence, Western blot, transfection, cell colony assay	Nuclear translocation of Atox1 potentiates activin A-induced cell migration and colony formation in colon cancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Nuclear translocation of Atox1 potentiates activin A-induced cell migration and colony formation in colon cancer		Nuclear translocation of Atox1 potentiates activin A-induced cell migration and colony formation in colon cancer	Immunohistochemical staining	Nuclear translocation of Atox1 potentiates activin A-induced cell migration and colony formation in colon cancer			免疫荧光，Western blot，转染，细胞集落实验				Atox1
31954402	chr7	148804633	148806633	EZH2	Expression of enhancer of zeste homolog 2 (EZH2) was significantly (P < 0.01) down regulated indicating that genes involved in epigenetic regulation are also differentially expressed in SD patients during the early stage of infection.	human	blood	High+Lowthroughput	Differential expression of microRNA, miR-150 and enhancer of zeste homolog 2 (EZH2) in peripheral blood cells as early prognostic markers of severe forms of dengue	否	无	dengue fever		E_01_0082	qRT-PCR	Expression of enhancer of zeste homolog 2 (EZH2) was significantly (P < 0.01) down regulated indicating that genes involved in epigenetic regulation are also differentially expressed in SD patients during the early stage of infection.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Expression of enhancer of zeste homolog 2 (EZH2) was significantly (P < 0.01) down regulated indicating that genes involved in epigenetic regulation are also differentially expressed in SD patients during the early stage of infection.	Immunohistochemical staining	Expression of enhancer of zeste homolog 2 (EZH2) was significantly (P < 0.01) down regulated indicating that genes involved in epigenetic regulation are also differentially expressed in SD patients during the early stage of infection.	EZH2		qRT-PCR	Expression of enhancer of zeste homolog 2 (EZH2) was significantly (P < 0.01) down regulated indicating that genes involved in epigenetic regulation are also differentially expressed in SD patients during the early stage of infection.			
31953940	chr4	108045068	108047068	LEF1	LEF1 is not expressed in most CD5-positive MZLs and LPLs; therefore, it is a reliable marker for distinguishing them from CLL/SLL. LEF1 may be expressed in CD5-positive FLs.	human		High+Lowthroughput	Immunohistochemical Expression of Lymphoid Enhancer Binding Factor 1 in CD5-Positive Marginal Zone, Lymphoplasmacytic, and Follicular Lymphomas.	否	无	Lymphoplasmacytoma, follicular lymphoma	tumor cell	E_01_0083	Immunohistochemistry, flow cytometry, fluorescence in situ hybridization, QRT PCR	LEF1 is not expressed in most CD5-positive MZLs and LPLs; therefore, it is a reliable marker for distinguishing them from CLL/SLL. LEF1 may be expressed in CD5-positive FLs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			LEF1 is not expressed in most CD5-positive MZLs and LPLs; therefore, it is a reliable marker for distinguishing them from CLL/SLL. LEF1 may be expressed in CD5-positive FLs.	Immunohistochemical staining	LEF1 is not expressed in most CD5-positive MZLs and LPLs; therefore, it is a reliable marker for distinguishing them from CLL/SLL. LEF1 may be expressed in CD5-positive FLs.	LEF1		免疫组化，流式细胞术，荧光原位杂交技术，qRT-PCR	LEF1 is not expressed in most CD5-positive MZLs and LPLs; therefore, it is a reliable marker for distinguishing them from CLL/SLL. LEF1 may be expressed in CD5-positive FLs.			
31953319	chr22	39516679	39518679	ATF4	Activating transcription factor 4 (ATF4) promotes skeletal muscle atrophy by forming a heterodimer with the transcriptional regulator C/EBPβ.	human	skeletal muscle	High+Lowthroughput	Activating transcription factor 4 (ATF4) promotes skeletal muscle atrophy by forming a heterodimer with the transcriptional regulator C/EBPβ	否	无	Skeletal muscle atrophy	mouse cell of skeletal muscle	E_01_0084	Western blot, transfection, qPCR, agarose gel electrophoresis	Activating transcription factor 4 (ATF4) promotes skeletal muscle atrophy by forming a heterodimer with the transcriptional regulator C/EBPβ.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Activating transcription factor 4 (ATF4) promotes skeletal muscle atrophy by forming a heterodimer with the transcriptional regulator C/EBPβ.	Immunohistochemical staining	Activating transcription factor 4 (ATF4) promotes skeletal muscle atrophy by forming a heterodimer with the transcriptional regulator C/EBPβ.	ATF4		Western Blot，转染，qPCR，琼脂糖凝胶电泳	Activating transcription factor 4 (ATF4) promotes skeletal muscle atrophy by forming a heterodimer with the transcriptional regulator C/EBPβ.			
31952907	chr7	148804371	148806371	EZH2	Taken together, EZH2 in CD4 T cells from RA patients was attenuated, which suppressed FOXP3 transcription through downregulating RUNX1 and upregulating SMAD7 in CD4 T cells, and ultimately suppressed Tregs differentiation. IL17 in RA synovial fluid might promote downregulation of EZH2 in CD4 T cells. Defective EZH2 in CD4 T cells might contribute to Treg deficiency in RA.	human	Connective tissue, peripheral blood	High+Lowthroughput	EZH2 deficiency attenuates Treg differentiation in rheumatoid arthritis	否	无	Rheumatoid arthritis	synovial cell，peripheral blood mononuclear cell，Jurkat T cell	E_01_0085	Western blot，RT-qPCR	Taken together, EZH2 in CD4 T cells from RA patients was attenuated, which suppressed FOXP3 transcription through downregulating RUNX1 and upregulating SMAD7 in CD4 T cells, and ultimately suppressed Tregs differentiation. IL17 in RA synovial fluid might promote downregulation of EZH2 in CD4 T cells. Defective EZH2 in CD4 T cells might contribute to Treg deficiency in RA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Taken together, EZH2 in CD4 T cells from RA patients was attenuated, which suppressed FOXP3 transcription through downregulating RUNX1 and upregulating SMAD7 in CD4 T cells, and ultimately suppressed Tregs differentiation. IL17 in RA synovial fluid might promote downregulation of EZH2 in CD4 T cells. Defective EZH2 in CD4 T cells might contribute to Treg deficiency in RA.	Immunohistochemical staining	Taken together, EZH2 in CD4 T cells from RA patients was attenuated, which suppressed FOXP3 transcription through downregulating RUNX1 and upregulating SMAD7 in CD4 T cells, and ultimately suppressed Tregs differentiation. IL17 in RA synovial fluid might promote downregulation of EZH2 in CD4 T cells. Defective EZH2 in CD4 T cells might contribute to Treg deficiency in RA.	EZH2		Western blot，RT-qPCR	Taken together, EZH2 in CD4 T cells from RA patients was attenuated, which suppressed FOXP3 transcription through downregulating RUNX1 and upregulating SMAD7 in CD4 T cells, and ultimately suppressed Tregs differentiation. IL17 in RA synovial fluid might promote downregulation of EZH2 in CD4 T cells. Defective EZH2 in CD4 T cells might contribute to Treg deficiency in RA.			
31951295	chr15	88633030	88635030	ISG20	Our findings suggest that ISG20 exerts the anti-HBV activity by acting as a putative repressor binding to the HBV EnhII/Cp region.	human	liver	High+Lowthroughput	Antiviral activity of interferon-stimulated gene 20, as a putative repressor binding to hepatitis B virus enhancer II and core promoter	否	无	hepatitis B	HepG2，HepG2 NTCP，HepAD38 cell	E_01_0086	Immunohistochemistry, luciferase analysis, transfection, Southern blot, Northern blot, Western blot, RT-PCR, chromatin immunoprecipitation analysis, microarray data analysis	Our findings suggest that ISG20 exerts the anti-HBV activity by acting as a putative repressor binding to the HBV EnhII/Cp region.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our findings suggest that ISG20 exerts the anti-HBV activity by acting as a putative repressor binding to the HBV EnhII/Cp region.		Our findings suggest that ISG20 exerts the anti-HBV activity by acting as a putative repressor binding to the HBV EnhII/Cp region.	Immunohistochemical staining	Our findings suggest that ISG20 exerts the anti-HBV activity by acting as a putative repressor binding to the HBV EnhII/Cp region.			免疫组化，荧光素酶分析，转染，Southern blot ，Northern blot，Western  blot，RT-PCR ，染色质免疫沉淀分析，微阵列数据分析				ISG20
31938642	chr9	81581120	81583120	TLE1	Frequency of Transducer-like Enhancer of Split 1 Immunohistochemical Expression in Synovial Sarcoma: An Institution-based Cross-sectional Study	human		High+Lowthroughput	Frequency of Transducer-like Enhancer of Split 1 Immunohistochemical Expression in Synovial Sarcoma: An Institution-based Cross-sectional Study	否	无	Soft tissue sarcoma		E_01_0087	Immunohistochemistry	Frequency of Transducer-like Enhancer of Split 1 Immunohistochemical Expression in Synovial Sarcoma: An Institution-based Cross-sectional Study	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Frequency of Transducer-like Enhancer of Split 1 Immunohistochemical Expression in Synovial Sarcoma: An Institution-based Cross-sectional Study	Immunohistochemical staining	Frequency of Transducer-like Enhancer of Split 1 Immunohistochemical Expression in Synovial Sarcoma: An Institution-based Cross-sectional Study	TLE1		免疫组化	Frequency of Transducer-like Enhancer of Split 1 Immunohistochemical Expression in Synovial Sarcoma: An Institution-based Cross-sectional Study			
31937792	chr9	78383023	78385023	Eef1a1	Efficient tissue-type specific expression of target genes in a tetracycline-controlled manner from the ubiquitously active Eef1a1 locus.	mouse	embryo	High+Lowthroughput	Efficient tissue-type specific expression of target genes in a tetracycline-controlled manner from the ubiquitously active Eef1a1 locus	否	无	tumour	embryonic stem cell	E_02_0054	Immunofluorescence, immunohistochemistry, he staining, Southern blot, PCR	Efficient tissue-type specific expression of target genes in a tetracycline-controlled manner from the ubiquitously active Eef1a1 locus.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Efficient tissue-type specific expression of target genes in a tetracycline-controlled manner from the ubiquitously active Eef1a1 locus.		Efficient tissue-type specific expression of target genes in a tetracycline-controlled manner from the ubiquitously active Eef1a1 locus.	Immunohistochemical staining	Efficient tissue-type specific expression of target genes in a tetracycline-controlled manner from the ubiquitously active Eef1a1 locus.			免疫荧光，免疫组化，HE染色，Southern blot，PCR				Eef1a1
31937612	chr5	69232027	69234027	CDK7	Targeting Super-Enhancer-Associated Oncogenes in Osteosarcoma with THZ2, a Covalent CDK7 Inhibitor	human	bone	High+Lowthroughput	Targeting Super-Enhancer-Associated Oncogenes in Osteosarcoma with THZ2, a Covalent CDK7 Inhibitor	否	无	Osteosarcoma	SJSA-1 cell，U2-OS cell，HOS cell，G-292 cell，MNNG/HOS cell，143B cell，MG-63 cell，cementoblast	E_01_0088	Chromatin immunoprecipitation, microarray, transfection, cell viability assay, Transwell, Western blot, RT qPCR	Targeting Super-Enhancer-Associated Oncogenes in Osteosarcoma with THZ2, a Covalent CDK7 Inhibitor	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Targeting Super-Enhancer-Associated Oncogenes in Osteosarcoma with THZ2, a Covalent CDK7 Inhibitor		Targeting Super-Enhancer-Associated Oncogenes in Osteosarcoma with THZ2, a Covalent CDK7 Inhibitor	Immunohistochemical staining	Targeting Super-Enhancer-Associated Oncogenes in Osteosarcoma with THZ2, a Covalent CDK7 Inhibitor			染色质免疫沉淀，微阵列，转染，细胞活力检测，Transwell，Western blot，RT-qPCR				CDK7
31933869	chr11	113406893	113408893	DRD2	This case-control evaluation involving the Chinese Han population suggests that the rs4648317 and rs7131056 polymorphisms and the haplotype GTGATCGCGCAGGC inside the DRD2 gene could be possible markers to forecast vulnerability to MDD.	human	Peripheral blood	High+Lowthroughput	Functional tag SNPs inside the DRD2 gene as a genetic risk factor for major depressive disorder in the Chinese Han population	是	rs4648317，rs7131056	Major depressive disorder	peripheral blood mononuclear cell	E_01_0089	PCR	This case-control evaluation involving the Chinese Han population suggests that the rs4648317 and rs7131056 polymorphisms and the haplotype GTGATCGCGCAGGC inside the DRD2 gene could be possible markers to forecast vulnerability to MDD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This case-control evaluation involving the Chinese Han population suggests that the rs4648317 and rs7131056 polymorphisms and the haplotype GTGATCGCGCAGGC inside the DRD2 gene could be possible markers to forecast vulnerability to MDD.		This case-control evaluation involving the Chinese Han population suggests that the rs4648317 and rs7131056 polymorphisms and the haplotype GTGATCGCGCAGGC inside the DRD2 gene could be possible markers to forecast vulnerability to MDD.	Immunohistochemical staining	This case-control evaluation involving the Chinese Han population suggests that the rs4648317 and rs7131056 polymorphisms and the haplotype GTGATCGCGCAGGC inside the DRD2 gene could be possible markers to forecast vulnerability to MDD.			PCR				DRD2
31933740	chr9	81580946	81582946	TLE1	TLE1 is a specific and sensitive diagnostic immunomarker for SS and can be helpful to distinguish SS from other mesenchymal neoplasms.	human		High+Lowthroughput	Transducer-like enhancer of split 1 (TLE1) as a novel biomarker for diagnosis of synovial sarcoma correlates with translocation t(X;18): a study of 155 cases in China	否	无	Synovial sarcoma		E_01_0090	Immunohistochemistry, fluorescence in situ hybridization	TLE1 is a specific and sensitive diagnostic immunomarker for SS and can be helpful to distinguish SS from other mesenchymal neoplasms.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TLE1 is a specific and sensitive diagnostic immunomarker for SS and can be helpful to distinguish SS from other mesenchymal neoplasms.	Immunohistochemical staining	TLE1 is a specific and sensitive diagnostic immunomarker for SS and can be helpful to distinguish SS from other mesenchymal neoplasms.	TLE1		免疫组化，荧光原位杂交	TLE1 is a specific and sensitive diagnostic immunomarker for SS and can be helpful to distinguish SS from other mesenchymal neoplasms.			
31932307	chr20	21508188	21510188	NKX2-2	The transcription factor NKX2-2 regulates oligodendrocyte differentiation through domain-specific interactions with transcriptional corepressors	mouse	brain	High+Lowthroughput	The transcription factor NKX2-2 regulates oligodendrocyte differentiation through domain-specific interactions with transcriptional corepressors	否	无		CG4 cell	E_02_0055	In situ hybridization, immunohistochemistry, immunofluorescence, CO immunoprecipitation, Western blot	The transcription factor NKX2-2 regulates oligodendrocyte differentiation through domain-specific interactions with transcriptional corepressors	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcription factor NKX2-2 regulates oligodendrocyte differentiation through domain-specific interactions with transcriptional corepressors		The transcription factor NKX2-2 regulates oligodendrocyte differentiation through domain-specific interactions with transcriptional corepressors	Immunohistochemical staining	The transcription factor NKX2-2 regulates oligodendrocyte differentiation through domain-specific interactions with transcriptional corepressors			原位杂交，免疫组化，免疫荧光，免疫共沉淀，Western blot				NKX2-2
31929803	chr4	108044497	108046497	LEF1	We conclude that high LEF1 expression was a favorable prognostic marker which can define AML patient risk and outcome independent from assessing the serum galectin.3 level.	human		High+Lowthroughput	Prognostic Impact of Lymphoid Enhancer Factor 1 Expression and Serum Galectin.3 in Egyptian AML Patients	否	无	Acute myeloid leukemia		E_01_0091	RT qPCR, ELISA	We conclude that high LEF1 expression was a favorable prognostic marker which can define AML patient risk and outcome independent from assessing the serum galectin.3 level.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We conclude that high LEF1 expression was a favorable prognostic marker which can define AML patient risk and outcome independent from assessing the serum galectin.3 level.	Immunohistochemical staining	We conclude that high LEF1 expression was a favorable prognostic marker which can define AML patient risk and outcome independent from assessing the serum galectin.3 level.	LEF1		RT-qPCR，联酶免疫吸附反应	We conclude that high LEF1 expression was a favorable prognostic marker which can define AML patient risk and outcome independent from assessing the serum galectin.3 level.			
31928966	chr6	10978082	10980082	ELOVL2	rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression	human	liver	High+Lowthroughput	rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression	是	rs953413	liver cancer	HepG2 cell	E_01_0092	As qPCR, chip SEQ, gene knockdown, QRT PCR, chromatin immunoprecipitation, luciferase reporter	rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression		rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression	Immunohistochemical staining	rs953413 Regulates Polyunsaturated Fatty Acid Metabolism by Modulating ELOVL2 Expression			AS-qPCR，ChIP-seq，基因敲除，qRT-PCR，染色质免疫沉淀，荧光素酶报告基因				ELOVL2
31927142	chr22	28791896	28793896	XBP1	Thus, XBP1 acts as an osmoprotective protein since it is activated by high osmolarity and upregulates lipid metabolism, membranes generation and the restoration of ER homeostasis.	mouse	kidney	High+Lowthroughput	X-box binding protein 1 (XBP1): A key protein for renal osmotic adaptation. Its role in lipogenic program regulation	否	无		MDCK cell	E_02_0056	Transfection, RT-PCR, Western blot, immunofluorescence	Thus, XBP1 acts as an osmoprotective protein since it is activated by high osmolarity and upregulates lipid metabolism, membranes generation and the restoration of ER homeostasis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, XBP1 acts as an osmoprotective protein since it is activated by high osmolarity and upregulates lipid metabolism, membranes generation and the restoration of ER homeostasis.		Thus, XBP1 acts as an osmoprotective protein since it is activated by high osmolarity and upregulates lipid metabolism, membranes generation and the restoration of ER homeostasis.	Immunohistochemical staining	Thus, XBP1 acts as an osmoprotective protein since it is activated by high osmolarity and upregulates lipid metabolism, membranes generation and the restoration of ER homeostasis.			转染，RT-PCR，Western blot，免疫荧光				XBP1
31915257	chr11	27652693	27654693	BDNF	CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons	mouse	brain	High+Lowthroughput	CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons	否	无			E_02_0057	RT qPCR, luciferase reporter assay, Western blot, immunocytochemistry, chromatin immunoprecipitation	CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons		CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons	Immunohistochemical staining	CREB family transcription factors are major mediators of BDNF transcriptional autoregulation in cortical neurons			RT-qPCR ，荧光素酶报告试验，Western blot，免疫细胞化学，染色质免疫沉淀				BDNF
31914694	chr7	148804420	148806420	EZH2	 In conclusion, our results proved that EZH2 inhibition alleviated renal pyroptosis by blocking Nox4-dependent ROS generation through ALK5/Smad2/3 signaling pathway, indicating that EZH2 could be a potential therapeutic target for renal I/R injury.	mouse	kidney	High+Lowthroughput	Enhancer of zeste homolog 2 modulates oxidative stress-mediated pyroptosis in vitro and in a mouse kidney ischemia-reperfusion injury model	否	无	Renal ischemia reperfusion injury	HK-2 cell	E_02_0058	RT-PCR, Western blot, he staining, immunohistochemistry, TUNEL staining, cell viability assay, luciferase reporter assay, transfection, immunofluorescence	 In conclusion, our results proved that EZH2 inhibition alleviated renal pyroptosis by blocking Nox4-dependent ROS generation through ALK5/Smad2/3 signaling pathway, indicating that EZH2 could be a potential therapeutic target for renal I/R injury.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 In conclusion, our results proved that EZH2 inhibition alleviated renal pyroptosis by blocking Nox4-dependent ROS generation through ALK5/Smad2/3 signaling pathway, indicating that EZH2 could be a potential therapeutic target for renal I/R injury.		 In conclusion, our results proved that EZH2 inhibition alleviated renal pyroptosis by blocking Nox4-dependent ROS generation through ALK5/Smad2/3 signaling pathway, indicating that EZH2 could be a potential therapeutic target for renal I/R injury.	Immunohistochemical staining	 In conclusion, our results proved that EZH2 inhibition alleviated renal pyroptosis by blocking Nox4-dependent ROS generation through ALK5/Smad2/3 signaling pathway, indicating that EZH2 could be a potential therapeutic target for renal I/R injury.			RT-PCR，Western blot，HE染色，免疫组化，TUNEL染色，细胞活力检测，荧光素酶报告分析，转染，免疫荧光				EZH2
31914533	chr19	19142448	19144448	MEF2B	The expression of MEF2B in MCL is related to the pathological subtypes, structural subtypes and the expression of SOX11, but not to the proliferation and prognosis. 	human		High+Lowthroughput	Expression of myocyte enhancer factor 2B in mantle cell lymphoma and its clinical significance	否	无	Mantle cell lymphoma		E_01_0093	He staining, immunohistochemistry, fluorescence in situ hybridization	The expression of MEF2B in MCL is related to the pathological subtypes, structural subtypes and the expression of SOX11, but not to the proliferation and prognosis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression of MEF2B in MCL is related to the pathological subtypes, structural subtypes and the expression of SOX11, but not to the proliferation and prognosis. 		The expression of MEF2B in MCL is related to the pathological subtypes, structural subtypes and the expression of SOX11, but not to the proliferation and prognosis. 	Immunohistochemical staining	The expression of MEF2B in MCL is related to the pathological subtypes, structural subtypes and the expression of SOX11, but not to the proliferation and prognosis. 			HE染色，免疫组化，荧光原位杂交				MEF2B
31914083	chr5	51380063	51382063	ISL1	ISL1 promotes cardiomyocyte differentiation and plays important roles in heart development.	human		High+Lowthroughput	Correlations between ISL1 rs1017 polymorphism and congenital heart disease risk: A PRISMA-compliant meta-analysis	是	rs1017	Congenital heart disease	cardiac muscle cell (sensu Arthopoda)	E_01_0094		ISL1 promotes cardiomyocyte differentiation and plays important roles in heart development.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			ISL1 promotes cardiomyocyte differentiation and plays important roles in heart development.	Immunohistochemical staining	ISL1 promotes cardiomyocyte differentiation and plays important roles in heart development.	ISL1			ISL1 promotes cardiomyocyte differentiation and plays important roles in heart development.			
31910882	chr11	306685	308685	IFITM1	Increased expression of the IFITM1 gene is required for LPS-stimulated hMSC migration. 	human	bone marrow	High+Lowthroughput	Epigenetic regulation of IFITM1 expression in lipopolysaccharide-stimulated human mesenchymal stromal cells	否	无		hMSC cell	E_01_0095	QRT PCR, ELISA, Western blot, immunocytochemistry, chromatin immunoprecipitation PCR, chip SEQ, scratch assay, gene knockdown, luciferase reporter assay	Increased expression of the IFITM1 gene is required for LPS-stimulated hMSC migration. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Increased expression of the IFITM1 gene is required for LPS-stimulated hMSC migration. 		Increased expression of the IFITM1 gene is required for LPS-stimulated hMSC migration. 	Immunohistochemical staining	Increased expression of the IFITM1 gene is required for LPS-stimulated hMSC migration. 			qRT-PCR，酶联免疫吸附试验，Western blot，免疫细胞化学，染色质免疫沉淀PCR，ChIP-seq，划痕实验，基因敲降，荧光素酶报告试验				IFITM1
31909872	chr5	177129035	177131035	NSD1	We also generated a mouse strain lacking one allele of Nsd1 and analyzed morphological and behavioral characteristics in these mice, showing behavioral characteristics reminiscent of some of the deficits seen in Sotos syndrome patients.	mouse		High+Lowthroughput	Investigating cortical features of Sotos syndrome using mice heterozygous for Nsd1.	否	无	Sotos syndrome		E_02_0059	Immunofluorescence, genotyping PCR, qPCR, hematoxylin staining,	We also generated a mouse strain lacking one allele of Nsd1 and analyzed morphological and behavioral characteristics in these mice, showing behavioral characteristics reminiscent of some of the deficits seen in Sotos syndrome patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We also generated a mouse strain lacking one allele of Nsd1 and analyzed morphological and behavioral characteristics in these mice, showing behavioral characteristics reminiscent of some of the deficits seen in Sotos syndrome patients.		We also generated a mouse strain lacking one allele of Nsd1 and analyzed morphological and behavioral characteristics in these mice, showing behavioral characteristics reminiscent of some of the deficits seen in Sotos syndrome patients.	Immunohistochemical staining	We also generated a mouse strain lacking one allele of Nsd1 and analyzed morphological and behavioral characteristics in these mice, showing behavioral characteristics reminiscent of some of the deficits seen in Sotos syndrome patients.			免疫荧光，基因分型PCR，qPCR，苏木精染色，				NSD1
31908011	chr2	199267108	199269108	SATB2	These findings indicate that maternal HFD-induced obesity may be associated with decreasing fetal pre-osteoblastic cell differentiation, under epigenetic control of SATB2 expression via Ezh2-dependent mechanisms.	mouse	Cord blood, skull	High+Lowthroughput	Maternal regulation of SATB2 in osteo-progeniters impairs skeletal development in offspring	否	无	Skeletal development	mesenchymal stem cell，skull cells	E_02_0060	Immunohistochemistry, chromatin immunoprecipitation, chip SEQ, RT qPCR, Western blot	These findings indicate that maternal HFD-induced obesity may be associated with decreasing fetal pre-osteoblastic cell differentiation, under epigenetic control of SATB2 expression via Ezh2-dependent mechanisms.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings indicate that maternal HFD-induced obesity may be associated with decreasing fetal pre-osteoblastic cell differentiation, under epigenetic control of SATB2 expression via Ezh2-dependent mechanisms.		These findings indicate that maternal HFD-induced obesity may be associated with decreasing fetal pre-osteoblastic cell differentiation, under epigenetic control of SATB2 expression via Ezh2-dependent mechanisms.	Immunohistochemical staining	These findings indicate that maternal HFD-induced obesity may be associated with decreasing fetal pre-osteoblastic cell differentiation, under epigenetic control of SATB2 expression via Ezh2-dependent mechanisms.			免疫组化，染色质免疫沉淀，ChIP-seq，RT-qPCR，Western blot				SATB2
31902945	chr22	27745785	27747785	MN1	Ectopia associated MN1 fusions and aberrant activation in myeloid neoplasms with t(12;22)(p13;q12)	human	bone marrow	High+Lowthroughput	Ectopia associated MN1 fusions and aberrant activation in myeloid neoplasms with t(12;22)(p13;q12)	否	无	Myeloid neoplasms	Bone marrow monocytes	E_01_0096	Whole genome sequencing, RT-PCR, fluorescence in situ hybridization, Sanger sequencing	Ectopia associated MN1 fusions and aberrant activation in myeloid neoplasms with t(12;22)(p13;q12)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ectopia associated MN1 fusions and aberrant activation in myeloid neoplasms with t(12;22)(p13;q12)		Ectopia associated MN1 fusions and aberrant activation in myeloid neoplasms with t(12;22)(p13;q12)	Immunohistochemical staining	Ectopia associated MN1 fusions and aberrant activation in myeloid neoplasms with t(12;22)(p13;q12)			全基因组测序，RT-PCR，荧光原位杂交，sanger测序				MN1
31900258	chr5	1250197	1252197	TERT	Epigenetically cotargeting Brd4 and Cdks suppresses human neuroblastoma with TERT overexpression by inhibiting the TERT-associated gene expression networks.	human		High+Lowthroughput		否	无	Neuroblastoma	neuroblastoma cells，SK-N-AS cell	E_01_0097	Chip – qPCR, RT qPCR, Western blot, cell viability assay	Epigenetically cotargeting Brd4 and Cdks suppresses human neuroblastoma with TERT overexpression by inhibiting the TERT-associated gene expression networks.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Epigenetically cotargeting Brd4 and Cdks suppresses human neuroblastoma with TERT overexpression by inhibiting the TERT-associated gene expression networks.	Immunohistochemical staining	Epigenetically cotargeting Brd4 and Cdks suppresses human neuroblastoma with TERT overexpression by inhibiting the TERT-associated gene expression networks.	TERT		ChIP–qPCR，RT-qPCR，Western blot，细胞活力检测	Epigenetically cotargeting Brd4 and Cdks suppresses human neuroblastoma with TERT overexpression by inhibiting the TERT-associated gene expression networks.			
31899875	chr14	100776332	100778332	MEG3	Furthermore, as a target gene of MIR-376B-3P, HMGA2 served as an oncogene in pituitary adenoma and could be negatively regulated by MEG3 via enriching MIR-376B-3P.	human	ovarian follicle	High+Lowthroughput	MEG3/MIR-376B-3P/HMGA2 axis is involved in pituitary tumor invasiveness	否	无	Pituitary tumors		E_01_0098	Dual luciferase reporter assay, immunofluorescence, IHC, RT qPCR, Western blot, flow cytometry, TUNEL staining, transfection, cell viability assay, Transwell, scratch assay	Furthermore, as a target gene of MIR-376B-3P, HMGA2 served as an oncogene in pituitary adenoma and could be negatively regulated by MEG3 via enriching MIR-376B-3P.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, as a target gene of MIR-376B-3P, HMGA2 served as an oncogene in pituitary adenoma and could be negatively regulated by MEG3 via enriching MIR-376B-3P.		Furthermore, as a target gene of MIR-376B-3P, HMGA2 served as an oncogene in pituitary adenoma and could be negatively regulated by MEG3 via enriching MIR-376B-3P.	Immunohistochemical staining	Furthermore, as a target gene of MIR-376B-3P, HMGA2 served as an oncogene in pituitary adenoma and could be negatively regulated by MEG3 via enriching MIR-376B-3P.			双荧光素酶报告基因，免疫荧光，，免疫组化，RT-qPCR，Western blot，流式细胞术，TUNEL染色，转染，细胞活力检测，Transwell，划痕实验				MEG3
31897846	chr19	2974615	2976615	TLE6	Expanding the genetic and phenotypic spectrum of female infertility caused by TLE6 mutations	human		High+Lowthroughput	Expanding the genetic and phenotypic spectrum of female infertility caused by TLE6 mutations	否	无	Infertility		E_01_0099	Whole exome sequencing, Sanger sequencing	Expanding the genetic and phenotypic spectrum of female infertility caused by TLE6 mutations	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Expanding the genetic and phenotypic spectrum of female infertility caused by TLE6 mutations		Expanding the genetic and phenotypic spectrum of female infertility caused by TLE6 mutations	Immunohistochemical staining	Expanding the genetic and phenotypic spectrum of female infertility caused by TLE6 mutations			全外显子组测序，Sanger测序				TLE6
31897220	chr1	6098734	6100734	CHD5	In conclusion, since CHD5 regulated multiple cancer-related targets, its expression may be a useful prognostic biomarker in patients with gastric cancer.	human	Stomach, cervix	High+Lowthroughput	Clinical significance of chromatin remodeling factor CHD5 expression in gastric cancer	否	无	gastric cancer	AGS cell, KATO III cell, MKN45 cell, NCI-N87 cell, NUGC-3 cell, OCUM‑1 cell,HeLa cell 	E_01_0100	Immunohistochemistry, scratch assay, cell viability assay, Transwell, Western blot, RT ＾ PCR	In conclusion, since CHD5 regulated multiple cancer-related targets, its expression may be a useful prognostic biomarker in patients with gastric cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, since CHD5 regulated multiple cancer-related targets, its expression may be a useful prognostic biomarker in patients with gastric cancer.		In conclusion, since CHD5 regulated multiple cancer-related targets, its expression may be a useful prognostic biomarker in patients with gastric cancer.	Immunohistochemical staining	In conclusion, since CHD5 regulated multiple cancer-related targets, its expression may be a useful prognostic biomarker in patients with gastric cancer.			免疫组化，划痕实验，细胞活力检测，Transwell，western blot，RT‑PCR				CHD5
31897216	chr4	7751333	7753333	AFAP1-AS1	 In conclusion, AFAP1-AS1 accelerates the proliferative and metastatic abilities of A549/DDP cells, whereas inhibits the apoptosis of A549/DDP cells, by interacting with EZH2 to activate the PI3K/AKT pathway; thus, inducing DDP resistance in NSCLC.	human	lung	High+Lowthroughput	AFAP1-AS1 induces cisplatin resistance in non-small cell lung cancer through PI3K/AKT pathway	否	无	Non small cell lung cancer	A549 cell	E_01_0101	RNA immunoprecipitation, flow cytometry, Western blot, Transwell, RT ‐qpcr	 In conclusion, AFAP1-AS1 accelerates the proliferative and metastatic abilities of A549/DDP cells, whereas inhibits the apoptosis of A549/DDP cells, by interacting with EZH2 to activate the PI3K/AKT pathway; thus, inducing DDP resistance in NSCLC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 In conclusion, AFAP1-AS1 accelerates the proliferative and metastatic abilities of A549/DDP cells, whereas inhibits the apoptosis of A549/DDP cells, by interacting with EZH2 to activate the PI3K/AKT pathway; thus, inducing DDP resistance in NSCLC.		 In conclusion, AFAP1-AS1 accelerates the proliferative and metastatic abilities of A549/DDP cells, whereas inhibits the apoptosis of A549/DDP cells, by interacting with EZH2 to activate the PI3K/AKT pathway; thus, inducing DDP resistance in NSCLC.	Immunohistochemical staining	 In conclusion, AFAP1-AS1 accelerates the proliferative and metastatic abilities of A549/DDP cells, whereas inhibits the apoptosis of A549/DDP cells, by interacting with EZH2 to activate the PI3K/AKT pathway; thus, inducing DDP resistance in NSCLC.			RNA免疫沉淀，流式细胞术，Western blot，Transwell，RT‑qPCR				AFAP1-AS1
31893185	chr9	81580729	81582729	TLE1	TLE1 may be a reliable immunostain for diagnosing SS, but its expression is not limited to SS. Its expression should be interpreted in the light of morphological features and a panel of antibodies.	human		High+Lowthroughput	Is TLE1 Expression Limited to Synovial Sarcoma? Our Experience at Shifa International Hospital, Pakistan	否	无	Synovial sarcoma		E_01_0102	Immunohistochemistry	TLE1 may be a reliable immunostain for diagnosing SS, but its expression is not limited to SS. Its expression should be interpreted in the light of morphological features and a panel of antibodies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TLE1 may be a reliable immunostain for diagnosing SS, but its expression is not limited to SS. Its expression should be interpreted in the light of morphological features and a panel of antibodies.	Immunohistochemical staining	TLE1 may be a reliable immunostain for diagnosing SS, but its expression is not limited to SS. Its expression should be interpreted in the light of morphological features and a panel of antibodies.	TLE1		免疫组化	TLE1 may be a reliable immunostain for diagnosing SS, but its expression is not limited to SS. Its expression should be interpreted in the light of morphological features and a panel of antibodies.			
31892537	chr10	102103573	102105573	LDB1	Our structural and biochemical data provide a much-anticipated structural basis for understanding how LDB1 and the LDB1/SSBP interactions form the structural core of diverse complexes mediating cell choice decisions and long-range enhancer-promoter interactions.	human	blood	High+Lowthroughput	Crystal structure of human LDB1 in complex with SSBP2	否	无		erythrocyte	E_01_0103	pull-down	Our structural and biochemical data provide a much-anticipated structural basis for understanding how LDB1 and the LDB1/SSBP interactions form the structural core of diverse complexes mediating cell choice decisions and long-range enhancer-promoter interactions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our structural and biochemical data provide a much-anticipated structural basis for understanding how LDB1 and the LDB1/SSBP interactions form the structural core of diverse complexes mediating cell choice decisions and long-range enhancer-promoter interactions.		Our structural and biochemical data provide a much-anticipated structural basis for understanding how LDB1 and the LDB1/SSBP interactions form the structural core of diverse complexes mediating cell choice decisions and long-range enhancer-promoter interactions.	Immunohistochemical staining	Our structural and biochemical data provide a much-anticipated structural basis for understanding how LDB1 and the LDB1/SSBP interactions form the structural core of diverse complexes mediating cell choice decisions and long-range enhancer-promoter interactions.			pull-down				LDB1
31891591	chr7	148804482	148806482	EZH2	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy	human		High+Lowthroughput	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy	否	无	epilepsy		E_01_0104	Western blot，qRT-PCR，LC-MS	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy	Immunohistochemical staining	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy	EZH2		Western blot，qRT-PCR，LC-MS	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy			
31890812	chr2	60447611	60449611	BCL11A	Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion.	human	Kidney, peripheral blood, bone marrow	High+Lowthroughput	Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion	否	无	β- Thalassemia disorders	HEK293T cell， KU812 cell，KG-1 cell	E_01_0105	Agarose gel electrophoresis, QRT PCR	Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion.		Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion.	Immunohistochemical staining	Expression analysis data of BCL11A and γ-globin genes in KU812 and KG-1 cell lines after CRISPR/Cas9-mediated BCL11A enhancer deletion.			琼脂糖凝胶电泳， qRT-PCR				BCL11A
31888703	chr3	12284215	12286215	PPARG	Enhancer polymorphism rs10865710 associated with traumatic sepsis is a regulator of PPARG gene expression	human		High+Lowthroughput	Enhancer polymorphism rs10865710 associated with traumatic sepsis is a regulator of PPARG gene expression	是	 rs10865710	Traumatic sepsis		E_01_0106	Western blot, dual luciferase gene reporter	Enhancer polymorphism rs10865710 associated with traumatic sepsis is a regulator of PPARG gene expression	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer polymorphism rs10865710 associated with traumatic sepsis is a regulator of PPARG gene expression	Immunohistochemical staining	Enhancer polymorphism rs10865710 associated with traumatic sepsis is a regulator of PPARG gene expression	PPARG		Western blot，双荧光素酶基因报告	Enhancer polymorphism rs10865710 associated with traumatic sepsis is a regulator of PPARG gene expression			
31886719	chr11	100684149	100686149	ARHGAP42	First, RBPJ and TEAD1 converge at an intronic enhancer to regulate ARHGAP42 expression in SMCs. Second, TEAD1 and RBPJ interact physically and bind cooperatively to the ARHGAP42 enhancer. Third, miR505 interacts with the ARHGAP42 3'-UTR to facilitate its degradation. Finally, LncRNA, AK124326, inhibits ARHGAP42 transcription.	human	Aortic smooth muscle, bronchial smooth muscle	High+Lowthroughput	Transcriptional and posttranscriptional regulation of the SMC-selective blood pressure-associated gene, ARHGAP42	是	rs604723	Blood pressure regulation	HUAOSMC cell，HUBRSMC cell	E_01_0107	Luciferase assay, immunoprecipitation, QRT PCR, chromatin immunoprecipitation assay, Western blot, electrophoretic mobility shift assay, immunofluorescence	First, RBPJ and TEAD1 converge at an intronic enhancer to regulate ARHGAP42 expression in SMCs. Second, TEAD1 and RBPJ interact physically and bind cooperatively to the ARHGAP42 enhancer. Third, miR505 interacts with the ARHGAP42 3'-UTR to facilitate its degradation. Finally, LncRNA, AK124326, inhibits ARHGAP42 transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	First, RBPJ and TEAD1 converge at an intronic enhancer to regulate ARHGAP42 expression in SMCs. Second, TEAD1 and RBPJ interact physically and bind cooperatively to the ARHGAP42 enhancer. Third, miR505 interacts with the ARHGAP42 3'-UTR to facilitate its degradation. Finally, LncRNA, AK124326, inhibits ARHGAP42 transcription.		First, RBPJ and TEAD1 converge at an intronic enhancer to regulate ARHGAP42 expression in SMCs. Second, TEAD1 and RBPJ interact physically and bind cooperatively to the ARHGAP42 enhancer. Third, miR505 interacts with the ARHGAP42 3'-UTR to facilitate its degradation. Finally, LncRNA, AK124326, inhibits ARHGAP42 transcription.	Immunohistochemical staining	First, RBPJ and TEAD1 converge at an intronic enhancer to regulate ARHGAP42 expression in SMCs. Second, TEAD1 and RBPJ interact physically and bind cooperatively to the ARHGAP42 enhancer. Third, miR505 interacts with the ARHGAP42 3'-UTR to facilitate its degradation. Finally, LncRNA, AK124326, inhibits ARHGAP42 transcription.			荧光素酶分析，免疫沉淀，qRT-PCR，染色质免疫沉淀实验，Western blot，电泳迁移率分析，免疫荧光				ARHGAP42
31886200	chr7	148804829	148806829	EZH2	Our results suggest a scale of measure for EZH2 expression in pediatric MDS, where aberrant EZH2 expression may be a potential biomarker of disease evolution.	human	bone marrow	High+Lowthroughput	Aberrant Expression of EZH2 in Pediatric Patients with Myelodysplastic Syndrome: A Potential Biomarker of Leukemic Evolution	否	无	Pediatric myelodysplastic syndrome	bone marrow cell	E_01_0108	qRT–PCR	Our results suggest a scale of measure for EZH2 expression in pediatric MDS, where aberrant EZH2 expression may be a potential biomarker of disease evolution.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our results suggest a scale of measure for EZH2 expression in pediatric MDS, where aberrant EZH2 expression may be a potential biomarker of disease evolution.	Immunohistochemical staining	Our results suggest a scale of measure for EZH2 expression in pediatric MDS, where aberrant EZH2 expression may be a potential biomarker of disease evolution.	EZH2		qRT–PCR	Our results suggest a scale of measure for EZH2 expression in pediatric MDS, where aberrant EZH2 expression may be a potential biomarker of disease evolution.			
31882553	chr19	15232668	15234668	BRD4	Since bromodomain-containing protein 4 (BRD4) facilitates the transcription of genes important for neoplastic cells in a cancer-type specific manner, BRD4-regulated molecules may also include therapeutic targets for mantle cell lymphoma (MCL), a treatment-refractory subtype of malignant lymphoma.	human	lymph	High+Lowthroughput	BRD4-Regulated Molecular Targets in Mantle Cell Lymphoma: Insights into Targeted Therapeutic Approach	否	无	Mantle cell lymphoma	JVM-2 cell，MINO cell，Z138 cell，KPUM-YY1 cell	E_01_0109	Cell viability assay, Western blot, QRT PCR, chromatin immunoprecipitation	Since bromodomain-containing protein 4 (BRD4) facilitates the transcription of genes important for neoplastic cells in a cancer-type specific manner, BRD4-regulated molecules may also include therapeutic targets for mantle cell lymphoma (MCL), a treatment-refractory subtype of malignant lymphoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Since bromodomain-containing protein 4 (BRD4) facilitates the transcription of genes important for neoplastic cells in a cancer-type specific manner, BRD4-regulated molecules may also include therapeutic targets for mantle cell lymphoma (MCL), a treatment-refractory subtype of malignant lymphoma.	Immunohistochemical staining	Since bromodomain-containing protein 4 (BRD4) facilitates the transcription of genes important for neoplastic cells in a cancer-type specific manner, BRD4-regulated molecules may also include therapeutic targets for mantle cell lymphoma (MCL), a treatment-refractory subtype of malignant lymphoma.	BRD4		细胞活力检测，Western blot，qRT-PCR，染色质免疫沉淀	Since bromodomain-containing protein 4 (BRD4) facilitates the transcription of genes important for neoplastic cells in a cancer-type specific manner, BRD4-regulated molecules may also include therapeutic targets for mantle cell lymphoma (MCL), a treatment-refractory subtype of malignant lymphoma.			
31878072	chr1	153659104	153661104	ILF2	Therefore, we present a distinct mechanism by which EV71 antagonizes ILF2-mediated antiviral effects by inhibiting ILF2 expression and promoting ILF2 translocation from the nucleus to the cytoplasm through its 2B protein.	human	Kidney, peripheral blood	High+Lowthroughput	Enterovirus 71 Represses Interleukin Enhancer-Binding Factor 2 Production and Nucleus Translocation to Antagonize ILF2 Antiviral Effects	否	无	antiviral	HEK293T cell、Vero cell、RD cell，thp-1 cell	E_01_0110	RT qPCR, Western blot, CO immunoprecipitation, immunofluorescence	Therefore, we present a distinct mechanism by which EV71 antagonizes ILF2-mediated antiviral effects by inhibiting ILF2 expression and promoting ILF2 translocation from the nucleus to the cytoplasm through its 2B protein.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, we present a distinct mechanism by which EV71 antagonizes ILF2-mediated antiviral effects by inhibiting ILF2 expression and promoting ILF2 translocation from the nucleus to the cytoplasm through its 2B protein.		Therefore, we present a distinct mechanism by which EV71 antagonizes ILF2-mediated antiviral effects by inhibiting ILF2 expression and promoting ILF2 translocation from the nucleus to the cytoplasm through its 2B protein.	Immunohistochemical staining	Therefore, we present a distinct mechanism by which EV71 antagonizes ILF2-mediated antiviral effects by inhibiting ILF2 expression and promoting ILF2 translocation from the nucleus to the cytoplasm through its 2B protein.			RT-qPCR，Western blot，免疫共沉淀，免疫荧光				ILF2
31866294	chr7	148804551	148806551	EZH2	Structural Basis of the Interaction Between Ubiquitin Specific Protease 7 and Enhancer of Zeste Homolog 2.	human	colon	High+Lowthroughput	Structural Basis of the Interaction Between Ubiquitin Specific Protease 7 and Enhancer of Zeste Homolog 2	否	无	tumour	HCT116 cell	E_01_0111	Fluorescence polarization assay, Western blot, CO immunoprecipitation	Structural Basis of the Interaction Between Ubiquitin Specific Protease 7 and Enhancer of Zeste Homolog 2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Structural Basis of the Interaction Between Ubiquitin Specific Protease 7 and Enhancer of Zeste Homolog 2.	Immunohistochemical staining	Structural Basis of the Interaction Between Ubiquitin Specific Protease 7 and Enhancer of Zeste Homolog 2.	EZH2		荧光偏振分析，Western Blot，共免疫沉淀	Structural Basis of the Interaction Between Ubiquitin Specific Protease 7 and Enhancer of Zeste Homolog 2.			
31866047	chr20	59860441	59862441	SYCP2	SYCP2 Translocation-Mediated Dysregulation and Frameshift Variants Cause Human Male Infertility	human	lymph	High+Lowthroughput	SYCP2 Translocation-Mediated Dysregulation and Frameshift Variants Cause Human Male Infertility	是	 rs568645874， rs199662252，rs45568532, rs551180067,  rs11549332		Lymphoblast	E_01_0112	QRT PCR, Western blot, Sanger sequencing, PAS staining, hematoxylin staining	SYCP2 Translocation-Mediated Dysregulation and Frameshift Variants Cause Human Male Infertility	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SYCP2 Translocation-Mediated Dysregulation and Frameshift Variants Cause Human Male Infertility		SYCP2 Translocation-Mediated Dysregulation and Frameshift Variants Cause Human Male Infertility	Immunohistochemical staining	SYCP2 Translocation-Mediated Dysregulation and Frameshift Variants Cause Human Male Infertility			qRT-PCR，Western Blot，Sanger测序，PAS染色，苏木精染色				SYCP2
31865141	chr3	3142136	3144136	CRBN	In conclusion, our study firstly provided a support that CRBN decrease effectively protected LPS-induced ALI against inflammatory response mainly through the repression of oxidative stress and ER stress.	mouse	lung	High+Lowthroughput	CRBN knockdown mitigates lipopolysaccharide-induced acute lung injury by suppression of oxidative stress and endoplasmic reticulum (ER) stress associated NF-κB signaling	否	无	acute lung injury 	A549 cell	E_02_0061	Biochemical analysis, he staining, immunofluorescence, ELISA, Western blot, QRT PCR, intracellular reactive oxygen species detection	In conclusion, our study firstly provided a support that CRBN decrease effectively protected LPS-induced ALI against inflammatory response mainly through the repression of oxidative stress and ER stress.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, our study firstly provided a support that CRBN decrease effectively protected LPS-induced ALI against inflammatory response mainly through the repression of oxidative stress and ER stress.		In conclusion, our study firstly provided a support that CRBN decrease effectively protected LPS-induced ALI against inflammatory response mainly through the repression of oxidative stress and ER stress.	Immunohistochemical staining	In conclusion, our study firstly provided a support that CRBN decrease effectively protected LPS-induced ALI against inflammatory response mainly through the repression of oxidative stress and ER stress.			生化分析，HE染色，免疫荧光，ELISA，Western blot，qRT-PCR，细胞内活性氧检测				CRBN
31864713	chr7	44101569	44103569	AEBP1	Adipocyte enhancer binding protein 1 (AEBP1) knockdown suppresses human glioma cell proliferation, invasion and induces early apoptosis	human	brain	High+Lowthroughput	Adipocyte enhancer binding protein 1 (AEBP1) knockdown suppresses human glioma cell proliferation, invasion and induces early apoptosis	否	无	Gliomas	U87MG cell，U251 MG cell	E_01_0113	Western blot, immunohistochemistry, QRT PCR, cell viability assay, Transwell, immunofluorescence, flow cytometry	Adipocyte enhancer binding protein 1 (AEBP1) knockdown suppresses human glioma cell proliferation, invasion and induces early apoptosis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Adipocyte enhancer binding protein 1 (AEBP1) knockdown suppresses human glioma cell proliferation, invasion and induces early apoptosis		Adipocyte enhancer binding protein 1 (AEBP1) knockdown suppresses human glioma cell proliferation, invasion and induces early apoptosis	Immunohistochemical staining	Adipocyte enhancer binding protein 1 (AEBP1) knockdown suppresses human glioma cell proliferation, invasion and induces early apoptosis			Western-blot，免疫组化，qRT-PCR，细胞活力检测，Transwell，免疫荧光，流式细胞术				AEBP1
31861475	chr9	36570240	36572240	MELK	Inhibition of MELK Protooncogene as an Innovative Treatment for Intrahepatic Cholangiocarcinoma	human	bile duct	High+Lowthroughput	Inhibition of MELK Protooncogene as an Innovative Treatment for Intrahepatic Cholangiocarcinoma	否	无	Intrahepatic cholangiocarcinoma	iCCA cell	E_01_0114	RT-PCR, immunohistochemistry	Inhibition of MELK Protooncogene as an Innovative Treatment for Intrahepatic Cholangiocarcinoma	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Inhibition of MELK Protooncogene as an Innovative Treatment for Intrahepatic Cholangiocarcinoma		Inhibition of MELK Protooncogene as an Innovative Treatment for Intrahepatic Cholangiocarcinoma	Immunohistochemical staining	Inhibition of MELK Protooncogene as an Innovative Treatment for Intrahepatic Cholangiocarcinoma			RT-PCR，免疫组织化学				MELK
31860165	chr4	52709533	52711533	DANCR	The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription	human	breast	High+Lowthroughput	The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription	否	无	mammary cancer	breast cancer cells，mammary gland epithelial cell	E_01_0115	QRT PCR, cell viability assay, ELISA, Western blot, RNA immunoprecipitation, chromatin immunoprecipitation, Transwell	The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription		The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription	Immunohistochemical staining	The long non-coding RNA DANCR regulates the inflammatory phenotype of breast cancer cells and promotes breast cancer progression via EZH2-dependent suppression of SOCS3 transcription			qRT-PCR，细胞活力检测，ELISA，Western blot，RNA免疫沉淀，染色质免疫沉淀，Transwell				DANCR
31858612	chr14	53946742	53948742	BMP4	The expression levels of ALP, runt-related transcription factor 2, bone morphogenetic protein 4, osterix and β-catenin were significantly increased in GSK-137647A-treated group, while the gene and protein levels of peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly reduced.	mouse	bone marrow	High+Lowthroughput	Effect of GSK-137647A, the first non-carboxylic FFA4 agonist, on the osteogenic and adipogenic differentiation of bone mesenchymal stem cells in db/db mice	否	无		mesenchymal stem cell of the bone marrow，cementoblast	E_02_0062	Flow cytometry, cell viability assay, oil red O staining, Western blot, RT qPCR	The expression levels of ALP, runt-related transcription factor 2, bone morphogenetic protein 4, osterix and β-catenin were significantly increased in GSK-137647A-treated group, while the gene and protein levels of peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly reduced.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression levels of ALP, runt-related transcription factor 2, bone morphogenetic protein 4, osterix and β-catenin were significantly increased in GSK-137647A-treated group, while the gene and protein levels of peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly reduced.		The expression levels of ALP, runt-related transcription factor 2, bone morphogenetic protein 4, osterix and β-catenin were significantly increased in GSK-137647A-treated group, while the gene and protein levels of peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly reduced.	Immunohistochemical staining	The expression levels of ALP, runt-related transcription factor 2, bone morphogenetic protein 4, osterix and β-catenin were significantly increased in GSK-137647A-treated group, while the gene and protein levels of peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly reduced.			流式细胞术，细胞活力检测，油红O染色，Western blot，RT-Qpcr				BMP4
31858557	chr15	42735912	42737912	TTBK2	Circ-TTBK2/miR-520b/EZH2 axis modulated cell proliferation, apoptosis, and invasion in glioma cell lines, and might serve as potential targets for glioma diagnosis and therapy.	human	brain	High+Lowthroughput	Circular RNA TTBK2 promotes the development of human glioma cells via miR-520b/EZH2 axis	否	无	Gliomas	A172 cell，U251 cell，astrocyte cell	E_01_0116	Transfection, QRT PCR, Western blot, flow cytometry, Transwell, dual luciferase reporter assay	Circ-TTBK2/miR-520b/EZH2 axis modulated cell proliferation, apoptosis, and invasion in glioma cell lines, and might serve as potential targets for glioma diagnosis and therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Circ-TTBK2/miR-520b/EZH2 axis modulated cell proliferation, apoptosis, and invasion in glioma cell lines, and might serve as potential targets for glioma diagnosis and therapy.	Immunohistochemical staining	Circ-TTBK2/miR-520b/EZH2 axis modulated cell proliferation, apoptosis, and invasion in glioma cell lines, and might serve as potential targets for glioma diagnosis and therapy.	TTBK2		转染，qRT-PCR，Western Blot，流式细胞术，Transwell，双荧光素酶报告分析	Circ-TTBK2/miR-520b/EZH2 axis modulated cell proliferation, apoptosis, and invasion in glioma cell lines, and might serve as potential targets for glioma diagnosis and therapy.			
31856860	chr20	50188118	50190118	CEBPB	 Analysis of transcription factor targets showed in both CS and SS patients, an enrichment of CCAAT-enhancer-binding protein beta (CEBPB) targets in genes downregulated over time and an enrichment of E2F targets in genes with an increasing expression trend.	human		High+Lowthroughput	A longitudinal study highlights shared aspects of the transcriptomic response to cardiogenic and septic shock	否	无	Cardiogenic and septic shock		E_01_0117	RNA sequencing	 Analysis of transcription factor targets showed in both CS and SS patients, an enrichment of CCAAT-enhancer-binding protein beta (CEBPB) targets in genes downregulated over time and an enrichment of E2F targets in genes with an increasing expression trend.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			 Analysis of transcription factor targets showed in both CS and SS patients, an enrichment of CCAAT-enhancer-binding protein beta (CEBPB) targets in genes downregulated over time and an enrichment of E2F targets in genes with an increasing expression trend.	Immunohistochemical staining	 Analysis of transcription factor targets showed in both CS and SS patients, an enrichment of CCAAT-enhancer-binding protein beta (CEBPB) targets in genes downregulated over time and an enrichment of E2F targets in genes with an increasing expression trend.	CEBPB		RNA测序	 Analysis of transcription factor targets showed in both CS and SS patients, an enrichment of CCAAT-enhancer-binding protein beta (CEBPB) targets in genes downregulated over time and an enrichment of E2F targets in genes with an increasing expression trend.			
31851943	chr19	1606379	1608379	TCF3	Loss-of-function studies of TCF3 confirm the role of TCF3 in mediating condition-specific enhancer-promoter interactions and gene regulation in fetal HSCs.	human	bone marrow	High+Lowthroughput	Spatial Genome Re-organization between Fetal and Adult Hematopoietic Stem Cells	否	无		HPC-7 cell	E_01_0118	Dna-fish, Western blot, flow cytometry	Loss-of-function studies of TCF3 confirm the role of TCF3 in mediating condition-specific enhancer-promoter interactions and gene regulation in fetal HSCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Loss-of-function studies of TCF3 confirm the role of TCF3 in mediating condition-specific enhancer-promoter interactions and gene regulation in fetal HSCs.	Immunohistochemical staining	Loss-of-function studies of TCF3 confirm the role of TCF3 in mediating condition-specific enhancer-promoter interactions and gene regulation in fetal HSCs.	TCF7L1		DNA-FISH， Western blot，流式细胞术	Loss-of-function studies of TCF3 confirm the role of TCF3 in mediating condition-specific enhancer-promoter interactions and gene regulation in fetal HSCs.			
31845224	chr2	26345405	26347405	Notch1	Taken together, these data suggest that Notch1 drives ICC formation and proliferation; downregulation of Notch1 induces apoptosis in ICC cells; Notch1 signaling may serve as a novel therapeutic target for the treatment of ICC.	human	gallbladder	High+Lowthroughput	Notch1 Drives the Formation and Proliferation of Intrahepatic Cholangiocarcinoma	否	无	Intrahepatic cholangiocarcinoma	BC-939 cell，RBE cell	E_01_0119	Western blot, flow cytometry, Western blot, immunohistochemistry, immunofluorescence, QRT PCR	Taken together, these data suggest that Notch1 drives ICC formation and proliferation; downregulation of Notch1 induces apoptosis in ICC cells; Notch1 signaling may serve as a novel therapeutic target for the treatment of ICC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, these data suggest that Notch1 drives ICC formation and proliferation; downregulation of Notch1 induces apoptosis in ICC cells; Notch1 signaling may serve as a novel therapeutic target for the treatment of ICC.		Taken together, these data suggest that Notch1 drives ICC formation and proliferation; downregulation of Notch1 induces apoptosis in ICC cells; Notch1 signaling may serve as a novel therapeutic target for the treatment of ICC.	Immunohistochemical staining	Taken together, these data suggest that Notch1 drives ICC formation and proliferation; downregulation of Notch1 induces apoptosis in ICC cells; Notch1 signaling may serve as a novel therapeutic target for the treatment of ICC.			Western blot， 流式细胞术，Western Blot，免疫组化，免疫荧光，qRT-PCR				Notch1
31845180	chr8	81475612	81477612	FABP4	Exogenous FABP4 interferes with differentiation, promotes lipolysis and inflammation in adipocytes	mouse		High+Lowthroughput	Exogenous FABP4 interferes with differentiation, promotes lipolysis and inflammation in adipocytes	否	无		3T3-LL cell	E_02_0063	Oil red O staining, Western blot	Exogenous FABP4 interferes with differentiation, promotes lipolysis and inflammation in adipocytes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Exogenous FABP4 interferes with differentiation, promotes lipolysis and inflammation in adipocytes		Exogenous FABP4 interferes with differentiation, promotes lipolysis and inflammation in adipocytes	Immunohistochemical staining	Exogenous FABP4 interferes with differentiation, promotes lipolysis and inflammation in adipocytes			油红O染色，Western blot				FABP4
31844321	chr5	129458078	129460078	ADAMTS19	Upregulation of endocardial Krüppel-like factor 2 in Adamts19 knockout mice precedes hemodynamic perturbation, showing that a tight balance in the Wnt-Adamts19-Klf2 axis is required for proper valve maturation and maintenance.	mouse	valve	High+Lowthroughput	Loss of ADAMTS19 causes progressive non-syndromic heart valve disease	否	无	Valvular heart disease	valve interstitial cells	E_02_0064	Immunohistochemistry, immunofluorescence,	Upregulation of endocardial Krüppel-like factor 2 in Adamts19 knockout mice precedes hemodynamic perturbation, showing that a tight balance in the Wnt-Adamts19-Klf2 axis is required for proper valve maturation and maintenance.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Upregulation of endocardial Krüppel-like factor 2 in Adamts19 knockout mice precedes hemodynamic perturbation, showing that a tight balance in the Wnt-Adamts19-Klf2 axis is required for proper valve maturation and maintenance.		Upregulation of endocardial Krüppel-like factor 2 in Adamts19 knockout mice precedes hemodynamic perturbation, showing that a tight balance in the Wnt-Adamts19-Klf2 axis is required for proper valve maturation and maintenance.	Immunohistochemical staining	Upregulation of endocardial Krüppel-like factor 2 in Adamts19 knockout mice precedes hemodynamic perturbation, showing that a tight balance in the Wnt-Adamts19-Klf2 axis is required for proper valve maturation and maintenance.			免疫组化，免疫荧光，				ADAMTS19
31843716	chr18	55219904	55221904	TCF4	3D-microenvironments initiate TCF4 expression rescuing nuclear β-catenin activity in MCF-7 breast cancer cells	human	breast	High+Lowthroughput	3D-microenvironments initiate TCF4 expression rescuing nuclear β-catenin activity in MCF-7 breast cancer cells	否	无	mammary cancer	MCF-7 cell，MDA-MB-231 cell	E_01_0120	Flow cytometry, immunofluorescence, Western blot	3D-microenvironments initiate TCF4 expression rescuing nuclear β-catenin activity in MCF-7 breast cancer cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			3D-microenvironments initiate TCF4 expression rescuing nuclear β-catenin activity in MCF-7 breast cancer cells	Immunohistochemical staining	3D-microenvironments initiate TCF4 expression rescuing nuclear β-catenin activity in MCF-7 breast cancer cells	TCF4		流式细胞术，免疫荧光，Western blot	3D-microenvironments initiate TCF4 expression rescuing nuclear β-catenin activity in MCF-7 breast cancer cells			
31843273	chr7	148804648	148806648	EZH2	Our results confirm the differential expression of EZH2 in uterine cancers compared to normal tissues.	human		High+Lowthroughput	Overexpression of enhance of Zeste homolog 2 (EZH2) in endometrial carcinoma: An NRG Oncology/Gynecologic Oncology Group Study	否	无	Endometrial cancer		E_01_0121	RT-PCR，Western blot	Our results confirm the differential expression of EZH2 in uterine cancers compared to normal tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our results confirm the differential expression of EZH2 in uterine cancers compared to normal tissues.	Immunohistochemical staining	Our results confirm the differential expression of EZH2 in uterine cancers compared to normal tissues.	EZH2		RT-PCR，Western blot	Our results confirm the differential expression of EZH2 in uterine cancers compared to normal tissues.			
31841397	chr7	148804351	148806351	EZH2	Mice lacking uterine enhancer of zeste homolog 2 have transcriptomic changes associated with uterine epithelial proliferation	mouse	uterus	High+Lowthroughput	Mice lacking uterine enhancer of zeste homolog 2 have transcriptomic changes associated with uterine epithelial proliferation	否	无	Uterine epithelial VAS	epithelial cell of uterus	E_02_0065	Immunohistochemistry, qPCR	Mice lacking uterine enhancer of zeste homolog 2 have transcriptomic changes associated with uterine epithelial proliferation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mice lacking uterine enhancer of zeste homolog 2 have transcriptomic changes associated with uterine epithelial proliferation		Mice lacking uterine enhancer of zeste homolog 2 have transcriptomic changes associated with uterine epithelial proliferation	Immunohistochemical staining	Mice lacking uterine enhancer of zeste homolog 2 have transcriptomic changes associated with uterine epithelial proliferation			免疫组化，qPCR				EZH2
31840569	chr17	80542354	80544354	RPTOR	Ultimately, atg7 rptor double-KO mice displayed decreased lipolysis, restored adipose tissue development, and upregulated thermogenic gene expression in brown and inguinal adipose tissue compared to RPTOR-deficient mice in vivo.	mouse	Fat	High+Lowthroughput	Sustained activation of autophagy suppresses adipocyte maturation via a lipolysis-dependent mechanism	否	无		fat cell	E_02_0066	Immunofluorescence, flow cytometry, oil red O staining, he staining, immunohistochemistry, Western blot	Ultimately, atg7 rptor double-KO mice displayed decreased lipolysis, restored adipose tissue development, and upregulated thermogenic gene expression in brown and inguinal adipose tissue compared to RPTOR-deficient mice in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ultimately, atg7 rptor double-KO mice displayed decreased lipolysis, restored adipose tissue development, and upregulated thermogenic gene expression in brown and inguinal adipose tissue compared to RPTOR-deficient mice in vivo.		Ultimately, atg7 rptor double-KO mice displayed decreased lipolysis, restored adipose tissue development, and upregulated thermogenic gene expression in brown and inguinal adipose tissue compared to RPTOR-deficient mice in vivo.	Immunohistochemical staining	Ultimately, atg7 rptor double-KO mice displayed decreased lipolysis, restored adipose tissue development, and upregulated thermogenic gene expression in brown and inguinal adipose tissue compared to RPTOR-deficient mice in vivo.			免疫荧光，流式细胞术，油红O染色，HE染色，免疫组化，western blot 				RPTOR
31836590	chr1	145918614	145920614	RBM8A	Thrombocytopenia-absent radii (TAR) syndrome, characterized by neonatal thrombocytopenia and bilateral radial aplasia with thumbs present, is typically caused by the inheritance of a 1q21.1 deletion and a single-nucelotide polymorphism in RBM8A on the nondeleted allele. 	human		High+Lowthroughput	1q21.1 deletion and a rare functional polymorphism in siblings with thrombocytopenia-absent radius-like phenotypes	是	rs61746197	Thrombocytopenia, radial hypoplasia		E_01_0122	Western blot	Thrombocytopenia-absent radii (TAR) syndrome, characterized by neonatal thrombocytopenia and bilateral radial aplasia with thumbs present, is typically caused by the inheritance of a 1q21.1 deletion and a single-nucelotide polymorphism in RBM8A on the nondeleted allele. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thrombocytopenia-absent radii (TAR) syndrome, characterized by neonatal thrombocytopenia and bilateral radial aplasia with thumbs present, is typically caused by the inheritance of a 1q21.1 deletion and a single-nucelotide polymorphism in RBM8A on the nondeleted allele. 		Thrombocytopenia-absent radii (TAR) syndrome, characterized by neonatal thrombocytopenia and bilateral radial aplasia with thumbs present, is typically caused by the inheritance of a 1q21.1 deletion and a single-nucelotide polymorphism in RBM8A on the nondeleted allele. 	Immunohistochemical staining	Thrombocytopenia-absent radii (TAR) syndrome, characterized by neonatal thrombocytopenia and bilateral radial aplasia with thumbs present, is typically caused by the inheritance of a 1q21.1 deletion and a single-nucelotide polymorphism in RBM8A on the nondeleted allele. 			Western blot				RBM8A
31833556	chr7	148804595	148806595	EZH2	By conducting TF enrichment analyses, we identified EZH2 as a common TF binding to osteoporosis-associated enhancers, and EZH2 was also associated with BMD in a Chinese population. EZH2 is functionally related to bone phenotypes. 	mouse		High+Lowthroughput	Transcription Factor Enrichment Analysis in Enhancers Identifies EZH2 as a Susceptibility Gene for Osteoporosis	是	rs111851041	Osteoporosis		E_02_0067		By conducting TF enrichment analyses, we identified EZH2 as a common TF binding to osteoporosis-associated enhancers, and EZH2 was also associated with BMD in a Chinese population. EZH2 is functionally related to bone phenotypes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	By conducting TF enrichment analyses, we identified EZH2 as a common TF binding to osteoporosis-associated enhancers, and EZH2 was also associated with BMD in a Chinese population. EZH2 is functionally related to bone phenotypes. 		By conducting TF enrichment analyses, we identified EZH2 as a common TF binding to osteoporosis-associated enhancers, and EZH2 was also associated with BMD in a Chinese population. EZH2 is functionally related to bone phenotypes. 	Immunohistochemical staining	By conducting TF enrichment analyses, we identified EZH2 as a common TF binding to osteoporosis-associated enhancers, and EZH2 was also associated with BMD in a Chinese population. EZH2 is functionally related to bone phenotypes. 							EZH2
31831267	chr7	148804596	148806596	EZH2	UNC6852 degrades both wild-type and mutant EZH2, and additionally displays anti-proliferative effects in this cancer model system.	human	Cervix, lymph, kidney	High+Lowthroughput	Degradation of Polycomb Repressive Complex 2 with an EED-Targeted Bivalent Chemical Degrader	否	无	cancer	Hela cell，DB cell，Pfeiffer cell，293T Cell 	E_01_0123	Western blot, cell viability assay	UNC6852 degrades both wild-type and mutant EZH2, and additionally displays anti-proliferative effects in this cancer model system.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			UNC6852 degrades both wild-type and mutant EZH2, and additionally displays anti-proliferative effects in this cancer model system.	Immunohistochemical staining	UNC6852 degrades both wild-type and mutant EZH2, and additionally displays anti-proliferative effects in this cancer model system.	EZH2		Western Blot，细胞活力检测	UNC6852 degrades both wild-type and mutant EZH2, and additionally displays anti-proliferative effects in this cancer model system.			
31827084	chrX	113613674	113615674	XACT	This ERV was hijacked by younger hominoid-specific ERVs that gave rise to the promoter of XACT, thus wiring its expression to the pluripotency network. This work illustrates how retroviral-derived sequences may intervene in species-specific regulatory pathways.	human	embryo	High+Lowthroughput	A primate-specific retroviral enhancer wires the XACT lncRNA into the core pluripotency network in humans	否	无		embryonic stem cell	E_01_0124	Rna-fish, RT qPCR, chromatin immunoprecipitation, Western blot,	This ERV was hijacked by younger hominoid-specific ERVs that gave rise to the promoter of XACT, thus wiring its expression to the pluripotency network. This work illustrates how retroviral-derived sequences may intervene in species-specific regulatory pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This ERV was hijacked by younger hominoid-specific ERVs that gave rise to the promoter of XACT, thus wiring its expression to the pluripotency network. This work illustrates how retroviral-derived sequences may intervene in species-specific regulatory pathways.		This ERV was hijacked by younger hominoid-specific ERVs that gave rise to the promoter of XACT, thus wiring its expression to the pluripotency network. This work illustrates how retroviral-derived sequences may intervene in species-specific regulatory pathways.	Immunohistochemical staining	This ERV was hijacked by younger hominoid-specific ERVs that gave rise to the promoter of XACT, thus wiring its expression to the pluripotency network. This work illustrates how retroviral-derived sequences may intervene in species-specific regulatory pathways.			RNA-FISH，RT-qPCR，染色质免疫沉淀，western blot，				XACT
31826955	chr14	37586693	37588693	FOXA1	Our study has uncovered high FOXA1-induced enhancer reprogramming and HIF-2α-dependent transcriptional programs as vulnerable targets for treating endocrine-resistant and metastatic breast cancer.	human	breast	High+Lowthroughput	FOXA1 upregulation promotes enhancer and transcriptional reprogramming in endocrine-resistant breast cancer	否	无	mammary cancer	MCF7L cell，T47D cell，600MPE cell	E_01_0125	Western blot, immunohistochemistry, QRT PCR	Our study has uncovered high FOXA1-induced enhancer reprogramming and HIF-2α-dependent transcriptional programs as vulnerable targets for treating endocrine-resistant and metastatic breast cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our study has uncovered high FOXA1-induced enhancer reprogramming and HIF-2α-dependent transcriptional programs as vulnerable targets for treating endocrine-resistant and metastatic breast cancer.	Immunohistochemical staining	Our study has uncovered high FOXA1-induced enhancer reprogramming and HIF-2α-dependent transcriptional programs as vulnerable targets for treating endocrine-resistant and metastatic breast cancer.	FOXA1		Western blot，免疫组化，qRT-PCR	Our study has uncovered high FOXA1-induced enhancer reprogramming and HIF-2α-dependent transcriptional programs as vulnerable targets for treating endocrine-resistant and metastatic breast cancer.			
31825847	chr20	64045290	64047290	SOX18	The SOX18 transcription factor (TF) coincided with a HGSOC-specific SE, and ectopic overexpression of SOX18 in FTSECs caused epithelial-to-mesenchymal transition, indicating that SOX18 plays a role in establishing the mesenchymal signature of fallopian-derived HGSOCs.	human	ovary	High+Lowthroughput	A Study of High-Grade Serous Ovarian Cancer Origins Implicates the SOX18 Transcription Factor in Tumor Development	否	无	oophoroma	FT246，FT282，FT318，CaOV3，COV318，EFO21，Kuramochi，FUOV1，OAW28，OV177，OVSAHO，TykNu，UWB1.289 cell	E_01_0126	western blot，qRT-PCR	The SOX18 transcription factor (TF) coincided with a HGSOC-specific SE, and ectopic overexpression of SOX18 in FTSECs caused epithelial-to-mesenchymal transition, indicating that SOX18 plays a role in establishing the mesenchymal signature of fallopian-derived HGSOCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The SOX18 transcription factor (TF) coincided with a HGSOC-specific SE, and ectopic overexpression of SOX18 in FTSECs caused epithelial-to-mesenchymal transition, indicating that SOX18 plays a role in establishing the mesenchymal signature of fallopian-derived HGSOCs.	Immunohistochemical staining	The SOX18 transcription factor (TF) coincided with a HGSOC-specific SE, and ectopic overexpression of SOX18 in FTSECs caused epithelial-to-mesenchymal transition, indicating that SOX18 plays a role in establishing the mesenchymal signature of fallopian-derived HGSOCs.	SOX18		western blot，qRT-PCR	The SOX18 transcription factor (TF) coincided with a HGSOC-specific SE, and ectopic overexpression of SOX18 in FTSECs caused epithelial-to-mesenchymal transition, indicating that SOX18 plays a role in establishing the mesenchymal signature of fallopian-derived HGSOCs.			
31819273	chr7	148804439	148806439	EZH2	Using a hydrophobic tagging approach, we generated MS1943, a first-in-class EZH2 selective degrader that effectively reduces EZH2 levels in cells. Importantly, MS1943 has a profound cytotoxic effect in multiple TNBC cells, while sparing normal cells, and is efficacious in vivo, suggesting that pharmacologic degradation of EZH2 can be advantageous for treating the cancers that are dependent on EZH2.	human	breast	High+Lowthroughput	Discovery of a first-in-class EZH2 selective degrader	否	无	cancer	MDA-MB-231，MDA-MB-468，BT549	E_01_0127	Western blot, cell viability assay, crystal violet staining, QRT PCR	Using a hydrophobic tagging approach, we generated MS1943, a first-in-class EZH2 selective degrader that effectively reduces EZH2 levels in cells. Importantly, MS1943 has a profound cytotoxic effect in multiple TNBC cells, while sparing normal cells, and is efficacious in vivo, suggesting that pharmacologic degradation of EZH2 can be advantageous for treating the cancers that are dependent on EZH2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Using a hydrophobic tagging approach, we generated MS1943, a first-in-class EZH2 selective degrader that effectively reduces EZH2 levels in cells. Importantly, MS1943 has a profound cytotoxic effect in multiple TNBC cells, while sparing normal cells, and is efficacious in vivo, suggesting that pharmacologic degradation of EZH2 can be advantageous for treating the cancers that are dependent on EZH2.	Immunohistochemical staining	Using a hydrophobic tagging approach, we generated MS1943, a first-in-class EZH2 selective degrader that effectively reduces EZH2 levels in cells. Importantly, MS1943 has a profound cytotoxic effect in multiple TNBC cells, while sparing normal cells, and is efficacious in vivo, suggesting that pharmacologic degradation of EZH2 can be advantageous for treating the cancers that are dependent on EZH2.	EZH2		western blot，细胞活力检测，结晶紫染色，qRT-PCR	Using a hydrophobic tagging approach, we generated MS1943, a first-in-class EZH2 selective degrader that effectively reduces EZH2 levels in cells. Importantly, MS1943 has a profound cytotoxic effect in multiple TNBC cells, while sparing normal cells, and is efficacious in vivo, suggesting that pharmacologic degradation of EZH2 can be advantageous for treating the cancers that are dependent on EZH2.			
31817839	chr1	115283204	115285204	NGF	NGF-Enhanced Vasculogenic Properties of Epithelial Ovarian Cancer Cells Is Reduced by Inhibition of the COX-2/PGE 2 Signaling Axis	human	ovary	High+Lowthroughput	NGF-Enhanced Vasculogenic Properties of Epithelial Ovarian Cancer Cells Is Reduced by Inhibition of the COX-2/PGE 2 Signaling Axis	否	无	Epithelial ovarian cancer	HOSE cell，A2780 cell，SKOV3 cell，OV90 cell，NIH-OVCAR3 cell	E_01_0128	Immunohistochemistry, immunocytochemistry, Western blot, QRT PCR, ELISA	NGF-Enhanced Vasculogenic Properties of Epithelial Ovarian Cancer Cells Is Reduced by Inhibition of the COX-2/PGE 2 Signaling Axis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	NGF-Enhanced Vasculogenic Properties of Epithelial Ovarian Cancer Cells Is Reduced by Inhibition of the COX-2/PGE 2 Signaling Axis		NGF-Enhanced Vasculogenic Properties of Epithelial Ovarian Cancer Cells Is Reduced by Inhibition of the COX-2/PGE 2 Signaling Axis	Immunohistochemical staining	NGF-Enhanced Vasculogenic Properties of Epithelial Ovarian Cancer Cells Is Reduced by Inhibition of the COX-2/PGE 2 Signaling Axis			免疫组织化学，免疫细胞化学，Western Blot，qRT-PCR， ELISA				NGF
31815603	chr6	133886394	133888394	TCF21	These data indicate that TCF21 antagonizes the MYOCD-SRF pathway through multiple mechanisms, further establishing a role for this coronary artery disease-associated gene in fundamental SMC processes and indicating the importance of smooth muscle response to vascular stress and phenotypic modulation of this cell type in coronary artery disease risk.	mouse	coronary artery	High+Lowthroughput	Coronary Disease-Associated Gene TCF21 Inhibits Smooth Muscle Cell Differentiation by Blocking the Myocardin-Serum Response Factor Pathway	否	无	coronary artery disease 	smooth muscle cell	E_02_0068	Western blot, chromatin immunoprecipitation sequencing, transfection	These data indicate that TCF21 antagonizes the MYOCD-SRF pathway through multiple mechanisms, further establishing a role for this coronary artery disease-associated gene in fundamental SMC processes and indicating the importance of smooth muscle response to vascular stress and phenotypic modulation of this cell type in coronary artery disease risk.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These data indicate that TCF21 antagonizes the MYOCD-SRF pathway through multiple mechanisms, further establishing a role for this coronary artery disease-associated gene in fundamental SMC processes and indicating the importance of smooth muscle response to vascular stress and phenotypic modulation of this cell type in coronary artery disease risk.		These data indicate that TCF21 antagonizes the MYOCD-SRF pathway through multiple mechanisms, further establishing a role for this coronary artery disease-associated gene in fundamental SMC processes and indicating the importance of smooth muscle response to vascular stress and phenotypic modulation of this cell type in coronary artery disease risk.	Immunohistochemical staining	These data indicate that TCF21 antagonizes the MYOCD-SRF pathway through multiple mechanisms, further establishing a role for this coronary artery disease-associated gene in fundamental SMC processes and indicating the importance of smooth muscle response to vascular stress and phenotypic modulation of this cell type in coronary artery disease risk.			Western Blot，染色质免疫沉淀测序，转染				TCF21
31804013	chr5	151027281	151029281	TNIP1	 Hypomorphic TNIP1 expression results from the combined concordant and opposing effects of multiple risk variants carried on the TNIP1 risk haplotype, with the strongest regulatory effect in B lymphoid lineage cells.	human	Peripheral blood	High+Lowthroughput	Role of Systemic Lupus Erythematosus Risk Variants With Opposing Functional Effects as a Driver of Hypomorphic Expression of TNIP1 and Other Genes Within a Three-Dimensional Chromatin Network	否	无	Systemic lupus erythematosus	Jurkat cell，THP-1cell	E_01_0129	Dual luciferase reporter assay, electrophoretic mobility shift assay, QRT PCR, Western blot, and pulldown	 Hypomorphic TNIP1 expression results from the combined concordant and opposing effects of multiple risk variants carried on the TNIP1 risk haplotype, with the strongest regulatory effect in B lymphoid lineage cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			 Hypomorphic TNIP1 expression results from the combined concordant and opposing effects of multiple risk variants carried on the TNIP1 risk haplotype, with the strongest regulatory effect in B lymphoid lineage cells.	Immunohistochemical staining	 Hypomorphic TNIP1 expression results from the combined concordant and opposing effects of multiple risk variants carried on the TNIP1 risk haplotype, with the strongest regulatory effect in B lymphoid lineage cells.	TNIP1		双荧光素酶报告分析，电泳迁移率分析，qRT-PCR，Western blot，pulldown 	 Hypomorphic TNIP1 expression results from the combined concordant and opposing effects of multiple risk variants carried on the TNIP1 risk haplotype, with the strongest regulatory effect in B lymphoid lineage cells.			
31799674	chr12	53959218	53961218	HOTAIR	LncRNA HOTAIR activates the expression of NF-κB in myeloma cells and promotes the proliferation of myeloma cells.	human	bone marrow	High+Lowthroughput	Effects of lncRNA HOTAIR on proliferation and apoptosis of myeloma cells through NF-κB pathway	否	无	Myeloma	Myeloma cell	E_01_0130	QRT PCR, flow cytometry, Western blot, cell viability assay, transfection	LncRNA HOTAIR activates the expression of NF-κB in myeloma cells and promotes the proliferation of myeloma cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			LncRNA HOTAIR activates the expression of NF-κB in myeloma cells and promotes the proliferation of myeloma cells.	Immunohistochemical staining	LncRNA HOTAIR activates the expression of NF-κB in myeloma cells and promotes the proliferation of myeloma cells.	HOTAIR		qRT-PCR，流式细胞术，Western blot，细胞活力检测，转染	LncRNA HOTAIR activates the expression of NF-κB in myeloma cells and promotes the proliferation of myeloma cells.			
31786140	chr7	27195600	27197600	HOTTIP	HOTTIP lncRNA Promotes Hematopoietic Stem Cell Self-Renewal Leading to AML-like Disease in Mice	mouse	Kidney, bone marrow	High+Lowthroughput	HOTTIP lncRNA Promotes Hematopoietic Stem Cell Self-Renewal Leading to AML-like Disease in Mice	否	无	Acute myeloid leukemia	HEK293T cell，OCI-AML3 cell	E_02_0069	QRT PCR, rip, flow cytometry, chromatin immunoprecipitation	HOTTIP lncRNA Promotes Hematopoietic Stem Cell Self-Renewal Leading to AML-like Disease in Mice	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HOTTIP lncRNA Promotes Hematopoietic Stem Cell Self-Renewal Leading to AML-like Disease in Mice		HOTTIP lncRNA Promotes Hematopoietic Stem Cell Self-Renewal Leading to AML-like Disease in Mice	Immunohistochemical staining	HOTTIP lncRNA Promotes Hematopoietic Stem Cell Self-Renewal Leading to AML-like Disease in Mice			qRT-PCR，RIP，流式细胞术，染色质免疫沉淀				HOTTIP
33081480	chr18	47806258	47808258	SMAD2	GLGZD was able to inhibit miR-155 upregulation, resulting in down-regulation of miR-155-targeted molecules in MCAO rats, including suppressor of cytokine signaling 1 (SOCS1), inhibitor of nuclear factor kappa-B kinase (IKK), mothers against decapentaplegic homolog 2 (SMAD2) and CCAAT/enhancer binding protein beta (CEBPβ).	mouse	brain tissue	High+Lowthroughput	The inhibitory effect of Gualou Guizhi Decoction on post-ischemic neuroinflammation via miR-155 in MCAO rats	否		stroke	Inflammatory cell	E_02_0070	RT-qPCR，Western blot，Immunohistochemistry	GLGZD was able to inhibit miR-155 upregulation, resulting in down-regulation of miR-155-targeted molecules in MCAO rats, including suppressor of cytokine signaling 1 (SOCS1), inhibitor of nuclear factor kappa-B kinase (IKK), mothers against decapentaplegic homolog 2 (SMAD2) and CCAAT/enhancer binding protein beta (CEBPβ).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	GLGZD was able to inhibit miR-155 upregulation, resulting in down-regulation of miR-155-targeted molecules in MCAO rats, including suppressor of cytokine signaling 1 (SOCS1), inhibitor of nuclear factor kappa-B kinase (IKK), mothers against decapentaplegic homolog 2 (SMAD2) and CCAAT/enhancer binding protein beta (CEBPβ).		GLGZD was able to inhibit miR-155 upregulation, resulting in down-regulation of miR-155-targeted molecules in MCAO rats, including suppressor of cytokine signaling 1 (SOCS1), inhibitor of nuclear factor kappa-B kinase (IKK), mothers against decapentaplegic homolog 2 (SMAD2) and CCAAT/enhancer binding protein beta (CEBPβ).	Immunohistochemical staining	GLGZD was able to inhibit miR-155 upregulation, resulting in down-regulation of miR-155-targeted molecules in MCAO rats, including suppressor of cytokine signaling 1 (SOCS1), inhibitor of nuclear factor kappa-B kinase (IKK), mothers against decapentaplegic homolog 2 (SMAD2) and CCAAT/enhancer binding protein beta (CEBPβ).			RT-qPCR，Western blot，Immunohistochemistry				SMAD2
29861522	chr3	149159891	149161891	CP	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.	mouse	Epithelial tissues	High+Lowthroughput	Effect of diethyldithiocarbamate in cyclophosphamide-induced nephrotoxicity: Immunohistochemical study of superoxide dismutase 1 in rat	否		Renal impairment	nephron tubule epithelial cell	E_02_0071	Biochemical analyses,Immunohistochemistry	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.		The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.	Immunohistochemical staining	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.			Biochemical analyses,Immunohistochemistry				CP
29861522	chr21	31656571	31658571	SOD1	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.	mouse	Epithelial tissues	High+Lowthroughput	Effect of diethyldithiocarbamate in cyclophosphamide-induced nephrotoxicity: Immunohistochemical study of superoxide dismutase 1 in rat	否		Renal impairment	nephron tubule epithelial cell	E_02_0071	Biochemical analyses,Immunohistochemistry	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.		The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.	Immunohistochemical staining	The present study indicates that DEDTC administration further exacerbated the CP-induced kidney damage in rat.			Biochemical analyses,Immunohistochemistry				SOD1
29861296	chr18	26013138	26015138	SS18	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.	human	Synovial sarcoma tissues	High+Lowthroughput	The SS18-SSX Fusion Oncoprotein Hijacks BAF Complex Targeting and Function to Drive Synovial Sarcoma	否		Synovial sarcoma (SS)	HEK293T LentiX cell	E_01_0131	Gene Knockdown,Western Blot,Immunoprecipitations,CRISPR/Cas9,Cell Proliferation Assay,Immunohistochemistry,Chromatin Immunoprecipitation (ChIP),RNA Isolation,RNA-seq,Assay for Transposase-Accessible Chromatin Sequencing (ATAC-seq),ChIP-Seq ,CHIP,Whole Exome Sequencing of Tumors	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.		These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.	Immunohistochemical staining	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.			Gene Knockdown,Western Blot,Immunoprecipitations,CRISPR/Cas9,Cell Proliferation Assay,Immunohistochemistry,Chromatin Immunoprecipitation (ChIP),RNA Isolation,RNA-seq,Assay for Transposase-Accessible Chromatin Sequencing (ATAC-seq),ChIP-Seq ,CHIP,Whole Exome Sequencing of Tumors				SS18
29861296	chr22	23783961	23785961	SMARCB1	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.	human	Synovial sarcoma tissues	High+Lowthroughput	The SS18-SSX Fusion Oncoprotein Hijacks BAF Complex Targeting and Function to Drive Synovial Sarcoma	否		Synovial sarcoma (SS)	HEK293T LentiX cell	E_01_0131	Gene Knockdown,Western Blot,Immunoprecipitations,CRISPR/Cas9,Cell Proliferation Assay,Immunohistochemistry,Chromatin Immunoprecipitation (ChIP),RNA Isolation,RNA-seq,Assay for Transposase-Accessible Chromatin Sequencing (ATAC-seq),ChIP-Seq ,CHIP,Whole Exome Sequencing of Tumors	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.		These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.	Immunohistochemical staining	These results establish a global hijacking mechanism for SS18-SSX on chromatin, and define the distinct contributions of two concurrent BAF complex perturbations.			Gene Knockdown,Western Blot,Immunoprecipitations,CRISPR/Cas9,Cell Proliferation Assay,Immunohistochemistry,Chromatin Immunoprecipitation (ChIP),RNA Isolation,RNA-seq,Assay for Transposase-Accessible Chromatin Sequencing (ATAC-seq),ChIP-Seq ,CHIP,Whole Exome Sequencing of Tumors				SMARCB1
29859467	chr10	67881752	67883752	SIRT1	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	mouse	Epididymal white adipose tissue	High+Lowthroughput	Qing Gan Zi Shen Tang alleviates adipose tissue dysfunction with up-regulation of SIRT1 in spontaneously hypertensive rat	否		Hypertension, obesity, hyperlipidemia, insulin resistance	fat cell	E_02_0072	ELISA,Western blot,Quantitative reverse transcription polymerase chain reaction (qRT-PCR),Immunohistochemistry analysis,HPLC	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.		Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	Immunohistochemical staining	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.			ELISA,Western blot,Quantitative reverse transcription polymerase chain reaction (qRT-PCR),Immunohistochemistry analysis,HPLC				SIRT1
29859467	chr13	40553149	40555149	FOXO1	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	mouse	Epididymal white adipose tissue	High+Lowthroughput	Qing Gan Zi Shen Tang alleviates adipose tissue dysfunction with up-regulation of SIRT1 in spontaneously hypertensive rat	否		Hypertension, obesity, hyperlipidemia, insulin resistance	fat cell	E_02_0072	ELISA,Western blot,Quantitative reverse transcription polymerase chain reaction (qRT-PCR),Immunohistochemistry analysis,HPLC	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.		Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	Immunohistochemical staining	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.			ELISA,Western blot,Quantitative reverse transcription polymerase chain reaction (qRT-PCR),Immunohistochemistry analysis,HPLC				FOXO1
29859467	chr8	81475508	81477508	FABP4	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	mouse	Epididymal white adipose tissue	High+Lowthroughput	Qing Gan Zi Shen Tang alleviates adipose tissue dysfunction with up-regulation of SIRT1 in spontaneously hypertensive rat	否		Hypertension, obesity, hyperlipidemia, insulin resistance	fat cell	E_02_0072	ELISA,Western blot,Quantitative reverse transcription polymerase chain reaction (qRT-PCR),Immunohistochemistry analysis,HPLC	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.		Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.	Immunohistochemical staining	Collectively, our research demonstrated for the first time that QGZST is able to alleviate eWAT dysfunction with up-regulation of SIRT1 in HFD-fed SHRs, which might supply further insight into QGZST-mediated anti-hypertension and anti-obesity effects.			ELISA,Western blot,Quantitative reverse transcription polymerase chain reaction (qRT-PCR),Immunohistochemistry analysis,HPLC				FABP4
29859124	chr1	11009935	11011935	TARDBP	Our study establishes possible mechanisms behind paraspeckle hyper-assembly in ALS and suggests their utility as therapeutic targets in ALS and other diseases with abnormal metabolism of microRNA and dsRNA.	human	Nervous tissue	High+Lowthroughput	Protective paraspeckle hyper-assembly downstream of TDP-43 loss of function in amyotrophic lateral sclerosis	否		Amyotrophic lateral sclerosis (ALS)	SH-SY5Y neuroblastoma cell	E_01_0132	Immunocytochemistry,RNA-FISH,RIP,PCR,Western blot,qRT-PCR,Real-time qPCR,transfection,Cell Viability Assay	Our study establishes possible mechanisms behind paraspeckle hyper-assembly in ALS and suggests their utility as therapeutic targets in ALS and other diseases with abnormal metabolism of microRNA and dsRNA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our study establishes possible mechanisms behind paraspeckle hyper-assembly in ALS and suggests their utility as therapeutic targets in ALS and other diseases with abnormal metabolism of microRNA and dsRNA.		Our study establishes possible mechanisms behind paraspeckle hyper-assembly in ALS and suggests their utility as therapeutic targets in ALS and other diseases with abnormal metabolism of microRNA and dsRNA.	Immunohistochemical staining	Our study establishes possible mechanisms behind paraspeckle hyper-assembly in ALS and suggests their utility as therapeutic targets in ALS and other diseases with abnormal metabolism of microRNA and dsRNA.			Immunocytochemistry,RNA-FISH,RIP,PCR,Western blot,qRT-PCR,Real-time qPCR,transfection,Cell Viability Assay				TARDBP
31484726	chr12	53959112	53961112	HOTAIR	Focusing on a well-known lncRNA, HOTAIR, four distinct epigenetic modification patterns were observed. The majority of HOTAIR binding sites (50.1%) were located within quiescent regions.	human,mouse		High+Lowthroughput	Comprehensive analysis of long noncoding RNA (lncRNA)-chromatin interactions reveals lncRNA functions dependent on binding diverse regulatory elements	否		cervical carcinoma	HeLa-S3 cell	E_02_0073	PCR,Flow cytometry	Focusing on a well-known lncRNA, HOTAIR, four distinct epigenetic modification patterns were observed. The majority of HOTAIR binding sites (50.1%) were located within quiescent regions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Focusing on a well-known lncRNA, HOTAIR, four distinct epigenetic modification patterns were observed. The majority of HOTAIR binding sites (50.1%) were located within quiescent regions.		Focusing on a well-known lncRNA, HOTAIR, four distinct epigenetic modification patterns were observed. The majority of HOTAIR binding sites (50.1%) were located within quiescent regions.	Immunohistochemical staining	Focusing on a well-known lncRNA, HOTAIR, four distinct epigenetic modification patterns were observed. The majority of HOTAIR binding sites (50.1%) were located within quiescent regions.			PCR,Flow cytometry				HOTAIR
31484079	chr7	150942398	150944398	KCNH2	The human ether-a-go-go-related gene KCNH2 encodes the voltage-gated potassium channel underlying IKr, a current critical for the repolarization phase of the cardiac action potential.	human,mouse	liver	High+Lowthroughput	Identification and Characterization of a Transcribed Distal Enhancer Involved in Cardiac Kcnh2 Regulation	是	rs9640171	liver cancer	hepatocellular carcinoma derived cell	E_02_0074	PCR,Flow cytometry	The human ether-a-go-go-related gene KCNH2 encodes the voltage-gated potassium channel underlying IKr, a current critical for the repolarization phase of the cardiac action potential.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The human ether-a-go-go-related gene KCNH2 encodes the voltage-gated potassium channel underlying IKr, a current critical for the repolarization phase of the cardiac action potential.		The human ether-a-go-go-related gene KCNH2 encodes the voltage-gated potassium channel underlying IKr, a current critical for the repolarization phase of the cardiac action potential.	Immunohistochemical staining	The human ether-a-go-go-related gene KCNH2 encodes the voltage-gated potassium channel underlying IKr, a current critical for the repolarization phase of the cardiac action potential.			PCR,Flow cytometry				KCNH2
32517740	chr4	153777966	153779966	SFRP2	We investigated the SFRP2 methylation in peripheral blood mononuclear cells (PBMCs), visceral adipose tissue (VAT), CRC tumor tissue, and adjacent tumor-free area. We also determined the relationship between SFRP2 methylation and methylation of carcinogenic and adipogenic genes.	human		High+Lowthroughput	Association between variation of circulating 25-OH vitamin D and methylation of secreted frizzled-related protein 2 in colorectal cancer	否		Colorectal cancer	Human colorectal carcinoma cell	E_01_0133	PCR	We investigated the SFRP2 methylation in peripheral blood mononuclear cells (PBMCs), visceral adipose tissue (VAT), CRC tumor tissue, and adjacent tumor-free area. We also determined the relationship between SFRP2 methylation and methylation of carcinogenic and adipogenic genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We investigated the SFRP2 methylation in peripheral blood mononuclear cells (PBMCs), visceral adipose tissue (VAT), CRC tumor tissue, and adjacent tumor-free area. We also determined the relationship between SFRP2 methylation and methylation of carcinogenic and adipogenic genes.		We investigated the SFRP2 methylation in peripheral blood mononuclear cells (PBMCs), visceral adipose tissue (VAT), CRC tumor tissue, and adjacent tumor-free area. We also determined the relationship between SFRP2 methylation and methylation of carcinogenic and adipogenic genes.	Immunohistochemical staining	We investigated the SFRP2 methylation in peripheral blood mononuclear cells (PBMCs), visceral adipose tissue (VAT), CRC tumor tissue, and adjacent tumor-free area. We also determined the relationship between SFRP2 methylation and methylation of carcinogenic and adipogenic genes.			PCR				SFRP2
32517078	chr10	112947720	112949720	TCF7L2	We report here that TCF7L2 transcription factor expression was found to be correlated to blast cell numbers during the progression of the disease.	human		High+Lowthroughput	Embryonic Program Activated during Blast Crisis of Chronic Myelogenous Leukemia (CML) Implicates a TCF7L2 and MYC Cooperative Chromatin Binding	否		Chronic Myelogenous Leukemia	K562 cell	E_01_0134	QRT-PCR，	We report here that TCF7L2 transcription factor expression was found to be correlated to blast cell numbers during the progression of the disease.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We report here that TCF7L2 transcription factor expression was found to be correlated to blast cell numbers during the progression of the disease.	Immunohistochemical staining	We report here that TCF7L2 transcription factor expression was found to be correlated to blast cell numbers during the progression of the disease.	TCF7L2		QRT-PCR，	We report here that TCF7L2 transcription factor expression was found to be correlated to blast cell numbers during the progression of the disease.			
32514254	chr12	56749082	56751082	HSD17B6	HSD17B6 inhibited tumor cell proliferation, migration and invasion in liver cancer cells and low expression of HSD17B6 correlated with high immune cells infltration, relative reduction of immune responses and multiple immune checkpoint genes expression in HCC, probably by regulating the expression of TGFB1.	human		High+Lowthroughput	Downexpression of HSD17B6 correlates with clinical prognosis and tumor immune infiltrates in hepatocellular carcinoma	否		Hepatocellular carcinoma	HCC cell	E_01_0135	Gene set enrichment analysis，RT‑qPCR，Western blot	HSD17B6 inhibited tumor cell proliferation, migration and invasion in liver cancer cells and low expression of HSD17B6 correlated with high immune cells infltration, relative reduction of immune responses and multiple immune checkpoint genes expression in HCC, probably by regulating the expression of TGFB1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HSD17B6 inhibited tumor cell proliferation, migration and invasion in liver cancer cells and low expression of HSD17B6 correlated with high immune cells infltration, relative reduction of immune responses and multiple immune checkpoint genes expression in HCC, probably by regulating the expression of TGFB1.		HSD17B6 inhibited tumor cell proliferation, migration and invasion in liver cancer cells and low expression of HSD17B6 correlated with high immune cells infltration, relative reduction of immune responses and multiple immune checkpoint genes expression in HCC, probably by regulating the expression of TGFB1.	Immunohistochemical staining	HSD17B6 inhibited tumor cell proliferation, migration and invasion in liver cancer cells and low expression of HSD17B6 correlated with high immune cells infltration, relative reduction of immune responses and multiple immune checkpoint genes expression in HCC, probably by regulating the expression of TGFB1.			Gene set enrichment analysis，RT‑qPCR，Western blot				HSD17B6
29945972	chrX	49025737	49027737	TFE3	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.	human,mouse		High+Lowthroughput	Protein phosphatase 2A stimulates activation of TFEB and TFE3 transcription factors in response to oxidative stress	否		cancer		E_02_0075	Western blot, immunofluorescence staining	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.		The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.	Immunohistochemical staining	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.			western blot,免疫荧光染色				TFE3
29945972	chr14	105848654	105850654	IGHM	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.	human,mouse		High+Lowthroughput	Protein phosphatase 2A stimulates activation of TFEB and TFE3 transcription factors in response to oxidative stress	否		cancer		E_02_0075	Western blot, immunofluorescence staining	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.		The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.	Immunohistochemical staining	The transcriptional regulators transcription factor EB (TFEB) and transcription factor binding to IGHM enhancer 3 (TFE3) play a key role in the control of these stress pathways.			western blot,免疫荧光染色				IGHM
29945888	chr11	120233455	120235455	POU2F3	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	human		High+Lowthroughput	POU2F3 is a master regulator of a tuft cell-like variant of small cell lung cancer	否		Small cell lung cancer (SCLC)	SCLC cell	E_01_0136	Rna-fish, human SCLC immunohistochemistry, Western blot, RNA SEQ, GSEA, chip SEQ, immunofluorescence staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Immunohistochemical staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	POU2F3		RNA-FISH,Human SCLC immunohistochemistry,Western blot,RNA-seq,GSEA,ChIP-seq,免疫荧光染色	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).			
29945888	chr12	102954806	102956806	ASCL1	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	human		High+Lowthroughput	POU2F3 is a master regulator of a tuft cell-like variant of small cell lung cancer	否		Small cell lung cancer (SCLC)	SCLC cell	E_01_0136	Rna-fish, human SCLC immunohistochemistry, Western blot, RNA SEQ, GSEA, chip SEQ, immunofluorescence staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Immunohistochemical staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	ASCL1		RNA-FISH,Human SCLC immunohistochemistry,Western blot,RNA-seq,GSEA,ChIP-seq,免疫荧光染色	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).			
29945888	chr2	181665466	181667466	NEUROD1	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	human		High+Lowthroughput	POU2F3 is a master regulator of a tuft cell-like variant of small cell lung cancer	否		Small cell lung cancer (SCLC)	SCLC cell	E_01_0136	Rna-fish, human SCLC immunohistochemistry, Western blot, RNA SEQ, GSEA, chip SEQ, immunofluorescence staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Immunohistochemical staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	NEUROD1		RNA-FISH,Human SCLC immunohistochemistry,Western blot,RNA-seq,GSEA,ChIP-seq,免疫荧光染色	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).			
29945888	chr20	20365577	20367577	INSM1	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	human		High+Lowthroughput	POU2F3 is a master regulator of a tuft cell-like variant of small cell lung cancer	否		Small cell lung cancer (SCLC)	SCLC cell	E_01_0136	Rna-fish, human SCLC immunohistochemistry, Western blot, RNA SEQ, GSEA, chip SEQ, immunofluorescence staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	Immunohistochemical staining	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).	INSM1		RNA-FISH,Human SCLC immunohistochemistry,Western blot,RNA-seq,GSEA,ChIP-seq,免疫荧光染色	An analysis of human SCLC specimens revealed that POU2F3 is expressed exclusively in variant SCLC tumors that lack expression of neuroendocrine markers and instead express markers of a chemosensory lineage known as tuft cells.                                                                                                                                                                                                                                                                                                                                                                                                        Moreover, we show that most SCLC tumors can be classified into one of three lineages based on the expression of POU2F3, ASCL1, or NEUROD1.                                                                                                                                                 Experiments in genetically engineered mice suggest a pulmonary neuroendocrine cell of origin for SCLC (Semenova et al. 2015), which is supported by the expression of neuroendocrine differentiation markers chromogranin A (CHGA) and insulinoma-associated protein 1 (INSM1) in human SCLC tumors (Gazdar et al. 2017).			
29945296	chr13	31737329	31739329	Foxq1	In particular, the Fox transcription factor binding motif was frequently observed within EWS FLI1 peaks and Foxq1 was identified as the cooperative partner that interacts with the EWS portion of EWS FLI1. 	human,mouse		High+Lowthroughput	EWS-FLI1 regulates a transcriptional program in cooperation with Foxq1 in mouse Ewing sarcoma	否		Ewing sarcoma		E_02_0076	Real ‐ time quantitative PCR, luciferase assay, chip ‐ SEQ, statistical analysis	In particular, the Fox transcription factor binding motif was frequently observed within EWS FLI1 peaks and Foxq1 was identified as the cooperative partner that interacts with the EWS portion of EWS FLI1. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In particular, the Fox transcription factor binding motif was frequently observed within EWS FLI1 peaks and Foxq1 was identified as the cooperative partner that interacts with the EWS portion of EWS FLI1. 		In particular, the Fox transcription factor binding motif was frequently observed within EWS FLI1 peaks and Foxq1 was identified as the cooperative partner that interacts with the EWS portion of EWS FLI1. 	Immunohistochemical staining	In particular, the Fox transcription factor binding motif was frequently observed within EWS FLI1 peaks and Foxq1 was identified as the cooperative partner that interacts with the EWS portion of EWS FLI1. 			Real‐time quantitative PCR,Luciferase assay,ChIP‐Seq,统计分析				Foxq1
29941955	chr1	186441221	186443221	PDC	Pyruvate decarboxylase (PDC), 1-amino cyclopropane 1-carboxylic acid oxidase (ACO), glutamine synthetase (GS), glutathione S-transferases (GST) and beta-1, 3-glucanase in adventitious, nodal and seminal roots were more abundant in TF58 than those in TF57 under waterlogging stress.	mouse		High+Lowthroughput	Elucidating the hypoxic stress response in barley (Hordeum vulgare L.) during waterlogging: A proteomics approach	否				E_02_0077	QRT PCR, Western blot, statistical analysis	Pyruvate decarboxylase (PDC), 1-amino cyclopropane 1-carboxylic acid oxidase (ACO), glutamine synthetase (GS), glutathione S-transferases (GST) and beta-1, 3-glucanase in adventitious, nodal and seminal roots were more abundant in TF58 than those in TF57 under waterlogging stress.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Pyruvate decarboxylase (PDC), 1-amino cyclopropane 1-carboxylic acid oxidase (ACO), glutamine synthetase (GS), glutathione S-transferases (GST) and beta-1, 3-glucanase in adventitious, nodal and seminal roots were more abundant in TF58 than those in TF57 under waterlogging stress.		Pyruvate decarboxylase (PDC), 1-amino cyclopropane 1-carboxylic acid oxidase (ACO), glutamine synthetase (GS), glutathione S-transferases (GST) and beta-1, 3-glucanase in adventitious, nodal and seminal roots were more abundant in TF58 than those in TF57 under waterlogging stress.	Immunohistochemical staining	Pyruvate decarboxylase (PDC), 1-amino cyclopropane 1-carboxylic acid oxidase (ACO), glutamine synthetase (GS), glutathione S-transferases (GST) and beta-1, 3-glucanase in adventitious, nodal and seminal roots were more abundant in TF58 than those in TF57 under waterlogging stress.			qRT-PCR,Western blot,统计分析				PDC
29594316	chr1	26690341	26692341	ARID1A	In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 	human,mouse	Lymphoid tissue, liver tissue	High+Lowthroughput	ARID1A loss in adult hepatocytes activates β-catenin-mediated erythropoietin transcription	否			erythrocyte，stem cell	E_02_0078	Immunohistochemistry and in situ hybridization experiments, enzyme-linked immunosorbent assay (ELISA), cell transfection, stimulation and luciferase assays, RNA extraction and quantitative RT-PCR, protein extracts and Western blotting, electrophoretic mobility shift assay (EMSA), flow cytometry and forming unit erythroid (CFU-E) assays, chromatin immunoprecipitation (chip) and ATAC qPCR assays were performed	In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 		In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 	Immunohistochemical staining	In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 			免疫组化和原位杂交实验，酶联免疫吸附测定（ELISA），细胞转染、刺激和荧光素酶检测，RNA 提取和定量 RT-PCR，蛋白质提取物和蛋白质印迹，电泳迁移率移位测定 （EMSA），流式细胞术和成形单元红系 （CFU-E） 检测，染色质免疫沉淀 （ChIP） 和 ATAC-qPCR 检测				ARID1A
29593713	chr17	27054976	27056976	Nkx2-5	We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.	mouse	Musculature	High+Lowthroughput	Divergent Transcription of the Nkx2-5 Locus Generates Two Enhancer RNAs with Opposing Functions	否		heart failure	cardiac muscle cell (sensu Arthopoda)	E_02_0079	RNA sequencing (RNA SEQ), quantitative PCR (qPCR), cell fractionation, rna-fish, Western blotting, fluorescent immunoassay	We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.		We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.	Immunohistochemical staining	We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.			RNA测序（RNA-seq），定量PCR（qPCR），细胞分馏，RNA-FISH，蛋白质印记，荧光免疫分析				Nkx2-5
29592873	chr13	73052423	73054423	KLF5	These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.	mouse	connective tissue	High+Lowthroughput	Regulation of adipocyte differentiation by clusterin-mediated Krüppel-like factor 5 stabilization	否			fat cell，mesenchymal stem cell	E_02_0080	RNA isolation and quantitative real_x0002_time PCR (qRT-PCR)，Luciferase reporter assay，20S proteasome activity assay	These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.		These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.	Immunohistochemical staining	These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.			RNA isolation and quantitative real_x0002_time PCR (qRT-PCR)，Luciferase reporter assay，20S proteasome activity assay				KLF5
29583017	chr6	47504032	47506032	Ezh2	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.	mouse	Bone marrow	High+Lowthroughput	Hematopoietic stem/progenitor cell senescence is associated with altered expression profiles of cellular memory-involved gene	否		senescence associated disease	progenitor cell	E_02_0081	qRT-PCR	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.		Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.	Immunohistochemical staining	Ezh2 is a key member of the PcG family. It can promote the survival of HSCs.			qRT-PCR				Ezh2
29580634	chr5	173229639	173231639	NKX2-5	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	human	Vascular tissue	High+Lowthroughput	Molecular Basis for Dysregulated Activation of NKX2-5 in the Vascular Remodeling of Systemic Sclerosis	是	rs3095870	scleroderma associated pulmonary hypertensio	smooth muscle cell of the pulmonary artery	E_01_0137	Western blot,qPCR	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	Immunohistochemical staining	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.	NKX2-5		Western blot,qPCR	NKX2-5 is a homeobox transcription factor required for the formation of the heart and vessels during development, with significant postnatal downregulation and reactivation in disease states characterised by vascular remodelling.			
29579222	chr11	12671903	12673903	TEAD1	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	human	Vascular tissue	High+Lowthroughput	Molecular Basis for Dysregulated Activation of NKX2-5 in the Vascular Remodeling of Systemic Sclerosis	是	rs3095870	scleroderma associated pulmonary hypertensio	smooth muscle cell of the pulmonary artery	E_01_0138	Western blot,qPCR	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	Immunohistochemical staining	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease	TEAD1		Western blot,qPCR	TEAD1 is a member of TEA/ATTS domain family transcription regulators with distinct and important roles in VSMC differentiation and in cardiovascular disease			
29579159	chr15	61854370	61856370	Myc	The transcription factor Myc is essential for the regulation of haematopoietic stem cells and progenitors and has a critical function in haematopoietic malignancies	mouse	Haematopoietic tissue	High+Lowthroughput	A Myc enhancer cluster regulates normal and leukaemic haematopoietic stem cell hierarchies	否		haematopoietic malignancies	hematopoietic stem cell	E_02_0082	RT–qPCR,ATAC-seq,RNA-seq,	The transcription factor Myc is essential for the regulation of haematopoietic stem cells and progenitors and has a critical function in haematopoietic malignancies	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcription factor Myc is essential for the regulation of haematopoietic stem cells and progenitors and has a critical function in haematopoietic malignancies		The transcription factor Myc is essential for the regulation of haematopoietic stem cells and progenitors and has a critical function in haematopoietic malignancies	Immunohistochemical staining	The transcription factor Myc is essential for the regulation of haematopoietic stem cells and progenitors and has a critical function in haematopoietic malignancies			RT–qPCR,ATAC-seq,RNA-seq,				Myc
29576612	chr17	42310573	42312573	STAT3	Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity	human		High+Lowthroughput	Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity	否				E_01_0139	 EZH2 	Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity	Immunohistochemical staining	Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity	STAT3		 EZH2 	Protein kinase A-mediated phosphorylation regulates STAT3 activation and oncogenic EZH2 activity			
29572261	chr12	54030375	54032375	HOXC5	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	human	Somatic tissue	High+Lowthroughput	HoxC5 and miR-615-3p target newly evolved genomic regions to repress hTERT and inhibit tumorigenesis	否		Tumor	somatic cell	E_01_0140	Luciferase reporter assay,Western blot,ChIP-Seq,qRT-PCR,3C-qPCR	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	Immunohistochemical staining	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.	HOXC5		Luciferase reporter assay,Western blot,ChIP-Seq,qRT-PCR,3C-qPCR	Deregulation of HOXC5 and mir-615-3p expression may contribute to the activation of hTERT in human cancers.			
29570423	chr19	19143043	19145043	MEF2B	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.	human	Lymphoid tissue	High+Lowthroughput	Comparison of Myocyte Enhancer Factor 2B Versus Other Germinal Center-associated Antigens in the Differential Diagnosis of B-Cell Non-Hodgkin Lymphomas	否		Lymphomas	B cell	E_01_0141	Immunohistochemical Staining	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.		Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.	Immunohistochemical staining	Myocyte enhancer binding factor 2B (MEF2B) is a transcriptional activator of the BCL6 proto-oncogene in normal germinal center (GC) B-cells.			Immunohistochemical Staining				MEF2B
29569934	chr17	43751254	43753254	SOST	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	human	Bone	High+Lowthroughput	Computational and functional characterization of four SNPs in the SOST locus associated with osteoporosis	是	rs1230399, rs7220711, rs1107748, rs75901553	osteoporosis	Germinal center B-cells	E_01_0142	Luciferase reporter assay,ChIP,qPCR	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.		The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.	Immunohistochemical staining	The SOST gene encodes sclerostin, a C-terminal cysteine knot-like domain containing key negative regulator of osteoblastic bone formation that inhibits LRP5/6-mediated canonical Wnt signaling.			Luciferase reporter assay,ChIP,qPCR				SOST
29568244	chr2	103785432	103787432	Lmo2	T controls the expression of Lmo2, a master regulator of hematopoietic and endothelial development	mouse	Embryo	High+Lowthroughput	BRACHYURY directs histone acetylation to target loci during mesoderm development	否		congenital diseases	hematopoietic and endothelial cell	E_02_0083	ChIP-Seq,RNA-Seq ,ChIP-qPCR	T controls the expression of Lmo2, a master regulator of hematopoietic and endothelial development	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	T controls the expression of Lmo2, a master regulator of hematopoietic and endothelial development		T controls the expression of Lmo2, a master regulator of hematopoietic and endothelial development	Immunohistochemical staining	T controls the expression of Lmo2, a master regulator of hematopoietic and endothelial development			ChIP-Seq,RNA-Seq ,ChIP-qPCR				Lmo2
29564771	chr7	148804053	148806053	EZH2	EZH2 plays an important role in this inflammatory process of dental pulp.	human,mouse	dental pulp tissue	High+Lowthroughput	EZH2 regulates dental pulp inflammation by direct effect on inflammatory factors	否		dental pulp inflammation	dental pulp cell	E_02_0084	qPCR,ChIP,Western blot	EZH2 plays an important role in this inflammatory process of dental pulp.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EZH2 plays an important role in this inflammatory process of dental pulp.		EZH2 plays an important role in this inflammatory process of dental pulp.	Immunohistochemical staining	EZH2 plays an important role in this inflammatory process of dental pulp.			qPCR,ChIP,Western blot				EZH2
29563873	chr14	100892224	100894224	MEG8	"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."	human		High+Lowthroughput	MEG8 long noncoding RNA contributes to epigenetic progression of the epithelial-mesenchymal transition of lung and pancreatic cancer cells	否		Lung and pancreatic cancer	A549 cell，  LC-2/ad cell，Panc1 cell	E_01_0143	"Quantitative PCR，Cell migration assay，Chromatin immunoprecipitation (ChIP) assays，RNA immunoprecipitation (RIP)，Chromatin isolation by RNA purification (ChIRP) 
assays"	"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."		"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."	Immunohistochemical staining	"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."			"Quantitative PCR，Cell migration assay，Chromatin immunoprecipitation (ChIP) assays，RNA immunoprecipitation (RIP)，Chromatin isolation by RNA purification (ChIRP) 
assays"				MEG8
29563767	chr12	55740444	55742444	GDF11	Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 	human		High+Lowthroughput	GDF11 Antagonizes Psoriasis-like Skin Inflammation via Suppression of NF-κB Signaling Pathway	否		Psoriasiform skin inflammation	Mouse leukemic monocyte macrophages	E_01_0144	miRNA transfection，Real-Time PCR,Western Blot,Immunofluorescence,ELISA Assays	Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 	Immunohistochemical staining	Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 	GDF11		miRNA transfection，Real-Time PCR,Western Blot,Immunofluorescence,ELISA Assays	Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 			
29563503	chr8	127077409	127079409	PRNCR1	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	human		High+Lowthroughput	LncRNA PRNCR1 interacts with HEY2 to abolish miR-448-mediated growth inhibition in non-small cell lung cancer	否		Non small cell lung cancer	A549 cell, SK-MES-1 cell, Calu-3 cell，H1299 cell，NHBE cell	E_01_0145	Cell transfection,RNA isolation,qRT-PCR analysi, Cell proliferation assays, Transwell assays,Luciferase reporter analysis,RIP assay, Western blot assay	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 		Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	Immunohistochemical staining	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 			Cell transfection,RNA isolation,qRT-PCR analysi, Cell proliferation assays, Transwell assays,Luciferase reporter analysis,RIP assay, Western blot assay				PRNCR1
29563503	chr6	125744658	125746658	HEY2	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	human		High+Lowthroughput	LncRNA PRNCR1 interacts with HEY2 to abolish miR-448-mediated growth inhibition in non-small cell lung cancer	否		Non small cell lung cancer	A549 cell, SK-MES-1 cell, Calu-3 cell，H1299 cell，NHBE cell	E_01_0145	Cell transfection,RNA isolation,qRT-PCR analysi, Cell proliferation assays, Transwell assays,Luciferase reporter analysis,RIP assay, Western blot assay	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	Immunohistochemical staining	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	HEY2		Cell transfection,RNA isolation,qRT-PCR analysi, Cell proliferation assays, Transwell assays,Luciferase reporter analysis,RIP assay, Western blot assay	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 			
29563192	chr16	67559679	67561679	CTCF	The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.	mouse		High+Lowthroughput	Stochastic Gene Choice during Cellular Differentiation	否			embryonic stem cell	E_02_0085	Single-Cell qRT-PCR,Chromatin Immunoprecipitation,Bisulfite Sequencing	The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.		The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.	Immunohistochemical staining	The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.			Single-Cell qRT-PCR,Chromatin Immunoprecipitation,Bisulfite Sequencing				CTCF
29563176	chr16	67559907	67561907	CTCF	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	human	blood	High+Lowthroughput	The first enhancer in an enhancer chain safeguards subsequent enhancer-promoter contacts from a distance	否			K562 cell	E_01_0146	PCR	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	Immunohistochemical staining	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	CTCF		PCR	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.			
29563122	chr9	21074270	21076270	IFNB1	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	human	uterus	High+Lowthroughput	The Nuclear Matrix Protein SAFA Surveils Viral RNA and Facilitates Immunity by Activating Antiviral Enhancers and Super-enhancers	否			HeLa cell	E_01_0147	PCR, Western blot, flow cytometry, immunofluorescence staining	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	Immunohistochemical staining	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	IFNB1		PCR,Western blot,Flow cytometry,免疫荧光染色	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).			
29563115	chr17	42310596	42312596	STAT3	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.	human,mouse	connective tissue	High+Lowthroughput	Generation of Nanog reporter mice that distinguish pluripotent stem cells from unipotent primordial germ cells	否			pluripotent stem cell	E_02_0086	PCR, flow cytometry, immunofluorescence staining	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.		Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.	Immunohistochemical staining	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.			PCR,Flow cytometry,免疫荧光染色				STAT3
29559957	chr7	99754049	99756049	CYP3A4	The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.	human		High+Lowthroughput	DNA methylation determines the regulation of pregnane X receptor on CYP3A4 expression	否			HepG2 cell	E_01_0148	Plasmid construction，In vitro methylation，Luciferase reporter assay，Transfection and rifampicin induction，RNA isolation and real-time quantitative polymerase chain reaction (RT-qPCR) ，ChIP assay	The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.		The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.	Immunohistochemical staining	The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.			Plasmid construction，In vitro methylation，Luciferase reporter assay，Transfection and rifampicin induction，RNA isolation and real-time quantitative polymerase chain reaction (RT-qPCR) ，ChIP assay				CYP3A4
29557377	chr1	156460952	156462952	MEF2D	We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 	human		High+Lowthroughput	A rare regulatory variant in the MEF2D gene affects gene regulation and splicing and is associated with a SLE sub-phenotype in Swedish cohorts	否			T, B, NK cell	E_01_0149	Gene array capture，Seq,Gene array capture	We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 		We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 	Immunohistochemical staining	We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 			Gene array capture，Seq,Gene array capture				MEF2D
29556394	chr8	144311848	144313848	DGAT1	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	mouse		High+Lowthroughput	Butyric acid induces spontaneous adipocytic differentiation of porcine bone marrow-derived mesenchymal stem cells	否			mesenchymal stem cell	E_02_0087	Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.		Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Immunohistochemical staining	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.			Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 				DGAT1
29556394	chr10	88950906	88952906	FAS	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	mouse		High+Lowthroughput	Butyric acid induces spontaneous adipocytic differentiation of porcine bone marrow-derived mesenchymal stem cells	否			mesenchymal stem cell	E_02_0087	Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.		Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Immunohistochemical staining	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.			Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 				FAS
29556394	chr1	53193789	53195789	CPT2	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	mouse		High+Lowthroughput	Butyric acid induces spontaneous adipocytic differentiation of porcine bone marrow-derived mesenchymal stem cells	否			mesenchymal stem cell	E_02_0087	Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.		Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Immunohistochemical staining	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.			Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 				CPT2
29556082	chr11	65494664	65496664	MALAT1	MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 	human		High+Lowthroughput	Transcriptional Profiling of Hypoxia-Regulated Non-coding RNAs in Human Primary Endothelial Cells	否			 Primary endothelial cell	E_01_0150	GRO-Seq and RNA-Seq,	MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 	Immunohistochemical staining	MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 	MALAT1		GRO-Seq and RNA-Seq,	MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 			
29554889	chr3	133743314	133745314	TF	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	human		High+Lowthroughput	Genomic analysis of transcriptional networks directing progression of cell states during MGE development.	否				E_01_0151	RT qPCR, in situ hybridization analysis, gene knockdown, chip SEQ, immunofluorescence staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.		Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Immunohistochemical staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.			RT-qPCR,原位杂交分析,基因敲降,ChIP-seq ,免疫荧光染色				TF
29554889	chr9	122199817	122201817	LHX6	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	human		High+Lowthroughput	Genomic analysis of transcriptional networks directing progression of cell states during MGE development.	否				E_01_0151	RT qPCR, in situ hybridization analysis, gene knockdown, chip SEQ, immunofluorescence staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.		Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Immunohistochemical staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.			RT-qPCR,原位杂交分析,基因敲降,ChIP-seq ,免疫荧光染色				LHX6
29554889	chr1	75125927	75127927	LHX8	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	human		High+Lowthroughput	Genomic analysis of transcriptional networks directing progression of cell states during MGE development.	否				E_01_0151	RT qPCR, in situ hybridization analysis, gene knockdown, chip SEQ, immunofluorescence staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.		Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Immunohistochemical staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.			RT-qPCR,原位杂交分析,基因敲降,ChIP-seq ,免疫荧光染色				LHX8
29552163	chr2	132413869	132415869	GPR39	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	human,mouse	adipose tissue	High+Lowthroughput	Improvement of Duchenne muscular dystrophy phenotype following obestatin treatment.	否		Duchenne muscular dystrophy (DMD)	satellite cell	E_02_0088	Real ‐ time PCR, Weston blot, immunofluorescence staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).		Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Immunohistochemical staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).			real‐time PCR,weston blot,免疫荧光染色				GPR39
29552153	chr2	132413957	132415957	GPR39	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	human,mouse		High+Lowthroughput	Improvement of Duchenne muscular dystrophy phenotype following obestatin treatment.	否		Duchenne muscular dystrophy (DMD)	muscle cell	E_02_0089	Real ‐ time PCR, Weston blot, immunofluorescence staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).		Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Immunohistochemical staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).			real‐time PCR,weston blot,免疫荧光染色				GPR39
29549111	chr14	21495511	21497511	METTL3	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	human		High+Lowthroughput	Disrupting the three-dimensional regulatory topology of the Pitx1 locus results in overtly normal development	否			Bone marrow stem cell	E_01_0152	flow cytometry ，Real-time quantitative PCR ， staining ，Protein extraction ，Western blot ，Cell transfection ，Immunofluorescence assay ，Quantitative analysis ，Chromatin immunoprecipitation assay ，Luciferase reporter assay	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 		The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	Immunohistochemical staining	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 			flow cytometry ，Real-time quantitative PCR ， staining ，Protein extraction ，Western blot ，Cell transfection ，Immunofluorescence assay ，Quantitative analysis ，Chromatin immunoprecipitation assay ，Luciferase reporter assay				METTL3
29545900	chr2	226728889	226730889	IRS1	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	human		High+Lowthroughput	Investigating a multigene prognostic assay based on significant pathways for Luminal A breast cancer through gene expression profile analysis	否			HeLa cell	E_01_0153	Nuclear magnetic resonance (NMR) spectroscopy analysis ，RNA extraction and real-time PCR ，Western blot analysis ，Histopathological analysis ,Analysis of glycated hemoglobin and β-cell function	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 		Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	Immunohistochemical staining	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 			Nuclear magnetic resonance (NMR) spectroscopy analysis ，RNA extraction and real-time PCR ，Western blot analysis ，Histopathological analysis ,Analysis of glycated hemoglobin and β-cell function				IRS1
29540569	chr7	148804523	148806523	EZH2	We report a distinct mechanism whereby p53-regulated MDM2 works together with MDMX to modulate sensitivity to DNA damage by controlling EZH2 (enhancer of zeste homolog 2) turnover.	mouse,	p53-dependent tissue	High+Lowthroughput	An EZH2-mediated epigenetic mechanism behind p53-dependent tissue sensitivity to DNA damage	否			Cancer cell	E_02_0090	qRT-PCR.	We report a distinct mechanism whereby p53-regulated MDM2 works together with MDMX to modulate sensitivity to DNA damage by controlling EZH2 (enhancer of zeste homolog 2) turnover.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We report a distinct mechanism whereby p53-regulated MDM2 works together with MDMX to modulate sensitivity to DNA damage by controlling EZH2 (enhancer of zeste homolog 2) turnover.		We report a distinct mechanism whereby p53-regulated MDM2 works together with MDMX to modulate sensitivity to DNA damage by controlling EZH2 (enhancer of zeste homolog 2) turnover.	Immunohistochemical staining	We report a distinct mechanism whereby p53-regulated MDM2 works together with MDMX to modulate sensitivity to DNA damage by controlling EZH2 (enhancer of zeste homolog 2) turnover.			qRT-PCR.				EZH2
29540468	chr17	66299977	66301977	PRKCA	The PRKCA enhancer contains two common genetic variants and 4 haplotypes;	human		High+Lowthroughput	Genetic Reduction in Left Ventricular Protein Kinase C-α and Adverse Ventricular Remodeling in Human Subjects	是	rs9912468		non-cardiac cell	E_01_0154	PCR	The PRKCA enhancer contains two common genetic variants and 4 haplotypes;	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The PRKCA enhancer contains two common genetic variants and 4 haplotypes;		The PRKCA enhancer contains two common genetic variants and 4 haplotypes;	Immunohistochemical staining	The PRKCA enhancer contains two common genetic variants and 4 haplotypes;			PCR				PRKCA
29535816	chr4	108044694	108046694	LEF1	The transcription factor lymphoid enhancer factor 1 (LEF1) and the secreted ligand WNT5A, expressed in NPC, were increased in EBV-infected NOK with sustained expression for more than 20 passages after viral loss. Increased LEF1 levels involved four LEF1 variants, and EBV-infected NOK showed a lack of responsiveness to 尾-catenin activation. Although forced expression of WNT5A and LEF1 enhanced the invasiveness of parental NOK, LEF1 knockdown reversed the invasive phenotype of EBV-infected NOK in the presence of WNT5A.	human,mouse		High+Lowthroughput	Epstein-Barr virus stably confers an invasive phenotype to epithelial cells through reprogramming of the WNT pathway	否			gastric cancer cell	E_02_0091	 RT-qPCR 	The transcription factor lymphoid enhancer factor 1 (LEF1) and the secreted ligand WNT5A, expressed in NPC, were increased in EBV-infected NOK with sustained expression for more than 20 passages after viral loss. Increased LEF1 levels involved four LEF1 variants, and EBV-infected NOK showed a lack of responsiveness to 尾-catenin activation. Although forced expression of WNT5A and LEF1 enhanced the invasiveness of parental NOK, LEF1 knockdown reversed the invasive phenotype of EBV-infected NOK in the presence of WNT5A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcription factor lymphoid enhancer factor 1 (LEF1) and the secreted ligand WNT5A, expressed in NPC, were increased in EBV-infected NOK with sustained expression for more than 20 passages after viral loss. Increased LEF1 levels involved four LEF1 variants, and EBV-infected NOK showed a lack of responsiveness to 尾-catenin activation. Although forced expression of WNT5A and LEF1 enhanced the invasiveness of parental NOK, LEF1 knockdown reversed the invasive phenotype of EBV-infected NOK in the presence of WNT5A.		The transcription factor lymphoid enhancer factor 1 (LEF1) and the secreted ligand WNT5A, expressed in NPC, were increased in EBV-infected NOK with sustained expression for more than 20 passages after viral loss. Increased LEF1 levels involved four LEF1 variants, and EBV-infected NOK showed a lack of responsiveness to 尾-catenin activation. Although forced expression of WNT5A and LEF1 enhanced the invasiveness of parental NOK, LEF1 knockdown reversed the invasive phenotype of EBV-infected NOK in the presence of WNT5A.	Immunohistochemical staining	The transcription factor lymphoid enhancer factor 1 (LEF1) and the secreted ligand WNT5A, expressed in NPC, were increased in EBV-infected NOK with sustained expression for more than 20 passages after viral loss. Increased LEF1 levels involved four LEF1 variants, and EBV-infected NOK showed a lack of responsiveness to 尾-catenin activation. Although forced expression of WNT5A and LEF1 enhanced the invasiveness of parental NOK, LEF1 knockdown reversed the invasive phenotype of EBV-infected NOK in the presence of WNT5A.			 RT-qPCR 				LEF1
29534682	chrX	21370203	21372203	CNKSR2	 The multi-functional scaffold protein Connector enhancer of kinase suppressor of ras 2 (CNKSR2) plays a key role in regulating cell proliferation, and differentiation through multiple receptor tyrosine kinase pathways.	human,		High+Lowthroughput	Regulation of CNKSR2 protein stability by the HECT E3 ubiquitin ligase Smurf2, and its role in breast cancer progression	否				E_02_0092	RT-PCR	 The multi-functional scaffold protein Connector enhancer of kinase suppressor of ras 2 (CNKSR2) plays a key role in regulating cell proliferation, and differentiation through multiple receptor tyrosine kinase pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 The multi-functional scaffold protein Connector enhancer of kinase suppressor of ras 2 (CNKSR2) plays a key role in regulating cell proliferation, and differentiation through multiple receptor tyrosine kinase pathways.		 The multi-functional scaffold protein Connector enhancer of kinase suppressor of ras 2 (CNKSR2) plays a key role in regulating cell proliferation, and differentiation through multiple receptor tyrosine kinase pathways.	Immunohistochemical staining	 The multi-functional scaffold protein Connector enhancer of kinase suppressor of ras 2 (CNKSR2) plays a key role in regulating cell proliferation, and differentiation through multiple receptor tyrosine kinase pathways.			RT-PCR				CNKSR2
29533787	chr2	132414173	132416173	GPR39	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	human,mouse		High+Lowthroughput	Improvement of Duchenne muscular dystrophy phenotype following obestatin treatment.	否			muscle cell	E_02_0093	Real ‐ time PCR, Weston blot, immunofluorescence staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).		Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Immunohistochemical staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).			real‐time PCR,weston blot,免疫荧光染色				GPR39
29531042	chr2	42492054	42494054	MTA3	The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.	human,mouse	Epithelial tissues	High+Lowthroughput	Acute and Cumulative Effects of Haze Fine Particles on Mortality and the Seasonal Characteristics in Beijing, China, 2005-2013: A Time-Stratified Case-Crossover Study	否			endothelial cell	E_02_0094	PCR, Western blot, gel electrophoresis	The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.		The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.	Immunohistochemical staining	The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.			PCR,Western blot,凝胶电泳				MTA3
29531012	chr6	36591744	36593744	SRSF3	SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.	human,mouse	kidney	High+Lowthroughput	The ameliorative effect of Protaetia brevitarsis Larvae in HFD-induced obese mice	否			HEK293T cell	E_02_0095	Western blot, gel electrophoresis, clip seq	SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.		SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.	Immunohistochemical staining	SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.			Western blot,凝胶电泳,CLIP-seq				SRSF3
29530927	chr12	113389472	113391472	SDS	Equal amounts (20 _xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.	human,mouse		High+Lowthroughput	Dephosphorylation of HDAC4 by PP2A-Bδ unravels a new role for the HDAC4/MEF2 axis in myoblast fusion	否			mesenchymal stem cell	E_02_0096	PCR, Western blot, gel electrophoresis	Equal amounts (20 _xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Equal amounts (20 _xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.		Equal amounts (20 _xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.	Immunohistochemical staining	Equal amounts (20 _xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.			PCR,Western blot,凝胶电泳				SDS
29530320	chr3	181709448	181711448	SOX2	Epigenomic Profifiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma	human	lung	High+Lowthroughput	Synthetically Scalable Poly(ampholyte) Which Dramatically Enhances Cellular Cryopreservation	否			Lung squamous cell	E_01_0155	Western blot, chip SEQ, RNA SEQ, flow cytometry, gene knockdown	Epigenomic Profifiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Epigenomic Profifiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma	Immunohistochemical staining	Epigenomic Profifiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma	SOX2		Western blot,ChIP-seq,RNA-seq,流式细胞术,基因敲降	Epigenomic Profifiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma			
29529279	chr8	94246645	94248645	GEM	In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).	human,mouse	liver	High+Lowthroughput	Toll-like receptor 2 stimulation augments esophageal barrier integrity	否			Huh 7 cell	E_02_0097	PCR, flow cytometry, gene knockdown, Western blot, gel electrophoresis, immunofluorescence staining	In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).		In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).	Immunohistochemical staining	In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).			PCR,流式细胞术,基因敲降,Western blot,凝胶电泳,免疫荧光染色				GEM
29526278	chr21	33540351	33542351	SON	Four AONs and a sense oligonucleotide (SON) were designed to block exonic splicing enhancers (ESEs).	human		High+Lowthroughput	Identification and Rescue of Splice Defects Caused by Two Neighboring Deep-Intronic ABCA4 Mutations Underlying Stargardt Disease	否				E_01_0156	RT-PCR	Four AONs and a sense oligonucleotide (SON) were designed to block exonic splicing enhancers (ESEs).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Four AONs and a sense oligonucleotide (SON) were designed to block exonic splicing enhancers (ESEs).		Four AONs and a sense oligonucleotide (SON) were designed to block exonic splicing enhancers (ESEs).	Immunohistochemical staining	Four AONs and a sense oligonucleotide (SON) were designed to block exonic splicing enhancers (ESEs).			RT-PCR				SON
29525407	chr7	148804989	148806989	EZH2	 It was shown that O-GlcNAcylation stabilizes histone methyltransferase enhancer of zeste homolog 2 (EZH2), which facilitates the formation of the trimethylation of histone 3 at lysine 27 (H3K27me3) thereby repressing gene expression in human MCF-7 cells [41].	human,mouse	 adipose tissue	High+Lowthroughput	Skeletal muscle O-GlcNAc transferase is important for muscle energy homeostasis and whole-body insulin sensitivity	否				E_02_0098	qPCR	 It was shown that O-GlcNAcylation stabilizes histone methyltransferase enhancer of zeste homolog 2 (EZH2), which facilitates the formation of the trimethylation of histone 3 at lysine 27 (H3K27me3) thereby repressing gene expression in human MCF-7 cells [41].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 It was shown that O-GlcNAcylation stabilizes histone methyltransferase enhancer of zeste homolog 2 (EZH2), which facilitates the formation of the trimethylation of histone 3 at lysine 27 (H3K27me3) thereby repressing gene expression in human MCF-7 cells [41].		 It was shown that O-GlcNAcylation stabilizes histone methyltransferase enhancer of zeste homolog 2 (EZH2), which facilitates the formation of the trimethylation of histone 3 at lysine 27 (H3K27me3) thereby repressing gene expression in human MCF-7 cells [41].	Immunohistochemical staining	 It was shown that O-GlcNAcylation stabilizes histone methyltransferase enhancer of zeste homolog 2 (EZH2), which facilitates the formation of the trimethylation of histone 3 at lysine 27 (H3K27me3) thereby repressing gene expression in human MCF-7 cells [41].			qPCR				EZH2
29524130	chr14	21495467	21497467	METTL3	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	human		High+Lowthroughput	Disrupting the three-dimensional regulatory topology of the Pitx1 locus results in overtly normal development	否			Bone marrow stem cell	E_01_0157	flow cytometry ，Real-time quantitative PCR ， staining ，Protein extraction ，Western blot ，Cell transfection ，Immunofluorescence assay ，Quantitative analysis ，Chromatin immunoprecipitation assay ，Luciferase reporter assay	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 		The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	Immunohistochemical staining	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 			flow cytometry ，Real-time quantitative PCR ， staining ，Protein extraction ，Western blot ，Cell transfection ，Immunofluorescence assay ，Quantitative analysis ，Chromatin immunoprecipitation assay ，Luciferase reporter assay				METTL3
29523836	chr2	226728284	226730284	IRS1	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	human		High+Lowthroughput	Investigating a multigene prognostic assay based on significant pathways for Luminal A breast cancer through gene expression profile analysis	否			HeLa cell	E_01_0158	Nuclear magnetic resonance (NMR) spectroscopy analysis ，RNA extraction and real-time PCR ，Western blot analysis ，Histopathological analysis ,Analysis of glycated hemoglobin and β-cell function	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 		Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	Immunohistochemical staining	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 			Nuclear magnetic resonance (NMR) spectroscopy analysis ，RNA extraction and real-time PCR ，Western blot analysis ，Histopathological analysis ,Analysis of glycated hemoglobin and β-cell function				IRS1
29521509	chr7	116522460	116524460	CAV1	CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 	mouse	lymphoid tissue	High+Lowthroughput	Rare Variant Burden Analysis within Enhancers Identifies CAV1 as an ALS Risk Gene	否			Lymphoblast	E_02_0099	Immunoblotting, fluorescent quantitative PCR (RT-PCR), immunocytochemistry, live cell imaging	CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 		CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 	Immunohistochemical staining	CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 			免疫印迹，荧光定量 PCR（RT-PCR），免疫细胞化学，活细胞成像				CAV1
29515369	chr1	145668268	145670268	PDZK1	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	human,fish		High+Lowthroughput	A non-coding genetic variant maximally associated with serum urate levels is functionally linked to HNF4A-dependent PDZK1 expression	否	rs1967017,rs1471633	hyperuricemia	HepG2 cell	E_02_0100	Quantitative PCR, immunoblot analysis, chip PCR, statistical analysis, Weston blot	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 		 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	Immunohistochemical staining	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 			Quantitative PCR,Immunoblot analysis, ChIP-PCR,统计分析,weston blot				PDZK1
29515369	chr20	44353272	44355272	HNF4A	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	human,fish		High+Lowthroughput	A non-coding genetic variant maximally associated with serum urate levels is functionally linked to HNF4A-dependent PDZK1 expression	否	rs1967017,rs1471633	hyperuricemia	HepG2 cell	E_02_0100	Quantitative PCR, immunoblot analysis, chip PCR, statistical analysis, Weston blot	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 		 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	Immunohistochemical staining	 siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 			Quantitative PCR,Immunoblot analysis, ChIP-PCR,统计分析,weston blot				HNF4A
29514910	chr11	73215408	73217408	P2RY2	P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 	human,		High+Lowthroughput	Enhancer RNA - P2RY2e induced by estrogen promotes malignant behaviors of bladder cancer	否		Breast, bladder, stomach, pancreas, prostate, lung	T24 cell	E_02_0101	RT qPCR, flow cytometry, ELISA, statistical analysis	P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 		P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 	Immunohistochemical staining	P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 			RT-qPCR,流式细胞术,ELISA,统计分析				P2RY2
29514101	chrX	67541320	67543320	AR	 For example, one human AR is an enhancer with putative roles in the evolution of the human thumb (Prabhakar et al., 2008). 	human,mouse		High+Lowthroughput	Accelerated Evolution in Distinctive Species Reveals Candidate Elements for Clinically Relevant Traits, Including Mutation and Cancer Resistance	否				E_02_0102	DNase-seq	 For example, one human AR is an enhancer with putative roles in the evolution of the human thumb (Prabhakar et al., 2008). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 For example, one human AR is an enhancer with putative roles in the evolution of the human thumb (Prabhakar et al., 2008). 		 For example, one human AR is an enhancer with putative roles in the evolution of the human thumb (Prabhakar et al., 2008). 	Immunohistochemical staining	 For example, one human AR is an enhancer with putative roles in the evolution of the human thumb (Prabhakar et al., 2008). 			DNase-seq				AR
29899112	chr6	47504499	47506499	Ezh2	Hence, genetic loss of Ezh2 in mouse pre-osteoblasts inhibits osteogenesis in part by inducing cell cycle changes. Our results suggest that Ezh2 serves a bifunctional role during bone formation by suppressing osteogenic lineage commitment while simultaneously facilitating proliferative expansion of osteoprogenitor cells.	mouse	Nervous tissue	High+Lowthroughput	Enhancer of zeste homolog 2 (Ezh2) controls bone formation and cell cycle progression during osteogenesis in mice	否			mesenchymal stem cell of the bone marrow	E_02_0103	"RNA-Seq,Western blot,staining,RT-qPCR,MTS assays,Flow cytometric analysis,Ex vivo assays,Histology,histomorphometric analysis,Micro-computed tomography analysis,Alkaline Phosphatase and Alizarin Red
Staining,Hoechst staining,"	Hence, genetic loss of Ezh2 in mouse pre-osteoblasts inhibits osteogenesis in part by inducing cell cycle changes. Our results suggest that Ezh2 serves a bifunctional role during bone formation by suppressing osteogenic lineage commitment while simultaneously facilitating proliferative expansion of osteoprogenitor cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hence, genetic loss of Ezh2 in mouse pre-osteoblasts inhibits osteogenesis in part by inducing cell cycle changes. Our results suggest that Ezh2 serves a bifunctional role during bone formation by suppressing osteogenic lineage commitment while simultaneously facilitating proliferative expansion of osteoprogenitor cells.		Hence, genetic loss of Ezh2 in mouse pre-osteoblasts inhibits osteogenesis in part by inducing cell cycle changes. Our results suggest that Ezh2 serves a bifunctional role during bone formation by suppressing osteogenic lineage commitment while simultaneously facilitating proliferative expansion of osteoprogenitor cells.	Immunohistochemical staining	Hence, genetic loss of Ezh2 in mouse pre-osteoblasts inhibits osteogenesis in part by inducing cell cycle changes. Our results suggest that Ezh2 serves a bifunctional role during bone formation by suppressing osteogenic lineage commitment while simultaneously facilitating proliferative expansion of osteoprogenitor cells.			"RNA-Seq,Western blot,staining,RT-qPCR,MTS assays,Flow cytometric analysis,Ex vivo assays,Histology,histomorphometric analysis,Micro-computed tomography analysis,Alkaline Phosphatase and Alizarin Red
Staining,Hoechst staining,"				Ezh2
29898989	chr3	36999364	37001216	CTCF	A CTCF-bound region within the MLH1-35 enhancer regulates MLH1 expression in colorectal cells and is worthy of scrutiny in future genetic screening strategies for suspected Lynch syndrome associated with loss of MLH1 expression.	human	Connective tissue	Low throughput	Disruption of a -35 kb Enhancer Impairs CTCF Binding and MLH1 Expression in Colorectal Cells	否	--	Lynch Syndrome		E_02_0104	ChIP-qPCR,3C,Luciferase Reporter Assay,CRISPR/Cas9	We provide the first description of an enhancer for the MLH1 gene. This -35kb enhancer was CTCF-bound, and disruption of the consensus binding site within the enhancer significantly impairs MLH1 expression in SW620 colorectal carcinoma cells.	Enhancer	3C,CRISPR/Cas9	ChIP-qPCR,Luciferase Reporter Assay	We deleted a DNA fragment corresponding to the -35kb region from SW620 cells,showed that the -35kb region functions as an MLH1 Enhancer in SW620 colorectal cells.	COCA2,FCC2,HNPCC,HNPCC2,hMLH1	--	--	--	CTCF	MRD21	CRISPR/Cas9	To evaluate the impact on endogenous MLH1 expression, we next deleted a region containing the CTCF binding motif in SW620 and K562 cells using CRISPR-Cas9 (Fig 3A, ΔCTCF). Similar to deletion of the entire Enhancer, we noted significant reduction in MLH1 expression in SW620 but not in K562 cells.	--	--	MLH1
29898989	chr3	36999364	37001216	MLH1	A CTCF-bound region within the MLH1-35 enhancer regulates MLH1 expression in colorectal cells and is worthy of scrutiny in future genetic screening strategies for suspected Lynch syndrome associated with loss of MLH1 expression.	human	Connective tissue	Low throughput	Disruption of a -35 kb Enhancer Impairs CTCF Binding and MLH1 Expression in Colorectal Cells	否	--	Lynch Syndrome		E_02_0104	ChIP-qPCR,3C,Luciferase Reporter Assay,CRISPR/Cas9	We provide the first description of an enhancer for the MLH1 gene. This -35kb enhancer was CTCF-bound, and disruption of the consensus binding site within the enhancer significantly impairs MLH1 expression in SW620 colorectal carcinoma cells.	Enhancer	3C,CRISPR/Cas9	ChIP-qPCR,Luciferase Reporter Assay	We deleted a DNA fragment corresponding to the -35kb region from SW620 cells,showed that the -35kb region functions as an MLH1 Enhancer in SW620 colorectal cells.	COCA2,FCC2,HNPCC,HNPCC2,hMLH1	--	--	--	CTCF	MRD21	CRISPR/Cas9	To evaluate the impact on endogenous MLH1 expression, we next deleted a region containing the CTCF binding motif in SW620 and K562 cells using CRISPR-Cas9 (Fig 3A, ΔCTCF). Similar to deletion of the entire Enhancer, we noted significant reduction in MLH1 expression in SW620 but not in K562 cells.	--	--	MLH1
29510148	chr14	30871809	30873809	COCH	COCH is the most abundantly expressed gene in the cochlea.	human,mouse		High+Lowthroughput	Novel loss-of-function mutations in COCH cause autosomal recessive nonsyndromic hearing loss	否			MDCK cell	E_02_0105	RT-PCR，PCR	COCH is the most abundantly expressed gene in the cochlea.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	COCH is the most abundantly expressed gene in the cochlea.		COCH is the most abundantly expressed gene in the cochlea.	Immunohistochemical staining	COCH is the most abundantly expressed gene in the cochlea.			RT-PCR，PCR				COCH
29503092	chr14	100235564	100237564	YY1	 We sorted YY1 peaks by H3K4me1 and H3K4me3 to distinguish enhancers from promoters, and observed that both enhancer and promoter regions enriched for YY1 were co-bound by SMARCA4 and OSN (Figure 5D). 	human,	 adult tissue	High+Lowthroughput	YY1 Positively Regulates Transcription by Targeting Promoters and Super-Enhancers through the BAF Complex in Embryonic Stem Cells	否			pre-B cell	E_02_0106	qPCR	 We sorted YY1 peaks by H3K4me1 and H3K4me3 to distinguish enhancers from promoters, and observed that both enhancer and promoter regions enriched for YY1 were co-bound by SMARCA4 and OSN (Figure 5D). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 We sorted YY1 peaks by H3K4me1 and H3K4me3 to distinguish enhancers from promoters, and observed that both enhancer and promoter regions enriched for YY1 were co-bound by SMARCA4 and OSN (Figure 5D). 		 We sorted YY1 peaks by H3K4me1 and H3K4me3 to distinguish enhancers from promoters, and observed that both enhancer and promoter regions enriched for YY1 were co-bound by SMARCA4 and OSN (Figure 5D). 	Immunohistochemical staining	 We sorted YY1 peaks by H3K4me1 and H3K4me3 to distinguish enhancers from promoters, and observed that both enhancer and promoter regions enriched for YY1 were co-bound by SMARCA4 and OSN (Figure 5D). 			qPCR				YY1
31223056	chr16	71843198	71845198	IST1	we demonstrate that MAPT accumulation suppresses IST1 transcription with the mechanisms involving the ANP32A-regulated mask of histone acetylation	human	connective tissue	High+Lowthroughput	MAPT/Tau accumulation represses autophagy flux by disrupting IST1-regulated ESCRT-III complex formation: a vicious cycle in Alzheimer neurodegeneration	否			macrophage	E_01_0159	PCR	we demonstrate that MAPT accumulation suppresses IST1 transcription with the mechanisms involving the ANP32A-regulated mask of histone acetylation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	we demonstrate that MAPT accumulation suppresses IST1 transcription with the mechanisms involving the ANP32A-regulated mask of histone acetylation		we demonstrate that MAPT accumulation suppresses IST1 transcription with the mechanisms involving the ANP32A-regulated mask of histone acetylation	Immunohistochemical staining	we demonstrate that MAPT accumulation suppresses IST1 transcription with the mechanisms involving the ANP32A-regulated mask of histone acetylation			PCR				IST1
31221974	chr7	148804781	148806781	EZH2	We have previously shown that the Enhancer-of-zeste-like protein Ezl1 is essential for programmed DNA elimination and viability of the sexual progeny 25 . Here, we provide evidence that, Paramecium Ezl1, which exhibits significant sequence and structural similarities with human EZH2, displays distinct enzy- matic properties.  	mouse	connective tissue	High+Lowthroughput	The Polycomb protein Ezl1 mediates H3K9 and H3K27 methylation to repress transposable elements in Paramecium	否			embryonic stem cell	E_02_0107	PCR	We have previously shown that the Enhancer-of-zeste-like protein Ezl1 is essential for programmed DNA elimination and viability of the sexual progeny 25 . Here, we provide evidence that, Paramecium Ezl1, which exhibits significant sequence and structural similarities with human EZH2, displays distinct enzy- matic properties.  	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We have previously shown that the Enhancer-of-zeste-like protein Ezl1 is essential for programmed DNA elimination and viability of the sexual progeny 25 . Here, we provide evidence that, Paramecium Ezl1, which exhibits significant sequence and structural similarities with human EZH2, displays distinct enzy- matic properties.  		We have previously shown that the Enhancer-of-zeste-like protein Ezl1 is essential for programmed DNA elimination and viability of the sexual progeny 25 . Here, we provide evidence that, Paramecium Ezl1, which exhibits significant sequence and structural similarities with human EZH2, displays distinct enzy- matic properties.  	Immunohistochemical staining	We have previously shown that the Enhancer-of-zeste-like protein Ezl1 is essential for programmed DNA elimination and viability of the sexual progeny 25 . Here, we provide evidence that, Paramecium Ezl1, which exhibits significant sequence and structural similarities with human EZH2, displays distinct enzy- matic properties.  			PCR				EZH2
31219650	chr7	44101654	44103654	AEBP1	In this study, we explored the clinical significance and biological function of AEBP1 in COAD. We observed that AEBP1 was overexpressed in COAD tissues and cells and that the expression of AEBP1 was correlated with tumor size, the level of histologic differentiation, lymph node metastasis, and cancer stage in COAD patients. 	human	Epithelial tissues	High+Lowthroughput	AEBP1, a prognostic indicator, promotes colon adenocarcinoma cell growth and metastasis through the NF-κB pathway	否			colon cancer cell	E_01_0160	PCR	In this study, we explored the clinical significance and biological function of AEBP1 in COAD. We observed that AEBP1 was overexpressed in COAD tissues and cells and that the expression of AEBP1 was correlated with tumor size, the level of histologic differentiation, lymph node metastasis, and cancer stage in COAD patients. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we explored the clinical significance and biological function of AEBP1 in COAD. We observed that AEBP1 was overexpressed in COAD tissues and cells and that the expression of AEBP1 was correlated with tumor size, the level of histologic differentiation, lymph node metastasis, and cancer stage in COAD patients. 		In this study, we explored the clinical significance and biological function of AEBP1 in COAD. We observed that AEBP1 was overexpressed in COAD tissues and cells and that the expression of AEBP1 was correlated with tumor size, the level of histologic differentiation, lymph node metastasis, and cancer stage in COAD patients. 	Immunohistochemical staining	In this study, we explored the clinical significance and biological function of AEBP1 in COAD. We observed that AEBP1 was overexpressed in COAD tissues and cells and that the expression of AEBP1 was correlated with tumor size, the level of histologic differentiation, lymph node metastasis, and cancer stage in COAD patients. 			PCR				AEBP1
31219209	chr7	148805028	148807028	EZH2	And lncRNA‐mediated epigenetic inhibition of antitumor gene via binding EZH2 in various cancers has been gradually detected. l	human	connective tissue	High+Lowthroughput	Long noncoding RNA OIP5-AS1 aggravates cell proliferation, migration in gastric cancer by epigenetically silencing NLRP6 expression via binding EZH2	否		Colon cancer	gastric cancer cell	E_01_0161	PCR	And lncRNA‐mediated epigenetic inhibition of antitumor gene via binding EZH2 in various cancers has been gradually detected. l	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			And lncRNA‐mediated epigenetic inhibition of antitumor gene via binding EZH2 in various cancers has been gradually detected. l	Immunohistochemical staining	And lncRNA‐mediated epigenetic inhibition of antitumor gene via binding EZH2 in various cancers has been gradually detected. l	EZH2		PCR	And lncRNA‐mediated epigenetic inhibition of antitumor gene via binding EZH2 in various cancers has been gradually detected. l			
31217031	chr1	26690366	26692366	ARID1A	We identify a previously unknown context-dependent tumor-supporting function of ARID1A in CRC downstream of KRAS signaling. 	mouse	connective tissue	High+Lowthroughput	ARID1A facilitates KRAS signaling-regulated?enhancer activity in an AP1-dependent manner in colorectal cancer cells	否			tumor cell	E_02_0108	PCR	We identify a previously unknown context-dependent tumor-supporting function of ARID1A in CRC downstream of KRAS signaling. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identify a previously unknown context-dependent tumor-supporting function of ARID1A in CRC downstream of KRAS signaling. 		We identify a previously unknown context-dependent tumor-supporting function of ARID1A in CRC downstream of KRAS signaling. 	Immunohistochemical staining	We identify a previously unknown context-dependent tumor-supporting function of ARID1A in CRC downstream of KRAS signaling. 			PCR				ARID1A
31216773	chr13	27958003	27960003	CDX2	It was found by chromatin immunoprecipitation experiments that CDX2 and HNF4α bind to the YAP1 enhancer in Caco-2 cells. These results reveal a previously unknown enhancer of the YAP1 promoter activity in the YAP1 gene, with importance for high expression levels in intestinal epithelial cells.	human	Colon tissue	High+Lowthroughput	HNF4α and CDX2 Regulate Intestinal YAP1 Promoter Activity	否			intestinal cell	E_01_0162	PCR	It was found by chromatin immunoprecipitation experiments that CDX2 and HNF4α bind to the YAP1 enhancer in Caco-2 cells. These results reveal a previously unknown enhancer of the YAP1 promoter activity in the YAP1 gene, with importance for high expression levels in intestinal epithelial cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			It was found by chromatin immunoprecipitation experiments that CDX2 and HNF4α bind to the YAP1 enhancer in Caco-2 cells. These results reveal a previously unknown enhancer of the YAP1 promoter activity in the YAP1 gene, with importance for high expression levels in intestinal epithelial cells.	Immunohistochemical staining	It was found by chromatin immunoprecipitation experiments that CDX2 and HNF4α bind to the YAP1 enhancer in Caco-2 cells. These results reveal a previously unknown enhancer of the YAP1 promoter activity in the YAP1 gene, with importance for high expression levels in intestinal epithelial cells.	CDX2		PCR	It was found by chromatin immunoprecipitation experiments that CDX2 and HNF4α bind to the YAP1 enhancer in Caco-2 cells. These results reveal a previously unknown enhancer of the YAP1 promoter activity in the YAP1 gene, with importance for high expression levels in intestinal epithelial cells.			
31216559	chr12	49973763	49975763	RACGAP1	Rac GTPase-activating protein 1 (RACGAP1) is as- sociated with cell proliferation, and there is much evidence of its oncogenic role. 	human	connective tissue	High+Lowthroughput	Rac GTPase-Activating Protein 1 (RACGAP1) as an Oncogenic Enhancer in Esophageal Carcinoma	否			cancer cell	E_01_0163	PCR	Rac GTPase-activating protein 1 (RACGAP1) is as- sociated with cell proliferation, and there is much evidence of its oncogenic role. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Rac GTPase-activating protein 1 (RACGAP1) is as- sociated with cell proliferation, and there is much evidence of its oncogenic role. 	Immunohistochemical staining	Rac GTPase-activating protein 1 (RACGAP1) is as- sociated with cell proliferation, and there is much evidence of its oncogenic role. 	RACGAP1		PCR	Rac GTPase-activating protein 1 (RACGAP1) is as- sociated with cell proliferation, and there is much evidence of its oncogenic role. 			
31216030	chr19	4171371	4173371	SIRT6	SIRT6 is critical for activating transcription of Nuclear factor (erythroid-derived 2)-like 2 (NRF2) re-sponsive genes during oxidative stress	human	connective tissue	High+Lowthroughput	SIRT6 promotes transcription of a subset of NRF2 targets by mono-ADP-ribosylating BAF170	否			stem cell	E_01_0164	PCR	SIRT6 is critical for activating transcription of Nuclear factor (erythroid-derived 2)-like 2 (NRF2) re-sponsive genes during oxidative stress	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SIRT6 is critical for activating transcription of Nuclear factor (erythroid-derived 2)-like 2 (NRF2) re-sponsive genes during oxidative stress		SIRT6 is critical for activating transcription of Nuclear factor (erythroid-derived 2)-like 2 (NRF2) re-sponsive genes during oxidative stress	Immunohistochemical staining	SIRT6 is critical for activating transcription of Nuclear factor (erythroid-derived 2)-like 2 (NRF2) re-sponsive genes during oxidative stress			PCR				SIRT6
31215771	chr20	56626718	56628718	TFAP2C	We found that the cooperations between regulators were much closer in lung‐metastatic cells. Moreover,regulators such as TFAP2C, GTF2I and LMO4 were found to have potential prognostic value for lung metastasis free (LMF) survival of breast cancer. 	human	connective tissue	High+Lowthroughput	Comprehensive epigenetic analyses reveal master regulators driving lung metastasis of breast cancer	否		mammary cancer	breast cancer cell	E_01_0165	PCR	We found that the cooperations between regulators were much closer in lung‐metastatic cells. Moreover,regulators such as TFAP2C, GTF2I and LMO4 were found to have potential prognostic value for lung metastasis free (LMF) survival of breast cancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found that the cooperations between regulators were much closer in lung‐metastatic cells. Moreover,regulators such as TFAP2C, GTF2I and LMO4 were found to have potential prognostic value for lung metastasis free (LMF) survival of breast cancer. 	Immunohistochemical staining	We found that the cooperations between regulators were much closer in lung‐metastatic cells. Moreover,regulators such as TFAP2C, GTF2I and LMO4 were found to have potential prognostic value for lung metastasis free (LMF) survival of breast cancer. 	TFAP2C		PCR	We found that the cooperations between regulators were much closer in lung‐metastatic cells. Moreover,regulators such as TFAP2C, GTF2I and LMO4 were found to have potential prognostic value for lung metastasis free (LMF) survival of breast cancer. 			
31213123	chr7	148804377	148806377	EZH2	Accumulating data demonstrated that Enhancer of zeste homolog 2 (EZH2) as an oncogenic pr otein is over-expressed in various human cancers, including PC.	human	connective tissue	High+Lowthroughput	Diosgenin exhibits tumor suppressive function via down-regulation of EZH2 in pancreatic cancer cells	否		tumour	tumor cell	E_01_0166	PCR	Accumulating data demonstrated that Enhancer of zeste homolog 2 (EZH2) as an oncogenic pr otein is over-expressed in various human cancers, including PC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Accumulating data demonstrated that Enhancer of zeste homolog 2 (EZH2) as an oncogenic pr otein is over-expressed in various human cancers, including PC.	Immunohistochemical staining	Accumulating data demonstrated that Enhancer of zeste homolog 2 (EZH2) as an oncogenic pr otein is over-expressed in various human cancers, including PC.	EZH2		PCR	Accumulating data demonstrated that Enhancer of zeste homolog 2 (EZH2) as an oncogenic pr otein is over-expressed in various human cancers, including PC.			
31205561	chr7	148804432	148806432	EZH2	Enhancer of zeste homolog 2 (EZH2) and Bcl-2 gene rearrangement or protein upregulation played pivotal roles in the carcinogenesis of various malignancies including lymphomas.	mouse	connective tissue	High+Lowthroughput	EZH2/Bcl-2 Coexpression Predicts Worse Survival in Diffuse Large B-cell Lymphomas and Demonstrates Poor Efficacy to Rituximab in Localized Lesions	否		tumour	tumor cell	E_02_0109	PCR	Enhancer of zeste homolog 2 (EZH2) and Bcl-2 gene rearrangement or protein upregulation played pivotal roles in the carcinogenesis of various malignancies including lymphomas.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of zeste homolog 2 (EZH2) and Bcl-2 gene rearrangement or protein upregulation played pivotal roles in the carcinogenesis of various malignancies including lymphomas.		Enhancer of zeste homolog 2 (EZH2) and Bcl-2 gene rearrangement or protein upregulation played pivotal roles in the carcinogenesis of various malignancies including lymphomas.	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2) and Bcl-2 gene rearrangement or protein upregulation played pivotal roles in the carcinogenesis of various malignancies including lymphomas.			PCR				EZH2
31202798	chr7	148804013	148806013	EZH2	Enhancer of zeste homolog-2 (EZH2), a histone methyltransferase, has been recognized to play a pivotal role in regulating the immune response in various diseases.	mouse	connective tissue	High+Lowthroughput	EZH2 inhibitor DZNep modulates microglial activation and protects against ischaemic brain injury after experimental stroke	否			microglial cell	E_02_0110	PCR	Enhancer of zeste homolog-2 (EZH2), a histone methyltransferase, has been recognized to play a pivotal role in regulating the immune response in various diseases.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of zeste homolog-2 (EZH2), a histone methyltransferase, has been recognized to play a pivotal role in regulating the immune response in various diseases.		Enhancer of zeste homolog-2 (EZH2), a histone methyltransferase, has been recognized to play a pivotal role in regulating the immune response in various diseases.	Immunohistochemical staining	Enhancer of zeste homolog-2 (EZH2), a histone methyltransferase, has been recognized to play a pivotal role in regulating the immune response in various diseases.			PCR				EZH2
31201420	chr7	148804563	148806563	EZH2	In summary, uterine EZH2 expression is developmentally and hormonally regulated, and its loss causes aberrant uterine epithelial proliferation, uterine hypertrophy and cystic endometrial hyperplasia, indicating a critical role in uterine development and function	mouse	connective tissue	High+Lowthroughput	The histone methyltransferase EZH2 is required for normal uterine development and function in mice?	否			epithelial cell of uterus	E_02_0111	PCR	In summary, uterine EZH2 expression is developmentally and hormonally regulated, and its loss causes aberrant uterine epithelial proliferation, uterine hypertrophy and cystic endometrial hyperplasia, indicating a critical role in uterine development and function	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In summary, uterine EZH2 expression is developmentally and hormonally regulated, and its loss causes aberrant uterine epithelial proliferation, uterine hypertrophy and cystic endometrial hyperplasia, indicating a critical role in uterine development and function		In summary, uterine EZH2 expression is developmentally and hormonally regulated, and its loss causes aberrant uterine epithelial proliferation, uterine hypertrophy and cystic endometrial hyperplasia, indicating a critical role in uterine development and function	Immunohistochemical staining	In summary, uterine EZH2 expression is developmentally and hormonally regulated, and its loss causes aberrant uterine epithelial proliferation, uterine hypertrophy and cystic endometrial hyperplasia, indicating a critical role in uterine development and function			PCR				EZH2
31189106	chrX	137563628	137565628	ZIC3	Our data therefore place ZIC3 upstream of a set of pro-differentiation transcriptional regulators and provide an important advance in our understanding of the regulatory factors governing the early steps in ESC differentiation	human	connective tissue	High+Lowthroughput	ZIC3 Controls the Transition from Naive to Primed Pluripotency	否			embryonic stem cell	E_01_0167	PCR	Our data therefore place ZIC3 upstream of a set of pro-differentiation transcriptional regulators and provide an important advance in our understanding of the regulatory factors governing the early steps in ESC differentiation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data therefore place ZIC3 upstream of a set of pro-differentiation transcriptional regulators and provide an important advance in our understanding of the regulatory factors governing the early steps in ESC differentiation		Our data therefore place ZIC3 upstream of a set of pro-differentiation transcriptional regulators and provide an important advance in our understanding of the regulatory factors governing the early steps in ESC differentiation	Immunohistochemical staining	Our data therefore place ZIC3 upstream of a set of pro-differentiation transcriptional regulators and provide an important advance in our understanding of the regulatory factors governing the early steps in ESC differentiation			PCR				ZIC3
31186776	chr1	205594870	205596870	ELK4	In addition, prognostic analysis demonstrated that ETV5 andELK4 expression levels were associated with the survival time of patients with GBM. These results suggested that ELK4 and ETV5 may be prognostic markers for GBM, and that their microRNAs may be candidate therapeutic targets.	human	connective tissue	High+Lowthroughput	ceRNA network analysis reveals prognostic markers for glioblastoma	否		cancer	cancer cell	E_01_0168	PCR	In addition, prognostic analysis demonstrated that ETV5 andELK4 expression levels were associated with the survival time of patients with GBM. These results suggested that ELK4 and ETV5 may be prognostic markers for GBM, and that their microRNAs may be candidate therapeutic targets.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, prognostic analysis demonstrated that ETV5 andELK4 expression levels were associated with the survival time of patients with GBM. These results suggested that ELK4 and ETV5 may be prognostic markers for GBM, and that their microRNAs may be candidate therapeutic targets.	Immunohistochemical staining	In addition, prognostic analysis demonstrated that ETV5 andELK4 expression levels were associated with the survival time of patients with GBM. These results suggested that ELK4 and ETV5 may be prognostic markers for GBM, and that their microRNAs may be candidate therapeutic targets.	ELK4		PCR	In addition, prognostic analysis demonstrated that ETV5 andELK4 expression levels were associated with the survival time of patients with GBM. These results suggested that ELK4 and ETV5 may be prognostic markers for GBM, and that their microRNAs may be candidate therapeutic targets.			
31186707	chr20	22578327	22580327	FOXA2	Long non-coding RNA-neighboring enhancer of FOXA2 (lncRNA-NEF) is a recently identified tumor suppressor in hepatocellular carcinoma. T	human	connective tissue	High+Lowthroughput	Long non-coding RNA-neighboring enhancer of FOXA2 inhibits the migration and invasion of small cell lung carcinoma cells by downregulating transforming growth factor-β1	否		lung cancer	Lung cancer cell	E_01_0169	PCR	Long non-coding RNA-neighboring enhancer of FOXA2 (lncRNA-NEF) is a recently identified tumor suppressor in hepatocellular carcinoma. T	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Long non-coding RNA-neighboring enhancer of FOXA2 (lncRNA-NEF) is a recently identified tumor suppressor in hepatocellular carcinoma. T	Immunohistochemical staining	Long non-coding RNA-neighboring enhancer of FOXA2 (lncRNA-NEF) is a recently identified tumor suppressor in hepatocellular carcinoma. T	FOXA2		PCR	Long non-coding RNA-neighboring enhancer of FOXA2 (lncRNA-NEF) is a recently identified tumor suppressor in hepatocellular carcinoma. T			
31182783	chr6	31161443	31163443	POU5F1	OCT4, also named POU5F1, is the main regulator of pluripotency in stem cells1 It also has a part in tumorigenesis, cellular stress response, and hence is linked to various diseases from cancer to autoimmune disorders 2–4 .OCT4 possesses several isoforms with different functions at both protein and transcript levels, and their expressions are regulated through different mechanisms and at various biological processes 5,6	human	connective tissue	High+Lowthroughput	lncRNA PSORS1C3 is regulated by glucocorticoids and fine-tunes OCT4 expression in non-pluripotent cells	否			stem cell	E_01_0170	PCR	OCT4, also named POU5F1, is the main regulator of pluripotency in stem cells1 It also has a part in tumorigenesis, cellular stress response, and hence is linked to various diseases from cancer to autoimmune disorders 2–4 .OCT4 possesses several isoforms with different functions at both protein and transcript levels, and their expressions are regulated through different mechanisms and at various biological processes 5,6	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			OCT4, also named POU5F1, is the main regulator of pluripotency in stem cells1 It also has a part in tumorigenesis, cellular stress response, and hence is linked to various diseases from cancer to autoimmune disorders 2–4 .OCT4 possesses several isoforms with different functions at both protein and transcript levels, and their expressions are regulated through different mechanisms and at various biological processes 5,6	Immunohistochemical staining	OCT4, also named POU5F1, is the main regulator of pluripotency in stem cells1 It also has a part in tumorigenesis, cellular stress response, and hence is linked to various diseases from cancer to autoimmune disorders 2–4 .OCT4 possesses several isoforms with different functions at both protein and transcript levels, and their expressions are regulated through different mechanisms and at various biological processes 5,6	POU5F1		PCR	OCT4, also named POU5F1, is the main regulator of pluripotency in stem cells1 It also has a part in tumorigenesis, cellular stress response, and hence is linked to various diseases from cancer to autoimmune disorders 2–4 .OCT4 possesses several isoforms with different functions at both protein and transcript levels, and their expressions are regulated through different mechanisms and at various biological processes 5,6			
31176714	chr18	63868870	63870870	SERPINB2	However, the further analysis demonstrated that the expression of the enhancer RNA encoded by the region of DNA 20 kbp upstream from the SERPINB2 gene was AhR-dependent	mouse	connective tissue	High+Lowthroughput	Expression of Serpin Peptidase Inhibitor B2 (SERPINB2) is regulated by Aryl hydrocarbon receptor (AhR)	否		tumour	tumor cell	E_02_0112	PCR	However, the further analysis demonstrated that the expression of the enhancer RNA encoded by the region of DNA 20 kbp upstream from the SERPINB2 gene was AhR-dependent	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, the further analysis demonstrated that the expression of the enhancer RNA encoded by the region of DNA 20 kbp upstream from the SERPINB2 gene was AhR-dependent		However, the further analysis demonstrated that the expression of the enhancer RNA encoded by the region of DNA 20 kbp upstream from the SERPINB2 gene was AhR-dependent	Immunohistochemical staining	However, the further analysis demonstrated that the expression of the enhancer RNA encoded by the region of DNA 20 kbp upstream from the SERPINB2 gene was AhR-dependent			PCR				SERPINB2
31174563	chr11	65495199	65497199	MALAT1	Microarray-based analysis initially provided data suggesting that the expression of MALAT1 was up regulated while that of the ABI family member 3 binding protein (ABI3BP) was down-regulated in GBC tissues and cell lines. 	human	connective tissue	High+Lowthroughput	Long noncoding RNA MALAT1 potentiates growth and inhibits senescence by antagonizing ABI3BP in gallbladder cancer cells	否		Gallbladder cancer	Gallbladder cancer cell	E_01_0171	PCR	Microarray-based analysis initially provided data suggesting that the expression of MALAT1 was up regulated while that of the ABI family member 3 binding protein (ABI3BP) was down-regulated in GBC tissues and cell lines. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Microarray-based analysis initially provided data suggesting that the expression of MALAT1 was up regulated while that of the ABI family member 3 binding protein (ABI3BP) was down-regulated in GBC tissues and cell lines. 	Immunohistochemical staining	Microarray-based analysis initially provided data suggesting that the expression of MALAT1 was up regulated while that of the ABI family member 3 binding protein (ABI3BP) was down-regulated in GBC tissues and cell lines. 	MALAT1		PCR	Microarray-based analysis initially provided data suggesting that the expression of MALAT1 was up regulated while that of the ABI family member 3 binding protein (ABI3BP) was down-regulated in GBC tissues and cell lines. 			
31173852	chr5	132437801	132439801	IRF1	In conclusion, the interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma progression by promoting interferon response through a positive regulatory loop with IRF1	mouse	connective tissue	High+Lowthroughput	Interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma by promoting interferon response	否		ESCC	Esophageal squamous cell carcinoma cell	E_02_0113	PCR	In conclusion, the interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma progression by promoting interferon response through a positive regulatory loop with IRF1	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, the interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma progression by promoting interferon response through a positive regulatory loop with IRF1		In conclusion, the interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma progression by promoting interferon response through a positive regulatory loop with IRF1	Immunohistochemical staining	In conclusion, the interferon-inducible lncRNA IRF1-AS represses esophageal squamous cell carcinoma progression by promoting interferon response through a positive regulatory loop with IRF1			PCR				IRF1
31171769	chr7	148803892	148805892	EZH2	We revealed that miR-708 was transcriptionally repressed by EZH2 (enhancer of zeste homolog 2)-induced histone H3 lysine 27 trimethylation and promoter methylation. 	human	connective tissue	High+Lowthroughput	Silencing of microRNA-708 promotes cell growth and epithelial-to-mesenchymal transition by activating the SPHK2/AKT/β-catenin pathway in glioma	否		Gliomas	Glioma cell	E_01_0172	PCR	We revealed that miR-708 was transcriptionally repressed by EZH2 (enhancer of zeste homolog 2)-induced histone H3 lysine 27 trimethylation and promoter methylation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We revealed that miR-708 was transcriptionally repressed by EZH2 (enhancer of zeste homolog 2)-induced histone H3 lysine 27 trimethylation and promoter methylation. 	Immunohistochemical staining	We revealed that miR-708 was transcriptionally repressed by EZH2 (enhancer of zeste homolog 2)-induced histone H3 lysine 27 trimethylation and promoter methylation. 	EZH2		PCR	We revealed that miR-708 was transcriptionally repressed by EZH2 (enhancer of zeste homolog 2)-induced histone H3 lysine 27 trimethylation and promoter methylation. 			
31164154	chr4	105142775	105144775	TET2	Together, our data demonstrated that AMPK is a critical regulator of myogenesis, partly through phosphorylating TET2.	mouse	connective tissue	High+Lowthroughput	Phosphorylation of TET2 by AMPK is indispensable in myogenic differentiation	否			myocyte	E_02_0114	PCR	Together, our data demonstrated that AMPK is a critical regulator of myogenesis, partly through phosphorylating TET2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Together, our data demonstrated that AMPK is a critical regulator of myogenesis, partly through phosphorylating TET2.		Together, our data demonstrated that AMPK is a critical regulator of myogenesis, partly through phosphorylating TET2.	Immunohistochemical staining	Together, our data demonstrated that AMPK is a critical regulator of myogenesis, partly through phosphorylating TET2.			PCR				TET2
31164150	chr16	67559426	67561426	CTCF	Our study suggests an intriguing model where cell type-specific transcription factors such as p63 cooperate with the genomeorganizer CTCF in the three dimensional chromatin space to regulate the transcription program important for the proper cell identity	human	epithelial cells	High+Lowthroughput	p63 cooperates with CTCF to modulate chromatin architecture in skin keratinocytes	否			glial cell	E_01_0173	PCR	Our study suggests an intriguing model where cell type-specific transcription factors such as p63 cooperate with the genomeorganizer CTCF in the three dimensional chromatin space to regulate the transcription program important for the proper cell identity	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our study suggests an intriguing model where cell type-specific transcription factors such as p63 cooperate with the genomeorganizer CTCF in the three dimensional chromatin space to regulate the transcription program important for the proper cell identity	Immunohistochemical staining	Our study suggests an intriguing model where cell type-specific transcription factors such as p63 cooperate with the genomeorganizer CTCF in the three dimensional chromatin space to regulate the transcription program important for the proper cell identity	CTCF		PCR	Our study suggests an intriguing model where cell type-specific transcription factors such as p63 cooperate with the genomeorganizer CTCF in the three dimensional chromatin space to regulate the transcription program important for the proper cell identity			
31162630	chr7	148804276	148806276	EZH2	EZH2 inhibition might be a potential therapeutic target for restenosis.	human	Myotome	High+Lowthroughput	Inhibition of polycomb repressor complex 2 ameliorates neointimal hyperplasia by suppressing trimethylation of H3K27 in vascular smooth muscle cells	否			smooth muscle cell	E_01_0174	PCR	EZH2 inhibition might be a potential therapeutic target for restenosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2 inhibition might be a potential therapeutic target for restenosis.	Immunohistochemical staining	EZH2 inhibition might be a potential therapeutic target for restenosis.	EZH2		PCR	EZH2 inhibition might be a potential therapeutic target for restenosis.			
31160593	chr7	148804085	148806085	EZH2	We report that suppressing EZH2 activity ameliorates experimental intestinal inflammation and delayed the onset of colitis-associated cancer. In a	human	connective tissue	High+Lowthroughput	Targeting EZH2 histone methyltransferase activity alleviates experimental intestinal inflammation	否		Colon cancer	colon cancer cell	E_01_0175	PCR	We report that suppressing EZH2 activity ameliorates experimental intestinal inflammation and delayed the onset of colitis-associated cancer. In a	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We report that suppressing EZH2 activity ameliorates experimental intestinal inflammation and delayed the onset of colitis-associated cancer. In a	Immunohistochemical staining	We report that suppressing EZH2 activity ameliorates experimental intestinal inflammation and delayed the onset of colitis-associated cancer. In a	EZH2		PCR	We report that suppressing EZH2 activity ameliorates experimental intestinal inflammation and delayed the onset of colitis-associated cancer. In a			
31155838	chr11	69767717	69769717	FGF4	Data suggest that FGF-4 signalling is involved in EWS-Oct-4-mediated tumorigenesis, and that its inhibition impairs tumour growth in vivo significantly	human	connective tissue	High+Lowthroughput	Critical role of the fibroblast growth factor signalling pathway in Ewing's sarcoma octamer-binding transcription factor 4-mediated cell proliferation and tumorigenesis	否		tumour	tumor cell	E_01_0176	PCR	Data suggest that FGF-4 signalling is involved in EWS-Oct-4-mediated tumorigenesis, and that its inhibition impairs tumour growth in vivo significantly	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Data suggest that FGF-4 signalling is involved in EWS-Oct-4-mediated tumorigenesis, and that its inhibition impairs tumour growth in vivo significantly		Data suggest that FGF-4 signalling is involved in EWS-Oct-4-mediated tumorigenesis, and that its inhibition impairs tumour growth in vivo significantly	Immunohistochemical staining	Data suggest that FGF-4 signalling is involved in EWS-Oct-4-mediated tumorigenesis, and that its inhibition impairs tumour growth in vivo significantly			PCR				FGF4
31141090	chr19	33297251	33299251	CEBPA	Moreover, this translocation is detected in 50% of T-ALL patients with gamma/delta T cell receptor rearrangement, frequently associated with low expression of transcription factor CCAAT/enhancer-binding protein alpha (CEBPA). 	mouse	connective tissue	High+Lowthroughput	CCAAT/enhancer-binding protein alpha (CEBPA) gene haploinsufficiency does not alter hematopoiesis or induce leukemia in Lck-CALM/AF10 transgenic mice	否			hematopoietic stem cell	E_02_0115	PCR	Moreover, this translocation is detected in 50% of T-ALL patients with gamma/delta T cell receptor rearrangement, frequently associated with low expression of transcription factor CCAAT/enhancer-binding protein alpha (CEBPA). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, this translocation is detected in 50% of T-ALL patients with gamma/delta T cell receptor rearrangement, frequently associated with low expression of transcription factor CCAAT/enhancer-binding protein alpha (CEBPA). 		Moreover, this translocation is detected in 50% of T-ALL patients with gamma/delta T cell receptor rearrangement, frequently associated with low expression of transcription factor CCAAT/enhancer-binding protein alpha (CEBPA). 	Immunohistochemical staining	Moreover, this translocation is detected in 50% of T-ALL patients with gamma/delta T cell receptor rearrangement, frequently associated with low expression of transcription factor CCAAT/enhancer-binding protein alpha (CEBPA). 			PCR				CEBPA
31081034	chr18	55219304	55221304	TCF4	The psychiatric risk-associated transcription factor 4 (TCF4) is linked to schizophrenia. Rare TCF4 coding variants are found in individuals with PittHopkins syndrome an intellectual disability and autism spectrum disorder.	human	connective tissue	High+Lowthroughput	Structural basis for preferential binding of human TCF4 to DNA containing 5-carboxylcytosine	否			neural cell	E_01_0177	PCR	The psychiatric risk-associated transcription factor 4 (TCF4) is linked to schizophrenia. Rare TCF4 coding variants are found in individuals with PittHopkins syndrome an intellectual disability and autism spectrum disorder.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The psychiatric risk-associated transcription factor 4 (TCF4) is linked to schizophrenia. Rare TCF4 coding variants are found in individuals with PittHopkins syndrome an intellectual disability and autism spectrum disorder.	Immunohistochemical staining	The psychiatric risk-associated transcription factor 4 (TCF4) is linked to schizophrenia. Rare TCF4 coding variants are found in individuals with PittHopkins syndrome an intellectual disability and autism spectrum disorder.	TCF4		PCR	The psychiatric risk-associated transcription factor 4 (TCF4) is linked to schizophrenia. Rare TCF4 coding variants are found in individuals with PittHopkins syndrome an intellectual disability and autism spectrum disorder.			
30995827	chr20	22578226	22580226	FOXA2	The role of FOXA2 is different, working as an activator in hepatic cells. As a tumour suppressor, FOXA2 could be responsible for SLC25A13 high expression levels in liver and its downregulation in hepatocellular carcinoma (HCC).	human	connective tissue	High+Lowthroughput	Transcriptional Regulation Factors of the Human Mitochondrial Aspartate/Glutamate Carrier Gene, Isoform 2 (SLC25A13): USF1 as Basal Factor and FOXA2 as Activator in Liver Cells	否			cancer cell	E_01_0178	PCR	The role of FOXA2 is different, working as an activator in hepatic cells. As a tumour suppressor, FOXA2 could be responsible for SLC25A13 high expression levels in liver and its downregulation in hepatocellular carcinoma (HCC).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The role of FOXA2 is different, working as an activator in hepatic cells. As a tumour suppressor, FOXA2 could be responsible for SLC25A13 high expression levels in liver and its downregulation in hepatocellular carcinoma (HCC).	Immunohistochemical staining	The role of FOXA2 is different, working as an activator in hepatic cells. As a tumour suppressor, FOXA2 could be responsible for SLC25A13 high expression levels in liver and its downregulation in hepatocellular carcinoma (HCC).	FOXA2		PCR	The role of FOXA2 is different, working as an activator in hepatic cells. As a tumour suppressor, FOXA2 could be responsible for SLC25A13 high expression levels in liver and its downregulation in hepatocellular carcinoma (HCC).			
31127282	chr16	67559749	67561749	CTCF	CTCF is an important regulator of the 3D chromatin ar- chitecture of interphase chromosomes, which guides gene expression (10–13).	human	connective tissue	High+Lowthroughput	Acute depletion of CTCF directly affects MYC regulation through loss of enhancer-promoter looping	否				E_01_0179	PCR	CTCF is an important regulator of the 3D chromatin ar- chitecture of interphase chromosomes, which guides gene expression (10–13).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			CTCF is an important regulator of the 3D chromatin ar- chitecture of interphase chromosomes, which guides gene expression (10–13).	Immunohistochemical staining	CTCF is an important regulator of the 3D chromatin ar- chitecture of interphase chromosomes, which guides gene expression (10–13).	CTCF		PCR	CTCF is an important regulator of the 3D chromatin ar- chitecture of interphase chromosomes, which guides gene expression (10–13).			
31064204	chr19	33297418	33299418	CEBPA	In this study, the coding domain sequences (CDS) of pigeon C/EBP-α and βwere cloned, 	mouse	connective tissue	High+Lowthroughput	Molecular cloning, characterisation, and expression patterns of pigeon CCAAT/enhancer binding protein-α and -β genes	否		cancer	cancer cell	E_02_0116	PCR	In this study, the coding domain sequences (CDS) of pigeon C/EBP-α and βwere cloned, 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, the coding domain sequences (CDS) of pigeon C/EBP-α and βwere cloned, 		In this study, the coding domain sequences (CDS) of pigeon C/EBP-α and βwere cloned, 	Immunohistochemical staining	In this study, the coding domain sequences (CDS) of pigeon C/EBP-α and βwere cloned, 			PCR				CEBPA
31053723	chr11	2126891	2128891	IGF2	This work suggests a mechanism for epigenetic regulation of dopamine levels in the brain. Epigenetic misregulation of an enhancer at IGF2 may underlie the dopaminergic abnormalities that drives psychotic symptoms. 	human	connective tissue	High+Lowthroughput	Differential methylation of enhancer at IGF2 is associated with abnormal dopamine synthesis in major psychosis	是			neural cell	E_01_0180	PCR	This work suggests a mechanism for epigenetic regulation of dopamine levels in the brain. Epigenetic misregulation of an enhancer at IGF2 may underlie the dopaminergic abnormalities that drives psychotic symptoms. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This work suggests a mechanism for epigenetic regulation of dopamine levels in the brain. Epigenetic misregulation of an enhancer at IGF2 may underlie the dopaminergic abnormalities that drives psychotic symptoms. 		This work suggests a mechanism for epigenetic regulation of dopamine levels in the brain. Epigenetic misregulation of an enhancer at IGF2 may underlie the dopaminergic abnormalities that drives psychotic symptoms. 	Immunohistochemical staining	This work suggests a mechanism for epigenetic regulation of dopamine levels in the brain. Epigenetic misregulation of an enhancer at IGF2 may underlie the dopaminergic abnormalities that drives psychotic symptoms. 			PCR				IGF2
31053176	chrX	153441659	153443659	TREX2	The data highlight a regulatory role of TREX2 DNA methylation for gene expression which might affect incidence and survival of laryngeal cancer. 	human	connective tissue	High+Lowthroughput	DNA methylation at an enhancer of the three prime repair exonuclease 2 gene (TREX2) is linked to gene expression and survival in laryngeal cancer	是			laryngeal carcinoma cell	E_01_0181	PCR	The data highlight a regulatory role of TREX2 DNA methylation for gene expression which might affect incidence and survival of laryngeal cancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The data highlight a regulatory role of TREX2 DNA methylation for gene expression which might affect incidence and survival of laryngeal cancer. 		The data highlight a regulatory role of TREX2 DNA methylation for gene expression which might affect incidence and survival of laryngeal cancer. 	Immunohistochemical staining	The data highlight a regulatory role of TREX2 DNA methylation for gene expression which might affect incidence and survival of laryngeal cancer. 			PCR				TREX2
31721105	chr12	117450290	117452290	KSR2	In order to understand biological roles of TE-derived miR-1269a, we examined expression pattern for miR-1269a and its target gene, KSR2, in various tissues of Sebastes schlegelii.	human	liver	High+Lowthroughput	Expression analysis of LTR-derived miR-1269a and target gene, KSR2 in Sebastes schlegelii	否	无	liver cancer	HCC cell	E_01_0182		In order to understand biological roles of TE-derived miR-1269a, we examined expression pattern for miR-1269a and its target gene, KSR2, in various tissues of Sebastes schlegelii.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In order to understand biological roles of TE-derived miR-1269a, we examined expression pattern for miR-1269a and its target gene, KSR2, in various tissues of Sebastes schlegelii.		In order to understand biological roles of TE-derived miR-1269a, we examined expression pattern for miR-1269a and its target gene, KSR2, in various tissues of Sebastes schlegelii.	Immunohistochemical staining	In order to understand biological roles of TE-derived miR-1269a, we examined expression pattern for miR-1269a and its target gene, KSR2, in various tissues of Sebastes schlegelii.							KSR2
31719045	chr13	63653269	63655269	Ptch1	We confirmed that, in comparison to wild-type (WT) littermates, SHH signalling was significantly decreased in the developing tongue of ShhMFCS4/− mice by E11.5, as demonstrated by reduced Shh and patched 1 (Ptch1) expression (Fig. 1A-D) and consistent with the known period of MFCS4 activity (Sagai et al., 2009).	human,mouse	Musculature	High+Lowthroughput	Temporospatial sonic hedgehog signalling is essential for neural crest-dependent patterning of the intrinsic tongue musculature	否	无		muscle precursor cell	E_02_0117	PCR、Western blot	We confirmed that, in comparison to wild-type (WT) littermates, SHH signalling was significantly decreased in the developing tongue of ShhMFCS4/− mice by E11.5, as demonstrated by reduced Shh and patched 1 (Ptch1) expression (Fig. 1A-D) and consistent with the known period of MFCS4 activity (Sagai et al., 2009).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We confirmed that, in comparison to wild-type (WT) littermates, SHH signalling was significantly decreased in the developing tongue of ShhMFCS4/− mice by E11.5, as demonstrated by reduced Shh and patched 1 (Ptch1) expression (Fig. 1A-D) and consistent with the known period of MFCS4 activity (Sagai et al., 2009).		We confirmed that, in comparison to wild-type (WT) littermates, SHH signalling was significantly decreased in the developing tongue of ShhMFCS4/− mice by E11.5, as demonstrated by reduced Shh and patched 1 (Ptch1) expression (Fig. 1A-D) and consistent with the known period of MFCS4 activity (Sagai et al., 2009).	Immunohistochemical staining	We confirmed that, in comparison to wild-type (WT) littermates, SHH signalling was significantly decreased in the developing tongue of ShhMFCS4/− mice by E11.5, as demonstrated by reduced Shh and patched 1 (Ptch1) expression (Fig. 1A-D) and consistent with the known period of MFCS4 activity (Sagai et al., 2009).			PCR、Western blot				Ptch1
31718595	chr7	148804304	148806304	EZH2	Overexpression of EZH2 is positively correlated with tissue pathological grade and stage,metastasis, and poor survival in many types of solid tumors, including lung cancer, breast cancer, gastric cancer, prostate cancer, and melanoma.	human	connective tissue	High+Lowthroughput	EZH2 upregulation by ERα induces proliferation and migration of papillary thyroid carcinoma	否	无	cancer	Cancer Stem Cell	E_01_0183	PCR, Western blot, immunofluorescence staining	Overexpression of EZH2 is positively correlated with tissue pathological grade and stage,metastasis, and poor survival in many types of solid tumors, including lung cancer, breast cancer, gastric cancer, prostate cancer, and melanoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Overexpression of EZH2 is positively correlated with tissue pathological grade and stage,metastasis, and poor survival in many types of solid tumors, including lung cancer, breast cancer, gastric cancer, prostate cancer, and melanoma.	Immunohistochemical staining	Overexpression of EZH2 is positively correlated with tissue pathological grade and stage,metastasis, and poor survival in many types of solid tumors, including lung cancer, breast cancer, gastric cancer, prostate cancer, and melanoma.	EZH2		PCR、Western blot、免疫荧光染色	Overexpression of EZH2 is positively correlated with tissue pathological grade and stage,metastasis, and poor survival in many types of solid tumors, including lung cancer, breast cancer, gastric cancer, prostate cancer, and melanoma.			
31718447	chr9	117701356	117703356	TLR4	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD2) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.	human,mouse	connective tissue	High+Lowthroughput	Sphingomyelin Synthase 2 Inhibition Ameliorates Cerebral Ischemic Reperfusion Injury Through Reducing the Recruitment of Toll-Like Receptor 4 to Lipid Rafts	否	无	cerebral ischemia	B cell	E_02_0118	PCR、Western blot	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD2) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD2) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.		Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD2) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.	Immunohistochemical staining	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD2) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.			PCR、Western blot				TLR4
31718447	chr1	223106431	223108431	TLR5	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD3) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.	human,mouse	brain	High+Lowthroughput	Sphingomyelin Synthase 2 Inhibition Ameliorates Cerebral Ischemic Reperfusion Injury Through Reducing the Recruitment of Toll-Like Receptor 5 to Lipid Rafts	否	无	cerebral ischemia	brain cell 	E_02_0118	PCR、Western blot	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD3) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD3) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.		Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD3) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.	Immunohistochemical staining	Activation of the TLR4 signaling pathway is initiated by the binding of its ligands to TLR4, causing TLR4 to relocate to lipid rafts, and then forming TLR4/myeloid differentiation factor 2 (MD3) complex in lipid rafts, leading to activation of nuclear factorkappa-light-chain-enhancer of activated B cells (NF-jB)and overproduction of proinflammatory cytokines.			PCR、Western blot				TLR5
31718444	chr3	43283601	43285601	SNRK	The SNRK (sucrose-nonfermenting–related kinase) enzyme is critical for cardiac function.	human,mouse	connective tissue	High+Lowthroughput	Cardiomyocyte-Specific Snrk Prevents Inflammation in the Heart	否	无	cancer	B cell	E_02_0119	PCR、Western blot	The SNRK (sucrose-nonfermenting–related kinase) enzyme is critical for cardiac function.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The SNRK (sucrose-nonfermenting–related kinase) enzyme is critical for cardiac function.		The SNRK (sucrose-nonfermenting–related kinase) enzyme is critical for cardiac function.	Immunohistochemical staining	The SNRK (sucrose-nonfermenting–related kinase) enzyme is critical for cardiac function.			PCR、Western blot				SNRK
31714653	chrX	123856867	123858867	XIAP	"In addition, expression of phospho-ERK (p-ERK), NF-κB p65 (Ser536), and tumor progression-associated proteins, such as matrix metallopeptidase 9 (MMP-9),
vascular endothelial growth factor (VEGF), X-linked inhibitor of apoptosis protein (XIAP), and CyclinD1 were all significantly decreased by magnolol."	human,mouse	connective tissue	High+Lowthroughput	Apoptosis induction and ERK/NF-κB inactivation are associated with magnolol-inhibited tumor progression in hepatocellular carcinoma in vivo	否	无	liver cancer	B cell	E_02_0120	PCR	"In addition, expression of phospho-ERK (p-ERK), NF-κB p65 (Ser536), and tumor progression-associated proteins, such as matrix metallopeptidase 9 (MMP-9),
vascular endothelial growth factor (VEGF), X-linked inhibitor of apoptosis protein (XIAP), and CyclinD1 were all significantly decreased by magnolol."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"In addition, expression of phospho-ERK (p-ERK), NF-κB p65 (Ser536), and tumor progression-associated proteins, such as matrix metallopeptidase 9 (MMP-9),
vascular endothelial growth factor (VEGF), X-linked inhibitor of apoptosis protein (XIAP), and CyclinD1 were all significantly decreased by magnolol."		"In addition, expression of phospho-ERK (p-ERK), NF-κB p65 (Ser536), and tumor progression-associated proteins, such as matrix metallopeptidase 9 (MMP-9),
vascular endothelial growth factor (VEGF), X-linked inhibitor of apoptosis protein (XIAP), and CyclinD1 were all significantly decreased by magnolol."	Immunohistochemical staining	"In addition, expression of phospho-ERK (p-ERK), NF-κB p65 (Ser536), and tumor progression-associated proteins, such as matrix metallopeptidase 9 (MMP-9),
vascular endothelial growth factor (VEGF), X-linked inhibitor of apoptosis protein (XIAP), and CyclinD1 were all significantly decreased by magnolol."			PCR				XIAP
31713877	chr17	27753488	27755488	NOS2	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS2 and TNF expression in diabetic mice.	human,mouse	connective tissue	High+Lowthroughput	Comparative effectiveness of different antiplatelet agents at reducing TNF-driven inflammatory responses in a mouse model	否	无	Ischemic disease	immune cell	E_02_0121	PCR、Western blot	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS2 and TNF expression in diabetic mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS2 and TNF expression in diabetic mice.		Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS2 and TNF expression in diabetic mice.	Immunohistochemical staining	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS2 and TNF expression in diabetic mice.			PCR、Western blot				NOS2
31713877	chr7	150988213	150990213	NOS3	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS3 and TNF expression in diabetic mice.	human,mouse	Epithelial tissues	High+Lowthroughput	Comparative effectiveness of different antiplatelet agents at reducing TNF-driven inflammatory responses in a mouse model	否	无	Ischemic disease	blood vessel endothelial cell	E_02_0121	PCR、Western blot	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS3 and TNF expression in diabetic mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS3 and TNF expression in diabetic mice.		Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS3 and TNF expression in diabetic mice.	Immunohistochemical staining	Clopidogrel reduced serum TNF and IL‐1β release in rats with coronary microembolization and experimental LPS-induced mouse model (25, 26). Sarpogrelate decreased immune cell infiltration and NOS3 and TNF expression in diabetic mice.			PCR、Western blot				NOS3
31712448	chr11	108808163	108810163	Axin2	In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells	human,mouse	Epithelial tissues	High+Lowthroughput	Hepatocyte nuclear factor-1β regulates Wnt signaling through genome-wide competition with β-catenin/lymphoid enhancer binding factor	否	无	Cystic kidney disease	epithelial cell	E_02_0122		In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells		In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells	Immunohistochemical staining	In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells							Axin2
31712448	chr16	44910716	44912716	Ccdc80	In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells	human,mouse	Epithelial tissues	High+Lowthroughput	Hepatocyte nuclear factor-1β regulates Wnt signaling through genome-wide competition with β-catenin/lymphoid enhancer binding factor	否	无	Cystic kidney disease	epithelial cell	E_02_0122		In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells		In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells	Immunohistochemical staining	In contrast, the expression of Axin2 and Ccdc80 was strongly up-regulated in Wnt3a-treated HNF-1β mutant cells compared to wild-type cells							Ccdc80
31712269	chr3	52218227	52220227	TLR9	pylori-induced NF-κB activation and IL-8 secretion are attributed to T4SS-dependent delivery of lipopolysaccharide metabolites and peptidoglycan into host cells, and Toll-like receptor 9 (TLR9) activation is attributed to delivery of bacterial DNA.	human,mouse	stomach	High+Lowthroughput	Bacterial Energetic Requirements for Helicobacter pylori Cag Type IV Secretion System-Dependent Alterations in Gastric Epithelial Cells	否	无	cancer	epithelial cell of stomach	E_02_0123		pylori-induced NF-κB activation and IL-8 secretion are attributed to T4SS-dependent delivery of lipopolysaccharide metabolites and peptidoglycan into host cells, and Toll-like receptor 9 (TLR9) activation is attributed to delivery of bacterial DNA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	pylori-induced NF-κB activation and IL-8 secretion are attributed to T4SS-dependent delivery of lipopolysaccharide metabolites and peptidoglycan into host cells, and Toll-like receptor 9 (TLR9) activation is attributed to delivery of bacterial DNA.		pylori-induced NF-κB activation and IL-8 secretion are attributed to T4SS-dependent delivery of lipopolysaccharide metabolites and peptidoglycan into host cells, and Toll-like receptor 9 (TLR9) activation is attributed to delivery of bacterial DNA.	Immunohistochemical staining	pylori-induced NF-κB activation and IL-8 secretion are attributed to T4SS-dependent delivery of lipopolysaccharide metabolites and peptidoglycan into host cells, and Toll-like receptor 9 (TLR9) activation is attributed to delivery of bacterial DNA.							TLR9
31711897	chr14	54839063	54841063	GCH1	GCH1 feedback regulatory protein (GFRP) inhibits GCH1 activity when BH4 levels increase [14];   dihydropteridin reductase (DHPR) and dihydrofolate reductase (DHFR) ensure the re_x0002_cycling of dihydrobiopterin (BH2) into BH4 [15], BH2 being an oxi_x0002_dized and inactive form of BH4.	mouse		High+Lowthroughput	Tetrahydrobiopterin administration facilitates amphetamine-induced dopamine release and motivation in mice	否				E_02_0124	PCR,Western blot	GCH1 feedback regulatory protein (GFRP) inhibits GCH1 activity when BH4 levels increase [14];   dihydropteridin reductase (DHPR) and dihydrofolate reductase (DHFR) ensure the re_x0002_cycling of dihydrobiopterin (BH2) into BH4 [15], BH2 being an oxi_x0002_dized and inactive form of BH4.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	GCH1 feedback regulatory protein (GFRP) inhibits GCH1 activity when BH4 levels increase [14];   dihydropteridin reductase (DHPR) and dihydrofolate reductase (DHFR) ensure the re_x0002_cycling of dihydrobiopterin (BH2) into BH4 [15], BH2 being an oxi_x0002_dized and inactive form of BH4.		GCH1 feedback regulatory protein (GFRP) inhibits GCH1 activity when BH4 levels increase [14];   dihydropteridin reductase (DHPR) and dihydrofolate reductase (DHFR) ensure the re_x0002_cycling of dihydrobiopterin (BH2) into BH4 [15], BH2 being an oxi_x0002_dized and inactive form of BH4.	Immunohistochemical staining	GCH1 feedback regulatory protein (GFRP) inhibits GCH1 activity when BH4 levels increase [14];   dihydropteridin reductase (DHPR) and dihydrofolate reductase (DHFR) ensure the re_x0002_cycling of dihydrobiopterin (BH2) into BH4 [15], BH2 being an oxi_x0002_dized and inactive form of BH4.			PCR,Western blot				GCH1
31711520	chr7	148804473	148806473	EZH2	We noticed that enhancer of zeste homologue 2 (EZH2) could afect the self-renewal and dif_x0002_ferentiation of hematopoietic stem cells [5] and may be an independent prognostic factor [6] related to a poor progno_x0002_sis [7].	human,mouse	connective tissue	High+Lowthroughput	HO-1 promotes resistance to an EZH2 inhibitor through the pRB-E2F pathway: correlation with the progression of myelodysplastic syndrome into acute myeloid leukemia	否		leukemia	tumor cell	E_02_0125	PCR, Western blot, immunofluorescence staining	We noticed that enhancer of zeste homologue 2 (EZH2) could afect the self-renewal and dif_x0002_ferentiation of hematopoietic stem cells [5] and may be an independent prognostic factor [6] related to a poor progno_x0002_sis [7].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We noticed that enhancer of zeste homologue 2 (EZH2) could afect the self-renewal and dif_x0002_ferentiation of hematopoietic stem cells [5] and may be an independent prognostic factor [6] related to a poor progno_x0002_sis [7].		We noticed that enhancer of zeste homologue 2 (EZH2) could afect the self-renewal and dif_x0002_ferentiation of hematopoietic stem cells [5] and may be an independent prognostic factor [6] related to a poor progno_x0002_sis [7].	Immunohistochemical staining	We noticed that enhancer of zeste homologue 2 (EZH2) could afect the self-renewal and dif_x0002_ferentiation of hematopoietic stem cells [5] and may be an independent prognostic factor [6] related to a poor progno_x0002_sis [7].			PCR,Western blot,免疫荧光染色				EZH2
31709534	chr1	164552565	164554565	PBX1	Low Nfe2l1 mRNA expression is unlikely caused by reduced mTOR signaling but could be the result of diminished pre‐B‐cell leukemia homeobox-1 transcription factor (PBX1) levels.	human,mouse	connective tissue	High+Lowthroughput	Decreased levels of constitutive proteasomes in experimental autoimmune encephalomyelitis may be caused by a combination of subunit displacement and reduced Nfe2l1 expression	否		inflammation	B cell	E_02_0126	PCR, Western blot, immunofluorescence staining	Low Nfe2l1 mRNA expression is unlikely caused by reduced mTOR signaling but could be the result of diminished pre‐B‐cell leukemia homeobox-1 transcription factor (PBX1) levels.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Low Nfe2l1 mRNA expression is unlikely caused by reduced mTOR signaling but could be the result of diminished pre‐B‐cell leukemia homeobox-1 transcription factor (PBX1) levels.		Low Nfe2l1 mRNA expression is unlikely caused by reduced mTOR signaling but could be the result of diminished pre‐B‐cell leukemia homeobox-1 transcription factor (PBX1) levels.	Immunohistochemical staining	Low Nfe2l1 mRNA expression is unlikely caused by reduced mTOR signaling but could be the result of diminished pre‐B‐cell leukemia homeobox-1 transcription factor (PBX1) levels.			PCR,Western blot,免疫荧光染色				PBX1
31709175	chr9	127084657	127086657	ANGPTL2	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.	human,mouse	connective tissue	High+Lowthroughput	Coagulation FXIII-A Protein Expression Defines Three Novel Sub-populations in Pediatric B-Cell Progenitor Acute Lymphoblastic Leukemia Characterized by Distinct Gene Expression Signatures	否		leukemia	B cell	E_02_0127	PCR,Flow cytometry	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.		Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.	Immunohistochemical staining	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.			PCR,Flow cytometry				ANGPTL2
31709175	chr7	22115708	22117708	RAPGEF5	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.	human,mouse	connective tissue	High+Lowthroughput	Coagulation FXIII-A Protein Expression Defines Three Novel Sub-populations in Pediatric B-Cell Progenitor Acute Lymphoblastic Leukemia Characterized by Distinct Gene Expression Signatures	否		leukemia	B cell	E_02_0127	PCR,Flow cytometry	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.		Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.	Immunohistochemical staining	Relative gene expression intensity of ANGPTL2, EHMT1 FOXO1, HAP1, NUCKS1, NUP43, PIK3CG,RAPGEF5, SEMA6A, SPIN1, TRH, and WASF2 followed the pattern of change in the intensity of the expression of the F13A1 gene.			PCR,Flow cytometry				RAPGEF5
31709175	chr17	35868982	35870982	CCL5	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	human,mouse	connective tissue	High+Lowthroughput	Coagulation FXIII-A Protein Expression Defines Three Novel Sub-populations in Pediatric B-Cell Progenitor Acute Lymphoblastic Leukemia Characterized by Distinct Gene Expression Signatures	否		leukemia	T cell	E_02_0127	PCR,Flow cytometry	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.		Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	Immunohistochemical staining	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.			PCR,Flow cytometry				CCL5
31709175	chr5	35849791	35851791	IL7R	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	human,mouse	connective tissue	High+Lowthroughput	Coagulation FXIII-A Protein Expression Defines Three Novel Sub-populations in Pediatric B-Cell Progenitor Acute Lymphoblastic Leukemia Characterized by Distinct Gene Expression Signatures	否		leukemia	T cell	E_02_0127	PCR,Flow cytometry	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.		Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	Immunohistochemical staining	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.			PCR,Flow cytometry				IL7R
31709175	chr3	39260841	39262841	CX3CR1	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	human,mouse	connective tissue	High+Lowthroughput	Coagulation FXIII-A Protein Expression Defines Three Novel Sub-populations in Pediatric B-Cell Progenitor Acute Lymphoblastic Leukemia Characterized by Distinct Gene Expression Signatures	否		leukemia	T cell	E_02_0127	PCR,Flow cytometry	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.		Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.	Immunohistochemical staining	Genes involved in lymphocyte and T-cell apoptotic processes (CCL5, CD3G,IL7R, PLAC8) were over-presented, as well as two others,CX3CR1, RORA, corresponding to macrophage migration.			PCR,Flow cytometry				CX3CR1
31708105	chr5	136274432	136276432	Cux1	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	human,mouse	connective tissue	High+Lowthroughput	Cux2 expression regulated by Lhx2 in the upper layer neurons of the developing cortex	否		autism	immune cell	E_02_0128	PCR, flow cytometry, immunofluorescence staining	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b		Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	Immunohistochemical staining	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b			PCR,Flow cytometry,免疫荧光染色				Cux1
31708105	chr5	121991850	121993850	Cux2	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	human,mouse	connective tissue	High+Lowthroughput	Cux2 expression regulated by Lhx2 in the upper layer neurons of the developing cortex	否		autism	immune cell	E_02_0128	PCR, flow cytometry, immunofluorescence staining	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b		Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	Immunohistochemical staining	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b			PCR,Flow cytometry,免疫荧光染色				Cux2
31708105	chrX	72233135	72235135	Xlr3b	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	human,mouse	connective tissue	High+Lowthroughput	Cux2 expression regulated by Lhx2 in the upper layer neurons of the developing cortex	否		autism	immune cell	E_02_0128	PCR, flow cytometry, immunofluorescence staining	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b		Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b	Immunohistochemical staining	Cux1 and Cux2, which are specifically expressed in cortical layer II-IV, have been shown to be involved in synapse formation, dendritic branching, and spine development by directly controlling the expression of Xlr3b and Xlr4b			PCR,Flow cytometry,免疫荧光染色				Xlr3b
31707045	chr16	56295383	56297383	Abi3bp	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Abi3bp
31707045	chr9	65169791	65171791	Cilp	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Cilp
31707045	chr9	95516985	95518985	Pcolce2	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Pcolce2
31707045	chr1	133962055	133964055	Fmod	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Fmod
31707045	chr13	49695201	49697201	Aspn	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Aspn
31707045	chr1	71621729	71623729	Fn1	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Fn1
31707045	chr17	34876882	34878882	Tnxb	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Tnxb
31707045	chr15	85088078	85090078	Fbln1	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	human,mouse	connective tissue	High+Lowthroughput	TonEBP-deficiency accelerates intervertebral disc degeneration underscored by matrix remodeling, cytoskeletal rearrangements, and changes in proinflammatory gene expression	否		cancer	cancer cell	E_02_0129	PCR, flow cytometry, immunofluorescence staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).		Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).	Immunohistochemical staining	Consistent with our histological and FTIR analyses, a number of downregulated extracellular matrix genes in the AF corresponded to collagen assembly and organization.  These genes included ABI family member 3 binding protein (Abi3bp), cartilage intermediate layer protein (Cilp, Cilp2), procollagen c-endopeptidase enhancer 2 (Pcolce2), fibromodulin (Fmod), asporin (Aspn), fibronectin 1 (Fn1), tenascin X (Tnxb), and fibulin 1 (Fbln1).			PCR,Flow cytometry,免疫荧光染色				Fbln1
31706027	chr16	67559869	67561869	CTCF	A popular model explaining loop formation in vertebrates has proposed that the cohesin complex can dynamically bind to DNA and move along the DNA strand, extruding chromatin to form loops until complex movement is stopped by CTCF [14]	human,mouse		High+Lowthroughput	Small Drosophila zinc finger C2H2 protein with an N-terminal zinc finger-associated domain demonstrates the architecture functions	否			S2 cell	E_02_0130	PCR, flow cytometry, immunofluorescence staining	A popular model explaining loop formation in vertebrates has proposed that the cohesin complex can dynamically bind to DNA and move along the DNA strand, extruding chromatin to form loops until complex movement is stopped by CTCF [14]	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A popular model explaining loop formation in vertebrates has proposed that the cohesin complex can dynamically bind to DNA and move along the DNA strand, extruding chromatin to form loops until complex movement is stopped by CTCF [14]		A popular model explaining loop formation in vertebrates has proposed that the cohesin complex can dynamically bind to DNA and move along the DNA strand, extruding chromatin to form loops until complex movement is stopped by CTCF [14]	Immunohistochemical staining	A popular model explaining loop formation in vertebrates has proposed that the cohesin complex can dynamically bind to DNA and move along the DNA strand, extruding chromatin to form loops until complex movement is stopped by CTCF [14]			PCR,Flow cytometry,免疫荧光染色				CTCF
31705954	chr3	115620608	115622608	GAP43	The aim of the present study was to evaluate the effect of fluoxetine, a widely used SSRI antidepressant, on the neurogenesis and the expression of Growth-Associated Protein 43 (GAP43), a synaptic protein, in the rat hippocampus exposed to Unpredictable Chronic Mild Stress	mouse,hippocampus	Nervous tissue	High+Lowthroughput	Fluoxetine attenuates stress-induced depressive-like behavior through modulation of hippocampal GAP43 and neurogenesis in male rats	否		depression	neural progenitor cell	E_02_0131	PCR, immunofluorescence staining	The aim of the present study was to evaluate the effect of fluoxetine, a widely used SSRI antidepressant, on the neurogenesis and the expression of Growth-Associated Protein 43 (GAP43), a synaptic protein, in the rat hippocampus exposed to Unpredictable Chronic Mild Stress	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The aim of the present study was to evaluate the effect of fluoxetine, a widely used SSRI antidepressant, on the neurogenesis and the expression of Growth-Associated Protein 43 (GAP43), a synaptic protein, in the rat hippocampus exposed to Unpredictable Chronic Mild Stress		The aim of the present study was to evaluate the effect of fluoxetine, a widely used SSRI antidepressant, on the neurogenesis and the expression of Growth-Associated Protein 43 (GAP43), a synaptic protein, in the rat hippocampus exposed to Unpredictable Chronic Mild Stress	Immunohistochemical staining	The aim of the present study was to evaluate the effect of fluoxetine, a widely used SSRI antidepressant, on the neurogenesis and the expression of Growth-Associated Protein 43 (GAP43), a synaptic protein, in the rat hippocampus exposed to Unpredictable Chronic Mild Stress			PCR,免疫荧光染色				GAP43
31704972	chr12	55964033	55966033	CDK2	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).	human,mouse		High+Lowthroughput	CDK2-mediated site-specific phosphorylation of EZH2 drives and maintains triple-negative breast cancer	否		mammary cancer	Triple-negative breast cancer cell	E_02_0132	PCR,Western blot	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).		Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).	Immunohistochemical staining	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).			PCR,Western blot				CDK2
31704972	chr7	148804376	148806376	EZH2	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).	human,mouse	breast	High+Lowthroughput	CDK2-mediated site-specific phosphorylation of EZH2 drives and maintains triple-negative breast cancer	否		mammary cancer	mammary gland epithelial cell	E_02_0132	PCR,Western blot	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).		Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).	Immunohistochemical staining	Previously, we and others report that cyclin E/cyclin-dependent kinase 2 (CDK2) phosphorylates enhancer of zeste homolog 2 (EZH2) at T416 (pT416-EZH2).			PCR,Western blot				EZH2
31699991	chr17	42697602	42699602	EZH1	Here we report that AML1-ETO-positive patients, with high histone lysine methyl_x0002_transferase Enhancer of zeste homolog 1 (EZH1) expression, show a worse overall survival than those with lower EZH1 expression. EZH1 knockdown impairs survival and proliferation of AML1-ETO-expressing cells in vitro and in vivo. 	human,mouse	connective tissue	High+Lowthroughput	Protein lysine 43 methylation by EZH1 promotes AML1-ETO transcriptional repression in leukemia	否		cancer	stem cell	E_02_0133	PCR,Western blot	Here we report that AML1-ETO-positive patients, with high histone lysine methyl_x0002_transferase Enhancer of zeste homolog 1 (EZH1) expression, show a worse overall survival than those with lower EZH1 expression. EZH1 knockdown impairs survival and proliferation of AML1-ETO-expressing cells in vitro and in vivo. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we report that AML1-ETO-positive patients, with high histone lysine methyl_x0002_transferase Enhancer of zeste homolog 1 (EZH1) expression, show a worse overall survival than those with lower EZH1 expression. EZH1 knockdown impairs survival and proliferation of AML1-ETO-expressing cells in vitro and in vivo. 		Here we report that AML1-ETO-positive patients, with high histone lysine methyl_x0002_transferase Enhancer of zeste homolog 1 (EZH1) expression, show a worse overall survival than those with lower EZH1 expression. EZH1 knockdown impairs survival and proliferation of AML1-ETO-expressing cells in vitro and in vivo. 	Immunohistochemical staining	Here we report that AML1-ETO-positive patients, with high histone lysine methyl_x0002_transferase Enhancer of zeste homolog 1 (EZH1) expression, show a worse overall survival than those with lower EZH1 expression. EZH1 knockdown impairs survival and proliferation of AML1-ETO-expressing cells in vitro and in vivo. 			PCR,Western blot				EZH1
31698854	chrX	25000875	25002875	ARX	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	human,mouse	connective tissue	High+Lowthroughput	Changes in Calcium Homeostasis and Gene Expression Implicated in Epilepsy in Hippocampi of Mice Overexpressing ORAI1	否		epilepsy	T cell	E_02_0134	PCR	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 		In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Immunohistochemical staining	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 			PCR				ARX
31698854	chr12	121623759	121625759	ORAI1	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	human,mouse	connective tissue	High+Lowthroughput	Changes in Calcium Homeostasis and Gene Expression Implicated in Epilepsy in Hippocampi of Mice Overexpressing ORAI1	否		epilepsy	T cell	E_02_0134	PCR	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 		In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Immunohistochemical staining	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 			PCR				ORAI1
31698854	chrX	159552038	159554038	Cdkl5	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	human,mouse	connective tissue	High+Lowthroughput	Changes in Calcium Homeostasis and Gene Expression Implicated in Epilepsy in Hippocampi of Mice Overexpressing ORAI1	否		epilepsy	T cell	E_02_0134	PCR	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 		In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Immunohistochemical staining	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 			PCR				Cdkl5
31698854	chr3	55147134	55149134	Dclk1	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	human,mouse	connective tissue	High+Lowthroughput	Changes in Calcium Homeostasis and Gene Expression Implicated in Epilepsy in Hippocampi of Mice Overexpressing ORAI1	否		epilepsy	T cell	E_02_0134	PCR	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 		In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 	Immunohistochemical staining	In humans, ARX, DCLK1, and CDLK5 were shown to be mutated in some rare epilepsy-associated disorders. We conclude that the occurrence of seizure-like events in aged mice overexpressing ORAI1 might be due to the down-regulation of Arx, and possibly of Cdkl5 and Dclk1 genes. 			PCR				Dclk1
31698100	chr20	13993019	13995019	MACROD2	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 	human		High+Lowthroughput	Split hand/foot malformation associated with 20p12.1 deletion: A case report	是		Split hand / foot malformation		E_01_0184	PCR	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 		Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 	Immunohistochemical staining	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 			PCR				MACROD2
31698100	chr20	16269065	16271065	KIF16B	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 	human		High+Lowthroughput	Split hand/foot malformation associated with 20p12.1 deletion: A case report	是		Split hand / foot malformation		E_01_0184	PCR	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 		Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 	Immunohistochemical staining	Although MACROD2 mutations have not been associated with limb malformation until now, it is located next to KIF16B, which is involved in fibroblast growth factor receptor (FGFR) signaling. 			PCR				KIF16B
31697837	chr5	88714150	88716150	MEF2C	In this context, SIK3maintains MEF2C function by directly phosphorylating histone deacetylase 4 (HDAC4), arepressive cofactor of MEF2C.	human,mouse	connective tissue	High+Lowthroughput	Salt-inducible kinase inhibition suppresses acute myeloid leukemia progression in vivo	否		Acute myeloid leukemia	mutant lymphoma cell	E_02_0135	PCR,Flow cytometry,Western blot	In this context, SIK3maintains MEF2C function by directly phosphorylating histone deacetylase 4 (HDAC4), arepressive cofactor of MEF2C.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this context, SIK3maintains MEF2C function by directly phosphorylating histone deacetylase 4 (HDAC4), arepressive cofactor of MEF2C.		In this context, SIK3maintains MEF2C function by directly phosphorylating histone deacetylase 4 (HDAC4), arepressive cofactor of MEF2C.	Immunohistochemical staining	In this context, SIK3maintains MEF2C function by directly phosphorylating histone deacetylase 4 (HDAC4), arepressive cofactor of MEF2C.			PCR,Flow cytometry,Western blot				MEF2C
31695501	chr7	148804320	148806320	EZH2	Enhancer of zeste 2 homolog (EZH2) is the catalytic subunit of the polycomb repressive complex 2, which is a complex that methylates lysine 27 of histone H3 (H3K27)to repress its gene expression.	human,mouse	connective tissue	High+Lowthroughput	Silencing Of hsa_circ_0008450 Represses Hepatocellular Carcinoma Progression Through Regulation Of microRNA-214-3p/EZH2 Axis	否		liver cancer	cancer cell	E_02_0136	PCR,Western blot	Enhancer of zeste 2 homolog (EZH2) is the catalytic subunit of the polycomb repressive complex 2, which is a complex that methylates lysine 27 of histone H3 (H3K27)to repress its gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of zeste 2 homolog (EZH2) is the catalytic subunit of the polycomb repressive complex 2, which is a complex that methylates lysine 27 of histone H3 (H3K27)to repress its gene expression.		Enhancer of zeste 2 homolog (EZH2) is the catalytic subunit of the polycomb repressive complex 2, which is a complex that methylates lysine 27 of histone H3 (H3K27)to repress its gene expression.	Immunohistochemical staining	Enhancer of zeste 2 homolog (EZH2) is the catalytic subunit of the polycomb repressive complex 2, which is a complex that methylates lysine 27 of histone H3 (H3K27)to repress its gene expression.			PCR,Western blot				EZH2
31695196	chr17	40016366	40018366	MED24	ERK triggers the reversible association and disassociation of RNA polymerase II and associated co-factors from genes and enhancers with the mediator component MED24 having an essential role in ERK-dependent transcriptional regulation.	human,mouse	connective tissue	High+Lowthroughput	Silencing Of hsa_circ_0008450 Represses Hepatocellular Carcinoma Progression Through Regulation Of microRNA-214-3p/EZH2 Axis	否	无		embryonic stem cell	E_02_0137	PCR,Flow cytometry	ERK triggers the reversible association and disassociation of RNA polymerase II and associated co-factors from genes and enhancers with the mediator component MED24 having an essential role in ERK-dependent transcriptional regulation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ERK triggers the reversible association and disassociation of RNA polymerase II and associated co-factors from genes and enhancers with the mediator component MED24 having an essential role in ERK-dependent transcriptional regulation.		ERK triggers the reversible association and disassociation of RNA polymerase II and associated co-factors from genes and enhancers with the mediator component MED24 having an essential role in ERK-dependent transcriptional regulation.	Immunohistochemical staining	ERK triggers the reversible association and disassociation of RNA polymerase II and associated co-factors from genes and enhancers with the mediator component MED24 having an essential role in ERK-dependent transcriptional regulation.			PCR,Flow cytometry				MED24
31694243	chr4	186066778	186068778	TLR3	Interestingly, the interaction of OAA with IκB kinase α/β (IKKα/β) strongly attenuated the production of certain proteins and inflammatory cytokines in the TLR3 signaling pathway, such as nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkBα),extracellular regulated kinases (ERK), and p38, in an in vitro model.	human,mouse	blood	High+Lowthroughput	Transcriptome analysis reveals a positive effect of brassinosteroids on the photosynthetic capacity of wucai under low temperature	否	无	leukemia	B cell	E_02_0138	PCR,Western blot	Interestingly, the interaction of OAA with IκB kinase α/β (IKKα/β) strongly attenuated the production of certain proteins and inflammatory cytokines in the TLR3 signaling pathway, such as nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkBα),extracellular regulated kinases (ERK), and p38, in an in vitro model.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Interestingly, the interaction of OAA with IκB kinase α/β (IKKα/β) strongly attenuated the production of certain proteins and inflammatory cytokines in the TLR3 signaling pathway, such as nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkBα),extracellular regulated kinases (ERK), and p38, in an in vitro model.		Interestingly, the interaction of OAA with IκB kinase α/β (IKKα/β) strongly attenuated the production of certain proteins and inflammatory cytokines in the TLR3 signaling pathway, such as nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkBα),extracellular regulated kinases (ERK), and p38, in an in vitro model.	Immunohistochemical staining	Interestingly, the interaction of OAA with IκB kinase α/β (IKKα/β) strongly attenuated the production of certain proteins and inflammatory cytokines in the TLR3 signaling pathway, such as nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkBα),extracellular regulated kinases (ERK), and p38, in an in vitro model.			PCR,Western blot				TLR3
31694013	chr7	148804620	148806620	EZH2	Enhancer of zeste homolog 2 (EZH2) is one central epigenetic silencer of the polycomb repressor complex 2 (PRC2) that is already in clinical use as a novel drug target and is associated with poorer prognosis in several cancer entities	human	intestines	High+Lowthroughput	Oleanolic Acid Acetate Exerts Anti-Inflammatory Activity via IKKα/β Suppression in TLR3-Mediated NF-κB Activation	否	无	Colon cancer	colon cancer cell	E_01_0185	PCR	Enhancer of zeste homolog 2 (EZH2) is one central epigenetic silencer of the polycomb repressor complex 2 (PRC2) that is already in clinical use as a novel drug target and is associated with poorer prognosis in several cancer entities	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2 (EZH2) is one central epigenetic silencer of the polycomb repressor complex 2 (PRC2) that is already in clinical use as a novel drug target and is associated with poorer prognosis in several cancer entities	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2) is one central epigenetic silencer of the polycomb repressor complex 2 (PRC2) that is already in clinical use as a novel drug target and is associated with poorer prognosis in several cancer entities	EZH2		PCR	Enhancer of zeste homolog 2 (EZH2) is one central epigenetic silencer of the polycomb repressor complex 2 (PRC2) that is already in clinical use as a novel drug target and is associated with poorer prognosis in several cancer entities			
31693890	chr7	148804304	148806304	EZH2	The histone methyl transferase enhancer of zeste ho_x0002_molog 2 (EZH2) is a master transcriptional regulatorinvolved in histone H3 lysine 27 trimethylation.	human	breast	High+Lowthroughput	Enhancer of Zeste Homolog 2 in Colorectal Cancer Development and Progression	否	无	mammary cancer	breast cancer cell	E_01_0186	PCR,Western blot,Flow cytometry	The histone methyl transferase enhancer of zeste ho_x0002_molog 2 (EZH2) is a master transcriptional regulatorinvolved in histone H3 lysine 27 trimethylation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The histone methyl transferase enhancer of zeste ho_x0002_molog 2 (EZH2) is a master transcriptional regulatorinvolved in histone H3 lysine 27 trimethylation.	Immunohistochemical staining	The histone methyl transferase enhancer of zeste ho_x0002_molog 2 (EZH2) is a master transcriptional regulatorinvolved in histone H3 lysine 27 trimethylation.	EZH2		PCR,Western blot,Flow cytometry	The histone methyl transferase enhancer of zeste ho_x0002_molog 2 (EZH2) is a master transcriptional regulatorinvolved in histone H3 lysine 27 trimethylation.			
31693439	chr15	90963083	90965083	PRC1	Four are the main epigenetic pathways involved in this kind of networks and considered in our analysis. The polycomb-repressive complex 1 (PRC1), a transcriptional-repressor complex consisting of several proteins among which an important role is played by the Polycomb group ring finger ones (in particular Bmi-1) and whose action is responsible of the ubiquitylation of H2AK119ub1	human	bone marrow	High+Lowthroughput	Regulation of EZH2 by SMYD2-Mediated Lysine Methylation Is Implicated in Tumorigenesis	否	无	Myeloma	Myeloma cell	E_01_0187	PCR,Western blot,Flow cytometry	Four are the main epigenetic pathways involved in this kind of networks and considered in our analysis. The polycomb-repressive complex 1 (PRC1), a transcriptional-repressor complex consisting of several proteins among which an important role is played by the Polycomb group ring finger ones (in particular Bmi-1) and whose action is responsible of the ubiquitylation of H2AK119ub1	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Four are the main epigenetic pathways involved in this kind of networks and considered in our analysis. The polycomb-repressive complex 1 (PRC1), a transcriptional-repressor complex consisting of several proteins among which an important role is played by the Polycomb group ring finger ones (in particular Bmi-1) and whose action is responsible of the ubiquitylation of H2AK119ub1		Four are the main epigenetic pathways involved in this kind of networks and considered in our analysis. The polycomb-repressive complex 1 (PRC1), a transcriptional-repressor complex consisting of several proteins among which an important role is played by the Polycomb group ring finger ones (in particular Bmi-1) and whose action is responsible of the ubiquitylation of H2AK119ub1	Immunohistochemical staining	Four are the main epigenetic pathways involved in this kind of networks and considered in our analysis. The polycomb-repressive complex 1 (PRC1), a transcriptional-repressor complex consisting of several proteins among which an important role is played by the Polycomb group ring finger ones (in particular Bmi-1) and whose action is responsible of the ubiquitylation of H2AK119ub1			PCR,Western blot,Flow cytometry				PRC1
31692936	chr4	1868930	1870930	NSD2	NSD2 (also known as WHSC1 and MMSET) was initially found to be deleted in Wolf-Hirschhorn syndrome (WHS) and rearranged with the immunoglobulin locus in 15%~20% multiple Ivyspring International Publisher myeloma (MM) cases [4-5].  Indeed, NSD2 gene,encoding two main isoforms, NSD2-long (1,365 aminoacid) and NSD2-short (647 amino acid), was located at chromosome 4p16.3, which exhibits strong cancerrelevance	human,mouse	kidney	High+Lowthroughput	Investigating the epi-miRNome: identification of epi-miRNAs using transfection experiments	否	无	renal cell carcinoma	Renal cell	E_02_0139	PCR,Western blot,Flow cytometry	NSD2 (also known as WHSC1 and MMSET) was initially found to be deleted in Wolf-Hirschhorn syndrome (WHS) and rearranged with the immunoglobulin locus in 15%~20% multiple Ivyspring International Publisher myeloma (MM) cases [4-5].  Indeed, NSD2 gene,encoding two main isoforms, NSD2-long (1,365 aminoacid) and NSD2-short (647 amino acid), was located at chromosome 4p16.3, which exhibits strong cancerrelevance	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	NSD2 (also known as WHSC1 and MMSET) was initially found to be deleted in Wolf-Hirschhorn syndrome (WHS) and rearranged with the immunoglobulin locus in 15%~20% multiple Ivyspring International Publisher myeloma (MM) cases [4-5].  Indeed, NSD2 gene,encoding two main isoforms, NSD2-long (1,365 aminoacid) and NSD2-short (647 amino acid), was located at chromosome 4p16.3, which exhibits strong cancerrelevance		NSD2 (also known as WHSC1 and MMSET) was initially found to be deleted in Wolf-Hirschhorn syndrome (WHS) and rearranged with the immunoglobulin locus in 15%~20% multiple Ivyspring International Publisher myeloma (MM) cases [4-5].  Indeed, NSD2 gene,encoding two main isoforms, NSD2-long (1,365 aminoacid) and NSD2-short (647 amino acid), was located at chromosome 4p16.3, which exhibits strong cancerrelevance	Immunohistochemical staining	NSD2 (also known as WHSC1 and MMSET) was initially found to be deleted in Wolf-Hirschhorn syndrome (WHS) and rearranged with the immunoglobulin locus in 15%~20% multiple Ivyspring International Publisher myeloma (MM) cases [4-5].  Indeed, NSD2 gene,encoding two main isoforms, NSD2-long (1,365 aminoacid) and NSD2-short (647 amino acid), was located at chromosome 4p16.3, which exhibits strong cancerrelevance			PCR,Western blot,Flow cytometry				NSD2
31692093	chr17	82215342	82217342	SLC16A3	Moreover, we demonstrate for the first time that HIF-1α directly activates an intronic enhancer in SLC16A3 under hypoxic conditions.	human,mouse	intervertebral disc	High+Lowthroughput	Combining GAL4 GFP enhancer trap with split luciferase to measure spatiotemporal promoter activity in Arabidopsis	否	无	Chronic intervertebral pain	intervertebral disc cells	E_02_0140	PCR, Western blot, flow cytometry, immunofluorescence staining	Moreover, we demonstrate for the first time that HIF-1α directly activates an intronic enhancer in SLC16A3 under hypoxic conditions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, we demonstrate for the first time that HIF-1α directly activates an intronic enhancer in SLC16A3 under hypoxic conditions.		Moreover, we demonstrate for the first time that HIF-1α directly activates an intronic enhancer in SLC16A3 under hypoxic conditions.	Immunohistochemical staining	Moreover, we demonstrate for the first time that HIF-1α directly activates an intronic enhancer in SLC16A3 under hypoxic conditions.			PCR,Western blot,Flow cytometry,免疫荧光染色				SLC16A3
31692040	chr12	55964023	55966023	CDK2	In this study, we show that cyclin‐dependent kinase 2 (CDK2) negatively regulates C/EBPα protein levels in myeloid leukemia cells	human,mouse	bone marrow	High+Lowthroughput	Lactate Efflux From Intervertebral Disc Cells Is Required for Maintenance of Spine Health	否	无	Myeloid leukemia	myeloid leukemia cells	E_02_0141	PCR, Western blot, flow cytometry, immunofluorescence staining	In this study, we show that cyclin‐dependent kinase 2 (CDK2) negatively regulates C/EBPα protein levels in myeloid leukemia cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we show that cyclin‐dependent kinase 2 (CDK2) negatively regulates C/EBPα protein levels in myeloid leukemia cells		In this study, we show that cyclin‐dependent kinase 2 (CDK2) negatively regulates C/EBPα protein levels in myeloid leukemia cells	Immunohistochemical staining	In this study, we show that cyclin‐dependent kinase 2 (CDK2) negatively regulates C/EBPα protein levels in myeloid leukemia cells			PCR,Western blot,Flow cytometry,免疫荧光染色				CDK2
31692040	chr19	33297357	33299357	CEBPA	Condi_x0002_tional disruption of CEBPA leads to differentiation block(transition from common myeloid to granulocyte mono_x0002_cyte progenitors), granulopoiesis in particular.	human,mouse	liver	High+Lowthroughput	Lactate Efflux From Intervertebral Disc Cells Is Required for Maintenance of Spine Health	否	无	tumour	hepatocyte	E_02_0141	PCR, Western blot, flow cytometry, immunofluorescence staining	Condi_x0002_tional disruption of CEBPA leads to differentiation block(transition from common myeloid to granulocyte mono_x0002_cyte progenitors), granulopoiesis in particular.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Condi_x0002_tional disruption of CEBPA leads to differentiation block(transition from common myeloid to granulocyte mono_x0002_cyte progenitors), granulopoiesis in particular.		Condi_x0002_tional disruption of CEBPA leads to differentiation block(transition from common myeloid to granulocyte mono_x0002_cyte progenitors), granulopoiesis in particular.	Immunohistochemical staining	Condi_x0002_tional disruption of CEBPA leads to differentiation block(transition from common myeloid to granulocyte mono_x0002_cyte progenitors), granulopoiesis in particular.			PCR,Western blot,Flow cytometry,免疫荧光染色				CEBPA
31691800	chr21	39443054	39445054	SH3BGR	Hi-C data show that rs2836411 is located in a sub-domain spanning from a region upstream of P3 till the 3_x0002_ end of ERG, which is part of a larger TAD spanning from the 3_x0002_ end of ERG to SH3BGR.	human,mouse	Epithelial tissues	High+Lowthroughput	Berberine Inhibits Adipogenesis in Porcine Adipocytes via AMP-Activated Protein Kinase-Dependent and -Independent Mechanisms	是	rs2836411	Abdominal aortic aneurysm	blood vessel endothelial cell	E_02_0142	PCR,Flow cytometry	Hi-C data show that rs2836411 is located in a sub-domain spanning from a region upstream of P3 till the 3_x0002_ end of ERG, which is part of a larger TAD spanning from the 3_x0002_ end of ERG to SH3BGR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hi-C data show that rs2836411 is located in a sub-domain spanning from a region upstream of P3 till the 3_x0002_ end of ERG, which is part of a larger TAD spanning from the 3_x0002_ end of ERG to SH3BGR.		Hi-C data show that rs2836411 is located in a sub-domain spanning from a region upstream of P3 till the 3_x0002_ end of ERG, which is part of a larger TAD spanning from the 3_x0002_ end of ERG to SH3BGR.	Immunohistochemical staining	Hi-C data show that rs2836411 is located in a sub-domain spanning from a region upstream of P3 till the 3_x0002_ end of ERG, which is part of a larger TAD spanning from the 3_x0002_ end of ERG to SH3BGR.			PCR,Flow cytometry				SH3BGR
31690584	chr17	72118178	72120178	SOX9	Knockdown of linc02095 results in decreased BC cell proliferation, whereas its overexpression promotes cells proliferation. Linc02095-depleted cells display reduced expression of SOX9 concomitant with reduced RNA polymerase	human	breast	High+Lowthroughput	The hTERT-VNTR2-2(nd) alleles are involved in genomic stability in gastrointestinal cancer	否	无	mammary cancer	breast cancer cell	E_01_0188	PCR, Western blot, gene knockdown	Knockdown of linc02095 results in decreased BC cell proliferation, whereas its overexpression promotes cells proliferation. Linc02095-depleted cells display reduced expression of SOX9 concomitant with reduced RNA polymerase	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Knockdown of linc02095 results in decreased BC cell proliferation, whereas its overexpression promotes cells proliferation. Linc02095-depleted cells display reduced expression of SOX9 concomitant with reduced RNA polymerase	Immunohistochemical staining	Knockdown of linc02095 results in decreased BC cell proliferation, whereas its overexpression promotes cells proliferation. Linc02095-depleted cells display reduced expression of SOX9 concomitant with reduced RNA polymerase	SOX9		PCR,Western blot,基因敲降	Knockdown of linc02095 results in decreased BC cell proliferation, whereas its overexpression promotes cells proliferation. Linc02095-depleted cells display reduced expression of SOX9 concomitant with reduced RNA polymerase			
31689455	chr7	100717697	100719697	EPO	EPO prevented the reduction of VSMC phenotypic markers, and reversed the increased calcium content and calcium salt deposition in the aortas of CKD rats and cultured calcified VSMCs.	human,mouse	Musculature	High+Lowthroughput	Erythropoietin attenuates vascular calcification by inhibiting endoplasmic reticulum stress in rats with chronic kidney disease	否	无	Vascular calcification	smooth muscle cell	E_02_0143	Western blot,PCR	EPO prevented the reduction of VSMC phenotypic markers, and reversed the increased calcium content and calcium salt deposition in the aortas of CKD rats and cultured calcified VSMCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EPO prevented the reduction of VSMC phenotypic markers, and reversed the increased calcium content and calcium salt deposition in the aortas of CKD rats and cultured calcified VSMCs.		EPO prevented the reduction of VSMC phenotypic markers, and reversed the increased calcium content and calcium salt deposition in the aortas of CKD rats and cultured calcified VSMCs.	Immunohistochemical staining	EPO prevented the reduction of VSMC phenotypic markers, and reversed the increased calcium content and calcium salt deposition in the aortas of CKD rats and cultured calcified VSMCs.			Western blot,PCR				EPO
31689455	chr19	11374596	11376596	EPOR	The EPO receptor (EPOR) mediates the pleiotropic effects of EPO in target cells	human,mouse	connective tissue	High+Lowthroughput	Erythropoietin attenuates vascular calcification by inhibiting endoplasmic reticulum stress in rats with chronic kidney disease	否	无	Vascular calcification	target cell	E_02_0143	Western blot,PCR	The EPO receptor (EPOR) mediates the pleiotropic effects of EPO in target cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The EPO receptor (EPOR) mediates the pleiotropic effects of EPO in target cells		The EPO receptor (EPOR) mediates the pleiotropic effects of EPO in target cells	Immunohistochemical staining	The EPO receptor (EPOR) mediates the pleiotropic effects of EPO in target cells			Western blot,PCR				EPOR
31686316	chr22	39516753	39518753	ATF4	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	mouse	connective tissue	High+Lowthroughput	CCAAT/enhancer-binding protein beta (C/EBPβ) knockdown reduces inflammation, ER stress, and apoptosis, and promotes autophagy in oxLDL-treated RAW264.7 macrophage cells	否	无	atherosclerosis	macrophage derived foam cell	E_02_0144	Western blot,PCR	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.		We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	Immunohistochemical staining	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.			Western blot,PCR				ATF4
31686316	chr1	161763620	161765620	ATF6	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	mouse	connective tissue	High+Lowthroughput	CCAAT/enhancer-binding protein beta (C/EBPβ) knockdown reduces inflammation, ER stress, and apoptosis, and promotes autophagy in oxLDL-treated RAW264.7 macrophage cells	否	无	atherosclerosis	macrophage derived foam cell	E_02_0144	Western blot,PCR	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.		We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	Immunohistochemical staining	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.			Western blot,PCR				ATF6
31686316	chr6	106042776	106044776	ATG5	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	mouse	connective tissue	High+Lowthroughput	CCAAT/enhancer-binding protein beta (C/EBPβ) knockdown reduces inflammation, ER stress, and apoptosis, and promotes autophagy in oxLDL-treated RAW264.7 macrophage cells	否	无	atherosclerosis	immune cell	E_02_0144	Western blot,PCR	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.		We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.	Immunohistochemical staining	We measured key genes CHOP, mTORC1, genes implicated in ERS [activat_x0002_ing transcription factor 4 & 6 (ATF4, ATF6)] and apopto_x0002_sis (caspase 1, caspase-3 and caspase 12), and autophagy (ATG5, LC3A, LC3B) in macrophage cells by qPCR.			Western blot,PCR				ATG5
31686214	chr16	86507862	86509862	FOXF1	Haploinsufciency of FOXF1 causes alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV), a lethal neonatal lung developmental disorder.  We describe two similar heterozygous CNV deletions involving the FOXF1 enhancer and re-analyze FOXF1 missense mutation, all associated with an unexpectedly mitigated disease phenotype.	human,mouse	Epithelial tissues	High+Lowthroughput	Association of rare non-coding SNVs in the lung-specific FOXF1 enhancer with a mitigation of the lethal ACDMPV phenotype	是	rs150502618-A	Misalignment of pulmonary veins	epithelial cell	E_02_0145	Flow cytometry,PCR	Haploinsufciency of FOXF1 causes alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV), a lethal neonatal lung developmental disorder.  We describe two similar heterozygous CNV deletions involving the FOXF1 enhancer and re-analyze FOXF1 missense mutation, all associated with an unexpectedly mitigated disease phenotype.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Haploinsufciency of FOXF1 causes alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV), a lethal neonatal lung developmental disorder.  We describe two similar heterozygous CNV deletions involving the FOXF1 enhancer and re-analyze FOXF1 missense mutation, all associated with an unexpectedly mitigated disease phenotype.		Haploinsufciency of FOXF1 causes alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV), a lethal neonatal lung developmental disorder.  We describe two similar heterozygous CNV deletions involving the FOXF1 enhancer and re-analyze FOXF1 missense mutation, all associated with an unexpectedly mitigated disease phenotype.	Immunohistochemical staining	Haploinsufciency of FOXF1 causes alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV), a lethal neonatal lung developmental disorder.  We describe two similar heterozygous CNV deletions involving the FOXF1 enhancer and re-analyze FOXF1 missense mutation, all associated with an unexpectedly mitigated disease phenotype.			Flow cytometry,PCR				FOXF1
31686214	chr16	67559674	67561674	CTCF	Sequencing of these alleles revealed two rare SNVs, rs150502618-A and rs79301423-T, mapping to the partially overlapping binding sites for TFAP2s and CTCF in the core region of the enhancer. 	human,mouse	lung	High+Lowthroughput	Association of rare non-coding SNVs in the lung-specific FOXF1 enhancer with a mitigation of the lethal ACDMPV phenotype	是	rs79301423-T	Misalignment of pulmonary veins	pneumocyte	E_02_0145	Flow cytometry,PCR	Sequencing of these alleles revealed two rare SNVs, rs150502618-A and rs79301423-T, mapping to the partially overlapping binding sites for TFAP2s and CTCF in the core region of the enhancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Sequencing of these alleles revealed two rare SNVs, rs150502618-A and rs79301423-T, mapping to the partially overlapping binding sites for TFAP2s and CTCF in the core region of the enhancer. 		Sequencing of these alleles revealed two rare SNVs, rs150502618-A and rs79301423-T, mapping to the partially overlapping binding sites for TFAP2s and CTCF in the core region of the enhancer. 	Immunohistochemical staining	Sequencing of these alleles revealed two rare SNVs, rs150502618-A and rs79301423-T, mapping to the partially overlapping binding sites for TFAP2s and CTCF in the core region of the enhancer. 			Flow cytometry,PCR				CTCF
31684161	chr4	153681439	153683439	TLR2	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 	human,mouse	blood	High+Lowthroughput	HP1717 Contributes to Streptococcus suis Virulence by Inducing an Excessive Inflammatory Response and Influencing the Biosynthesis of the Capsule	否	无	inflammation	B cell	E_02_0146	Western blot,PCR	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 		The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 	Immunohistochemical staining	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 			Western blot,PCR				TLR2
31684161	chr9	117701075	117703075	TLR4	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 	human,mouse	connective tissue	High+Lowthroughput	HP1717 Contributes to Streptococcus suis Virulence by Inducing an Excessive Inflammatory Response and Influencing the Biosynthesis of the Capsule	否	无	inflammation	immune cell	E_02_0146	Western blot,PCR	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 		The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 	Immunohistochemical staining	The qRT-PCR results show that TLR2 transcription was significantly upregulated in RAW264.7 cells stimulated by HP1717, but TLR4 transcription did not significantly change (Figure 4A). 			Western blot,PCR				TLR4
31682213	chr20	44582166	44584166	ADA	Azodicarbonamide (ADA) is a dough-enhancer, which in Nigeria is an approved replacement for potassium bromate (a dough-enhancer that has been banned in a number of coun_x0002_tries due to its nephrotoxic potential).	human	connective tissue	High+Lowthroughput	An Assessment of the Effects of Azodicarbonamide-containing Diet on Neurobehaviour, Brain Antioxidant Status and Membrane Lipid Peroxidation Status in Rats	否	无			E_01_0189	PCR	Azodicarbonamide (ADA) is a dough-enhancer, which in Nigeria is an approved replacement for potassium bromate (a dough-enhancer that has been banned in a number of coun_x0002_tries due to its nephrotoxic potential).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Azodicarbonamide (ADA) is a dough-enhancer, which in Nigeria is an approved replacement for potassium bromate (a dough-enhancer that has been banned in a number of coun_x0002_tries due to its nephrotoxic potential).		Azodicarbonamide (ADA) is a dough-enhancer, which in Nigeria is an approved replacement for potassium bromate (a dough-enhancer that has been banned in a number of coun_x0002_tries due to its nephrotoxic potential).	Immunohistochemical staining	Azodicarbonamide (ADA) is a dough-enhancer, which in Nigeria is an approved replacement for potassium bromate (a dough-enhancer that has been banned in a number of coun_x0002_tries due to its nephrotoxic potential).			PCR				ADA
31681405	chr14	100235887	100237887	YY1	The promoters interacting with elncRNA-associated enhancers were rich in RNA polymerase II and YY1 transcription factor binding sites. We clustered enhancer–promoter pairs into different groups to reflect the different ways in which elncRNAs could influence enhancer–promoter pairs.	human,mouse		High+Lowthroughput	Enhancer LncRNAs Influence Chromatin Interactions in Different Ways	是	无		GM12878 cell	E_02_0147	Flow cytometry	The promoters interacting with elncRNA-associated enhancers were rich in RNA polymerase II and YY1 transcription factor binding sites. We clustered enhancer–promoter pairs into different groups to reflect the different ways in which elncRNAs could influence enhancer–promoter pairs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The promoters interacting with elncRNA-associated enhancers were rich in RNA polymerase II and YY1 transcription factor binding sites. We clustered enhancer–promoter pairs into different groups to reflect the different ways in which elncRNAs could influence enhancer–promoter pairs.		The promoters interacting with elncRNA-associated enhancers were rich in RNA polymerase II and YY1 transcription factor binding sites. We clustered enhancer–promoter pairs into different groups to reflect the different ways in which elncRNAs could influence enhancer–promoter pairs.	Immunohistochemical staining	The promoters interacting with elncRNA-associated enhancers were rich in RNA polymerase II and YY1 transcription factor binding sites. We clustered enhancer–promoter pairs into different groups to reflect the different ways in which elncRNAs could influence enhancer–promoter pairs.			Flow cytometry				YY1
31681009	chr8	19899234	19901234	LPL	For instance, lipoprotein lipase (LPL) reveals lipid storage in the early stages of differentiation, whereas fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and glycerol-3-phosphate dehydrogenase (G-3-PDH) are involved in triglyceride metabolism in late stages	human,mouse	connective tissue	High+Lowthroughput	Ghrelin Promotes Proliferation and Inhibits Differentiation of 3T3-L1 and Human Primary Preadipocytes	否	无		pluripotent stem cell	E_02_0148	Western blot,PCR	For instance, lipoprotein lipase (LPL) reveals lipid storage in the early stages of differentiation, whereas fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and glycerol-3-phosphate dehydrogenase (G-3-PDH) are involved in triglyceride metabolism in late stages	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	For instance, lipoprotein lipase (LPL) reveals lipid storage in the early stages of differentiation, whereas fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and glycerol-3-phosphate dehydrogenase (G-3-PDH) are involved in triglyceride metabolism in late stages		For instance, lipoprotein lipase (LPL) reveals lipid storage in the early stages of differentiation, whereas fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and glycerol-3-phosphate dehydrogenase (G-3-PDH) are involved in triglyceride metabolism in late stages	Immunohistochemical staining	For instance, lipoprotein lipase (LPL) reveals lipid storage in the early stages of differentiation, whereas fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and glycerol-3-phosphate dehydrogenase (G-3-PDH) are involved in triglyceride metabolism in late stages			Western blot,PCR				LPL
31680128	chr11	1155000	1157000	MUC5AC	 MUC5AC and MUC5B is a major gel-forming mucin that is linked to increased morbidity and mortality in respiratory diseases	human	Epithelial tissues	High+Lowthroughput	Fipronil upregulates inflammatory cytokines and MUC5AC expression in human nasal epithelial cells	否	无	airway inflammation 	epithelial cell	E_01_0190	Western blot,PCR	 MUC5AC and MUC5B is a major gel-forming mucin that is linked to increased morbidity and mortality in respiratory diseases	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 MUC5AC and MUC5B is a major gel-forming mucin that is linked to increased morbidity and mortality in respiratory diseases		 MUC5AC and MUC5B is a major gel-forming mucin that is linked to increased morbidity and mortality in respiratory diseases	Immunohistochemical staining	 MUC5AC and MUC5B is a major gel-forming mucin that is linked to increased morbidity and mortality in respiratory diseases			Western blot,PCR				MUC5AC
31679819	chr12	48826675	48828675	DDX23	Even when formed, R-loops may be removed either by RNase H1 ac_x0002_tivity that selectively degrades RNA hybridized to DNA (Cerritelli and Crouch, 2009) or alternatively by various helicases such as Senataxin (SETX;  Skourti-Stathaki et al., 2011), Aquarius (Sollier et al., 2014), DDX23 (Sridhara et al., 2017), and DHX9 (Cristini et al., 2018), which have all been shown to restrict R-loop accu_x0002_mulation.	human,mouse	uterus	High+Lowthroughput	R-Loops Promote Antisense Transcription across the Mammalian Genome	否	无		HeLa cell	E_02_0149	Western blot,PCR,Flow cytometry	Even when formed, R-loops may be removed either by RNase H1 ac_x0002_tivity that selectively degrades RNA hybridized to DNA (Cerritelli and Crouch, 2009) or alternatively by various helicases such as Senataxin (SETX;  Skourti-Stathaki et al., 2011), Aquarius (Sollier et al., 2014), DDX23 (Sridhara et al., 2017), and DHX9 (Cristini et al., 2018), which have all been shown to restrict R-loop accu_x0002_mulation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Even when formed, R-loops may be removed either by RNase H1 ac_x0002_tivity that selectively degrades RNA hybridized to DNA (Cerritelli and Crouch, 2009) or alternatively by various helicases such as Senataxin (SETX;  Skourti-Stathaki et al., 2011), Aquarius (Sollier et al., 2014), DDX23 (Sridhara et al., 2017), and DHX9 (Cristini et al., 2018), which have all been shown to restrict R-loop accu_x0002_mulation.		Even when formed, R-loops may be removed either by RNase H1 ac_x0002_tivity that selectively degrades RNA hybridized to DNA (Cerritelli and Crouch, 2009) or alternatively by various helicases such as Senataxin (SETX;  Skourti-Stathaki et al., 2011), Aquarius (Sollier et al., 2014), DDX23 (Sridhara et al., 2017), and DHX9 (Cristini et al., 2018), which have all been shown to restrict R-loop accu_x0002_mulation.	Immunohistochemical staining	Even when formed, R-loops may be removed either by RNase H1 ac_x0002_tivity that selectively degrades RNA hybridized to DNA (Cerritelli and Crouch, 2009) or alternatively by various helicases such as Senataxin (SETX;  Skourti-Stathaki et al., 2011), Aquarius (Sollier et al., 2014), DDX23 (Sridhara et al., 2017), and DHX9 (Cristini et al., 2018), which have all been shown to restrict R-loop accu_x0002_mulation.			Western blot,PCR,Flow cytometry				DDX23
31679819	chr2	144361373	144363373	ZEB2	Similarly, the ZEB2 gene, which is associated with stem celldevelopment and reprogramming, generates a lncRNA (referred to as a native AS RNA or NAT) initiating in the ZEB2 intron 1 that plays a positive role in activating ZEB2 expression.	human,mouse	connective tissue	High+Lowthroughput	R-Loops Promote Antisense Transcription across the Mammalian Genome	否	无		stem cell	E_02_0149	Western blot,PCR,Flow cytometry	Similarly, the ZEB2 gene, which is associated with stem celldevelopment and reprogramming, generates a lncRNA (referred to as a native AS RNA or NAT) initiating in the ZEB2 intron 1 that plays a positive role in activating ZEB2 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Similarly, the ZEB2 gene, which is associated with stem celldevelopment and reprogramming, generates a lncRNA (referred to as a native AS RNA or NAT) initiating in the ZEB2 intron 1 that plays a positive role in activating ZEB2 expression.		Similarly, the ZEB2 gene, which is associated with stem celldevelopment and reprogramming, generates a lncRNA (referred to as a native AS RNA or NAT) initiating in the ZEB2 intron 1 that plays a positive role in activating ZEB2 expression.	Immunohistochemical staining	Similarly, the ZEB2 gene, which is associated with stem celldevelopment and reprogramming, generates a lncRNA (referred to as a native AS RNA or NAT) initiating in the ZEB2 intron 1 that plays a positive role in activating ZEB2 expression.			Western blot,PCR,Flow cytometry				ZEB2
31678303	chr1	156461181	156463181	MEF2D	MEF2D protein acetylation and proteins that interact with MEF2D were identified by co-immunoprecipitation and pull-down assays. H22 cells, with MEF2D knockout or without (controls) were transplanted into BALB/c mice, some mice were given antibodies to deplete T cells. 	human,mouse	liver	High+Lowthroughput	Disruption of SIRT7 Increases the Efficacy of Checkpoint Inhibitor via MEF2D Regulation of Programmed Cell Death 1 Ligand 1 in Hepatocellular Carcinoma Cells	否	无	liver cancer	hepatocellular carcinoma cell	E_02_0150	Western blot, PCR, flow cytometry, immunofluorescence staining	MEF2D protein acetylation and proteins that interact with MEF2D were identified by co-immunoprecipitation and pull-down assays. H22 cells, with MEF2D knockout or without (controls) were transplanted into BALB/c mice, some mice were given antibodies to deplete T cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MEF2D protein acetylation and proteins that interact with MEF2D were identified by co-immunoprecipitation and pull-down assays. H22 cells, with MEF2D knockout or without (controls) were transplanted into BALB/c mice, some mice were given antibodies to deplete T cells. 		MEF2D protein acetylation and proteins that interact with MEF2D were identified by co-immunoprecipitation and pull-down assays. H22 cells, with MEF2D knockout or without (controls) were transplanted into BALB/c mice, some mice were given antibodies to deplete T cells. 	Immunohistochemical staining	MEF2D protein acetylation and proteins that interact with MEF2D were identified by co-immunoprecipitation and pull-down assays. H22 cells, with MEF2D knockout or without (controls) were transplanted into BALB/c mice, some mice were given antibodies to deplete T cells. 			Western blot,PCR,Flow cytometry,免疫荧光染色				MEF2D
31678303	chr17	81909215	81911215	SIRT7	Mice bearing orthotopic tumors grown from HCC cells with or without knockout of SIRT7, were given injections of an antibody against PD1.	human,mouse	blood	High+Lowthroughput	Disruption of SIRT7 Increases the Efficacy of Checkpoint Inhibitor via MEF2D Regulation of Programmed Cell Death 1 Ligand 1 in Hepatocellular Carcinoma Cells	否	无	liver cancer	T cell	E_02_0150	Western blot, PCR, flow cytometry, immunofluorescence staining	Mice bearing orthotopic tumors grown from HCC cells with or without knockout of SIRT7, were given injections of an antibody against PD1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mice bearing orthotopic tumors grown from HCC cells with or without knockout of SIRT7, were given injections of an antibody against PD1.		Mice bearing orthotopic tumors grown from HCC cells with or without knockout of SIRT7, were given injections of an antibody against PD1.	Immunohistochemical staining	Mice bearing orthotopic tumors grown from HCC cells with or without knockout of SIRT7, were given injections of an antibody against PD1.			Western blot,PCR,Flow cytometry,免疫荧光染色				SIRT7
31678303	chr9	5447414	5449414	CD274	MEF2D bound the promoter region of the CD274 gene (encodes PD-L1) and activated its transcription. 	human,mouse	connective tissue	High+Lowthroughput	Disruption of SIRT7 Increases the Efficacy of Checkpoint Inhibitor via MEF2D Regulation of Programmed Cell Death 1 Ligand 1 in Hepatocellular Carcinoma Cells	否	无	liver cancer	immune cell	E_02_0150	Western blot, PCR, flow cytometry, immunofluorescence staining	MEF2D bound the promoter region of the CD274 gene (encodes PD-L1) and activated its transcription. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MEF2D bound the promoter region of the CD274 gene (encodes PD-L1) and activated its transcription. 		MEF2D bound the promoter region of the CD274 gene (encodes PD-L1) and activated its transcription. 	Immunohistochemical staining	MEF2D bound the promoter region of the CD274 gene (encodes PD-L1) and activated its transcription. 			Western blot,PCR,Flow cytometry,免疫荧光染色				CD274
31676868	chr20	40683274	40685274	MAFB	Thus, we took advantage of published ChIP_x0002_seq datasets of islet-specific transcription factors (MAFB, PDX1, FOXA2, NKX6.1 and NKX2.2) mapped in unstimulated human pancreatic islets9 to measure transcription factor occupancy in primed and neo-enhancers before the proinflammatory stimu_x0002_lus.	human	blood	High+Lowthroughput	The impact of proinflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabetes	是	rs78037977	diabetes	B cell	E_01_0191	Flow cytometry,PCR	Thus, we took advantage of published ChIP_x0002_seq datasets of islet-specific transcription factors (MAFB, PDX1, FOXA2, NKX6.1 and NKX2.2) mapped in unstimulated human pancreatic islets9 to measure transcription factor occupancy in primed and neo-enhancers before the proinflammatory stimu_x0002_lus.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, we took advantage of published ChIP_x0002_seq datasets of islet-specific transcription factors (MAFB, PDX1, FOXA2, NKX6.1 and NKX2.2) mapped in unstimulated human pancreatic islets9 to measure transcription factor occupancy in primed and neo-enhancers before the proinflammatory stimu_x0002_lus.	Immunohistochemical staining	Thus, we took advantage of published ChIP_x0002_seq datasets of islet-specific transcription factors (MAFB, PDX1, FOXA2, NKX6.1 and NKX2.2) mapped in unstimulated human pancreatic islets9 to measure transcription factor occupancy in primed and neo-enhancers before the proinflammatory stimu_x0002_lus.	MAFB		Flow cytometry,PCR	Thus, we took advantage of published ChIP_x0002_seq datasets of islet-specific transcription factors (MAFB, PDX1, FOXA2, NKX6.1 and NKX2.2) mapped in unstimulated human pancreatic islets9 to measure transcription factor occupancy in primed and neo-enhancers before the proinflammatory stimu_x0002_lus.			
31676868	chr16	11251612	11253612	SOCS1	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	human	connective tissue	High+Lowthroughput	The impact of proinflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabetes	是	rs193778	diabetes	EC cell	E_01_0191	Flow cytometry,PCR	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	Immunohistochemical staining	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	SOCS1		Flow cytometry,PCR	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.			
31676868	chr16	10925964	10927964	DEXI	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	human	connective tissue	High+Lowthroughput	The impact of proinflammatory cytokines on the β-cell regulatory landscape provides insights into the genetics of type 1 diabetes	是	rs193778	diabetes	EC cell	E_01_0191	Flow cytometry,PCR	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.		The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.	Immunohistochemical staining	The locus includes several upregulated genes (SOCS1, DEXI, CIITA, RMI2) that could represent potential targets of this IRE. Recent research points to DEXI as a T1D candidate gene in immune cells and β cells31,32.			Flow cytometry,PCR				DEXI
31676828	chr1	92469783	92471783	GFI1	In erythro–megakaryocyte lineage leukemia cells, activation of the SE of GFI1 (GFI1-SE) is related to induction of myeloid differentiation by LSD1 inhibitors NCD38 and NCD25 and to their antileukemia effect. 	human,mouse	blood	High+Lowthroughput	LSD1-mediated repression of GFI1 super-enhancer plays an essential role in erythroleukemia	否	无	leukemia	leukemic cell	E_02_0151	Flow cytometry,PCR	In erythro–megakaryocyte lineage leukemia cells, activation of the SE of GFI1 (GFI1-SE) is related to induction of myeloid differentiation by LSD1 inhibitors NCD38 and NCD25 and to their antileukemia effect. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In erythro–megakaryocyte lineage leukemia cells, activation of the SE of GFI1 (GFI1-SE) is related to induction of myeloid differentiation by LSD1 inhibitors NCD38 and NCD25 and to their antileukemia effect. 		In erythro–megakaryocyte lineage leukemia cells, activation of the SE of GFI1 (GFI1-SE) is related to induction of myeloid differentiation by LSD1 inhibitors NCD38 and NCD25 and to their antileukemia effect. 	Immunohistochemical staining	In erythro–megakaryocyte lineage leukemia cells, activation of the SE of GFI1 (GFI1-SE) is related to induction of myeloid differentiation by LSD1 inhibitors NCD38 and NCD25 and to their antileukemia effect. 			Flow cytometry,PCR				GFI1
31676673	chrX	49025404	49027404	TFE3	Our results reveal that Fnip1 coordinates multiple metabolic pathways regulated by AMPK, mTORC1, and transcription factor binding to IgHM enhancer 3 (TFE3) to maintain metabolic ho_x0002_meostasis necessary for pre–B cell survival and differentiation during metabolic stress.	human,mouse	blood	High+Lowthroughput	Folliculin Interacting Protein 1 Maintains Metabolic Homeostasis during B Cell Development by Modulating AMPK, mTORC1, and TFE3	否	无		B cell	E_02_0152	Flow cytometry,PCR	Our results reveal that Fnip1 coordinates multiple metabolic pathways regulated by AMPK, mTORC1, and transcription factor binding to IgHM enhancer 3 (TFE3) to maintain metabolic ho_x0002_meostasis necessary for pre–B cell survival and differentiation during metabolic stress.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results reveal that Fnip1 coordinates multiple metabolic pathways regulated by AMPK, mTORC1, and transcription factor binding to IgHM enhancer 3 (TFE3) to maintain metabolic ho_x0002_meostasis necessary for pre–B cell survival and differentiation during metabolic stress.		Our results reveal that Fnip1 coordinates multiple metabolic pathways regulated by AMPK, mTORC1, and transcription factor binding to IgHM enhancer 3 (TFE3) to maintain metabolic ho_x0002_meostasis necessary for pre–B cell survival and differentiation during metabolic stress.	Immunohistochemical staining	Our results reveal that Fnip1 coordinates multiple metabolic pathways regulated by AMPK, mTORC1, and transcription factor binding to IgHM enhancer 3 (TFE3) to maintain metabolic ho_x0002_meostasis necessary for pre–B cell survival and differentiation during metabolic stress.			Flow cytometry,PCR				TFE3
31675590	chr7	148804429	148806429	EZH2	Our results indicate that Cd at1 mM concentration increases the viability of HepG2 and MCF7 cells and significantly upregulates the expression of PRMT5 and EZH2, leading to an increased global level of symmetric dimethylarginine(SDMA), H4R3me2s, and H3K27me3.	human,mouse	connective tissue	High+Lowthroughput	The carcinogen cadmium elevates CpG-demethylation and enrichment of NFYA and E2F1 in the promoter of oncogenic PRMT5 and EZH2 methyltransferases resulting in their elevated expression in?vitro	否	无	cancer	HepG2 cell	E_02_0153	Western blot,PCR,Flow cytometry	Our results indicate that Cd at1 mM concentration increases the viability of HepG2 and MCF7 cells and significantly upregulates the expression of PRMT5 and EZH2, leading to an increased global level of symmetric dimethylarginine(SDMA), H4R3me2s, and H3K27me3.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results indicate that Cd at1 mM concentration increases the viability of HepG2 and MCF7 cells and significantly upregulates the expression of PRMT5 and EZH2, leading to an increased global level of symmetric dimethylarginine(SDMA), H4R3me2s, and H3K27me3.		Our results indicate that Cd at1 mM concentration increases the viability of HepG2 and MCF7 cells and significantly upregulates the expression of PRMT5 and EZH2, leading to an increased global level of symmetric dimethylarginine(SDMA), H4R3me2s, and H3K27me3.	Immunohistochemical staining	Our results indicate that Cd at1 mM concentration increases the viability of HepG2 and MCF7 cells and significantly upregulates the expression of PRMT5 and EZH2, leading to an increased global level of symmetric dimethylarginine(SDMA), H4R3me2s, and H3K27me3.			Western blot,PCR,Flow cytometry				EZH2
31672165	chr17	47197711	47199711	MYL4	Interestingly, while HEK293 cells are not thought to express MYL4, human MYL4 is known to be slightly larger than the mouse protein.	mouse	blood	High+Lowthroughput	Contaminating reactivity of a monoclonal CCAAT/Enhancer Binding Protein β antibody in differentiating myoblasts	否	无		B cell	E_02_0154	Western blot	Interestingly, while HEK293 cells are not thought to express MYL4, human MYL4 is known to be slightly larger than the mouse protein.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Interestingly, while HEK293 cells are not thought to express MYL4, human MYL4 is known to be slightly larger than the mouse protein.		Interestingly, while HEK293 cells are not thought to express MYL4, human MYL4 is known to be slightly larger than the mouse protein.	Immunohistochemical staining	Interestingly, while HEK293 cells are not thought to express MYL4, human MYL4 is known to be slightly larger than the mouse protein.			Western blot				MYL4
31668620	chr13	118804154	118806154	Fgf10	Analyzing open chromatin revealsdifferentially active regulatory elements near Fgf10 and Sall-1 in the emu wing, and the Sall-1 enhancer ac_x0002_tivity is dependent on a likely Fgf-mediated Ets tran_x0002_scription factor-binding site. 	mouse	Musculature	High+Lowthroughput	Attenuated Fgf Signaling Underlies the Forelimb Heterochrony in the Emu Dromaius novaehollandiae	否	无		muscle cell	E_02_0155	Flow cytometry, PCR, immunofluorescence staining	Analyzing open chromatin revealsdifferentially active regulatory elements near Fgf10 and Sall-1 in the emu wing, and the Sall-1 enhancer ac_x0002_tivity is dependent on a likely Fgf-mediated Ets tran_x0002_scription factor-binding site. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Analyzing open chromatin revealsdifferentially active regulatory elements near Fgf10 and Sall-1 in the emu wing, and the Sall-1 enhancer ac_x0002_tivity is dependent on a likely Fgf-mediated Ets tran_x0002_scription factor-binding site. 		Analyzing open chromatin revealsdifferentially active regulatory elements near Fgf10 and Sall-1 in the emu wing, and the Sall-1 enhancer ac_x0002_tivity is dependent on a likely Fgf-mediated Ets tran_x0002_scription factor-binding site. 	Immunohistochemical staining	Analyzing open chromatin revealsdifferentially active regulatory elements near Fgf10 and Sall-1 in the emu wing, and the Sall-1 enhancer ac_x0002_tivity is dependent on a likely Fgf-mediated Ets tran_x0002_scription factor-binding site. 			Flow cytometry,PCR,免疫荧光染色				Fgf10
31666694	chr11	69983276	69985276	ANO1	By contrast, ANO1 was bi-allelically expressed, suggesting that the biased FGF expression reflected allele_x0002_specific insulator loss. Consistently, in one SDH-deficient tumour with a heterozygous SNP near the CTCF site, we confirmed that only one allele of the FGF insulator was methylated (Extended Data Fig. 4d).	human	Stomach, gut	High+Lowthroughput	Altered chromosomal topology drives oncogenic programs in SDH-deficient GISTs	否	无	Gastrointestinal stromal tumors	GIST-T1 cell	E_01_0192	Flow cytometry	By contrast, ANO1 was bi-allelically expressed, suggesting that the biased FGF expression reflected allele_x0002_specific insulator loss. Consistently, in one SDH-deficient tumour with a heterozygous SNP near the CTCF site, we confirmed that only one allele of the FGF insulator was methylated (Extended Data Fig. 4d).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			By contrast, ANO1 was bi-allelically expressed, suggesting that the biased FGF expression reflected allele_x0002_specific insulator loss. Consistently, in one SDH-deficient tumour with a heterozygous SNP near the CTCF site, we confirmed that only one allele of the FGF insulator was methylated (Extended Data Fig. 4d).	Immunohistochemical staining	By contrast, ANO1 was bi-allelically expressed, suggesting that the biased FGF expression reflected allele_x0002_specific insulator loss. Consistently, in one SDH-deficient tumour with a heterozygous SNP near the CTCF site, we confirmed that only one allele of the FGF insulator was methylated (Extended Data Fig. 4d).	ANO1		Flow cytometry	By contrast, ANO1 was bi-allelically expressed, suggesting that the biased FGF expression reflected allele_x0002_specific insulator loss. Consistently, in one SDH-deficient tumour with a heterozygous SNP near the CTCF site, we confirmed that only one allele of the FGF insulator was methylated (Extended Data Fig. 4d).			
31666665	chr7	148804251	148806251	EZH2	Enhancer of zester homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 (PCR2), and its-terminal SET domain exhibits methyl transferase activity9	human,mouse	lung	High+Lowthroughput	Cigarette smoke affects the onco-suppressor DAB2IP expression in bronchial epithelial cells of COPD patients	否	无	lung cancer	Lung cancer cell	E_02_0156	PCR, Western blot, immunofluorescence staining	Enhancer of zester homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 (PCR2), and its-terminal SET domain exhibits methyl transferase activity9	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of zester homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 (PCR2), and its-terminal SET domain exhibits methyl transferase activity9		Enhancer of zester homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 (PCR2), and its-terminal SET domain exhibits methyl transferase activity9	Immunohistochemical staining	Enhancer of zester homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 (PCR2), and its-terminal SET domain exhibits methyl transferase activity9			PCR,Western blot,免疫荧光染色				EZH2
31666509	chr3	38545360	38547360	SCN5A	Mutations and variations in and around SCN5A, encoding the major cardiac sodium channel, influence impulse conduction and are associated with a broad spectrum of arrhythmia dis_x0002_orders.	human,mouse	heart	High+Lowthroughput	An enhancer cluster controls gene activity and topology of the SCN5A-SCN10A locus in vivo	是	rs6810361	Arrhythmia	cardiac muscle cell (sensu Arthopoda)	E_02_0157	Flow cytometry,PCR	Mutations and variations in and around SCN5A, encoding the major cardiac sodium channel, influence impulse conduction and are associated with a broad spectrum of arrhythmia dis_x0002_orders.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mutations and variations in and around SCN5A, encoding the major cardiac sodium channel, influence impulse conduction and are associated with a broad spectrum of arrhythmia dis_x0002_orders.		Mutations and variations in and around SCN5A, encoding the major cardiac sodium channel, influence impulse conduction and are associated with a broad spectrum of arrhythmia dis_x0002_orders.	Immunohistochemical staining	Mutations and variations in and around SCN5A, encoding the major cardiac sodium channel, influence impulse conduction and are associated with a broad spectrum of arrhythmia dis_x0002_orders.			Flow cytometry,PCR				SCN5A
31666509	chr3	38694445	38696445	SCN10A	The activity of REs is largely limited to target genes that fall within the same TAD8, including SCN5A, SCN10A, EXOG, SCN11A, and WDR48.	human,mouse	connective tissue	High+Lowthroughput	An enhancer cluster controls gene activity and topology of the SCN5A-SCN10A locus in vivo	是	rs6781009	Arrhythmia	embryonic stem cell	E_02_0157	Flow cytometry,PCR	The activity of REs is largely limited to target genes that fall within the same TAD8, including SCN5A, SCN10A, EXOG, SCN11A, and WDR48.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The activity of REs is largely limited to target genes that fall within the same TAD8, including SCN5A, SCN10A, EXOG, SCN11A, and WDR48.		The activity of REs is largely limited to target genes that fall within the same TAD8, including SCN5A, SCN10A, EXOG, SCN11A, and WDR48.	Immunohistochemical staining	The activity of REs is largely limited to target genes that fall within the same TAD8, including SCN5A, SCN10A, EXOG, SCN11A, and WDR48.			Flow cytometry,PCR				SCN10A
31666072	chr17	50181276	50183276	COL1A1	Many mutations associated with these conditions (e.g., col_x0002_lagen [COL1A1] in patients with Ehlers-Danlos syndrome)affect the structural integrity of the vasculature or the abil_x0002_ity of the vessel walls to maintain homeostasis [12, 13].	human	Epithelial tissues	High+Lowthroughput	Epigenetic landscapes suggest that genetic risk for intracranial aneurysm operates on the endothelium	是	rs1333040	inflammation	endothelial cell	E_01_0193	ChIP-Seq	Many mutations associated with these conditions (e.g., col_x0002_lagen [COL1A1] in patients with Ehlers-Danlos syndrome)affect the structural integrity of the vasculature or the abil_x0002_ity of the vessel walls to maintain homeostasis [12, 13].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Many mutations associated with these conditions (e.g., col_x0002_lagen [COL1A1] in patients with Ehlers-Danlos syndrome)affect the structural integrity of the vasculature or the abil_x0002_ity of the vessel walls to maintain homeostasis [12, 13].	Immunohistochemical staining	Many mutations associated with these conditions (e.g., col_x0002_lagen [COL1A1] in patients with Ehlers-Danlos syndrome)affect the structural integrity of the vasculature or the abil_x0002_ity of the vessel walls to maintain homeostasis [12, 13].	COL1A1		ChIP-Seq	Many mutations associated with these conditions (e.g., col_x0002_lagen [COL1A1] in patients with Ehlers-Danlos syndrome)affect the structural integrity of the vasculature or the abil_x0002_ity of the vessel walls to maintain homeostasis [12, 13].			
31665646	chrX	73818246	73820246	XIST	"HEK293 are female cells and, therefore, one of the two X chromosomes is subject to X chromosome inactivation, a process that is dependent on the expression of the XIST lncRNA (da Rocha and Heard, 2017; Jégu et al., 2017). Both MapR and RHΔC&R signals are clearly higher than the respective controls at the 5′ end of the 
XIST gene (Figure 2E). "	human,mouse	connective tissue	High+Lowthroughput	Mapping Native R-Loops Genome-wide Using a Targeted Nuclease Approach	否	无	cancer	HEK293 cell	E_02_0158	Flow cytometry,PCR	"HEK293 are female cells and, therefore, one of the two X chromosomes is subject to X chromosome inactivation, a process that is dependent on the expression of the XIST lncRNA (da Rocha and Heard, 2017; Jégu et al., 2017). Both MapR and RHΔC&R signals are clearly higher than the respective controls at the 5′ end of the 
XIST gene (Figure 2E). "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"HEK293 are female cells and, therefore, one of the two X chromosomes is subject to X chromosome inactivation, a process that is dependent on the expression of the XIST lncRNA (da Rocha and Heard, 2017; Jégu et al., 2017). Both MapR and RHΔC&R signals are clearly higher than the respective controls at the 5′ end of the 
XIST gene (Figure 2E). "		"HEK293 are female cells and, therefore, one of the two X chromosomes is subject to X chromosome inactivation, a process that is dependent on the expression of the XIST lncRNA (da Rocha and Heard, 2017; Jégu et al., 2017). Both MapR and RHΔC&R signals are clearly higher than the respective controls at the 5′ end of the 
XIST gene (Figure 2E). "	Immunohistochemical staining	"HEK293 are female cells and, therefore, one of the two X chromosomes is subject to X chromosome inactivation, a process that is dependent on the expression of the XIST lncRNA (da Rocha and Heard, 2017; Jégu et al., 2017). Both MapR and RHΔC&R signals are clearly higher than the respective controls at the 5′ end of the 
XIST gene (Figure 2E). "			Flow cytometry,PCR				XIST
31665330	chr16	68733997	68735997	CDH1	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 	human,mouse	Epithelial tissues	High+Lowthroughput	Human Endometrial Transcriptome and Progesterone Receptor Cistrome Reveal Important Pathways and Epithelial Regulators	否	无	Infertility	epithelial cell	E_02_0159	PCR	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 		On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 	Immunohistochemical staining	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 			PCR				CDH1
31665330	chr13	73052330	73054330	KLF5	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 	human,mouse	Epithelial tissues	High+Lowthroughput	Human Endometrial Transcriptome and Progesterone Receptor Cistrome Reveal Important Pathways and Epithelial Regulators	否	无	Infertility	epithelial cell	E_02_0159	PCR	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 		On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 	Immunohistochemical staining	On the other hand, numerous epithelial cell markers including CDH1, CLDN1, CLDN4, CLDN8, CLDN10, KLF4 and KLF5 were all upregulated during MS. 			PCR				KLF5
31665330	chr16	28529423	28531423	NUPR1	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.	mouse	blood	High+Lowthroughput	Human Endometrial Transcriptome and Progesterone Receptor Cistrome Reveal Important Pathways and Epithelial Regulators	否	无	Infertility	B cell	E_02_0159	PCR	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.		Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.	Immunohistochemical staining	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.			PCR				NUPR1
31665330	chr12	131947347	131949347	EP400	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.	mouse	blood	High+Lowthroughput	Human Endometrial Transcriptome and Progesterone Receptor Cistrome Reveal Important Pathways and Epithelial Regulators	否	无	Infertility	B cell	E_02_0159	PCR	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.		Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.	Immunohistochemical staining	Additionally, the majority of the epithelial transcription regulators identified in our study have yet to be studied for functional relevance in mediating implantation in the human endometrium, including NUPR1, TBX2, SMARCA4, CEBPA, RABL6 and EP400. Interestingly, the Estrogen Receptors ESR1 and ESR2 showed repression and activation during WOI in the epithelium, respectively.			PCR				EP400
31665135	chr8	116842944	116844944	RAD21	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.	human,mouse	blood	High+Lowthroughput	EAGLE: An algorithm that utilizes a small number of genomic features to predict tissue/cell type-specific enhancer-gene interactions	否	无			E_02_0160	Flow cytometry,PCR	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.		Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.	Immunohistochemical staining	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.			Flow cytometry,PCR				RAD21
31665135	chr16	67559548	67561548	CTCF	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.	human,mouse	uterus	High+Lowthroughput	EAGLE: An algorithm that utilizes a small number of genomic features to predict tissue/cell type-specific enhancer-gene interactions	否	无		Hela-S3 cell	E_02_0160	Flow cytometry,PCR	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.		Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.	Immunohistochemical staining	Similarly, CTCF, RAD21, and H3K4me3 occurred more often at interacting pro_x0002_moters than non-interacting promoters (Fig 7). Taken together, histone marks and relevant factors suggested that our prediction of enhancer-target relationships were likely biologically functional.			Flow cytometry,PCR				CTCF
31665067	chr18	55219450	55221450	TCF4	While pro_x0002_moting the transcription of tumor suppressors genes,RUVBL1 was revealed to promote β-catenin-mediated neoplastic transformation by forming chromatin remod_x0002_eling complex with TIP60 and thus promotes histone H4 acetylation in the promoter region of ITF-2 gene and enhances the transcriptional activity of TCF4 [42].	human	bone	High+Lowthroughput	CircMYO10 promotes osteosarcoma progression by regulating miR-370-3p/RUVBL1 axis to enhance the transcriptional activity of β-catenin/LEF1 complex via effects on chromatin remodeling	否	无	Osteosarcoma	osteosarcoma cell	E_01_0194	Flow cytometry,PCR,Western blot	While pro_x0002_moting the transcription of tumor suppressors genes,RUVBL1 was revealed to promote β-catenin-mediated neoplastic transformation by forming chromatin remod_x0002_eling complex with TIP60 and thus promotes histone H4 acetylation in the promoter region of ITF-2 gene and enhances the transcriptional activity of TCF4 [42].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			While pro_x0002_moting the transcription of tumor suppressors genes,RUVBL1 was revealed to promote β-catenin-mediated neoplastic transformation by forming chromatin remod_x0002_eling complex with TIP60 and thus promotes histone H4 acetylation in the promoter region of ITF-2 gene and enhances the transcriptional activity of TCF4 [42].	Immunohistochemical staining	While pro_x0002_moting the transcription of tumor suppressors genes,RUVBL1 was revealed to promote β-catenin-mediated neoplastic transformation by forming chromatin remod_x0002_eling complex with TIP60 and thus promotes histone H4 acetylation in the promoter region of ITF-2 gene and enhances the transcriptional activity of TCF4 [42].	TCF4		Flow cytometry,PCR,Western blot	While pro_x0002_moting the transcription of tumor suppressors genes,RUVBL1 was revealed to promote β-catenin-mediated neoplastic transformation by forming chromatin remod_x0002_eling complex with TIP60 and thus promotes histone H4 acetylation in the promoter region of ITF-2 gene and enhances the transcriptional activity of TCF4 [42].			
31665067	chr5	16658965	16660965	MYO10	In this study, we identified the oncogenic role of cir_x0002_cMYO10, a circRNA that is upregulated in OS [44].	human	connective tissue	High+Lowthroughput	CircMYO10 promotes osteosarcoma progression by regulating miR-370-3p/RUVBL1 axis to enhance the transcriptional activity of β-catenin/LEF1 complex via effects on chromatin remodeling	否	无	Osteosarcoma	mesenchymal stem cell	E_01_0194	Flow cytometry,PCR,Western blot	In this study, we identified the oncogenic role of cir_x0002_cMYO10, a circRNA that is upregulated in OS [44].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we identified the oncogenic role of cir_x0002_cMYO10, a circRNA that is upregulated in OS [44].		In this study, we identified the oncogenic role of cir_x0002_cMYO10, a circRNA that is upregulated in OS [44].	Immunohistochemical staining	In this study, we identified the oncogenic role of cir_x0002_cMYO10, a circRNA that is upregulated in OS [44].			Flow cytometry,PCR,Western blot				MYO10
31664109	chrX	154007840	154009840	IRAK1	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 	human	blood	High+Lowthroughput	IRAK3 modulates downstream innate immune signalling through its guanylate cyclase activity	是	无	inflammation	B cell	E_01_0195	PCR	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 		IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 	Immunohistochemical staining	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 			PCR				IRAK1
31664109	chr12	43756484	43758484	IRAK4	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 	human	blood	High+Lowthroughput	IRAK3 modulates downstream innate immune signalling through its guanylate cyclase activity	是	无	inflammation	B cell	E_01_0195	PCR	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 		IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 	Immunohistochemical staining	IRAK1, IRAK2 and IRAK4 work in concert to stimulate myeloid diferentiation primary response 88 (MyD88) dependent activation of nuclear factor kappa-light-chain enhancer of activated B cells (NFκB) and thus pro-infammatory cytokine production12. 			PCR				IRAK4
31662342	chr16	86508235	86510235	FOXF1	Tran_x0002_scriptional profiling of lung samples obtained from normal human fetal lung tissues ranging from 53 to 140 days of gesta_x0002_tion demonstrated that FOXF1 has robust, stable expression throughout early human lung development (online supplemen_x0002_tary figure 4,11).	human,mouse	Epithelial tissues	High+Lowthroughput	Disruption of normal patterns of FOXF1 expression in a lethal disorder of lung development	否	无	cancer	endothelial cell	E_02_0161	Flow cytometry,PCR,Western blot	Tran_x0002_scriptional profiling of lung samples obtained from normal human fetal lung tissues ranging from 53 to 140 days of gesta_x0002_tion demonstrated that FOXF1 has robust, stable expression throughout early human lung development (online supplemen_x0002_tary figure 4,11).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Tran_x0002_scriptional profiling of lung samples obtained from normal human fetal lung tissues ranging from 53 to 140 days of gesta_x0002_tion demonstrated that FOXF1 has robust, stable expression throughout early human lung development (online supplemen_x0002_tary figure 4,11).		Tran_x0002_scriptional profiling of lung samples obtained from normal human fetal lung tissues ranging from 53 to 140 days of gesta_x0002_tion demonstrated that FOXF1 has robust, stable expression throughout early human lung development (online supplemen_x0002_tary figure 4,11).	Immunohistochemical staining	Tran_x0002_scriptional profiling of lung samples obtained from normal human fetal lung tissues ranging from 53 to 140 days of gesta_x0002_tion demonstrated that FOXF1 has robust, stable expression throughout early human lung development (online supplemen_x0002_tary figure 4,11).			Flow cytometry,PCR,Western blot				FOXF1
31661141	chr12	2855382	2857382	FOXM1	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).	human,mouse	uterus	High+Lowthroughput	Crosstalk between histone modification and DNA methylation orchestrates the epigenetic regulation of the costimulatory factors, Tim?3 and galectin?9, in cervical cancer	否	无	cervical carcinoma	HeLa cell	E_02_0162	PCR,Western blot	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).		In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).	Immunohistochemical staining	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).			PCR,Western blot				FOXM1
31661141	chr7	148804354	148806354	EZH2	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).	human,mouse	blood	High+Lowthroughput	Crosstalk between histone modification and DNA methylation orchestrates the epigenetic regulation of the costimulatory factors, Tim?3 and galectin?9, in cervical cancer	否	无	cervical carcinoma	T cell	E_02_0162	PCR,Western blot	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).		In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).	Immunohistochemical staining	In this study, we report that E2F-1 and FOXM1 mediated by HPV18 E6 and E7 can enhance the transcriptional activity of Enhancer of zeste homolog 2 (EZH2) by binding to its promoter region, resulting in the induced expression of the EZH2‑specific target protein, H3K27me3, which consequently reduces the expression of the downstream target gene, DNA (cytosine-5)-methyltransferase 3A (DNMT3A).			PCR,Western blot				EZH2
31661121	chr17	58267209	58269209	MPO	Measurement of myeloperoxidase (MPO), malondialde‑hyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) levels. The MPO, MDA, SOD and GSH levels were detected using the related kits (MPO: cat. no. A044; MDA: cat. no. A003; SOD: cat. no. A001; GSH: cat. no. A005; Nanjing Jiancheng Bioengineering Institute). 	human,mouse	Epithelial tissues	High+Lowthroughput	Dihydroartemisinin attenuates lipopolysaccharide?induced acute lung injury in mice by suppressing NF?κB signaling in an Nrf2?dependent manner	否	无	inflammation	epithelial cell	E_02_0163	PCR, Western blot, immunofluorescence staining	Measurement of myeloperoxidase (MPO), malondialde‑hyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) levels. The MPO, MDA, SOD and GSH levels were detected using the related kits (MPO: cat. no. A044; MDA: cat. no. A003; SOD: cat. no. A001; GSH: cat. no. A005; Nanjing Jiancheng Bioengineering Institute). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Measurement of myeloperoxidase (MPO), malondialde‑hyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) levels. The MPO, MDA, SOD and GSH levels were detected using the related kits (MPO: cat. no. A044; MDA: cat. no. A003; SOD: cat. no. A001; GSH: cat. no. A005; Nanjing Jiancheng Bioengineering Institute). 		Measurement of myeloperoxidase (MPO), malondialde‑hyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) levels. The MPO, MDA, SOD and GSH levels were detected using the related kits (MPO: cat. no. A044; MDA: cat. no. A003; SOD: cat. no. A001; GSH: cat. no. A005; Nanjing Jiancheng Bioengineering Institute). 	Immunohistochemical staining	Measurement of myeloperoxidase (MPO), malondialde‑hyde (MDA), superoxide dismutase (SOD) and glutathione (GSH) levels. The MPO, MDA, SOD and GSH levels were detected using the related kits (MPO: cat. no. A044; MDA: cat. no. A003; SOD: cat. no. A001; GSH: cat. no. A005; Nanjing Jiancheng Bioengineering Institute). 			PCR,Western blot,免疫荧光染色				MPO
31659808	chr2	237482764	237484764	MLPH	To determine the potential effect of rs13426236 genotypes on MLPH alternative splicing, we performed splicing variant‐specific qPCRs in 87 benign prostate tissues.	human	prostate	High+Lowthroughput	Single-nucleotide polymorphism rs13426236 contributes to an increased prostate cancer risk via regulating MLPH splicing variant 4	是	rs13426236	prostatic cancer	prostate cancer cell	E_01_0196	Flow cytometry,Western blot,PCR	To determine the potential effect of rs13426236 genotypes on MLPH alternative splicing, we performed splicing variant‐specific qPCRs in 87 benign prostate tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To determine the potential effect of rs13426236 genotypes on MLPH alternative splicing, we performed splicing variant‐specific qPCRs in 87 benign prostate tissues.		To determine the potential effect of rs13426236 genotypes on MLPH alternative splicing, we performed splicing variant‐specific qPCRs in 87 benign prostate tissues.	Immunohistochemical staining	To determine the potential effect of rs13426236 genotypes on MLPH alternative splicing, we performed splicing variant‐specific qPCRs in 87 benign prostate tissues.			Flow cytometry,Western blot,PCR				MLPH
31659207	chr11	128455802	128457802	ETS1	ETS1 is involved in B cell and T17 cell diferentiation, and an association between rs1128334 and SLE has been reported in Asian SLE cohorts39.	human	blood	High+Lowthroughput	Rare variants in non-coding regulatory regions of the genome that affect gene expression in systemic lupus erythematosus	是	rs9888739	Systemic lupus erythematosus	T cell	E_01_0197	Flow cytometry,PCR	ETS1 is involved in B cell and T17 cell diferentiation, and an association between rs1128334 and SLE has been reported in Asian SLE cohorts39.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			ETS1 is involved in B cell and T17 cell diferentiation, and an association between rs1128334 and SLE has been reported in Asian SLE cohorts39.	Immunohistochemical staining	ETS1 is involved in B cell and T17 cell diferentiation, and an association between rs1128334 and SLE has been reported in Asian SLE cohorts39.	ETS1		Flow cytometry,PCR	ETS1 is involved in B cell and T17 cell diferentiation, and an association between rs1128334 and SLE has been reported in Asian SLE cohorts39.			
31659207	chrX	49247778	49249778	FOXP3	Te rare variant we identifed at this locus was located in a lower information nucleotide in a FOXP3 motif and was found to increase ETS1 expression via luciferase assay (Fig. 1D and Supplementary Table 1).	human	connective tissue	High+Lowthroughput	Rare variants in non-coding regulatory regions of the genome that affect gene expression in systemic lupus erythematosus	是	rs1143679	Systemic lupus erythematosus	stem cell	E_01_0197	Flow cytometry,PCR	Te rare variant we identifed at this locus was located in a lower information nucleotide in a FOXP3 motif and was found to increase ETS1 expression via luciferase assay (Fig. 1D and Supplementary Table 1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Te rare variant we identifed at this locus was located in a lower information nucleotide in a FOXP3 motif and was found to increase ETS1 expression via luciferase assay (Fig. 1D and Supplementary Table 1).	Immunohistochemical staining	Te rare variant we identifed at this locus was located in a lower information nucleotide in a FOXP3 motif and was found to increase ETS1 expression via luciferase assay (Fig. 1D and Supplementary Table 1).	FOXP3		Flow cytometry,PCR	Te rare variant we identifed at this locus was located in a lower information nucleotide in a FOXP3 motif and was found to increase ETS1 expression via luciferase assay (Fig. 1D and Supplementary Table 1).			
31659207	chr5	151027114	151029114	TNIP1	We found a rare variant near rs10036748, within the TNIP1 gene, which impaired TNIP1 expression according to a luciferase reporter assay (Fig. 1E and Supplementary Table 1).	human	blood	High+Lowthroughput	Rare variants in non-coding regulatory regions of the genome that affect gene expression in systemic lupus erythematosus	是	rs10488631	Systemic lupus erythematosus	B cell	E_01_0197	Flow cytometry,PCR	We found a rare variant near rs10036748, within the TNIP1 gene, which impaired TNIP1 expression according to a luciferase reporter assay (Fig. 1E and Supplementary Table 1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found a rare variant near rs10036748, within the TNIP1 gene, which impaired TNIP1 expression according to a luciferase reporter assay (Fig. 1E and Supplementary Table 1).	Immunohistochemical staining	We found a rare variant near rs10036748, within the TNIP1 gene, which impaired TNIP1 expression according to a luciferase reporter assay (Fig. 1E and Supplementary Table 1).	TNIP1		Flow cytometry,PCR	We found a rare variant near rs10036748, within the TNIP1 gene, which impaired TNIP1 expression according to a luciferase reporter assay (Fig. 1E and Supplementary Table 1).			
31659207	chr7	128934736	128936736	IRF5	We identifed novel variants in the loci of IRF5, ETS1, ITGAM1 and TNIP1, each of which caused alterations in the expression levels of the association genes.	human	connective tissue	High+Lowthroughput	Rare variants in non-coding regulatory regions of the genome that affect gene expression in systemic lupus erythematosus	是	rs4728142	Systemic lupus erythematosus	B-lymphoblastoid cells	E_01_0197	Flow cytometry,PCR	We identifed novel variants in the loci of IRF5, ETS1, ITGAM1 and TNIP1, each of which caused alterations in the expression levels of the association genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We identifed novel variants in the loci of IRF5, ETS1, ITGAM1 and TNIP1, each of which caused alterations in the expression levels of the association genes.	Immunohistochemical staining	We identifed novel variants in the loci of IRF5, ETS1, ITGAM1 and TNIP1, each of which caused alterations in the expression levels of the association genes.	IRF5		Flow cytometry,PCR	We identifed novel variants in the loci of IRF5, ETS1, ITGAM1 and TNIP1, each of which caused alterations in the expression levels of the association genes.			
31659207	chrX	12864199	12866199	TLR7	Moreover, mice lacking Gf1 have recently been reported to develop a TLR7-dependent lupus-like phenotype, which the authors showed to involve excess NFκB signaling45.	human	connective tissue	High+Lowthroughput	Rare variants in non-coding regulatory regions of the genome that affect gene expression in systemic lupus erythematosus	是	rs1128334	Systemic lupus erythematosus	immune cell	E_01_0197	Flow cytometry,PCR	Moreover, mice lacking Gf1 have recently been reported to develop a TLR7-dependent lupus-like phenotype, which the authors showed to involve excess NFκB signaling45.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, mice lacking Gf1 have recently been reported to develop a TLR7-dependent lupus-like phenotype, which the authors showed to involve excess NFκB signaling45.		Moreover, mice lacking Gf1 have recently been reported to develop a TLR7-dependent lupus-like phenotype, which the authors showed to involve excess NFκB signaling45.	Immunohistochemical staining	Moreover, mice lacking Gf1 have recently been reported to develop a TLR7-dependent lupus-like phenotype, which the authors showed to involve excess NFκB signaling45.			Flow cytometry,PCR				TLR7
31659207	chr7	128951769	128953769	TNPO3	The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share.	human	blood	High+Lowthroughput	Rare variants in non-coding regulatory regions of the genome that affect gene expression in systemic lupus erythematosus	是	rs6590330	Systemic lupus erythematosus		E_01_0197	Flow cytometry,PCR	The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share.		The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share.	Immunohistochemical staining	The IRF5-TNPO3 association with systemic lupus erythematosus has two components that other autoimmune disorders variably share.			Flow cytometry,PCR				TNPO3
31659164	chr8	11673920	11675920	GATA4	Mapping the chromatin occupancy of transcription factors (TFs) is a key step in deciphering developmental transcriptional programs. Here we use biotinylated knockin alleles of seven key cardiac TFs (GATA4, NKX2-5, MEF2A, MEF2C, SRF, TBX5, TEAD1) to sensitively and reproducibly map their genome-wide occupancy in the fetal and adult mouse heart. 	human	connective tissue	High+Lowthroughput	A reference map of murine cardiac transcription factor chromatin occupancy identifies dynamic and conserved enhancers	否	无	cancer	stem cell	E_01_0198	PCR,Flow cytometry	Mapping the chromatin occupancy of transcription factors (TFs) is a key step in deciphering developmental transcriptional programs. Here we use biotinylated knockin alleles of seven key cardiac TFs (GATA4, NKX2-5, MEF2A, MEF2C, SRF, TBX5, TEAD1) to sensitively and reproducibly map their genome-wide occupancy in the fetal and adult mouse heart. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mapping the chromatin occupancy of transcription factors (TFs) is a key step in deciphering developmental transcriptional programs. Here we use biotinylated knockin alleles of seven key cardiac TFs (GATA4, NKX2-5, MEF2A, MEF2C, SRF, TBX5, TEAD1) to sensitively and reproducibly map their genome-wide occupancy in the fetal and adult mouse heart. 	Immunohistochemical staining	Mapping the chromatin occupancy of transcription factors (TFs) is a key step in deciphering developmental transcriptional programs. Here we use biotinylated knockin alleles of seven key cardiac TFs (GATA4, NKX2-5, MEF2A, MEF2C, SRF, TBX5, TEAD1) to sensitively and reproducibly map their genome-wide occupancy in the fetal and adult mouse heart. 	GATA4		PCR,Flow cytometry	Mapping the chromatin occupancy of transcription factors (TFs) is a key step in deciphering developmental transcriptional programs. Here we use biotinylated knockin alleles of seven key cardiac TFs (GATA4, NKX2-5, MEF2A, MEF2C, SRF, TBX5, TEAD1) to sensitively and reproducibly map their genome-wide occupancy in the fetal and adult mouse heart. 			
31659164	chr5	173229614	173231614	NKX2-5	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	human	Musculature	High+Lowthroughput	A reference map of murine cardiac transcription factor chromatin occupancy identifies dynamic and conserved enhancers	否	无	cancer	muscle cell	E_01_0198	PCR,Flow cytometry	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	Immunohistochemical staining	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	NKX2-5		PCR,Flow cytometry	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 			
31659164	chr15	99562305	99564305	MEF2A	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	human	Musculature	High+Lowthroughput	A reference map of murine cardiac transcription factor chromatin occupancy identifies dynamic and conserved enhancers	否	无	cancer	muscle cell	E_01_0198	PCR,Flow cytometry	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	Immunohistochemical staining	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 	MEF2A		PCR,Flow cytometry	The development of the heart is orchestrated by intricate transcriptional programs, so that mutations in TFs and epigenetic regulators are important causes of congenital heart disease5. Among the well known cardiac TFs are NKX2-5, TBX5, GATA4,MEF2A, MEF2C, and SRF6–11. 			
31659118	chr7	97849158	97851158	ASNS	"Insufficient expression of ASNS leads to asparagine deficiency, which facilitates an ATF4-independent induction of C/EBP homologous protein (CHOP) that triggers
apoptosis. "	human,mouse	tumour	High+Lowthroughput	Promoter demethylation of the asparagine synthetase gene is required for ATF4-dependent adaptation to asparagine depletion	否	无	acute lymphoblastic leukemia	tumor cell	E_02_0164	Flow cytometry,Western blot,PCR	"Insufficient expression of ASNS leads to asparagine deficiency, which facilitates an ATF4-independent induction of C/EBP homologous protein (CHOP) that triggers
apoptosis. "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Insufficient expression of ASNS leads to asparagine deficiency, which facilitates an ATF4-independent induction of C/EBP homologous protein (CHOP) that triggers
apoptosis. "		"Insufficient expression of ASNS leads to asparagine deficiency, which facilitates an ATF4-independent induction of C/EBP homologous protein (CHOP) that triggers
apoptosis. "	Immunohistochemical staining	"Insufficient expression of ASNS leads to asparagine deficiency, which facilitates an ATF4-independent induction of C/EBP homologous protein (CHOP) that triggers
apoptosis. "			Flow cytometry,Western blot,PCR				ASNS
31659118	chr1	28257099	28259099	SESN2	As a control, there was induced recruitment of ATF4 to the promoter region of another target gene, SESN2 (Figure 3E), following asparagine depletion in both the RS4;11 and RS4;11/R cells (Figure 4G, right).	human,mouse	blood	High+Lowthroughput	Promoter demethylation of the asparagine synthetase gene is required for ATF4-dependent adaptation to asparagine depletion	否	无	acute lymphoblastic leukemia	Nalm-6 cell	E_02_0164	Flow cytometry,Western blot,PCR	As a control, there was induced recruitment of ATF4 to the promoter region of another target gene, SESN2 (Figure 3E), following asparagine depletion in both the RS4;11 and RS4;11/R cells (Figure 4G, right).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	As a control, there was induced recruitment of ATF4 to the promoter region of another target gene, SESN2 (Figure 3E), following asparagine depletion in both the RS4;11 and RS4;11/R cells (Figure 4G, right).		As a control, there was induced recruitment of ATF4 to the promoter region of another target gene, SESN2 (Figure 3E), following asparagine depletion in both the RS4;11 and RS4;11/R cells (Figure 4G, right).	Immunohistochemical staining	As a control, there was induced recruitment of ATF4 to the promoter region of another target gene, SESN2 (Figure 3E), following asparagine depletion in both the RS4;11 and RS4;11/R cells (Figure 4G, right).			Flow cytometry,Western blot,PCR				SESN2
31658410	chr14	48891897	48893897	Otx2	Homeodomain transcription factor Otx2 is essential for embryonic development of multiple head tissues, including retinal pigment epithelium (RPE) and neuroretina. Temporospatial regulation of Otx2 expression is critical for its functions.	human,mouse	connective tissue	High+Lowthroughput	A distal enhancer that directs Otx2 expression in the retinal pigment epithelium and neuroretina	否	无		pluripotent stem cell	E_02_0165	Flow cytometry, immunofluorescence staining	Homeodomain transcription factor Otx2 is essential for embryonic development of multiple head tissues, including retinal pigment epithelium (RPE) and neuroretina. Temporospatial regulation of Otx2 expression is critical for its functions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Homeodomain transcription factor Otx2 is essential for embryonic development of multiple head tissues, including retinal pigment epithelium (RPE) and neuroretina. Temporospatial regulation of Otx2 expression is critical for its functions.		Homeodomain transcription factor Otx2 is essential for embryonic development of multiple head tissues, including retinal pigment epithelium (RPE) and neuroretina. Temporospatial regulation of Otx2 expression is critical for its functions.	Immunohistochemical staining	Homeodomain transcription factor Otx2 is essential for embryonic development of multiple head tissues, including retinal pigment epithelium (RPE) and neuroretina. Temporospatial regulation of Otx2 expression is critical for its functions.			Flow cytometry，免疫荧光染色				Otx2
31658410	chr11	31781903	31783903	PAX6	In the 392-bp mouse hs1150 element, recognition sites for transcription factors PAX6, CHX10, CRX, BLIMP1, and OTX were found (Fig. 6A, B), suggesting that hs1150 enhancer could be regulated by these transcription factors thatare essential for neuroretinal cell differentiation	human,mouse	Nervous tissue	High+Lowthroughput	A distal enhancer that directs Otx2 expression in the retinal pigment epithelium and neuroretina	否	无		photoreceptor cell	E_02_0165	Flow cytometry, immunofluorescence staining	In the 392-bp mouse hs1150 element, recognition sites for transcription factors PAX6, CHX10, CRX, BLIMP1, and OTX were found (Fig. 6A, B), suggesting that hs1150 enhancer could be regulated by these transcription factors thatare essential for neuroretinal cell differentiation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the 392-bp mouse hs1150 element, recognition sites for transcription factors PAX6, CHX10, CRX, BLIMP1, and OTX were found (Fig. 6A, B), suggesting that hs1150 enhancer could be regulated by these transcription factors thatare essential for neuroretinal cell differentiation		In the 392-bp mouse hs1150 element, recognition sites for transcription factors PAX6, CHX10, CRX, BLIMP1, and OTX were found (Fig. 6A, B), suggesting that hs1150 enhancer could be regulated by these transcription factors thatare essential for neuroretinal cell differentiation	Immunohistochemical staining	In the 392-bp mouse hs1150 element, recognition sites for transcription factors PAX6, CHX10, CRX, BLIMP1, and OTX were found (Fig. 6A, B), suggesting that hs1150 enhancer could be regulated by these transcription factors thatare essential for neuroretinal cell differentiation			Flow cytometry，免疫荧光染色				PAX6
31657619	chr1	26690155	26692155	ARID1A	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"	human,mouse	connective tissue	High+Lowthroughput	Altered 5-Hydroxymethylcytosine Landscape in Primary Gastric Adenocarcinoma	否	无	gastric cancer	embryonic stem cell	E_02_0166	PCR	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"		"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"	Immunohistochemical staining	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"			PCR				ARID1A
31657619	chr10	121475438	121477438	FGFR2	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"	human,mouse	connective tissue	High+Lowthroughput	Altered 5-Hydroxymethylcytosine Landscape in Primary Gastric Adenocarcinoma	否	无	gastric cancer	embryonic stem cell	E_02_0166	PCR	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"		"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"	Immunohistochemical staining	"For example, previous studies have identified several key genetic alterations that are linked to gastric malignancy, including mutations in the chromatin modifier gene AT-rich interaction domain 1A (ARID1A) and amplifications in human epidermal growth factor receptor 2 (HER2), fibroblast growth factor receptor 2 (FGFR2),
and mesenchymal–epithelial transition (MET)"			PCR				FGFR2
31654083	chr17	44073800	44075800	HDAC5	"HDAC5 is recruited to its target genesthrough interactions with transcription factors, i.e., myocyte en_x0002_hancer factor 2 (MEF2), to repress target gene transcription
(Parra and Verdin 2010). "	human,mouse	blood	High+Lowthroughput	Early-life blockade of NMDA receptors induces epigenetic abnormalities in the adult medial prefrontal cortex: possible involvement in memory impairment in trace fear conditioning	否	无	Schizophrenia		E_02_0167	PCR,Western blot 	"HDAC5 is recruited to its target genesthrough interactions with transcription factors, i.e., myocyte en_x0002_hancer factor 2 (MEF2), to repress target gene transcription
(Parra and Verdin 2010). "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"HDAC5 is recruited to its target genesthrough interactions with transcription factors, i.e., myocyte en_x0002_hancer factor 2 (MEF2), to repress target gene transcription
(Parra and Verdin 2010). "		"HDAC5 is recruited to its target genesthrough interactions with transcription factors, i.e., myocyte en_x0002_hancer factor 2 (MEF2), to repress target gene transcription
(Parra and Verdin 2010). "	Immunohistochemical staining	"HDAC5 is recruited to its target genesthrough interactions with transcription factors, i.e., myocyte en_x0002_hancer factor 2 (MEF2), to repress target gene transcription
(Parra and Verdin 2010). "			PCR,Western blot 				HDAC5
31653691	chr12	107873350	107875350	Bcl11b	To com_x0002_pare the molecular mechanisms through which Bcl11b controls cell type–specific gene regulation in the two contexts, we first examined the DNA binding patterns of Bcl11b across the genome in pro-T cells with those in ILC2 cells.	human,mouse	blood	High+Lowthroughput	Cell type-specific actions of Bcl11b in early T-lineage and group 2 innate lymphoid cells	否	无		mutant lymphoma cell	E_02_0168	Flow cytometry,Western blot,PCR	To com_x0002_pare the molecular mechanisms through which Bcl11b controls cell type–specific gene regulation in the two contexts, we first examined the DNA binding patterns of Bcl11b across the genome in pro-T cells with those in ILC2 cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To com_x0002_pare the molecular mechanisms through which Bcl11b controls cell type–specific gene regulation in the two contexts, we first examined the DNA binding patterns of Bcl11b across the genome in pro-T cells with those in ILC2 cells.		To com_x0002_pare the molecular mechanisms through which Bcl11b controls cell type–specific gene regulation in the two contexts, we first examined the DNA binding patterns of Bcl11b across the genome in pro-T cells with those in ILC2 cells.	Immunohistochemical staining	To com_x0002_pare the molecular mechanisms through which Bcl11b controls cell type–specific gene regulation in the two contexts, we first examined the DNA binding patterns of Bcl11b across the genome in pro-T cells with those in ILC2 cells.			Flow cytometry,Western blot,PCR				Bcl11b
31653691	chr16	92395674	92397674	Runx1	Thus, globally, Runx1, Runx3, and Bcl11b binding sites across the genome were often coincident within a cell type, but differed markedly between pro-T and ILC2 contexts.	human,mouse	lymph	High+Lowthroughput	Cell type-specific actions of Bcl11b in early T-lineage and group 2 innate lymphoid cells	否	无		lymphocyte	E_02_0168	Flow cytometry,Western blot,PCR	Thus, globally, Runx1, Runx3, and Bcl11b binding sites across the genome were often coincident within a cell type, but differed markedly between pro-T and ILC2 contexts.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, globally, Runx1, Runx3, and Bcl11b binding sites across the genome were often coincident within a cell type, but differed markedly between pro-T and ILC2 contexts.		Thus, globally, Runx1, Runx3, and Bcl11b binding sites across the genome were often coincident within a cell type, but differed markedly between pro-T and ILC2 contexts.	Immunohistochemical staining	Thus, globally, Runx1, Runx3, and Bcl11b binding sites across the genome were often coincident within a cell type, but differed markedly between pro-T and ILC2 contexts.			Flow cytometry,Western blot,PCR				Runx1
31653691	chr10	8042938	8044938	GATA3	These results show sharp lineagespecific binding differences both for the Runx factors, usually co-recruited with Bcl11b, and for GATA3, often recruited inde pendently of Bcl11b. They also indicate a likely role for a bZIP family member in defining ILC2-specific occupancy sites of Bcl11b, Runx factors, and GATA3	human,mouse	blood	High+Lowthroughput	Cell type-specific actions of Bcl11b in early T-lineage and group 2 innate lymphoid cells	否	无		T cell	E_02_0168	Flow cytometry,Western blot,PCR	These results show sharp lineagespecific binding differences both for the Runx factors, usually co-recruited with Bcl11b, and for GATA3, often recruited inde pendently of Bcl11b. They also indicate a likely role for a bZIP family member in defining ILC2-specific occupancy sites of Bcl11b, Runx factors, and GATA3	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results show sharp lineagespecific binding differences both for the Runx factors, usually co-recruited with Bcl11b, and for GATA3, often recruited inde pendently of Bcl11b. They also indicate a likely role for a bZIP family member in defining ILC2-specific occupancy sites of Bcl11b, Runx factors, and GATA3		These results show sharp lineagespecific binding differences both for the Runx factors, usually co-recruited with Bcl11b, and for GATA3, often recruited inde pendently of Bcl11b. They also indicate a likely role for a bZIP family member in defining ILC2-specific occupancy sites of Bcl11b, Runx factors, and GATA3	Immunohistochemical staining	These results show sharp lineagespecific binding differences both for the Runx factors, usually co-recruited with Bcl11b, and for GATA3, often recruited inde pendently of Bcl11b. They also indicate a likely role for a bZIP family member in defining ILC2-specific occupancy sites of Bcl11b, Runx factors, and GATA3			Flow cytometry,Western blot,PCR				GATA3
31652979	chr8	127732500	127734500	MYC	Gene set enrichment analysis revealed that DKI cells were enriched over single mutant cells for genes that characterize a MYC target gene signature.	human,mouse	breast	High+Lowthroughput	PIK3CA Cooperates with KRAS to Promote MYC Activity and Tumorigenesis via the Bromodomain Protein BRD9	否	无	tumour	mammary gland epithelial cell	E_02_0169	Western blot	Gene set enrichment analysis revealed that DKI cells were enriched over single mutant cells for genes that characterize a MYC target gene signature.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gene set enrichment analysis revealed that DKI cells were enriched over single mutant cells for genes that characterize a MYC target gene signature.		Gene set enrichment analysis revealed that DKI cells were enriched over single mutant cells for genes that characterize a MYC target gene signature.	Immunohistochemical staining	Gene set enrichment analysis revealed that DKI cells were enriched over single mutant cells for genes that characterize a MYC target gene signature.			Western blot				MYC
31652453	chr7	148804156	148806156	EZH2	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	human	bone	High+Lowthroughput	Ketamine induces endoplasmic reticulum stress in rats and SV-HUC-1 human uroepithelial cells by activating NLRP3/TXNIP aix	否	无	Osteosarcoma	osteosarcoma cell	E_01_0199	Flow cytometry, Western blot, PCR, immunofluorescence light staining	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	Immunohistochemical staining	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	EZH2		Flow cytometry,Western blot,PCR,免疫荧光光染色	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23			
31652453	chr9	94600340	94602340	FBP1	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	human	bone	High+Lowthroughput	Ketamine induces endoplasmic reticulum stress in rats and SV-HUC-1 human uroepithelial cells by activating NLRP3/TXNIP aix	否	无	Osteosarcoma	osteosarcoma cell	E_01_0199	Flow cytometry, Western blot, PCR, immunofluorescence light staining	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23		FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23	Immunohistochemical staining	FBP1 expression in tumor cells is linked to poor patient survival.27,32 Recently, we demonstrated that FBP1 physically interacted with EZH2 in osteosarcoma cells and that GSK343 treatment inhibited the expression of EZH2 and FBP1.23			Flow cytometry,Western blot,PCR,免疫荧光光染色				FBP1
31651209	chr2	236162410	236164410	GBX2	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.	human,mouse		High+Lowthroughput	GSK343 induces programmed cell death through the inhibition of EZH2 and FBP1 in osteosarcoma cells	否	无	Nerve injury	Schwann cell	E_02_0170	PCR, Western blot, immunofluorescence staining	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.		A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.	Immunohistochemical staining	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.			PCR,Western blot ,免疫荧光染色				GBX2
31651209	chr11	114056802	114058802	ZBTB16	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.	human,mouse		High+Lowthroughput	GSK343 induces programmed cell death through the inhibition of EZH2 and FBP1 in osteosarcoma cells	否	无	Nerve injury	Schwann cell	E_02_0170	PCR, Western blot, immunofluorescence staining	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.		A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.	Immunohistochemical staining	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. TFAP2A, a gene encoding transcription factor activating enhancer binding protein 2 alpha, was found to be critical in the regulatory network.			PCR,Western blot ,免疫荧光染色				ZBTB16
31650361	chr2	236162780	236164780	GBX2	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. -	human,mouse	connective tissue	High+Lowthroughput	Dysregulated Transcription Factor TFAP2A After Peripheral Nerve Injury Modulated Schwann Cell Phenotype	否	无		Schwann cell	E_02_0171	Western blot, PCR, gene knockdown	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. -	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. -		A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. -	Immunohistochemical staining	A total of 9 transcription factor genes, including GBX2, HIF3A, IRF8, LRRC63, SNAI3, SPIB, TBX21, TFAP2A, and ZBTB16 were identifed to be commonly diferentially expressed at 1, 4, 7, and 14 days after nerve injury. -			Western blot,PCR,基因敲降				GBX2
31649847	chr11	70018598	70020598	Mgl2	Kin increased the expression of M2-related genes Mgl1, Mgl2,Pgc1-β, Arg-1, Il-10 and Cd206 (Fig. 3A).	human,mouse	connective tissue	High+Lowthroughput	Kinsenoside attenuates osteoarthritis by repolarizing macrophages through inactivating NF-κB/MAPK signaling and protecting chondrocytes	否	无	Osteoarthritis	macrophage	E_02_0172	PCR, Western blot, flow cytometry, gene knockdown	Kin increased the expression of M2-related genes Mgl1, Mgl2,Pgc1-β, Arg-1, Il-10 and Cd206 (Fig. 3A).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Kin increased the expression of M2-related genes Mgl1, Mgl2,Pgc1-β, Arg-1, Il-10 and Cd206 (Fig. 3A).		Kin increased the expression of M2-related genes Mgl1, Mgl2,Pgc1-β, Arg-1, Il-10 and Cd206 (Fig. 3A).	Immunohistochemical staining	Kin increased the expression of M2-related genes Mgl1, Mgl2,Pgc1-β, Arg-1, Il-10 and Cd206 (Fig. 3A).			PCR,Western blot,Flow cytometry,基因敲降				Mgl2
31649059	chr1	8001795	8003795	ERRFI1	"As exemplified by the ERRFI1 locus (Fig.3A) and summarized genome-wide for all TSSs (Fig. 3B), both transient and stable transcript TSSs are accurately captured by
csRNA-seq. "	human	blood	High+Lowthroughput	Identification and dynamic quantification of regulatory elements using total RNA	否	无	leukemia	myelogenous leukemia cell	E_01_0200	Flow cytometry	"As exemplified by the ERRFI1 locus (Fig.3A) and summarized genome-wide for all TSSs (Fig. 3B), both transient and stable transcript TSSs are accurately captured by
csRNA-seq. "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"As exemplified by the ERRFI1 locus (Fig.3A) and summarized genome-wide for all TSSs (Fig. 3B), both transient and stable transcript TSSs are accurately captured by
csRNA-seq. "		"As exemplified by the ERRFI1 locus (Fig.3A) and summarized genome-wide for all TSSs (Fig. 3B), both transient and stable transcript TSSs are accurately captured by
csRNA-seq. "	Immunohistochemical staining	"As exemplified by the ERRFI1 locus (Fig.3A) and summarized genome-wide for all TSSs (Fig. 3B), both transient and stable transcript TSSs are accurately captured by
csRNA-seq. "			Flow cytometry				ERRFI1
31649055	chr2	47342302	47344302	EPCAM	"The significantly differentially expressed genes include common clinical biomarkers for macrophages (CD68 and CD163) and DCIS cells (EPCAM, KRT7, KRT18, and
ERBB2 [also known as HER2]) (Fig. 4C; Supplemental File 3). The single-cell samples generally have gene expression profiles similar to the cell type–matched bulk samples. "	human	connective tissue	High+Lowthroughput	FFPEcap-seq: a method for sequencing capped RNAs in formalin-fixed paraffin-embedded samples	是	无	leukemia	stromal macrophage cell	E_01_0201	Flow cytometry	"The significantly differentially expressed genes include common clinical biomarkers for macrophages (CD68 and CD163) and DCIS cells (EPCAM, KRT7, KRT18, and
ERBB2 [also known as HER2]) (Fig. 4C; Supplemental File 3). The single-cell samples generally have gene expression profiles similar to the cell type–matched bulk samples. "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"The significantly differentially expressed genes include common clinical biomarkers for macrophages (CD68 and CD163) and DCIS cells (EPCAM, KRT7, KRT18, and
ERBB2 [also known as HER2]) (Fig. 4C; Supplemental File 3). The single-cell samples generally have gene expression profiles similar to the cell type–matched bulk samples. "	Immunohistochemical staining	"The significantly differentially expressed genes include common clinical biomarkers for macrophages (CD68 and CD163) and DCIS cells (EPCAM, KRT7, KRT18, and
ERBB2 [also known as HER2]) (Fig. 4C; Supplemental File 3). The single-cell samples generally have gene expression profiles similar to the cell type–matched bulk samples. "	EPCAM		Flow cytometry	"The significantly differentially expressed genes include common clinical biomarkers for macrophages (CD68 and CD163) and DCIS cells (EPCAM, KRT7, KRT18, and
ERBB2 [also known as HER2]) (Fig. 4C; Supplemental File 3). The single-cell samples generally have gene expression profiles similar to the cell type–matched bulk samples. "			
31649032	chr3	66876146	66878146	Shox2	Using mice, here we report that deficiency in short stature homeobox 2 (Shox2), a transcriptional regulator whose expression is restricted to the anterior palatal mesenchyme, leads to a defective palatine process of the maxilla, but does not affect the palatine. 	human	connective tissue	High+Lowthroughput	Shox2 regulates osteogenic differentiation and pattern formation during hard palate development in mice	否	无		mesenchymal cell	E_01_0202	Flow cytometry, PCR, immunofluorescence staining	Using mice, here we report that deficiency in short stature homeobox 2 (Shox2), a transcriptional regulator whose expression is restricted to the anterior palatal mesenchyme, leads to a defective palatine process of the maxilla, but does not affect the palatine. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Using mice, here we report that deficiency in short stature homeobox 2 (Shox2), a transcriptional regulator whose expression is restricted to the anterior palatal mesenchyme, leads to a defective palatine process of the maxilla, but does not affect the palatine. 		Using mice, here we report that deficiency in short stature homeobox 2 (Shox2), a transcriptional regulator whose expression is restricted to the anterior palatal mesenchyme, leads to a defective palatine process of the maxilla, but does not affect the palatine. 	Immunohistochemical staining	Using mice, here we report that deficiency in short stature homeobox 2 (Shox2), a transcriptional regulator whose expression is restricted to the anterior palatal mesenchyme, leads to a defective palatine process of the maxilla, but does not affect the palatine. 			Flow cytometry,PCR,免疫荧光染色				Shox2
31644911	chr8	101489945	101491945	GRHL2	Motif enrichment analysis of sequences within the ‘‘gained’’ DHSs in TAMR indicated that the transcription factors most likely to be interacting at these genomic loci include those that bind bZip motifs, GRHL2, AP2 factors, ER, and FOXA family members (Figure 1B).	human,mouse	breast	High+Lowthroughput	The Lineage Determining Factor GRHL2 Collaborates with FOXA1 to Establish a Targetable Pathway in Endocrine Therapy-Resistant Breast Cancer	否	无	mammary cancer	breast cancer cell	E_02_0173	PCR,Western blot,Flow cytometry	Motif enrichment analysis of sequences within the ‘‘gained’’ DHSs in TAMR indicated that the transcription factors most likely to be interacting at these genomic loci include those that bind bZip motifs, GRHL2, AP2 factors, ER, and FOXA family members (Figure 1B).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Motif enrichment analysis of sequences within the ‘‘gained’’ DHSs in TAMR indicated that the transcription factors most likely to be interacting at these genomic loci include those that bind bZip motifs, GRHL2, AP2 factors, ER, and FOXA family members (Figure 1B).		Motif enrichment analysis of sequences within the ‘‘gained’’ DHSs in TAMR indicated that the transcription factors most likely to be interacting at these genomic loci include those that bind bZip motifs, GRHL2, AP2 factors, ER, and FOXA family members (Figure 1B).	Immunohistochemical staining	Motif enrichment analysis of sequences within the ‘‘gained’’ DHSs in TAMR indicated that the transcription factors most likely to be interacting at these genomic loci include those that bind bZip motifs, GRHL2, AP2 factors, ER, and FOXA family members (Figure 1B).			PCR,Western blot,Flow cytometry				GRHL2
31644352	chr16	28929347	28931347	CD19	"Wounds were digested as described above. Single cell suspen_x0002_sions were incubated with fluorescein isothiocyanate–labeled anti-CD3, anti-CD19, and anti-Ly6G (BioLegend) followed by antifluorescein isothiocyanate microbeads (Miltenyi Biotec). 
"	human	blood	High+Lowthroughput	Sepsis Induces Prolonged Epigenetic Modifications in Bone Marrow and Peripheral Macrophages Impairing Inflammation and Wound Healing	否	无	septicemia	B cell	E_01_0203	PCR, flow cytometry, immunofluorescence staining	"Wounds were digested as described above. Single cell suspen_x0002_sions were incubated with fluorescein isothiocyanate–labeled anti-CD3, anti-CD19, and anti-Ly6G (BioLegend) followed by antifluorescein isothiocyanate microbeads (Miltenyi Biotec). 
"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Wounds were digested as described above. Single cell suspen_x0002_sions were incubated with fluorescein isothiocyanate–labeled anti-CD3, anti-CD19, and anti-Ly6G (BioLegend) followed by antifluorescein isothiocyanate microbeads (Miltenyi Biotec). 
"		"Wounds were digested as described above. Single cell suspen_x0002_sions were incubated with fluorescein isothiocyanate–labeled anti-CD3, anti-CD19, and anti-Ly6G (BioLegend) followed by antifluorescein isothiocyanate microbeads (Miltenyi Biotec). 
"	Immunohistochemical staining	"Wounds were digested as described above. Single cell suspen_x0002_sions were incubated with fluorescein isothiocyanate–labeled anti-CD3, anti-CD19, and anti-Ly6G (BioLegend) followed by antifluorescein isothiocyanate microbeads (Miltenyi Biotec). 
"			PCR,Flow cytometry,免疫荧光染色				CD19
31642979	chr4	184382613	184384613	IRF2	Similarly, IRF2 was predicted to bind to the sequence with the T allele at rs7071351 (Fig. 3d) and IRF2 ChIP-seq peak was also found in the SNP region (Fig. 3b).	human	colon	High+Lowthroughput	Three functional variants were identified to affect RPS24 expression and significantly associated with risk of colorectal cancer	是	rs7071351	Colon cancer	Human colorectal carcinoma cell	E_01_0204	PCR,Flow cytometry	Similarly, IRF2 was predicted to bind to the sequence with the T allele at rs7071351 (Fig. 3d) and IRF2 ChIP-seq peak was also found in the SNP region (Fig. 3b).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Similarly, IRF2 was predicted to bind to the sequence with the T allele at rs7071351 (Fig. 3d) and IRF2 ChIP-seq peak was also found in the SNP region (Fig. 3b).	Immunohistochemical staining	Similarly, IRF2 was predicted to bind to the sequence with the T allele at rs7071351 (Fig. 3d) and IRF2 ChIP-seq peak was also found in the SNP region (Fig. 3b).	IRF2		PCR,Flow cytometry	Similarly, IRF2 was predicted to bind to the sequence with the T allele at rs7071351 (Fig. 3d) and IRF2 ChIP-seq peak was also found in the SNP region (Fig. 3b).			
31642979	chr10	79066184	79068184	ZMIZ1	However, ZMIZ1-AS1 is a miscellaneous RNA gene with unknown function and both ZMIZ1 and ZMIZ1-AS1 failed to afect cell growth in our functionalinterrogation.	human	colon	High+Lowthroughput	Three functional variants were identified to affect RPS24 expression and significantly associated with risk of colorectal cancer	是	rs704017	Colon cancer	Human colorectal carcinoma cell	E_01_0204	PCR,Flow cytometry	However, ZMIZ1-AS1 is a miscellaneous RNA gene with unknown function and both ZMIZ1 and ZMIZ1-AS1 failed to afect cell growth in our functionalinterrogation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			However, ZMIZ1-AS1 is a miscellaneous RNA gene with unknown function and both ZMIZ1 and ZMIZ1-AS1 failed to afect cell growth in our functionalinterrogation.	Immunohistochemical staining	However, ZMIZ1-AS1 is a miscellaneous RNA gene with unknown function and both ZMIZ1 and ZMIZ1-AS1 failed to afect cell growth in our functionalinterrogation.	ZMIZ1		PCR,Flow cytometry	However, ZMIZ1-AS1 is a miscellaneous RNA gene with unknown function and both ZMIZ1 and ZMIZ1-AS1 failed to afect cell growth in our functionalinterrogation.			
31642363	chr7	148804489	148806489	EZH2	Enhancer of zeste homolog 2 (EZH2), a catalytic component of the polycomb repressive complex 2, acts as a methyltrans_x0002_ferase for H3 lysine 27 trimethylation, mod_x0002_ulates chromatin structure and gene expression, and recruits DNA methyltrans_x0002_ferases for gene silencing.2	human	connective tissue	High+Lowthroughput	Sepsis Induces Prolonged Epigenetic Modifications in Bone Marrow and Peripheral Macrophages Impairing Inflammation and Wound Healing	否	无		mesenchymal stem cell	E_01_0205	PCR,Western blot	Enhancer of zeste homolog 2 (EZH2), a catalytic component of the polycomb repressive complex 2, acts as a methyltrans_x0002_ferase for H3 lysine 27 trimethylation, mod_x0002_ulates chromatin structure and gene expression, and recruits DNA methyltrans_x0002_ferases for gene silencing.2	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2 (EZH2), a catalytic component of the polycomb repressive complex 2, acts as a methyltrans_x0002_ferase for H3 lysine 27 trimethylation, mod_x0002_ulates chromatin structure and gene expression, and recruits DNA methyltrans_x0002_ferases for gene silencing.2	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2), a catalytic component of the polycomb repressive complex 2, acts as a methyltrans_x0002_ferase for H3 lysine 27 trimethylation, mod_x0002_ulates chromatin structure and gene expression, and recruits DNA methyltrans_x0002_ferases for gene silencing.2	EZH2		PCR,Western blot	Enhancer of zeste homolog 2 (EZH2), a catalytic component of the polycomb repressive complex 2, acts as a methyltrans_x0002_ferase for H3 lysine 27 trimethylation, mod_x0002_ulates chromatin structure and gene expression, and recruits DNA methyltrans_x0002_ferases for gene silencing.2			
31641208	chr16	68734197	68736197	CDH1	Here, through comprehensive filtration, we prioritized rs7198799, a common SNP in the second intron of the CDH1, as the putative causal variant. In addition, we found an association of CRC_x0002_risk allele C of rs7198799 with elevated transcript level of biological plausible candidate gene ZFP90 via expression quantitative trait loci analysis.	human	blood	High+Lowthroughput	Enhancer of zeste homolog 2 enhances the migration and chemotaxis of dental mesenchymal stem cells	是	rs7198799,	tumour		E_01_0206	PCR,Western blot	Here, through comprehensive filtration, we prioritized rs7198799, a common SNP in the second intron of the CDH1, as the putative causal variant. In addition, we found an association of CRC_x0002_risk allele C of rs7198799 with elevated transcript level of biological plausible candidate gene ZFP90 via expression quantitative trait loci analysis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, through comprehensive filtration, we prioritized rs7198799, a common SNP in the second intron of the CDH1, as the putative causal variant. In addition, we found an association of CRC_x0002_risk allele C of rs7198799 with elevated transcript level of biological plausible candidate gene ZFP90 via expression quantitative trait loci analysis.	Immunohistochemical staining	Here, through comprehensive filtration, we prioritized rs7198799, a common SNP in the second intron of the CDH1, as the putative causal variant. In addition, we found an association of CRC_x0002_risk allele C of rs7198799 with elevated transcript level of biological plausible candidate gene ZFP90 via expression quantitative trait loci analysis.	CDH1		PCR,Western blot	Here, through comprehensive filtration, we prioritized rs7198799, a common SNP in the second intron of the CDH1, as the putative causal variant. In addition, we found an association of CRC_x0002_risk allele C of rs7198799 with elevated transcript level of biological plausible candidate gene ZFP90 via expression quantitative trait loci analysis.			
31636473	chr10	67881712	67883712	SIRT1	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases. However, the role of SIRT1 in ulcerative colitis (UC) is still confusing	human	Epithelial tissues	High+Lowthroughput	Sirtuin 1 alleviates endoplasmic reticulum stress-mediated apoptosis of intestinal epithelial cells in ulcerative colitis	否	无		epithelial cell	E_01_0207	Flow cytometry,PCR,Western blot	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases. However, the role of SIRT1 in ulcerative colitis (UC) is still confusing	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases. However, the role of SIRT1 in ulcerative colitis (UC) is still confusing	Immunohistochemical staining	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases. However, the role of SIRT1 in ulcerative colitis (UC) is still confusing	SIRT1		Flow cytometry,PCR,Western blot	Sirtuin 1 (SIRT1) is a nicotinamide adenine dinucleotide (NAD+)-dependent protein deacetylase that is involved in various diseases, including cancers, metabolic diseases, and inflammation-associated diseases. However, the role of SIRT1 in ulcerative colitis (UC) is still confusing			
31636429	chr5	70046788	70048788	SMN2	The adenine base was substi_x0002_tuted in the SMN2 mini-gene and the effect of these mutations was evaluated in human cellular models (Fig. 3a).	human	Epithelial tissues	High+Lowthroughput	Structural basis of a small molecule targeting RNA for a specific splicing correction	否	无	Spinal muscular atrophy	HEK293T	E_01_0208	Western blot	The adenine base was substi_x0002_tuted in the SMN2 mini-gene and the effect of these mutations was evaluated in human cellular models (Fig. 3a).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The adenine base was substi_x0002_tuted in the SMN2 mini-gene and the effect of these mutations was evaluated in human cellular models (Fig. 3a).		The adenine base was substi_x0002_tuted in the SMN2 mini-gene and the effect of these mutations was evaluated in human cellular models (Fig. 3a).	Immunohistochemical staining	The adenine base was substi_x0002_tuted in the SMN2 mini-gene and the effect of these mutations was evaluated in human cellular models (Fig. 3a).			Western blot				SMN2
31636200	chr4	110614447	110616447	PITX2	Genome-wide association studies found that increased risk for atrial fibrillation (AF), the most common human heart arrhythmia,is associated with noncoding sequence variants located in proxim_x0002_ity to PITX2.	human	connective tissue	High+Lowthroughput	Long-range Pitx2c enhancer-promoter interactions prevent predisposition to atrial fibrillation	是	rs2595104	Atrial fibrillation	embryonic stem cell	E_01_0209	Flow cytometry,PCR,Western blot	Genome-wide association studies found that increased risk for atrial fibrillation (AF), the most common human heart arrhythmia,is associated with noncoding sequence variants located in proxim_x0002_ity to PITX2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Genome-wide association studies found that increased risk for atrial fibrillation (AF), the most common human heart arrhythmia,is associated with noncoding sequence variants located in proxim_x0002_ity to PITX2.	Immunohistochemical staining	Genome-wide association studies found that increased risk for atrial fibrillation (AF), the most common human heart arrhythmia,is associated with noncoding sequence variants located in proxim_x0002_ity to PITX2.	PITX2		Flow cytometry,PCR,Western blot	Genome-wide association studies found that increased risk for atrial fibrillation (AF), the most common human heart arrhythmia,is associated with noncoding sequence variants located in proxim_x0002_ity to PITX2.			
31634421	chr16	92395428	92397428	Runx1	Runx1 is an important haematopoietic transcription factor as stressed by its involve_x0002_ment in a number of haematological malignancies.	human	blood	High+Lowthroughput	Gata3 targets Runx1 in the embryonic haematopoietic stem cell niche	否	无	Hematologic disorders	hematopoietic stem cell	E_01_0210	Flow cytometry,PCR,Western blot	Runx1 is an important haematopoietic transcription factor as stressed by its involve_x0002_ment in a number of haematological malignancies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Runx1 is an important haematopoietic transcription factor as stressed by its involve_x0002_ment in a number of haematological malignancies.		Runx1 is an important haematopoietic transcription factor as stressed by its involve_x0002_ment in a number of haematological malignancies.	Immunohistochemical staining	Runx1 is an important haematopoietic transcription factor as stressed by its involve_x0002_ment in a number of haematological malignancies.			Flow cytometry,PCR,Western blot				Runx1
31633376	chr6	84684753	84686753	TBX18	Transcription factor TBX18 is a member of the TBX subfamily of the T-box family, which is involved in the formation and development of sinus node head.	human	Musculature	High+Lowthroughput	Transcription Factor TBX18 Reprograms Vascular Smooth Muscle Cells of Ascending Aorta to Pacemaker-Like Cells	否	无		smooth muscle cell	E_01_0211	Flow cytometry, PCR, immunofluorescence staining	Transcription factor TBX18 is a member of the TBX subfamily of the T-box family, which is involved in the formation and development of sinus node head.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Transcription factor TBX18 is a member of the TBX subfamily of the T-box family, which is involved in the formation and development of sinus node head.	Immunohistochemical staining	Transcription factor TBX18 is a member of the TBX subfamily of the T-box family, which is involved in the formation and development of sinus node head.	TBX18		Flow cytometry,PCR,免疫荧光染色	Transcription factor TBX18 is a member of the TBX subfamily of the T-box family, which is involved in the formation and development of sinus node head.			
31632241	chr20	50885804	50887804	ADNP	Activity-dependent neuroprotective protein (ADNP) has been initially discovered through its eight amino acid sequence NAPVSIPQ (Bassan et al., 1999), which shares SIP motif with SALLRSIPA – a peptide derived from activity-dependent neurotrophic factor (ADNF) (Brenneman and Gozes, 1996; Zamostiano et al., 1999). 	human,mouse		High+Lowthroughput	A Novel Microtubule-Tau Association Enhancer and Neuroprotective Drug Candidate: Ac-SKIP	否	无	Alzheimer		E_02_0174	Flow cytometry,PCR,Western blot	Activity-dependent neuroprotective protein (ADNP) has been initially discovered through its eight amino acid sequence NAPVSIPQ (Bassan et al., 1999), which shares SIP motif with SALLRSIPA – a peptide derived from activity-dependent neurotrophic factor (ADNF) (Brenneman and Gozes, 1996; Zamostiano et al., 1999). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Activity-dependent neuroprotective protein (ADNP) has been initially discovered through its eight amino acid sequence NAPVSIPQ (Bassan et al., 1999), which shares SIP motif with SALLRSIPA – a peptide derived from activity-dependent neurotrophic factor (ADNF) (Brenneman and Gozes, 1996; Zamostiano et al., 1999). 		Activity-dependent neuroprotective protein (ADNP) has been initially discovered through its eight amino acid sequence NAPVSIPQ (Bassan et al., 1999), which shares SIP motif with SALLRSIPA – a peptide derived from activity-dependent neurotrophic factor (ADNF) (Brenneman and Gozes, 1996; Zamostiano et al., 1999). 	Immunohistochemical staining	Activity-dependent neuroprotective protein (ADNP) has been initially discovered through its eight amino acid sequence NAPVSIPQ (Bassan et al., 1999), which shares SIP motif with SALLRSIPA – a peptide derived from activity-dependent neurotrophic factor (ADNF) (Brenneman and Gozes, 1996; Zamostiano et al., 1999). 			Flow cytometry,PCR,Western blot				ADNP
31631036	chr7	148804245	148806245	EZH2	To ascertain whether EZH2 expression was correlated with CEP degeneration, immunohistochemical analysis of human CEP tissue was used to compare the level of EZH2 in normal and degenerated human CEP. It was found that the expression of EZH2 increased in degenerated human CEP (Fig. 1D and 1E).	human,mouse	connective tissue	High+Lowthroughput	Inhibition of EZH2 ameliorates cartilage endplate degeneration and attenuates the progression of intervertebral disc degeneration via demethylation of Sox-9	否	无	Disc degeneration	stem cell	E_02_0175	PCR,Western blot	To ascertain whether EZH2 expression was correlated with CEP degeneration, immunohistochemical analysis of human CEP tissue was used to compare the level of EZH2 in normal and degenerated human CEP. It was found that the expression of EZH2 increased in degenerated human CEP (Fig. 1D and 1E).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To ascertain whether EZH2 expression was correlated with CEP degeneration, immunohistochemical analysis of human CEP tissue was used to compare the level of EZH2 in normal and degenerated human CEP. It was found that the expression of EZH2 increased in degenerated human CEP (Fig. 1D and 1E).		To ascertain whether EZH2 expression was correlated with CEP degeneration, immunohistochemical analysis of human CEP tissue was used to compare the level of EZH2 in normal and degenerated human CEP. It was found that the expression of EZH2 increased in degenerated human CEP (Fig. 1D and 1E).	Immunohistochemical staining	To ascertain whether EZH2 expression was correlated with CEP degeneration, immunohistochemical analysis of human CEP tissue was used to compare the level of EZH2 in normal and degenerated human CEP. It was found that the expression of EZH2 increased in degenerated human CEP (Fig. 1D and 1E).			PCR,Western blot				EZH2
31631026	chr1	23017098	23019098	KDM1A	We conduct a CRISPR screen revealing that knockout of KDM1A encoding lysine-specific demethylase 1 (LSD1) sensitizes DIPG cells to histone deacetylase (HDAC) inhibitors. Consistently, Corin, a bifunctional inhibitor of HDACs and LSD1, potently inhibits DIPG growth in vitro and in xenografts.	human	connective tissue	High+Lowthroughput	Re-programing Chromatin with a Bifunctional LSD1/HDAC Inhibitor Induces Therapeutic Differentiation in DIPG	否	无	Desmosomas	melanoma cells	E_01_0212	Western blot,PCR,Flow cytometry	We conduct a CRISPR screen revealing that knockout of KDM1A encoding lysine-specific demethylase 1 (LSD1) sensitizes DIPG cells to histone deacetylase (HDAC) inhibitors. Consistently, Corin, a bifunctional inhibitor of HDACs and LSD1, potently inhibits DIPG growth in vitro and in xenografts.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We conduct a CRISPR screen revealing that knockout of KDM1A encoding lysine-specific demethylase 1 (LSD1) sensitizes DIPG cells to histone deacetylase (HDAC) inhibitors. Consistently, Corin, a bifunctional inhibitor of HDACs and LSD1, potently inhibits DIPG growth in vitro and in xenografts.	Immunohistochemical staining	We conduct a CRISPR screen revealing that knockout of KDM1A encoding lysine-specific demethylase 1 (LSD1) sensitizes DIPG cells to histone deacetylase (HDAC) inhibitors. Consistently, Corin, a bifunctional inhibitor of HDACs and LSD1, potently inhibits DIPG growth in vitro and in xenografts.	KDM1A		Western blot,PCR,Flow cytometry	We conduct a CRISPR screen revealing that knockout of KDM1A encoding lysine-specific demethylase 1 (LSD1) sensitizes DIPG cells to histone deacetylase (HDAC) inhibitors. Consistently, Corin, a bifunctional inhibitor of HDACs and LSD1, potently inhibits DIPG growth in vitro and in xenografts.			
31631012	chr2	209421458	209423458	MAP2	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	human	connective tissue	High+Lowthroughput	Identification and Massively Parallel Characterization of Regulatory Elements Driving Neural Induction	是	rs2176546		pluripotent stem cell	E_01_0213	Flow cytometry,PCR	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).		Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	Immunohistochemical staining	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).			Flow cytometry,PCR				MAP2
31631012	chr9	91560120	91562120	ROR2	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	human	connective tissue	High+Lowthroughput	Identification and Massively Parallel Characterization of Regulatory Elements Driving Neural Induction	是	rs2176546		pluripotent stem cell	E_01_0213	Flow cytometry,PCR	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	Immunohistochemical staining	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).	ROR2		Flow cytometry,PCR	Specif_x0002_ically, examination of potential enhancers within these clusters that are located near neural marker genes, MAP2 (Herzog and Weber, 1978) and ROR2 (Endo et al., 2012), found them to be en_x0002_riched for ATAC-seq signal at 12–24 h, H3K27ac signal at 48–72h, and their expression to peak at 72 h (Figures S2A and S2B).			
31631012	chr12	7784977	7786977	NANOG	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	human	Nervous tissue	High+Lowthroughput	Identification and Massively Parallel Characterization of Regulatory Elements Driving Neural Induction	是	rs6545663		neural progenitor cell	E_01_0213	Flow cytometry,PCR	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.		Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	Immunohistochemical staining	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.			Flow cytometry,PCR				NANOG
31631012	chr6	31161576	31163576	POU5F1	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	human	Nervous tissue	High+Lowthroughput	Identification and Massively Parallel Characterization of Regulatory Elements Driving Neural Induction	是	rs6545663		neural progenitor cell	E_01_0213	Flow cytometry,PCR	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	Immunohistochemical staining	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	POU5F1		Flow cytometry,PCR	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.			
31631012	chr1	212563135	212565135	ATF3	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	human	connective tissue	High+Lowthroughput	Identification and Massively Parallel Characterization of Regulatory Elements Driving Neural Induction	是	rs6545664		stem cell	E_01_0213	Flow cytometry,PCR	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.		Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.	Immunohistochemical staining	Pluripotent markers (NANOG and POU5F1) and direct targets of transforming growth factor b (TGF-b) and bone morphogenetic protein (BMP) signaling(SMAD7, ID1, and LEFTY2) were downregulated, and immediate early genes (ATF3, FOS, FOSB, and EGR1/2/3) were transiently upregulated at 3 h, corresponding to the cell’s stress response against differentiation stimuli.			Flow cytometry,PCR				ATF3
31629814	chrX	47632617	47634617	ELK1	Furthermore, ELK1 supports cell-cycle entry during liver regeneration because Elk1-/- mice show reduced hepatocyte proliferation after PHx.40	human	liver	High+Lowthroughput	The Dynamic Chromatin Architecture of the Regenerating Liver	否	无	Obesity	hepatocyte	E_01_0214	Flow cytometry,PCR	Furthermore, ELK1 supports cell-cycle entry during liver regeneration because Elk1-/- mice show reduced hepatocyte proliferation after PHx.40	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Furthermore, ELK1 supports cell-cycle entry during liver regeneration because Elk1-/- mice show reduced hepatocyte proliferation after PHx.40	Immunohistochemical staining	Furthermore, ELK1 supports cell-cycle entry during liver regeneration because Elk1-/- mice show reduced hepatocyte proliferation after PHx.40	KCNH4		Flow cytometry,PCR	Furthermore, ELK1 supports cell-cycle entry during liver regeneration because Elk1-/- mice show reduced hepatocyte proliferation after PHx.40			
31629687	chr1	35867480	35869480	AGO1	A study showed AGO1 binding with RNA polymerase II and active promoters (Huang et al.,2013), while another report indicated that AGO1 association with active enhancers did not explain the observed widespread changes in gene expression in AGO1 depleted cells	human	liver	High+Lowthroughput	Nuclear AGO1 Regulates Gene Expression by Affecting Chromatin Architecture in Human Cells	否	无	cancer	HepG2 cell	E_01_0215	Western blot,Flow cytometry,PCR	A study showed AGO1 binding with RNA polymerase II and active promoters (Huang et al.,2013), while another report indicated that AGO1 association with active enhancers did not explain the observed widespread changes in gene expression in AGO1 depleted cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A study showed AGO1 binding with RNA polymerase II and active promoters (Huang et al.,2013), while another report indicated that AGO1 association with active enhancers did not explain the observed widespread changes in gene expression in AGO1 depleted cells		A study showed AGO1 binding with RNA polymerase II and active promoters (Huang et al.,2013), while another report indicated that AGO1 association with active enhancers did not explain the observed widespread changes in gene expression in AGO1 depleted cells	Immunohistochemical staining	A study showed AGO1 binding with RNA polymerase II and active promoters (Huang et al.,2013), while another report indicated that AGO1 association with active enhancers did not explain the observed widespread changes in gene expression in AGO1 depleted cells			Western blot,Flow cytometry,PCR				AGO1
31628347	chr5	147234799	147236799	Cdx2	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.	human	connective tissue	High+Lowthroughput	Super-enhancer-guided mapping of regulatory networks controlling mouse trophoblast stem cells	否	无		Trophoblast stem cell	E_01_0216	Flow cytometry	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.		We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.	Immunohistochemical staining	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.			Flow cytometry				Cdx2
31628347	chr6	128198651	128200651	Tead4	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.	human	connective tissue	High+Lowthroughput	Super-enhancer-guided mapping of regulatory networks controlling mouse trophoblast stem cells	否	无		Trophoblast stem cell	E_01_0216	Flow cytometry	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.		We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.	Immunohistochemical staining	We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated.			Flow cytometry				Tead4
31628324	chr16	72780389	72782389	ZFHX3	A third locus we examined is 16q22. The most highly AF_x0002_associated risk SNPs in this locus are found in the first intron of ZFHX3, which codes for a TF that plays key roles in development and in adult tissues56,57. 	human,mouse	Musculature	High+Lowthroughput	Identification of atrial fibrillation associated genes and functional non-coding variants	是	rs281766	Arrhythmia	muscle cell	E_02_0176	Flow cytometry,PCR	A third locus we examined is 16q22. The most highly AF_x0002_associated risk SNPs in this locus are found in the first intron of ZFHX3, which codes for a TF that plays key roles in development and in adult tissues56,57. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A third locus we examined is 16q22. The most highly AF_x0002_associated risk SNPs in this locus are found in the first intron of ZFHX3, which codes for a TF that plays key roles in development and in adult tissues56,57. 		A third locus we examined is 16q22. The most highly AF_x0002_associated risk SNPs in this locus are found in the first intron of ZFHX3, which codes for a TF that plays key roles in development and in adult tissues56,57. 	Immunohistochemical staining	A third locus we examined is 16q22. The most highly AF_x0002_associated risk SNPs in this locus are found in the first intron of ZFHX3, which codes for a TF that plays key roles in development and in adult tissues56,57. 			Flow cytometry,PCR				ZFHX3
31626715	chr4	108044853	108046853	LEF1	Here we identify the EMT transcription factor LEF1 as a critical regulator of glutathione (GSH) metabolism aside from its well-known role as EMT inducer. 	human,mouse	breast	High+Lowthroughput	LEF1 supports metastatic brain colonization by regulating glutathione metabolism and increasing ROS resistance in breast cancer	否	无	mammary cancer	breast cancer cell	E_02_0177	Western blot,PCR,Flow cytometry	Here we identify the EMT transcription factor LEF1 as a critical regulator of glutathione (GSH) metabolism aside from its well-known role as EMT inducer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we identify the EMT transcription factor LEF1 as a critical regulator of glutathione (GSH) metabolism aside from its well-known role as EMT inducer. 		Here we identify the EMT transcription factor LEF1 as a critical regulator of glutathione (GSH) metabolism aside from its well-known role as EMT inducer. 	Immunohistochemical staining	Here we identify the EMT transcription factor LEF1 as a critical regulator of glutathione (GSH) metabolism aside from its well-known role as EMT inducer. 			Western blot,PCR,Flow cytometry				LEF1
31624269	chr14	95707296	95709296	TCL1A	Wright et al.identified a total of 19 loci associated with mLOY9, including TCL1A and other genes involved in cell cycle regulation and DNA damage response.	human,mouse	blood	High+Lowthroughput	GWAS of mosaic loss of chromosome Y highlights genetic effects on blood cell differentiation	是	rs17758695		hematopoietic stem cell	E_02_0178	Flow cytometry	Wright et al.identified a total of 19 loci associated with mLOY9, including TCL1A and other genes involved in cell cycle regulation and DNA damage response.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Wright et al.identified a total of 19 loci associated with mLOY9, including TCL1A and other genes involved in cell cycle regulation and DNA damage response.		Wright et al.identified a total of 19 loci associated with mLOY9, including TCL1A and other genes involved in cell cycle regulation and DNA damage response.	Immunohistochemical staining	Wright et al.identified a total of 19 loci associated with mLOY9, including TCL1A and other genes involved in cell cycle regulation and DNA damage response.			Flow cytometry				TCL1A
31624086	chr6	45325657	45327657	RUNX2	RUNX2 is a mammalian RUNT-related transcription factor (TF) required during embryogenesis for skeletal development and for the morphogenesis of many organs such as breast and thy_x0002_roid (13, 14).	human,mouse	connective tissue	High+Lowthroughput	RAIN Is a Novel Enhancer-Associated lncRNA That Controls RUNX2 Expression and Promotes Breast and Thyroid Cancer	否	无	cancer	cancer cell	E_02_0179	Flow cytometry,PCR	RUNX2 is a mammalian RUNT-related transcription factor (TF) required during embryogenesis for skeletal development and for the morphogenesis of many organs such as breast and thy_x0002_roid (13, 14).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RUNX2 is a mammalian RUNT-related transcription factor (TF) required during embryogenesis for skeletal development and for the morphogenesis of many organs such as breast and thy_x0002_roid (13, 14).		RUNX2 is a mammalian RUNT-related transcription factor (TF) required during embryogenesis for skeletal development and for the morphogenesis of many organs such as breast and thy_x0002_roid (13, 14).	Immunohistochemical staining	RUNX2 is a mammalian RUNT-related transcription factor (TF) required during embryogenesis for skeletal development and for the morphogenesis of many organs such as breast and thy_x0002_roid (13, 14).			Flow cytometry,PCR				RUNX2
31623059	chr1	998360	1000360	ISG15	However, knockdown of lncRNA ISR had little effect on the expression of several ISGs, including myxovirus resistance protein A (MxA), Interferon-stimulated gene 15 (ISG15) and human 20-50-oligoadenylate synthetase 2 (OAS2) (Figure 3b).	human	blood	High+Lowthroughput	Identification of an Interferon-Stimulated Long Noncoding RNA (LncRNA ISR) Involved in Regulation of Influenza A Virus Replication	否	无	influenza	B cell	E_01_0217	PCR,Western blot	However, knockdown of lncRNA ISR had little effect on the expression of several ISGs, including myxovirus resistance protein A (MxA), Interferon-stimulated gene 15 (ISG15) and human 20-50-oligoadenylate synthetase 2 (OAS2) (Figure 3b).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, knockdown of lncRNA ISR had little effect on the expression of several ISGs, including myxovirus resistance protein A (MxA), Interferon-stimulated gene 15 (ISG15) and human 20-50-oligoadenylate synthetase 2 (OAS2) (Figure 3b).		However, knockdown of lncRNA ISR had little effect on the expression of several ISGs, including myxovirus resistance protein A (MxA), Interferon-stimulated gene 15 (ISG15) and human 20-50-oligoadenylate synthetase 2 (OAS2) (Figure 3b).	Immunohistochemical staining	However, knockdown of lncRNA ISR had little effect on the expression of several ISGs, including myxovirus resistance protein A (MxA), Interferon-stimulated gene 15 (ISG15) and human 20-50-oligoadenylate synthetase 2 (OAS2) (Figure 3b).			PCR,Western blot				ISG15
31622687	chr3	101825749	101827749	NFKBIZ	No alteration in NFKBIZ mRNA expression was observed in the PBMCs of the psoriatic patients during secukinumab treatment (Fig 3, B).	human	blood	High+Lowthroughput	IκBζ is a key player in the antipsoriatic effects of secukinumab	否	无	Psoriasis	B cell	E_01_0218	PCR,Western blot	No alteration in NFKBIZ mRNA expression was observed in the PBMCs of the psoriatic patients during secukinumab treatment (Fig 3, B).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	No alteration in NFKBIZ mRNA expression was observed in the PBMCs of the psoriatic patients during secukinumab treatment (Fig 3, B).		No alteration in NFKBIZ mRNA expression was observed in the PBMCs of the psoriatic patients during secukinumab treatment (Fig 3, B).	Immunohistochemical staining	No alteration in NFKBIZ mRNA expression was observed in the PBMCs of the psoriatic patients during secukinumab treatment (Fig 3, B).			PCR,Western blot				NFKBIZ
31621893	chr12	6531600	6533600	GAPDH	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	human	liver	High+Lowthroughput	Costunolide represses hepatic fibrosis through WW domain-containing protein 2-mediated Notch3 degradation	否	无		hepatic stellate cell	E_01_0219	PCR, Western blot, immunofluorescence staining	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	Immunohistochemical staining	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	GAPDH		PCR,Western blot,免疫荧光染色	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .			
31621893	chr6	125135892	125137892	Gapdh	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	human	kidney	High+Lowthroughput	Costunolide represses hepatic fibrosis through WW domain-containing protein 2-mediated Notch3 degradation	否	无		HEK293T	E_01_0219	PCR, Western blot, immunofluorescence staining	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .		The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .	Immunohistochemical staining	The GAPDH/Gapdh served as an internal control for mRNA expression. The fold change in target mRNA expression was calculated using the equation 2−ΔΔCt .			PCR,Western blot,免疫荧光染色				Gapdh
31621133	chr17	42310525	42312525	STAT3	Via CSF1‐R and CD138, IL‐34 promoted the proliferation and migration of hepatoma cells, and contributed to the activation of  ERK and STAT3 pathways and the upregulation of Bcl‐xl and c‐Myc mediated by HBX.	human	liver	High+Lowthroughput	Interleukin-34 mediated by hepatitis B virus X protein via CCAAT/enhancer-binding protein α contributes to the proliferation and migration of hepatoma cells	否	无	liver cancer	HCC cell	E_01_0220	PCR, gene knockdown, Western blot	Via CSF1‐R and CD138, IL‐34 promoted the proliferation and migration of hepatoma cells, and contributed to the activation of  ERK and STAT3 pathways and the upregulation of Bcl‐xl and c‐Myc mediated by HBX.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Via CSF1‐R and CD138, IL‐34 promoted the proliferation and migration of hepatoma cells, and contributed to the activation of  ERK and STAT3 pathways and the upregulation of Bcl‐xl and c‐Myc mediated by HBX.	Immunohistochemical staining	Via CSF1‐R and CD138, IL‐34 promoted the proliferation and migration of hepatoma cells, and contributed to the activation of  ERK and STAT3 pathways and the upregulation of Bcl‐xl and c‐Myc mediated by HBX.	STAT3		PCR,基因敲降,Western blot	Via CSF1‐R and CD138, IL‐34 promoted the proliferation and migration of hepatoma cells, and contributed to the activation of  ERK and STAT3 pathways and the upregulation of Bcl‐xl and c‐Myc mediated by HBX.			
31620967	chr12	6531445	6533445	GAPDH	Membranes were incubated with primary antibody solution diluted 1:1000 in 5% (w/v) nonfat dry milk in TBS-T (mouse anti-ATP synthase subunit beta, ab14730, Abcam; rabbit anti-GAPDH, ab9485, Abcam; rabbit anti-ETFDH, ab91508, Abcam;	mouse	heart	High+Lowthroughput	One year of exercise training promotes distinct adaptations in right and left ventricle of female Sprague-Dawley rats	否	无		Cardiac progenitor cell	E_02_0180	PCR,Western blot	Membranes were incubated with primary antibody solution diluted 1:1000 in 5% (w/v) nonfat dry milk in TBS-T (mouse anti-ATP synthase subunit beta, ab14730, Abcam; rabbit anti-GAPDH, ab9485, Abcam; rabbit anti-ETFDH, ab91508, Abcam;	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Membranes were incubated with primary antibody solution diluted 1:1000 in 5% (w/v) nonfat dry milk in TBS-T (mouse anti-ATP synthase subunit beta, ab14730, Abcam; rabbit anti-GAPDH, ab9485, Abcam; rabbit anti-ETFDH, ab91508, Abcam;		Membranes were incubated with primary antibody solution diluted 1:1000 in 5% (w/v) nonfat dry milk in TBS-T (mouse anti-ATP synthase subunit beta, ab14730, Abcam; rabbit anti-GAPDH, ab9485, Abcam; rabbit anti-ETFDH, ab91508, Abcam;	Immunohistochemical staining	Membranes were incubated with primary antibody solution diluted 1:1000 in 5% (w/v) nonfat dry milk in TBS-T (mouse anti-ATP synthase subunit beta, ab14730, Abcam; rabbit anti-GAPDH, ab9485, Abcam; rabbit anti-ETFDH, ab91508, Abcam;			PCR,Western blot				GAPDH
31619507	chr4	147635062	147637062	PRMT9	Increased expression of PRMT isoforms, for example, PRMT1, CARM1, PRMT5, PRMT6, and PRMT9, in several tumor types has been correlated with poor overall survival. 	human	lung	High+Lowthroughput	PRMT6 Promotes Lung Tumor Progression via the Alternate Activation of Tumor-Associated Macrophages	否	无	tumour	NSCLC cell	E_01_0221	PCR, gene knockdown, Western blot	Increased expression of PRMT isoforms, for example, PRMT1, CARM1, PRMT5, PRMT6, and PRMT9, in several tumor types has been correlated with poor overall survival. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Increased expression of PRMT isoforms, for example, PRMT1, CARM1, PRMT5, PRMT6, and PRMT9, in several tumor types has been correlated with poor overall survival. 		Increased expression of PRMT isoforms, for example, PRMT1, CARM1, PRMT5, PRMT6, and PRMT9, in several tumor types has been correlated with poor overall survival. 	Immunohistochemical staining	Increased expression of PRMT isoforms, for example, PRMT1, CARM1, PRMT5, PRMT6, and PRMT9, in several tumor types has been correlated with poor overall survival. 			PCR,基因敲降,Western blot				PRMT9
31619182	chr7	148804718	148806718	EZH2	In mammals, gain-of-function mutations as well as overexpression of EZH2 have been associated with several tumors, therefore making this subunit a suitable target for the development of selective inhibitors. Indeed, highly specific small-molecule inhibitors of EZH2 have been reported. In plants, mutations in some PRC2 components lead to embryonic lethality, but no trial with any inhibitor has ever been reported.	human	blood	High+Lowthroughput	Inhibition of Polycomb Repressive Complex 2 activity reduces trimethylation of H3K27 and affects development in Arabidopsis seedlings	否	无	leukemia	leukemic cell	E_01_0222	PCR, Western blot, immunofluorescence staining	In mammals, gain-of-function mutations as well as overexpression of EZH2 have been associated with several tumors, therefore making this subunit a suitable target for the development of selective inhibitors. Indeed, highly specific small-molecule inhibitors of EZH2 have been reported. In plants, mutations in some PRC2 components lead to embryonic lethality, but no trial with any inhibitor has ever been reported.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In mammals, gain-of-function mutations as well as overexpression of EZH2 have been associated with several tumors, therefore making this subunit a suitable target for the development of selective inhibitors. Indeed, highly specific small-molecule inhibitors of EZH2 have been reported. In plants, mutations in some PRC2 components lead to embryonic lethality, but no trial with any inhibitor has ever been reported.	Immunohistochemical staining	In mammals, gain-of-function mutations as well as overexpression of EZH2 have been associated with several tumors, therefore making this subunit a suitable target for the development of selective inhibitors. Indeed, highly specific small-molecule inhibitors of EZH2 have been reported. In plants, mutations in some PRC2 components lead to embryonic lethality, but no trial with any inhibitor has ever been reported.	EZH2		PCR,Western blot,免疫荧光染色	In mammals, gain-of-function mutations as well as overexpression of EZH2 have been associated with several tumors, therefore making this subunit a suitable target for the development of selective inhibitors. Indeed, highly specific small-molecule inhibitors of EZH2 have been reported. In plants, mutations in some PRC2 components lead to embryonic lethality, but no trial with any inhibitor has ever been reported.			
31618980	chr10	67881914	67883914	SIRT1	SIRT1 couples the deacetylation of various transcription factors and co- factors to the cleavage of NAD+, an indicator of cellular metabolic status, playing a vital role in metabolism, including fat storage, gluconeogenesis, fatty acid oxidation, lipogenesis, insulin secretion, food intake, circadian rhythm, and inflammation [40].	human	Musculature	High+Lowthroughput	Gynostemma Pentaphyllum Extract Ameliorates High-Fat Diet-Induced Obesity in C57BL/6N Mice by Upregulating SIRT1	否	无	Obesity	mouse cell of skeletal muscle	E_01_0223	PCR,Western blot	SIRT1 couples the deacetylation of various transcription factors and co- factors to the cleavage of NAD+, an indicator of cellular metabolic status, playing a vital role in metabolism, including fat storage, gluconeogenesis, fatty acid oxidation, lipogenesis, insulin secretion, food intake, circadian rhythm, and inflammation [40].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			SIRT1 couples the deacetylation of various transcription factors and co- factors to the cleavage of NAD+, an indicator of cellular metabolic status, playing a vital role in metabolism, including fat storage, gluconeogenesis, fatty acid oxidation, lipogenesis, insulin secretion, food intake, circadian rhythm, and inflammation [40].	Immunohistochemical staining	SIRT1 couples the deacetylation of various transcription factors and co- factors to the cleavage of NAD+, an indicator of cellular metabolic status, playing a vital role in metabolism, including fat storage, gluconeogenesis, fatty acid oxidation, lipogenesis, insulin secretion, food intake, circadian rhythm, and inflammation [40].	SIRT1		PCR,Western blot	SIRT1 couples the deacetylation of various transcription factors and co- factors to the cleavage of NAD+, an indicator of cellular metabolic status, playing a vital role in metabolism, including fat storage, gluconeogenesis, fatty acid oxidation, lipogenesis, insulin secretion, food intake, circadian rhythm, and inflammation [40].			
31618627	chr12	2956471	2958471	TEAD4	Here, we mapped DSBs at high resolution in cancer and non-tumorigenic cells and found a transcrip_x0002_tion-coupled repair mechanism at oncogeni super_x0002_enhancers. At these super-enhancers the transcrip_x0002_tion factor TEAD4, together with various transcription factors and co-factors, co-localizes with the repair factor RAD51 of the homologous recombination pathway.	human	connective tissue	High+Lowthroughput	Activation of Oncogenic Super-Enhancers Is Coupled with DNA Repair by RAD51	否	无	cancer		E_01_0224	PCR,Flow cytometry	Here, we mapped DSBs at high resolution in cancer and non-tumorigenic cells and found a transcrip_x0002_tion-coupled repair mechanism at oncogeni super_x0002_enhancers. At these super-enhancers the transcrip_x0002_tion factor TEAD4, together with various transcription factors and co-factors, co-localizes with the repair factor RAD51 of the homologous recombination pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we mapped DSBs at high resolution in cancer and non-tumorigenic cells and found a transcrip_x0002_tion-coupled repair mechanism at oncogeni super_x0002_enhancers. At these super-enhancers the transcrip_x0002_tion factor TEAD4, together with various transcription factors and co-factors, co-localizes with the repair factor RAD51 of the homologous recombination pathway.	Immunohistochemical staining	Here, we mapped DSBs at high resolution in cancer and non-tumorigenic cells and found a transcrip_x0002_tion-coupled repair mechanism at oncogeni super_x0002_enhancers. At these super-enhancers the transcrip_x0002_tion factor TEAD4, together with various transcription factors and co-factors, co-localizes with the repair factor RAD51 of the homologous recombination pathway.	TEAD4		PCR,Flow cytometry	Here, we mapped DSBs at high resolution in cancer and non-tumorigenic cells and found a transcrip_x0002_tion-coupled repair mechanism at oncogeni super_x0002_enhancers. At these super-enhancers the transcrip_x0002_tion factor TEAD4, together with various transcription factors and co-factors, co-localizes with the repair factor RAD51 of the homologous recombination pathway.			
31616042	chr16	54280654	54282654	IRX3	"The mechanism underlying the link between IRX3 and these conditions was since established using both 4-C and CRISPR-Cas9 based methods, which showed that
the SNP in the FTO region de-repressed IRX3 expression, leading to altered energy metabolism and increased lipid storage [18, 19]."	human	connective tissue	High+Lowthroughput	Understanding the genetics of neuropsychiatric disorders: the potential role of genomic regulatory blocks	是	rs75059851	tumour	tumor cell	E_01_0225	Flow cytometry	"The mechanism underlying the link between IRX3 and these conditions was since established using both 4-C and CRISPR-Cas9 based methods, which showed that
the SNP in the FTO region de-repressed IRX3 expression, leading to altered energy metabolism and increased lipid storage [18, 19]."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"The mechanism underlying the link between IRX3 and these conditions was since established using both 4-C and CRISPR-Cas9 based methods, which showed that
the SNP in the FTO region de-repressed IRX3 expression, leading to altered energy metabolism and increased lipid storage [18, 19]."		"The mechanism underlying the link between IRX3 and these conditions was since established using both 4-C and CRISPR-Cas9 based methods, which showed that
the SNP in the FTO region de-repressed IRX3 expression, leading to altered energy metabolism and increased lipid storage [18, 19]."	Immunohistochemical staining	"The mechanism underlying the link between IRX3 and these conditions was since established using both 4-C and CRISPR-Cas9 based methods, which showed that
the SNP in the FTO region de-repressed IRX3 expression, leading to altered energy metabolism and increased lipid storage [18, 19]."			Flow cytometry				IRX3
31616042	chr2	57904994	57906994	VRK2	A notable example of an SNP involved in long-range reg_x0002_ulation of gene expression is a locus obtained by merging two SNPs in LD, with two nearby VRK2 and FANCL genes highlighted as putative targets of these variants.	human	Nervous tissue	High+Lowthroughput	Understanding the genetics of neuropsychiatric disorders: the potential role of genomic regulatory blocks	是	rs10791097	Schizophrenia	neural cell	E_01_0225	Flow cytometry	A notable example of an SNP involved in long-range reg_x0002_ulation of gene expression is a locus obtained by merging two SNPs in LD, with two nearby VRK2 and FANCL genes highlighted as putative targets of these variants.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A notable example of an SNP involved in long-range reg_x0002_ulation of gene expression is a locus obtained by merging two SNPs in LD, with two nearby VRK2 and FANCL genes highlighted as putative targets of these variants.		A notable example of an SNP involved in long-range reg_x0002_ulation of gene expression is a locus obtained by merging two SNPs in LD, with two nearby VRK2 and FANCL genes highlighted as putative targets of these variants.	Immunohistochemical staining	A notable example of an SNP involved in long-range reg_x0002_ulation of gene expression is a locus obtained by merging two SNPs in LD, with two nearby VRK2 and FANCL genes highlighted as putative targets of these variants.			Flow cytometry				VRK2
31615896	chr17	39401537	39403537	MED1	In addition, other TFs and cofactors, such as KLFs, STAT5, PBX1, Krox20, AP1 , ATFs, GATA2/3 , TAF8 , and Mediator subunits (MED1, MED14 and NED23), have been reported to be involved in regulating either adipocyte commitment or differentiation in cell line and/or mouse models.	human	connective tissue	High+Lowthroughput	The transcription factor NKX1-2 promotes adipogenesis and may contribute to a balance between adipocyte and osteoblast differentiation	否	无	Thyroid cancer	ear mesenchymal stem cell	E_01_0226	Western blot,PCR	In addition, other TFs and cofactors, such as KLFs, STAT5, PBX1, Krox20, AP1 , ATFs, GATA2/3 , TAF8 , and Mediator subunits (MED1, MED14 and NED23), have been reported to be involved in regulating either adipocyte commitment or differentiation in cell line and/or mouse models.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, other TFs and cofactors, such as KLFs, STAT5, PBX1, Krox20, AP1 , ATFs, GATA2/3 , TAF8 , and Mediator subunits (MED1, MED14 and NED23), have been reported to be involved in regulating either adipocyte commitment or differentiation in cell line and/or mouse models.	Immunohistochemical staining	In addition, other TFs and cofactors, such as KLFs, STAT5, PBX1, Krox20, AP1 , ATFs, GATA2/3 , TAF8 , and Mediator subunits (MED1, MED14 and NED23), have been reported to be involved in regulating either adipocyte commitment or differentiation in cell line and/or mouse models.	MED1		Western blot,PCR	In addition, other TFs and cofactors, such as KLFs, STAT5, PBX1, Krox20, AP1 , ATFs, GATA2/3 , TAF8 , and Mediator subunits (MED1, MED14 and NED23), have been reported to be involved in regulating either adipocyte commitment or differentiation in cell line and/or mouse models.			
31615655	chr17	39458277	39460277	CDK12	CDK12 is a transcription-related CDK that complexes with cyclinK to regulate gene transcription [6]. CDK12 has been demonstrated to be essential for DNA damage response (DDR), mRNA processing, and differentiation [7e9]. Several recent studies also implicated CDK12 in cancer pathology [10,11].	human,mouse	thyroid	High+Lowthroughput	Targeting CDK12-mediated transcription regulation in anaplastic thyroid carcinoma	否	无	Anaplastic thyroid cancer	Anaplastic thyroid carcinoma cell	E_02_0181	PCR, Western blot, flow cytometry, immunofluorescence staining	CDK12 is a transcription-related CDK that complexes with cyclinK to regulate gene transcription [6]. CDK12 has been demonstrated to be essential for DNA damage response (DDR), mRNA processing, and differentiation [7e9]. Several recent studies also implicated CDK12 in cancer pathology [10,11].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CDK12 is a transcription-related CDK that complexes with cyclinK to regulate gene transcription [6]. CDK12 has been demonstrated to be essential for DNA damage response (DDR), mRNA processing, and differentiation [7e9]. Several recent studies also implicated CDK12 in cancer pathology [10,11].		CDK12 is a transcription-related CDK that complexes with cyclinK to regulate gene transcription [6]. CDK12 has been demonstrated to be essential for DNA damage response (DDR), mRNA processing, and differentiation [7e9]. Several recent studies also implicated CDK12 in cancer pathology [10,11].	Immunohistochemical staining	CDK12 is a transcription-related CDK that complexes with cyclinK to regulate gene transcription [6]. CDK12 has been demonstrated to be essential for DNA damage response (DDR), mRNA processing, and differentiation [7e9]. Several recent studies also implicated CDK12 in cancer pathology [10,11].			PCR,Western blot,Flow cytometry,免疫荧光染色				CDK12
31615341	chr1	204393890	204395890	PPP1R15B	However, levels of TGFβR1 did not show any change and therefore is possibly not a direct target of miR-98-5p. miR-98-5p also significantly decreased the mRNA levels of PPP1R15B (Figure 3(b)) further suggesting that this gene is targeted by miR-98-5p.	human,mouse	Epithelial tissues	High+Lowthroughput	Circulatory miR-98-5p levels are deregulated during diabetes and it inhibits proliferation and promotes apoptosis by targeting PPP1R15B in keratinocytes	否	无	diabetes	HaCaT cell	E_02_0182	Flow cytometry,PCR,Western blot	However, levels of TGFβR1 did not show any change and therefore is possibly not a direct target of miR-98-5p. miR-98-5p also significantly decreased the mRNA levels of PPP1R15B (Figure 3(b)) further suggesting that this gene is targeted by miR-98-5p.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, levels of TGFβR1 did not show any change and therefore is possibly not a direct target of miR-98-5p. miR-98-5p also significantly decreased the mRNA levels of PPP1R15B (Figure 3(b)) further suggesting that this gene is targeted by miR-98-5p.		However, levels of TGFβR1 did not show any change and therefore is possibly not a direct target of miR-98-5p. miR-98-5p also significantly decreased the mRNA levels of PPP1R15B (Figure 3(b)) further suggesting that this gene is targeted by miR-98-5p.	Immunohistochemical staining	However, levels of TGFβR1 did not show any change and therefore is possibly not a direct target of miR-98-5p. miR-98-5p also significantly decreased the mRNA levels of PPP1R15B (Figure 3(b)) further suggesting that this gene is targeted by miR-98-5p.			Flow cytometry,PCR,Western blot				PPP1R15B
31614133	chr5	88713906	88715906	MEF2C	Additionally, chromatin immunoprecipitation experiments and luciferase assays confirmed MEF2C interaction and direct binding of the CAIII promoter between -416 to -200 base pair.	human,mouse	Musculature	High+Lowthroughput	CAIII expression in skeletal muscle is regulated by Ca(2+)-CaMKII-MEF2C signaling	否	无		mouse cell of skeletal muscle	E_02_0183	PCR,Western blot	Additionally, chromatin immunoprecipitation experiments and luciferase assays confirmed MEF2C interaction and direct binding of the CAIII promoter between -416 to -200 base pair.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, chromatin immunoprecipitation experiments and luciferase assays confirmed MEF2C interaction and direct binding of the CAIII promoter between -416 to -200 base pair.		Additionally, chromatin immunoprecipitation experiments and luciferase assays confirmed MEF2C interaction and direct binding of the CAIII promoter between -416 to -200 base pair.	Immunohistochemical staining	Additionally, chromatin immunoprecipitation experiments and luciferase assays confirmed MEF2C interaction and direct binding of the CAIII promoter between -416 to -200 base pair.			PCR,Western blot				MEF2C
31614133	chr15	99563007	99565007	MEF2A	Therefore, we evaluated the role of different MEF2 homologs in CAIII expression. Plasmids containing RNAi sequences targeting MEF2A, MEF2C, and MEF2D were transfected into C2C12 cells, and CAIII expression was evaluated. 	human,mouse	Musculature	High+Lowthroughput	CAIII expression in skeletal muscle is regulated by Ca(2+)-CaMKII-MEF2C signaling	否	无		C2C12 cell	E_02_0183	PCR,Western blot	Therefore, we evaluated the role of different MEF2 homologs in CAIII expression. Plasmids containing RNAi sequences targeting MEF2A, MEF2C, and MEF2D were transfected into C2C12 cells, and CAIII expression was evaluated. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, we evaluated the role of different MEF2 homologs in CAIII expression. Plasmids containing RNAi sequences targeting MEF2A, MEF2C, and MEF2D were transfected into C2C12 cells, and CAIII expression was evaluated. 		Therefore, we evaluated the role of different MEF2 homologs in CAIII expression. Plasmids containing RNAi sequences targeting MEF2A, MEF2C, and MEF2D were transfected into C2C12 cells, and CAIII expression was evaluated. 	Immunohistochemical staining	Therefore, we evaluated the role of different MEF2 homologs in CAIII expression. Plasmids containing RNAi sequences targeting MEF2A, MEF2C, and MEF2D were transfected into C2C12 cells, and CAIII expression was evaluated. 			PCR,Western blot				MEF2A
31610176	chr6	131945597	131947597	CCN2	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	human	connective tissue	High+Lowthroughput	Insights into Fibroblast Plasticity: Cellular Communication Network 2 Is Required for Activation of Cancer-Associated Fibroblasts in a Murine Model of Melanoma	否	无	tumour	melanoma cells	E_01_0227	Flow cytometry,PCR,Western blot	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	Immunohistochemical staining	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	CCN2		Flow cytometry,PCR,Western blot	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.			
31610176	chr3	34702118	34704118	Sox2	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	human	connective tissue	High+Lowthroughput	Insights into Fibroblast Plasticity: Cellular Communication Network 2 Is Required for Activation of Cancer-Associated Fibroblasts in a Murine Model of Melanoma	否	无	tumour	stem cell	E_01_0227	Flow cytometry,PCR,Western blot	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.		Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.	Immunohistochemical staining	Conversely, fibroblast activation was impaired in mice with a fibroblast-specific deletion of Ccn2, associated with reduced expression of alpha-smooth muscle actin and Sox2.			Flow cytometry,PCR,Western blot				Sox2
31610176	chr7	140716436	140718436	BRAF	Although drugs, including those targeting specific mutations (eg, in BRAF) and checkpoint inhibitors, have been discovered that can retard melanoma progression in some patients, ultimately patients develop resistance to these regimens.	human	connective tissue	High+Lowthroughput	Insights into Fibroblast Plasticity: Cellular Communication Network 2 Is Required for Activation of Cancer-Associated Fibroblasts in a Murine Model of Melanoma	否	无	tumour	tumor cell	E_01_0227	Flow cytometry,PCR,Western blot	Although drugs, including those targeting specific mutations (eg, in BRAF) and checkpoint inhibitors, have been discovered that can retard melanoma progression in some patients, ultimately patients develop resistance to these regimens.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Although drugs, including those targeting specific mutations (eg, in BRAF) and checkpoint inhibitors, have been discovered that can retard melanoma progression in some patients, ultimately patients develop resistance to these regimens.	Immunohistochemical staining	Although drugs, including those targeting specific mutations (eg, in BRAF) and checkpoint inhibitors, have been discovered that can retard melanoma progression in some patients, ultimately patients develop resistance to these regimens.	BRAF		Flow cytometry,PCR,Western blot	Although drugs, including those targeting specific mutations (eg, in BRAF) and checkpoint inhibitors, have been discovered that can retard melanoma progression in some patients, ultimately patients develop resistance to these regimens.			
31610176	chr8	76678526	76680526	ZFHX4	This resulted in a 9-gene score composed of the following genes: ZFHX4, DCN, ITGA11, COL6A3, COL1A1, ITGBL1, COL8A1, INHBA, and, MEG3. CAF-specific CCN2 scores were dichotimized with 13 receiver operating characteristics (ROC) curves to determine the optimal cutoff for the endpoint of overall survival censorship.	human	connective tissue	High+Lowthroughput	Insights into Fibroblast Plasticity: Cellular Communication Network 2 Is Required for Activation of Cancer-Associated Fibroblasts in a Murine Model of Melanoma	否	无	tumour	dermal progenitor cell	E_01_0227	Flow cytometry,PCR,Western blot	This resulted in a 9-gene score composed of the following genes: ZFHX4, DCN, ITGA11, COL6A3, COL1A1, ITGBL1, COL8A1, INHBA, and, MEG3. CAF-specific CCN2 scores were dichotimized with 13 receiver operating characteristics (ROC) curves to determine the optimal cutoff for the endpoint of overall survival censorship.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This resulted in a 9-gene score composed of the following genes: ZFHX4, DCN, ITGA11, COL6A3, COL1A1, ITGBL1, COL8A1, INHBA, and, MEG3. CAF-specific CCN2 scores were dichotimized with 13 receiver operating characteristics (ROC) curves to determine the optimal cutoff for the endpoint of overall survival censorship.		This resulted in a 9-gene score composed of the following genes: ZFHX4, DCN, ITGA11, COL6A3, COL1A1, ITGBL1, COL8A1, INHBA, and, MEG3. CAF-specific CCN2 scores were dichotimized with 13 receiver operating characteristics (ROC) curves to determine the optimal cutoff for the endpoint of overall survival censorship.	Immunohistochemical staining	This resulted in a 9-gene score composed of the following genes: ZFHX4, DCN, ITGA11, COL6A3, COL1A1, ITGBL1, COL8A1, INHBA, and, MEG3. CAF-specific CCN2 scores were dichotimized with 13 receiver operating characteristics (ROC) curves to determine the optimal cutoff for the endpoint of overall survival censorship.			Flow cytometry,PCR,Western blot				ZFHX4
31608710	chr1	173855753	173857753	GAS5	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	human	eye	High+Lowthroughput	Silencing of GAS5 Alleviates Glaucoma in Rat Models by Reducing Retinal Ganglion Cell Apoptosis	否	无	glaucoma	retinal ganglion cell	E_01_0228	PCR, Western blot, immunofluorescence light staining, flow cytometry	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	Immunohistochemical staining	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	GAS5		PCR,Western blot,免疫荧光光染色,Flow cytometry	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.			
31608710	chr7	148804386	148806386	EZH2	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	human	kidney	High+Lowthroughput	Silencing of GAS5 Alleviates Glaucoma in Rat Models by Reducing Retinal Ganglion Cell Apoptosis	否	无	glaucoma	HEK293 cell	E_01_0228	PCR, Western blot, immunofluorescence light staining, flow cytometry	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	Immunohistochemical staining	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.	EZH2		PCR,Western blot,免疫荧光光染色,Flow cytometry	The overexpression vector or short hairpin RNA for GAS5 or enhancer of zeste homolog 2 (EZH2) were transfected into RGCs after in vitro pressurization culture to exam the function of GAS5 in RGC apoptosis.			
31608710	chr9	104778194	104780194	ABCA1	In addition, up-regulation of EZH2 promoted trimethylation of lysine 27 on histone H3, therefore suppressing ABCA1 expression, eventually leading to the inhibition of RGC apoptosis.	human	connective tissue	High+Lowthroughput	Silencing of GAS5 Alleviates Glaucoma in Rat Models by Reducing Retinal Ganglion Cell Apoptosis	否	无	glaucoma	neuroblastoma cell	E_01_0228	PCR, Western blot, immunofluorescence light staining, flow cytometry	In addition, up-regulation of EZH2 promoted trimethylation of lysine 27 on histone H3, therefore suppressing ABCA1 expression, eventually leading to the inhibition of RGC apoptosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, up-regulation of EZH2 promoted trimethylation of lysine 27 on histone H3, therefore suppressing ABCA1 expression, eventually leading to the inhibition of RGC apoptosis.		In addition, up-regulation of EZH2 promoted trimethylation of lysine 27 on histone H3, therefore suppressing ABCA1 expression, eventually leading to the inhibition of RGC apoptosis.	Immunohistochemical staining	In addition, up-regulation of EZH2 promoted trimethylation of lysine 27 on histone H3, therefore suppressing ABCA1 expression, eventually leading to the inhibition of RGC apoptosis.			PCR,Western blot,免疫荧光光染色,Flow cytometry				ABCA1
31608546	chr6	88136910	88138910	CNR1	Previous studies have shown that the coding regions of the CNR1 gene, that encodes CB1, lack common non-synonymous polymorphisms that might account for differences in cannabinoid response.	human	connective tissue	High+Lowthroughput	Disease-associated polymorphisms within the conserved ECR1 enhancer differentially regulate the tissue-specific activity of the cannabinoid-1 receptor gene promoter; implications for cannabinoid pharmacogenetics	是	rs2023239	Obesity	SH-SY5Y (human neuroblastoma cell)	E_01_0229	PCR immunofluorescence staining	Previous studies have shown that the coding regions of the CNR1 gene, that encodes CB1, lack common non-synonymous polymorphisms that might account for differences in cannabinoid response.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Previous studies have shown that the coding regions of the CNR1 gene, that encodes CB1, lack common non-synonymous polymorphisms that might account for differences in cannabinoid response.		Previous studies have shown that the coding regions of the CNR1 gene, that encodes CB1, lack common non-synonymous polymorphisms that might account for differences in cannabinoid response.	Immunohistochemical staining	Previous studies have shown that the coding regions of the CNR1 gene, that encodes CB1, lack common non-synonymous polymorphisms that might account for differences in cannabinoid response.			PCR免疫荧光染色				CNR1
31606392	chr1	247413593	247415593	NLRP3	Several experiments have confirmed that changes in intracellular ion concentration and the content of reactive oxygen species (ROS) play an important role in the activation of the NLRP3 inflammasome, while inhibition of Ca2+ inflow/K+ outflow and decreased ROS production can block the activation of NLRP3 to a certain extent [18-21].	human,mouse	blood	High+Lowthroughput	Nickel-refining fumes induce NLRP3 activation dependent on mitochondrial damage and ROS production in Beas-2B cells	否	无	inflammation	B cell	E_02_0184	PCR, Western blot, immunofluorescence staining	Several experiments have confirmed that changes in intracellular ion concentration and the content of reactive oxygen species (ROS) play an important role in the activation of the NLRP3 inflammasome, while inhibition of Ca2+ inflow/K+ outflow and decreased ROS production can block the activation of NLRP3 to a certain extent [18-21].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Several experiments have confirmed that changes in intracellular ion concentration and the content of reactive oxygen species (ROS) play an important role in the activation of the NLRP3 inflammasome, while inhibition of Ca2+ inflow/K+ outflow and decreased ROS production can block the activation of NLRP3 to a certain extent [18-21].		Several experiments have confirmed that changes in intracellular ion concentration and the content of reactive oxygen species (ROS) play an important role in the activation of the NLRP3 inflammasome, while inhibition of Ca2+ inflow/K+ outflow and decreased ROS production can block the activation of NLRP3 to a certain extent [18-21].	Immunohistochemical staining	Several experiments have confirmed that changes in intracellular ion concentration and the content of reactive oxygen species (ROS) play an important role in the activation of the NLRP3 inflammasome, while inhibition of Ca2+ inflow/K+ outflow and decreased ROS production can block the activation of NLRP3 to a certain extent [18-21].			PCR,Western blot,免疫荧光染色				NLRP3
31606247	chr16	30955158	30957158	SETD1A	Our findings advance understanding of how SETD1A mutations predispose to schizophrenia (SCZ) and point to novel therapeutic interventions.	human	Nervous tissue	High+Lowthroughput	Recapitulation and Reversal of Schizophrenia-Related Phenotypes in Setd1a-Deficient Mice	是	无	Schizophrenia	neural progenitor cell	E_01_0230	Flow cytometry, PCR, immunofluorescence staining, Western blot	Our findings advance understanding of how SETD1A mutations predispose to schizophrenia (SCZ) and point to novel therapeutic interventions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our findings advance understanding of how SETD1A mutations predispose to schizophrenia (SCZ) and point to novel therapeutic interventions.		Our findings advance understanding of how SETD1A mutations predispose to schizophrenia (SCZ) and point to novel therapeutic interventions.	Immunohistochemical staining	Our findings advance understanding of how SETD1A mutations predispose to schizophrenia (SCZ) and point to novel therapeutic interventions.			Flow cytometry,PCR,免疫荧光染色,Western blot				SETD1A
31605138	chr9	21964977	21966977	CDKN2A	The existence of genetic risk factors common to NB and CMM has been suggested by the finding of the loss of function mutation E27X in CDKN2A in melanoma families who display NB (7).	human	blood	High+Lowthroughput	Neural crest-derived tumor neuroblastoma and melanoma share 1p13.2 as susceptibility locus that shows a long-range interaction with the SLC16A1 gene	是	rs2153977	cancer		E_01_0231	Flow cytometry,PCR,Western blot	The existence of genetic risk factors common to NB and CMM has been suggested by the finding of the loss of function mutation E27X in CDKN2A in melanoma families who display NB (7).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The existence of genetic risk factors common to NB and CMM has been suggested by the finding of the loss of function mutation E27X in CDKN2A in melanoma families who display NB (7).	Immunohistochemical staining	The existence of genetic risk factors common to NB and CMM has been suggested by the finding of the loss of function mutation E27X in CDKN2A in melanoma families who display NB (7).	CDKN2A		Flow cytometry,PCR,Western blot	The existence of genetic risk factors common to NB and CMM has been suggested by the finding of the loss of function mutation E27X in CDKN2A in melanoma families who display NB (7).			
31601918	chr7	44101861	44103861	AEBP1	We had observed earlier that adipocyte enhancer binding protein 1 (AEBP1) expression to be up-regulated in primary GBMs as opposed to progressive secondary GBMs through transcriptome analysis1 .	human,mouse	Nervous tissue	High+Lowthroughput	AEBP1 down regulation induced cell death pathway depends on PTEN status of glioma cells	否	无	tumour	glioma cell	E_02_0185	PCR, Western blot, immunofluorescence light staining, flow cytometry	We had observed earlier that adipocyte enhancer binding protein 1 (AEBP1) expression to be up-regulated in primary GBMs as opposed to progressive secondary GBMs through transcriptome analysis1 .	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We had observed earlier that adipocyte enhancer binding protein 1 (AEBP1) expression to be up-regulated in primary GBMs as opposed to progressive secondary GBMs through transcriptome analysis1 .		We had observed earlier that adipocyte enhancer binding protein 1 (AEBP1) expression to be up-regulated in primary GBMs as opposed to progressive secondary GBMs through transcriptome analysis1 .	Immunohistochemical staining	We had observed earlier that adipocyte enhancer binding protein 1 (AEBP1) expression to be up-regulated in primary GBMs as opposed to progressive secondary GBMs through transcriptome analysis1 .			PCR,Western blot,免疫荧光光染色,Flow cytometry				AEBP1
31601151	chr11	35136538	35138538	CD44	The expression levels of ASCs markers CD44, SMA, and Vimentin were decreased dur_x0002_ing the differentiation process (Figure 2(Ea–c)).	human,mouse	connective tissue	High+Lowthroughput	Cl- channels regulate lipid droplet formation via Rab8a expression during adipocyte differentiation	否	无		stem cell	E_02_0186	PCR, flow cytometry, Western blot, immunofluorescence staining	The expression levels of ASCs markers CD44, SMA, and Vimentin were decreased dur_x0002_ing the differentiation process (Figure 2(Ea–c)).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression levels of ASCs markers CD44, SMA, and Vimentin were decreased dur_x0002_ing the differentiation process (Figure 2(Ea–c)).		The expression levels of ASCs markers CD44, SMA, and Vimentin were decreased dur_x0002_ing the differentiation process (Figure 2(Ea–c)).	Immunohistochemical staining	The expression levels of ASCs markers CD44, SMA, and Vimentin were decreased dur_x0002_ing the differentiation process (Figure 2(Ea–c)).			PCR,Flow cytometry,Western blot,免疫荧光染色				CD44
31601151	chr1	11854664	11856664	NPPB	The morphology of the differentiated cells treated with NPPB was similar to that of those untreated with NPPB (Figure 3(Aa and b)).	human,mouse	connective tissue	High+Lowthroughput	Cl- channels regulate lipid droplet formation via Rab8a expression during adipocyte differentiation	否	无		3T3-L1 cell	E_02_0186	PCR, flow cytometry, Western blot, immunofluorescence staining	The morphology of the differentiated cells treated with NPPB was similar to that of those untreated with NPPB (Figure 3(Aa and b)).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The morphology of the differentiated cells treated with NPPB was similar to that of those untreated with NPPB (Figure 3(Aa and b)).		The morphology of the differentiated cells treated with NPPB was similar to that of those untreated with NPPB (Figure 3(Aa and b)).	Immunohistochemical staining	The morphology of the differentiated cells treated with NPPB was similar to that of those untreated with NPPB (Figure 3(Aa and b)).			PCR,Flow cytometry,Western blot,免疫荧光染色				NPPB
31599948	chr12	4365800	4367800	FGF23	Fibroblast growth factor 23 (FGF23) is a newly dis_x0002_covered member of the endocrine subfamily of sys_x0002_temic FGF hormones that in humans include FGF19 and FGF21 (1, 2).	human	Epithelial tissues	High+Lowthroughput	A Control Region Near the Fibroblast Growth Factor 23 Gene Mediates Response to Phosphate, 1,25(OH)2D3, and LPS In Vivo	否	无	cancer	epithelial cell	E_01_0232	PCR 	Fibroblast growth factor 23 (FGF23) is a newly dis_x0002_covered member of the endocrine subfamily of sys_x0002_temic FGF hormones that in humans include FGF19 and FGF21 (1, 2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Fibroblast growth factor 23 (FGF23) is a newly dis_x0002_covered member of the endocrine subfamily of sys_x0002_temic FGF hormones that in humans include FGF19 and FGF21 (1, 2).		Fibroblast growth factor 23 (FGF23) is a newly dis_x0002_covered member of the endocrine subfamily of sys_x0002_temic FGF hormones that in humans include FGF19 and FGF21 (1, 2).	Immunohistochemical staining	Fibroblast growth factor 23 (FGF23) is a newly dis_x0002_covered member of the endocrine subfamily of sys_x0002_temic FGF hormones that in humans include FGF19 and FGF21 (1, 2).			PCR 				FGF23
31599948	chr20	54150645	54152645	CYP24A1	Accordingly, FGF23 has been shown to inhibit both the synthesis and se_x0002_cretion of PTH and to suppress CYP27B1 while induc_x0002_ing CYP24A1, the renal enzymes responsible for the synthesis and homeostatic maintenance of circulating 1,25(OH)2D3.	human	blood	High+Lowthroughput	A Control Region Near the Fibroblast Growth Factor 23 Gene Mediates Response to Phosphate, 1,25(OH)2D3, and LPS In Vivo	否	无	cancer	T cell	E_01_0232	PCR 	Accordingly, FGF23 has been shown to inhibit both the synthesis and se_x0002_cretion of PTH and to suppress CYP27B1 while induc_x0002_ing CYP24A1, the renal enzymes responsible for the synthesis and homeostatic maintenance of circulating 1,25(OH)2D3.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Accordingly, FGF23 has been shown to inhibit both the synthesis and se_x0002_cretion of PTH and to suppress CYP27B1 while induc_x0002_ing CYP24A1, the renal enzymes responsible for the synthesis and homeostatic maintenance of circulating 1,25(OH)2D3.		Accordingly, FGF23 has been shown to inhibit both the synthesis and se_x0002_cretion of PTH and to suppress CYP27B1 while induc_x0002_ing CYP24A1, the renal enzymes responsible for the synthesis and homeostatic maintenance of circulating 1,25(OH)2D3.	Immunohistochemical staining	Accordingly, FGF23 has been shown to inhibit both the synthesis and se_x0002_cretion of PTH and to suppress CYP27B1 while induc_x0002_ing CYP24A1, the renal enzymes responsible for the synthesis and homeostatic maintenance of circulating 1,25(OH)2D3.			PCR 				CYP24A1
31599948	chr10	126881570	126883570	Cyp27b1	Be_x0002_cause both PTH and 1,25(OH)2D3 also modulate P homeostasis and PTH represents a primary inducer of the Cyp27b1 gene (11, 14, 15), these activities of FGF23 constitute key negative feedback loops that serve to limit the activity of both hormones in the target tissues de_x0002_scribed previously.	human	bone	High+Lowthroughput	A Control Region Near the Fibroblast Growth Factor 23 Gene Mediates Response to Phosphate, 1,25(OH)2D3, and LPS In Vivo	否	无	cancer	osteocyte	E_01_0232	PCR 	Be_x0002_cause both PTH and 1,25(OH)2D3 also modulate P homeostasis and PTH represents a primary inducer of the Cyp27b1 gene (11, 14, 15), these activities of FGF23 constitute key negative feedback loops that serve to limit the activity of both hormones in the target tissues de_x0002_scribed previously.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Be_x0002_cause both PTH and 1,25(OH)2D3 also modulate P homeostasis and PTH represents a primary inducer of the Cyp27b1 gene (11, 14, 15), these activities of FGF23 constitute key negative feedback loops that serve to limit the activity of both hormones in the target tissues de_x0002_scribed previously.		Be_x0002_cause both PTH and 1,25(OH)2D3 also modulate P homeostasis and PTH represents a primary inducer of the Cyp27b1 gene (11, 14, 15), these activities of FGF23 constitute key negative feedback loops that serve to limit the activity of both hormones in the target tissues de_x0002_scribed previously.	Immunohistochemical staining	Be_x0002_cause both PTH and 1,25(OH)2D3 also modulate P homeostasis and PTH represents a primary inducer of the Cyp27b1 gene (11, 14, 15), these activities of FGF23 constitute key negative feedback loops that serve to limit the activity of both hormones in the target tissues de_x0002_scribed previously.			PCR 				Cyp27b1
31598701	chr7	55016371	55018371	EGFR	Other relevant genes such as EGFR and BCL-X, also known to be regulated by pro_x0002_gestins (56,64) exhibited a similar transcriptional activity in response to R5020 in both cell lines (Supplementary Figure S4B), pointing to a gene-specific GR-PR modulation.	human,mouse	breast	High+Lowthroughput	Exogenous pyruvate represses histone gene expression and inhibits cancer cell proliferation via the NAMPT-NAD+-SIRT1 pathway	否	无	mammary cancer	breast cancer cell	E_02_0187	PCR,Flow cytometry,Western blot	Other relevant genes such as EGFR and BCL-X, also known to be regulated by pro_x0002_gestins (56,64) exhibited a similar transcriptional activity in response to R5020 in both cell lines (Supplementary Figure S4B), pointing to a gene-specific GR-PR modulation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Other relevant genes such as EGFR and BCL-X, also known to be regulated by pro_x0002_gestins (56,64) exhibited a similar transcriptional activity in response to R5020 in both cell lines (Supplementary Figure S4B), pointing to a gene-specific GR-PR modulation.		Other relevant genes such as EGFR and BCL-X, also known to be regulated by pro_x0002_gestins (56,64) exhibited a similar transcriptional activity in response to R5020 in both cell lines (Supplementary Figure S4B), pointing to a gene-specific GR-PR modulation.	Immunohistochemical staining	Other relevant genes such as EGFR and BCL-X, also known to be regulated by pro_x0002_gestins (56,64) exhibited a similar transcriptional activity in response to R5020 in both cell lines (Supplementary Figure S4B), pointing to a gene-specific GR-PR modulation.			PCR,Flow cytometry,Western blot				EGFR
31595632	chr12	6531857	6533857	GAPDH	The RNA concentration was detected by a microplate reader, and RNA was reverse transcribed to cDNA using the QIAGEN miRNA reverse transcription (miScript II RT Kit) and Thermo reverse transcription kits. Using cDNA as a template, the gene expression of U6, miR-326, C/EBPα, PPARγ, and GAPDH was detected by qPCR.	human	connective tissue	High+Lowthroughput	The Role of miR-326 in Adipogenic Differentiation of Human Adipose-Derived Stem Cells by Targeting C/EBPα in vitro	否	无	Obesity	mesenchymal stem cell	E_01_0233	PCR, Western blot	The RNA concentration was detected by a microplate reader, and RNA was reverse transcribed to cDNA using the QIAGEN miRNA reverse transcription (miScript II RT Kit) and Thermo reverse transcription kits. Using cDNA as a template, the gene expression of U6, miR-326, C/EBPα, PPARγ, and GAPDH was detected by qPCR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The RNA concentration was detected by a microplate reader, and RNA was reverse transcribed to cDNA using the QIAGEN miRNA reverse transcription (miScript II RT Kit) and Thermo reverse transcription kits. Using cDNA as a template, the gene expression of U6, miR-326, C/EBPα, PPARγ, and GAPDH was detected by qPCR.	Immunohistochemical staining	The RNA concentration was detected by a microplate reader, and RNA was reverse transcribed to cDNA using the QIAGEN miRNA reverse transcription (miScript II RT Kit) and Thermo reverse transcription kits. Using cDNA as a template, the gene expression of U6, miR-326, C/EBPα, PPARγ, and GAPDH was detected by qPCR.	GAPDH		PCR, Western blot	The RNA concentration was detected by a microplate reader, and RNA was reverse transcribed to cDNA using the QIAGEN miRNA reverse transcription (miScript II RT Kit) and Thermo reverse transcription kits. Using cDNA as a template, the gene expression of U6, miR-326, C/EBPα, PPARγ, and GAPDH was detected by qPCR.			
31592235	chr12	57744934	57746934	CDK4	Not only cyclin-dependent kinase (CDK) 1 and phosphorylated forkhead box protein (FOX) O1 but also CDK4, CDK6 and phosphorylated retinoblastoma-associated protein (RB) had similar increase trends, so did epidermal growth factor receptor (EGFR), AKT serine/threonine kinase (AKT), and their respective phosphorylation levels.	mouse	Musculature	High+Lowthroughput	P21 and P27 promote tumorigenesis and progression via cell cycle acceleration in seminal vesicles of TRAMP mice	否	无	prostatic cancer	smooth muscle cell	E_02_0188	Western blot	Not only cyclin-dependent kinase (CDK) 1 and phosphorylated forkhead box protein (FOX) O1 but also CDK4, CDK6 and phosphorylated retinoblastoma-associated protein (RB) had similar increase trends, so did epidermal growth factor receptor (EGFR), AKT serine/threonine kinase (AKT), and their respective phosphorylation levels.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Not only cyclin-dependent kinase (CDK) 1 and phosphorylated forkhead box protein (FOX) O1 but also CDK4, CDK6 and phosphorylated retinoblastoma-associated protein (RB) had similar increase trends, so did epidermal growth factor receptor (EGFR), AKT serine/threonine kinase (AKT), and their respective phosphorylation levels.		Not only cyclin-dependent kinase (CDK) 1 and phosphorylated forkhead box protein (FOX) O1 but also CDK4, CDK6 and phosphorylated retinoblastoma-associated protein (RB) had similar increase trends, so did epidermal growth factor receptor (EGFR), AKT serine/threonine kinase (AKT), and their respective phosphorylation levels.	Immunohistochemical staining	Not only cyclin-dependent kinase (CDK) 1 and phosphorylated forkhead box protein (FOX) O1 but also CDK4, CDK6 and phosphorylated retinoblastoma-associated protein (RB) had similar increase trends, so did epidermal growth factor receptor (EGFR), AKT serine/threonine kinase (AKT), and their respective phosphorylation levels.			Western blot				CDK4
31592235	chr7	55016191	55018191	EGFR	The results indicated that EGFR, AKT, STAT3, and EZH2 all play a crucial role in promoting cell proliferation and tumor growth in seminal vesicles of TRAMP mice.	mouse	connective tissue	High+Lowthroughput	P21 and P27 promote tumorigenesis and progression via cell cycle acceleration in seminal vesicles of TRAMP mice	否	无	tumour	tumor cell	E_02_0188	Western blot	The results indicated that EGFR, AKT, STAT3, and EZH2 all play a crucial role in promoting cell proliferation and tumor growth in seminal vesicles of TRAMP mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The results indicated that EGFR, AKT, STAT3, and EZH2 all play a crucial role in promoting cell proliferation and tumor growth in seminal vesicles of TRAMP mice.		The results indicated that EGFR, AKT, STAT3, and EZH2 all play a crucial role in promoting cell proliferation and tumor growth in seminal vesicles of TRAMP mice.	Immunohistochemical staining	The results indicated that EGFR, AKT, STAT3, and EZH2 all play a crucial role in promoting cell proliferation and tumor growth in seminal vesicles of TRAMP mice.			Western blot				EGFR
31592229	chr7	148804549	148806549	EZH2	In our previous study, we have demonstrated that circular RNA circEZH2 was down-regulated during TGEV infection and promoted the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) via targeting miR-22 in porcine intestinal epithelial cell line (IPEC-J2).	human,Pig	intestine	High+Lowthroughput	Circular RNA CircEZH2 Suppresses Transmissible Gastroenteritis Coronavirus-induced Opening of Mitochondrial Permeability Transition Pore via Targeting MiR-22 in IPEC-J2	否	无	Infectious gastroenteritis	porcine intestinal epthelial cell	E_02_0189	Western blot, flow cytometry, PCR, immunofluorescence staining	In our previous study, we have demonstrated that circular RNA circEZH2 was down-regulated during TGEV infection and promoted the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) via targeting miR-22 in porcine intestinal epithelial cell line (IPEC-J2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In our previous study, we have demonstrated that circular RNA circEZH2 was down-regulated during TGEV infection and promoted the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) via targeting miR-22 in porcine intestinal epithelial cell line (IPEC-J2).		In our previous study, we have demonstrated that circular RNA circEZH2 was down-regulated during TGEV infection and promoted the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) via targeting miR-22 in porcine intestinal epithelial cell line (IPEC-J2).	Immunohistochemical staining	In our previous study, we have demonstrated that circular RNA circEZH2 was down-regulated during TGEV infection and promoted the activation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) via targeting miR-22 in porcine intestinal epithelial cell line (IPEC-J2).			Western blot,Flow cytometry,PCR,免疫荧光染色				EZH2
31592229	chr10	74821853	74823853	KAT6B	miR-22 has a strong correlation with NF-κB pathway and mitochondrial damage. Recently, it was reported that miR-22 inhibited PI3K/Akt/NF-κB signaling in tongue squamous cell carcinoma (TSCC) cells via targeting KAT6B[22].	human,Pig	kidney	High+Lowthroughput	Circular RNA CircEZH2 Suppresses Transmissible Gastroenteritis Coronavirus-induced Opening of Mitochondrial Permeability Transition Pore via Targeting MiR-22 in IPEC-J2	否	无	cancer	PK-15 cell	E_02_0189	Western blot, flow cytometry, PCR, immunofluorescence staining	miR-22 has a strong correlation with NF-κB pathway and mitochondrial damage. Recently, it was reported that miR-22 inhibited PI3K/Akt/NF-κB signaling in tongue squamous cell carcinoma (TSCC) cells via targeting KAT6B[22].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	miR-22 has a strong correlation with NF-κB pathway and mitochondrial damage. Recently, it was reported that miR-22 inhibited PI3K/Akt/NF-κB signaling in tongue squamous cell carcinoma (TSCC) cells via targeting KAT6B[22].		miR-22 has a strong correlation with NF-κB pathway and mitochondrial damage. Recently, it was reported that miR-22 inhibited PI3K/Akt/NF-κB signaling in tongue squamous cell carcinoma (TSCC) cells via targeting KAT6B[22].	Immunohistochemical staining	miR-22 has a strong correlation with NF-κB pathway and mitochondrial damage. Recently, it was reported that miR-22 inhibited PI3K/Akt/NF-κB signaling in tongue squamous cell carcinoma (TSCC) cells via targeting KAT6B[22].			Western blot,Flow cytometry,PCR,免疫荧光染色				KAT6B
31592229	chr2	74831204	74833204	HK2	However, HK2 does not regulate NK-κB activation. Not only HK2, IL-6 was also identified as the target of miR-22 and suppressed TGEV-induced mPTP opening via activating NF-κB pathway, suggesting that miR-22 regulates TGEV-induced mPTP opening via at least two pathways.	human,Pig	blood	High+Lowthroughput	Circular RNA CircEZH2 Suppresses Transmissible Gastroenteritis Coronavirus-induced Opening of Mitochondrial Permeability Transition Pore via Targeting MiR-22 in IPEC-J2	否	无	cancer	B cell	E_02_0189	Western blot, flow cytometry, PCR, immunofluorescence staining	However, HK2 does not regulate NK-κB activation. Not only HK2, IL-6 was also identified as the target of miR-22 and suppressed TGEV-induced mPTP opening via activating NF-κB pathway, suggesting that miR-22 regulates TGEV-induced mPTP opening via at least two pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, HK2 does not regulate NK-κB activation. Not only HK2, IL-6 was also identified as the target of miR-22 and suppressed TGEV-induced mPTP opening via activating NF-κB pathway, suggesting that miR-22 regulates TGEV-induced mPTP opening via at least two pathways.		However, HK2 does not regulate NK-κB activation. Not only HK2, IL-6 was also identified as the target of miR-22 and suppressed TGEV-induced mPTP opening via activating NF-κB pathway, suggesting that miR-22 regulates TGEV-induced mPTP opening via at least two pathways.	Immunohistochemical staining	However, HK2 does not regulate NK-κB activation. Not only HK2, IL-6 was also identified as the target of miR-22 and suppressed TGEV-induced mPTP opening via activating NF-κB pathway, suggesting that miR-22 regulates TGEV-induced mPTP opening via at least two pathways.			Western blot,Flow cytometry,PCR,免疫荧光染色				HK2
31592021	chr10	100370073	100372073	OLMALINC	maturation-associated long intergenic noncoding RNA (OLMALINC) in a statin- and triglyceride (TG)- associated liver co-expression network using liver RNA sequencing (RNA-seq) from 259 Finnish patients who had undergone bariatric surgery.	human	liver	High+Lowthroughput	Novel Lipid Long Intervening Noncoding RNA, Oligodendrocyte Maturation-Associated Long Intergenic Noncoding RNA, Regulates the Liver Steatosis Gene Stearoyl-Coenzyme A Desaturase As an Enhancer RNA	否	无	liver cancer	HepG2 cell	E_01_0234	Flow cytometry,Western blot	maturation-associated long intergenic noncoding RNA (OLMALINC) in a statin- and triglyceride (TG)- associated liver co-expression network using liver RNA sequencing (RNA-seq) from 259 Finnish patients who had undergone bariatric surgery.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	maturation-associated long intergenic noncoding RNA (OLMALINC) in a statin- and triglyceride (TG)- associated liver co-expression network using liver RNA sequencing (RNA-seq) from 259 Finnish patients who had undergone bariatric surgery.		maturation-associated long intergenic noncoding RNA (OLMALINC) in a statin- and triglyceride (TG)- associated liver co-expression network using liver RNA sequencing (RNA-seq) from 259 Finnish patients who had undergone bariatric surgery.	Immunohistochemical staining	maturation-associated long intergenic noncoding RNA (OLMALINC) in a statin- and triglyceride (TG)- associated liver co-expression network using liver RNA sequencing (RNA-seq) from 259 Finnish patients who had undergone bariatric surgery.			Flow cytometry,Western blot				OLMALINC
31591447	chr4	53777000	53779000	Tal2	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes	human,mouse	Epithelial tissues	High+Lowthroughput	Distinct enhancer signatures in the mouse gastrula delineate progressive cell fate continuum during embryo development	否	无		anterior epiblast cell	E_02_0190	Flow cytometry,PCR	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes		We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes	Immunohistochemical staining	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes			Flow cytometry,PCR				Tal2
31591447	chr5	120566993	120568993	Lhx5	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes	human,mouse	blood	High+Lowthroughput	Distinct enhancer signatures in the mouse gastrula delineate progressive cell fate continuum during embryo development	否	无			E_02_0190	Flow cytometry,PCR	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes		We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes	Immunohistochemical staining	We first analyzed gene expression dynamics during the development of each lineage (Fig. 1b–e; Supplementary informa_x0002_tion, Table S2) and found that expression of ectodermal genes (e.g., Tal2 and Lhx5), mesendodermal genes			Flow cytometry,PCR				Lhx5
31591447	chr3	34701896	34703896	Sox2	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).	human,mouse	connective tissue	High+Lowthroughput	Distinct enhancer signatures in the mouse gastrula delineate progressive cell fate continuum during embryo development	否	无		EpiSC细胞	E_02_0190	Flow cytometry,PCR	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).		These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).	Immunohistochemical staining	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).			Flow cytometry,PCR				Sox2
31591447	chr7	79439406	79441406	Mesp1	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).	human,mouse	Musculature	High+Lowthroughput	Distinct enhancer signatures in the mouse gastrula delineate progressive cell fate continuum during embryo development	否	无		muscle cell	E_02_0190	Flow cytometry,PCR	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).		These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).	Immunohistochemical staining	These gastrula-specific enhancer bins were enriched near genes that are related to embryonic pattern formation, gastrulation and primary germ layer specification, and are highly expressed at the gastrulation stage, such as Sox2, Eomes and Mesp1 (Fig. 5b–e).			Flow cytometry,PCR				Mesp1
31590652	chr12	7785003	7787003	NANOG	We train our models on p300 co-activator binding sites; H1-specific, transcription factor binding sites (TFBS): NANOG, OCT4, and SOX2; and uncondensed, cleavage sensitive, DNase I Hypersensitivity Regions (DHS); which are all distal to TSS; as positive examples.	human	connective tissue	High+Lowthroughput	AIKYATAN: mapping distal regulatory elements using convolutional learning on GPU	否	无	cancer	embryonic stem cell	E_01_0235	PCR	We train our models on p300 co-activator binding sites; H1-specific, transcription factor binding sites (TFBS): NANOG, OCT4, and SOX2; and uncondensed, cleavage sensitive, DNase I Hypersensitivity Regions (DHS); which are all distal to TSS; as positive examples.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We train our models on p300 co-activator binding sites; H1-specific, transcription factor binding sites (TFBS): NANOG, OCT4, and SOX2; and uncondensed, cleavage sensitive, DNase I Hypersensitivity Regions (DHS); which are all distal to TSS; as positive examples.		We train our models on p300 co-activator binding sites; H1-specific, transcription factor binding sites (TFBS): NANOG, OCT4, and SOX2; and uncondensed, cleavage sensitive, DNase I Hypersensitivity Regions (DHS); which are all distal to TSS; as positive examples.	Immunohistochemical staining	We train our models on p300 co-activator binding sites; H1-specific, transcription factor binding sites (TFBS): NANOG, OCT4, and SOX2; and uncondensed, cleavage sensitive, DNase I Hypersensitivity Regions (DHS); which are all distal to TSS; as positive examples.			PCR				NANOG
31589602	chr12	80713954	80715954	MYF5	We also compared motifs within H3K27ac or ATAC-seq peaks and found similar representations of jun proto-oncogene (JUN), myogenic factor 5 (MYF5), MEF2, specificity protein 1 (SP1), nuclear transcription fac_x0002_tor Y (NFY), and E-twenty-six family transcription factor (ETS) elements in MT and Quad, whereas factors critical for progenitor functions including runt-related transcription factor (RUNX), paired box (PAX), and TEA domain transcription factor 1 (TEAD) were more con_x0002_centrated in MT (Fig 4G).	human,mouse	blood	High+Lowthroughput	Dynamic enhancers control skeletal muscle identity and reprogramming	否	无	cancer	T cell	E_02_0191	Flow cytometry,PCR	We also compared motifs within H3K27ac or ATAC-seq peaks and found similar representations of jun proto-oncogene (JUN), myogenic factor 5 (MYF5), MEF2, specificity protein 1 (SP1), nuclear transcription fac_x0002_tor Y (NFY), and E-twenty-six family transcription factor (ETS) elements in MT and Quad, whereas factors critical for progenitor functions including runt-related transcription factor (RUNX), paired box (PAX), and TEA domain transcription factor 1 (TEAD) were more con_x0002_centrated in MT (Fig 4G).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We also compared motifs within H3K27ac or ATAC-seq peaks and found similar representations of jun proto-oncogene (JUN), myogenic factor 5 (MYF5), MEF2, specificity protein 1 (SP1), nuclear transcription fac_x0002_tor Y (NFY), and E-twenty-six family transcription factor (ETS) elements in MT and Quad, whereas factors critical for progenitor functions including runt-related transcription factor (RUNX), paired box (PAX), and TEA domain transcription factor 1 (TEAD) were more con_x0002_centrated in MT (Fig 4G).		We also compared motifs within H3K27ac or ATAC-seq peaks and found similar representations of jun proto-oncogene (JUN), myogenic factor 5 (MYF5), MEF2, specificity protein 1 (SP1), nuclear transcription fac_x0002_tor Y (NFY), and E-twenty-six family transcription factor (ETS) elements in MT and Quad, whereas factors critical for progenitor functions including runt-related transcription factor (RUNX), paired box (PAX), and TEA domain transcription factor 1 (TEAD) were more con_x0002_centrated in MT (Fig 4G).	Immunohistochemical staining	We also compared motifs within H3K27ac or ATAC-seq peaks and found similar representations of jun proto-oncogene (JUN), myogenic factor 5 (MYF5), MEF2, specificity protein 1 (SP1), nuclear transcription fac_x0002_tor Y (NFY), and E-twenty-six family transcription factor (ETS) elements in MT and Quad, whereas factors critical for progenitor functions including runt-related transcription factor (RUNX), paired box (PAX), and TEA domain transcription factor 1 (TEAD) were more con_x0002_centrated in MT (Fig 4G).			Flow cytometry,PCR				MYF5
31589096	chr17	42697169	42699169	EZH1	Furthermore, the treatment of G. glabra root extract was also capable of augmenting the production of EZH1 in C666-1 cells (Figure 3(c)), thereby providing a potential mechanism that AK027294 silencing sup_x0002_presses C666-1 proliferation by increasing EZH1 expression levels.	human	nasopharynx	High+Lowthroughput	Glycyrrhiza glabra suppresses nasopharyngeal carcinoma cell proliferation through inhibiting the expression of lncRNA, AK027294	否	无	Nasopharyngeal carcinoma	nasopharyngeal carcinoma cell	E_01_0236	Western blot,Flow cytometry,PCR	Furthermore, the treatment of G. glabra root extract was also capable of augmenting the production of EZH1 in C666-1 cells (Figure 3(c)), thereby providing a potential mechanism that AK027294 silencing sup_x0002_presses C666-1 proliferation by increasing EZH1 expression levels.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, the treatment of G. glabra root extract was also capable of augmenting the production of EZH1 in C666-1 cells (Figure 3(c)), thereby providing a potential mechanism that AK027294 silencing sup_x0002_presses C666-1 proliferation by increasing EZH1 expression levels.		Furthermore, the treatment of G. glabra root extract was also capable of augmenting the production of EZH1 in C666-1 cells (Figure 3(c)), thereby providing a potential mechanism that AK027294 silencing sup_x0002_presses C666-1 proliferation by increasing EZH1 expression levels.	Immunohistochemical staining	Furthermore, the treatment of G. glabra root extract was also capable of augmenting the production of EZH1 in C666-1 cells (Figure 3(c)), thereby providing a potential mechanism that AK027294 silencing sup_x0002_presses C666-1 proliferation by increasing EZH1 expression levels.			Western blot,Flow cytometry,PCR				EZH1
31588347	chr5	113018862	113020862	MCC	Mucociliary clearance (MCC) in the respiratory tract acts as the first physical barrier of the innate immune defense mecha_x0002_nism, by which inhaled environmental stimuli, including microbes and irritants.5 MCC depends on two important con_x0002_stituents: mucus production and mucus transport.	human	Epithelial tissues	High+Lowthroughput	Benzisothiazolinone upregulates the MUC5AC expression via ERK1/2, p38, and NF-κB pathways in airway epithelial cells	否	无	asthma	epithelial cell	E_01_0237	PCR,Western blot 	Mucociliary clearance (MCC) in the respiratory tract acts as the first physical barrier of the innate immune defense mecha_x0002_nism, by which inhaled environmental stimuli, including microbes and irritants.5 MCC depends on two important con_x0002_stituents: mucus production and mucus transport.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mucociliary clearance (MCC) in the respiratory tract acts as the first physical barrier of the innate immune defense mecha_x0002_nism, by which inhaled environmental stimuli, including microbes and irritants.5 MCC depends on two important con_x0002_stituents: mucus production and mucus transport.		Mucociliary clearance (MCC) in the respiratory tract acts as the first physical barrier of the innate immune defense mecha_x0002_nism, by which inhaled environmental stimuli, including microbes and irritants.5 MCC depends on two important con_x0002_stituents: mucus production and mucus transport.	Immunohistochemical staining	Mucociliary clearance (MCC) in the respiratory tract acts as the first physical barrier of the innate immune defense mecha_x0002_nism, by which inhaled environmental stimuli, including microbes and irritants.5 MCC depends on two important con_x0002_stituents: mucus production and mucus transport.			PCR,Western blot 				MCC
31588046	chr12	7785776	7787776	NANOG	After 48 h of TGF-bi treatment, the transcriptional downre_x0002_gulation of key pluripotency genes, including NANOG, OCT4 (POU5F1), and PRDM14 was evident (Figure S1A)	human	connective tissue	High+Lowthroughput	The RNA Helicase DDX6 Controls Cellular Plasticity by Modulating P-Body Homeostasis	否	无	cancer	cancer cell	E_01_0238	Flow cytometry, PCR, immunofluorescence staining	After 48 h of TGF-bi treatment, the transcriptional downre_x0002_gulation of key pluripotency genes, including NANOG, OCT4 (POU5F1), and PRDM14 was evident (Figure S1A)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	After 48 h of TGF-bi treatment, the transcriptional downre_x0002_gulation of key pluripotency genes, including NANOG, OCT4 (POU5F1), and PRDM14 was evident (Figure S1A)		After 48 h of TGF-bi treatment, the transcriptional downre_x0002_gulation of key pluripotency genes, including NANOG, OCT4 (POU5F1), and PRDM14 was evident (Figure S1A)	Immunohistochemical staining	After 48 h of TGF-bi treatment, the transcriptional downre_x0002_gulation of key pluripotency genes, including NANOG, OCT4 (POU5F1), and PRDM14 was evident (Figure S1A)			Flow cytometry,PCR,免疫荧光染色				NANOG
31588023	chr1	170660059	170662059	PRRX1	Motifs for the SE-associated TFs PRRX1, NFIC, and NFIX were enriched in both H3K27M sub_x0002_groups over normal pons (Figure 2D)	human	connective tissue	High+Lowthroughput	Histone Variant and Cell Context Determine H3K27M Reprogramming of the Enhancer Landscape and Oncogenic State	否	无	Malignancy	immune cell	E_01_0239	Flow cytometry, PCR, immunofluorescence staining	Motifs for the SE-associated TFs PRRX1, NFIC, and NFIX were enriched in both H3K27M sub_x0002_groups over normal pons (Figure 2D)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Motifs for the SE-associated TFs PRRX1, NFIC, and NFIX were enriched in both H3K27M sub_x0002_groups over normal pons (Figure 2D)		Motifs for the SE-associated TFs PRRX1, NFIC, and NFIX were enriched in both H3K27M sub_x0002_groups over normal pons (Figure 2D)	Immunohistochemical staining	Motifs for the SE-associated TFs PRRX1, NFIC, and NFIX were enriched in both H3K27M sub_x0002_groups over normal pons (Figure 2D)			Flow cytometry,PCR,免疫荧光染色				PRRX1
31588020	chr17	39685586	39687586	ERBB2	However, the National Comprehensive Can_x0002_cer Network guidelines for non-small cell lung cancer (NSCLC) recommend that newly diagnosed patients undergo broad mo_x0002_lecular profiling to detect ERBB2 mutations (Ettinger et al., 2018).	mouse	blood	High+Lowthroughput	Pan-Cancer Landscape and Analysis of ERBB2 Mutations Identifies Poziotinib as a Clinically Active Inhibitor and Enhancer of T-DM1 Activity	否	无	cancer	Ba/F3 cell	E_02_0192	PCR,Western blot	However, the National Comprehensive Can_x0002_cer Network guidelines for non-small cell lung cancer (NSCLC) recommend that newly diagnosed patients undergo broad mo_x0002_lecular profiling to detect ERBB2 mutations (Ettinger et al., 2018).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, the National Comprehensive Can_x0002_cer Network guidelines for non-small cell lung cancer (NSCLC) recommend that newly diagnosed patients undergo broad mo_x0002_lecular profiling to detect ERBB2 mutations (Ettinger et al., 2018).		However, the National Comprehensive Can_x0002_cer Network guidelines for non-small cell lung cancer (NSCLC) recommend that newly diagnosed patients undergo broad mo_x0002_lecular profiling to detect ERBB2 mutations (Ettinger et al., 2018).	Immunohistochemical staining	However, the National Comprehensive Can_x0002_cer Network guidelines for non-small cell lung cancer (NSCLC) recommend that newly diagnosed patients undergo broad mo_x0002_lecular profiling to detect ERBB2 mutations (Ettinger et al., 2018).			PCR,Western blot				ERBB2
31586130	chr3	194133931	194135931	HES1	Furthermore, NRARP overexpression blocked NOTCH transcriptional activity as shown by the overall decreased expression of NOTCH1 downstream tar_x0002_gets HES1 and DTX1 in NRARP-overexpressing cells (Fig. 1f).	human	blood	High+Lowthroughput	NRARP displays either pro- or anti-tumoral roles in T-cell acute lymphoblastic leukemia depending on Notch and Wnt signaling	否	无	Acute lymphoblastic leukemia	T cell	E_01_0240	PCR,Western blot	Furthermore, NRARP overexpression blocked NOTCH transcriptional activity as shown by the overall decreased expression of NOTCH1 downstream tar_x0002_gets HES1 and DTX1 in NRARP-overexpressing cells (Fig. 1f).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Furthermore, NRARP overexpression blocked NOTCH transcriptional activity as shown by the overall decreased expression of NOTCH1 downstream tar_x0002_gets HES1 and DTX1 in NRARP-overexpressing cells (Fig. 1f).	Immunohistochemical staining	Furthermore, NRARP overexpression blocked NOTCH transcriptional activity as shown by the overall decreased expression of NOTCH1 downstream tar_x0002_gets HES1 and DTX1 in NRARP-overexpressing cells (Fig. 1f).	HES1		PCR,Western blot	Furthermore, NRARP overexpression blocked NOTCH transcriptional activity as shown by the overall decreased expression of NOTCH1 downstream tar_x0002_gets HES1 and DTX1 in NRARP-overexpressing cells (Fig. 1f).			
31586130	chr4	108044223	108046223	LEF1	Thus, we next dissected the impact of LEF1 downstream from NRARP by silencing LEF1 in DND4.1 and Loucy cells with and without NRARP overexpression (Supplementary Fig. S4A, B).	mouse	Nervous tissue	High+Lowthroughput	NRARP displays either pro- or anti-tumoral roles in T-cell acute lymphoblastic leukemia depending on Notch and Wnt signaling	否	无	Acute lymphoblastic leukemia	neural crest cell	E_01_0240	PCR,Western blot	Thus, we next dissected the impact of LEF1 downstream from NRARP by silencing LEF1 in DND4.1 and Loucy cells with and without NRARP overexpression (Supplementary Fig. S4A, B).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, we next dissected the impact of LEF1 downstream from NRARP by silencing LEF1 in DND4.1 and Loucy cells with and without NRARP overexpression (Supplementary Fig. S4A, B).		Thus, we next dissected the impact of LEF1 downstream from NRARP by silencing LEF1 in DND4.1 and Loucy cells with and without NRARP overexpression (Supplementary Fig. S4A, B).	Immunohistochemical staining	Thus, we next dissected the impact of LEF1 downstream from NRARP by silencing LEF1 in DND4.1 and Loucy cells with and without NRARP overexpression (Supplementary Fig. S4A, B).			PCR,Western blot				LEF1
31586043	chr5	1389936	1391936	SLC6A3	Many environmental factors can regulate dopaminergic (DAergic) activity including SLC6A3, the gene encoding the dopamine transporter (DAT)1–7 .	human,mouse	Nervous tissue	High+Lowthroughput	Identification of HIVEP2 as a dopaminergic transcription factor related to substance use disorders in rats and humans	是	rs67175440	Immunodeficiencies	SH-SH5Y cell	E_02_0193	PCR,Western blot	Many environmental factors can regulate dopaminergic (DAergic) activity including SLC6A3, the gene encoding the dopamine transporter (DAT)1–7 .	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Many environmental factors can regulate dopaminergic (DAergic) activity including SLC6A3, the gene encoding the dopamine transporter (DAT)1–7 .		Many environmental factors can regulate dopaminergic (DAergic) activity including SLC6A3, the gene encoding the dopamine transporter (DAT)1–7 .	Immunohistochemical staining	Many environmental factors can regulate dopaminergic (DAergic) activity including SLC6A3, the gene encoding the dopamine transporter (DAT)1–7 .			PCR,Western blot				SLC6A3
31586043	chr10	102227203	102229203	PITX3	Recently, several TFs for SLC6A3 have been cloned, including Nurr1 (NR4A2), paired-like homeobox 3 pro_x0002_tein (PITX3), HEY1, SP1, SP3, AZI23′UTR, SRP54, and Nfe2l18–13.	human,mouse	Nervous tissue	High+Lowthroughput	Identification of HIVEP2 as a dopaminergic transcription factor related to substance use disorders in rats and humans	是	rs748209	Immunodeficiencies	SK-N-AS cell	E_02_0193	PCR,Western blot	Recently, several TFs for SLC6A3 have been cloned, including Nurr1 (NR4A2), paired-like homeobox 3 pro_x0002_tein (PITX3), HEY1, SP1, SP3, AZI23′UTR, SRP54, and Nfe2l18–13.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Recently, several TFs for SLC6A3 have been cloned, including Nurr1 (NR4A2), paired-like homeobox 3 pro_x0002_tein (PITX3), HEY1, SP1, SP3, AZI23′UTR, SRP54, and Nfe2l18–13.		Recently, several TFs for SLC6A3 have been cloned, including Nurr1 (NR4A2), paired-like homeobox 3 pro_x0002_tein (PITX3), HEY1, SP1, SP3, AZI23′UTR, SRP54, and Nfe2l18–13.	Immunohistochemical staining	Recently, several TFs for SLC6A3 have been cloned, including Nurr1 (NR4A2), paired-like homeobox 3 pro_x0002_tein (PITX3), HEY1, SP1, SP3, AZI23′UTR, SRP54, and Nfe2l18–13.			PCR,Western blot				PITX3
31586032	chr16	67559931	67561931	CTCF	Since enhancer-promoter looping is mediated by various transcription factors (69) and chromatin remodelers such as Mediator, Cohesin (70), CTCF proteins (71) and YY1(72), it is possible that the acidic and PEST domains interact with different factors to establish enhancer_x0002_promoter interactions in a gene and cell type_x0002_specific manner.	mouse	tumour	High+Lowthroughput	The transcription factor PU.1 mediates enhancer-promoter looping that is required for IL-1β eRNA and mRNA transcription in mouse melanoma and macrophage cell lines	否	无	tumour	melanoma cells	E_02_0194	PCR,Western blot,Flow cytometry	Since enhancer-promoter looping is mediated by various transcription factors (69) and chromatin remodelers such as Mediator, Cohesin (70), CTCF proteins (71) and YY1(72), it is possible that the acidic and PEST domains interact with different factors to establish enhancer_x0002_promoter interactions in a gene and cell type_x0002_specific manner.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Since enhancer-promoter looping is mediated by various transcription factors (69) and chromatin remodelers such as Mediator, Cohesin (70), CTCF proteins (71) and YY1(72), it is possible that the acidic and PEST domains interact with different factors to establish enhancer_x0002_promoter interactions in a gene and cell type_x0002_specific manner.		Since enhancer-promoter looping is mediated by various transcription factors (69) and chromatin remodelers such as Mediator, Cohesin (70), CTCF proteins (71) and YY1(72), it is possible that the acidic and PEST domains interact with different factors to establish enhancer_x0002_promoter interactions in a gene and cell type_x0002_specific manner.	Immunohistochemical staining	Since enhancer-promoter looping is mediated by various transcription factors (69) and chromatin remodelers such as Mediator, Cohesin (70), CTCF proteins (71) and YY1(72), it is possible that the acidic and PEST domains interact with different factors to establish enhancer_x0002_promoter interactions in a gene and cell type_x0002_specific manner.			PCR,Western blot,Flow cytometry				CTCF
31585804	chrX	100840244	100842244	NOX1	Endo_x0002_thelial cells express 4 ROS-generating NOX isoforms (eg, NOX1, NOX2, NOX4, and NOX5).	mouse	Epithelial tissues	High+Lowthroughput	Sildenafil Protects Endothelial Cells From Radiation-Induced Oxidative Stress	否	无	atherosclerosis	endothelial cell	E_02_0195	PCR	Endo_x0002_thelial cells express 4 ROS-generating NOX isoforms (eg, NOX1, NOX2, NOX4, and NOX5).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Endo_x0002_thelial cells express 4 ROS-generating NOX isoforms (eg, NOX1, NOX2, NOX4, and NOX5).		Endo_x0002_thelial cells express 4 ROS-generating NOX isoforms (eg, NOX1, NOX2, NOX4, and NOX5).	Immunohistochemical staining	Endo_x0002_thelial cells express 4 ROS-generating NOX isoforms (eg, NOX1, NOX2, NOX4, and NOX5).			PCR				NOX1
31585741	chrX	48506512	48508512	PORCN	To explore kidney_x0002_specific functions of PORCN in UUO pathogenesis, we first confirmed that expression of Wnt pathway components were induced in the obstructed kidney	mouse	bone	High+Lowthroughput	Opposing actions of renal tubular- and myeloid-derived porcupine in obstruction-induced?kidney fibrosis	否	无		infiltrating myeloid cell	E_02_0196	PCR,Western blot	To explore kidney_x0002_specific functions of PORCN in UUO pathogenesis, we first confirmed that expression of Wnt pathway components were induced in the obstructed kidney	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To explore kidney_x0002_specific functions of PORCN in UUO pathogenesis, we first confirmed that expression of Wnt pathway components were induced in the obstructed kidney		To explore kidney_x0002_specific functions of PORCN in UUO pathogenesis, we first confirmed that expression of Wnt pathway components were induced in the obstructed kidney	Immunohistochemical staining	To explore kidney_x0002_specific functions of PORCN in UUO pathogenesis, we first confirmed that expression of Wnt pathway components were induced in the obstructed kidney			PCR,Western blot				PORCN
31585741	chr11	108808537	108810537	Axin2	Accordingly, ablation of PORCN in the obstructed KKO kidneys led not only to reduced expression of Wnt target genes, Axin2 and Nkd1, but also several Wnt ligands including Wnt3, Wnt4, Wnt7a, and Wnt9b.	mouse	Epithelial tissues	High+Lowthroughput	Opposing actions of renal tubular- and myeloid-derived porcupine in obstruction-induced?kidney fibrosis	否	无	Renal fibrosis	epithelial cell	E_02_0196	PCR,Western blot	Accordingly, ablation of PORCN in the obstructed KKO kidneys led not only to reduced expression of Wnt target genes, Axin2 and Nkd1, but also several Wnt ligands including Wnt3, Wnt4, Wnt7a, and Wnt9b.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Accordingly, ablation of PORCN in the obstructed KKO kidneys led not only to reduced expression of Wnt target genes, Axin2 and Nkd1, but also several Wnt ligands including Wnt3, Wnt4, Wnt7a, and Wnt9b.		Accordingly, ablation of PORCN in the obstructed KKO kidneys led not only to reduced expression of Wnt target genes, Axin2 and Nkd1, but also several Wnt ligands including Wnt3, Wnt4, Wnt7a, and Wnt9b.	Immunohistochemical staining	Accordingly, ablation of PORCN in the obstructed KKO kidneys led not only to reduced expression of Wnt target genes, Axin2 and Nkd1, but also several Wnt ligands including Wnt3, Wnt4, Wnt7a, and Wnt9b.			PCR,Western blot				Axin2
31584754	chr3	41191952	41193952	CTNNB1	It is well established that the central genetic event in the tumorigenesis of SPN is a gain-of-function mutation within the CTNNB1 gene that prevents β-catenin phos_x0002_phorylation and its subsequent proteasomal degradation through ubiquitination.1	human	tumour	High+Lowthroughput	The usefulness of lymphoid enhancer-binding factor 1 and androgen receptor in diagnosing solid pseudopapillary neoplasm of the pancreas on cytopathology	否	无	tumour	tumor cell	E_01_0241	Immunohistochemistry	It is well established that the central genetic event in the tumorigenesis of SPN is a gain-of-function mutation within the CTNNB1 gene that prevents β-catenin phos_x0002_phorylation and its subsequent proteasomal degradation through ubiquitination.1	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			It is well established that the central genetic event in the tumorigenesis of SPN is a gain-of-function mutation within the CTNNB1 gene that prevents β-catenin phos_x0002_phorylation and its subsequent proteasomal degradation through ubiquitination.1	Immunohistochemical staining	It is well established that the central genetic event in the tumorigenesis of SPN is a gain-of-function mutation within the CTNNB1 gene that prevents β-catenin phos_x0002_phorylation and its subsequent proteasomal degradation through ubiquitination.1	CTNNB1		免疫组化	It is well established that the central genetic event in the tumorigenesis of SPN is a gain-of-function mutation within the CTNNB1 gene that prevents β-catenin phos_x0002_phorylation and its subsequent proteasomal degradation through ubiquitination.1			
31583122	chr11	35136216	35138216	CD44	It has been suggested that the expression of stem cell-associated markers, such as CD44 and Oct4, may support their roles in therapy evasion, tumor recur_x0002_rence, and metastasis11.	human	lung	High+Lowthroughput	Targeting Wnt/EZH2/microRNA-708 signaling pathway inhibits neuroendocrine differentiation in prostate cancer	否	无	Lung adenocarcinoma	adenocarcinoma cell	E_01_0242	PCR,Western blot	It has been suggested that the expression of stem cell-associated markers, such as CD44 and Oct4, may support their roles in therapy evasion, tumor recur_x0002_rence, and metastasis11.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	It has been suggested that the expression of stem cell-associated markers, such as CD44 and Oct4, may support their roles in therapy evasion, tumor recur_x0002_rence, and metastasis11.		It has been suggested that the expression of stem cell-associated markers, such as CD44 and Oct4, may support their roles in therapy evasion, tumor recur_x0002_rence, and metastasis11.	Immunohistochemical staining	It has been suggested that the expression of stem cell-associated markers, such as CD44 and Oct4, may support their roles in therapy evasion, tumor recur_x0002_rence, and metastasis11.			PCR,Western blot				CD44
31582835	chr7	148804794	148806794	EZH2	Histone 3 trimethylated on lysine 27 (H3K27me3), a marker of silent chromatin conformation is present at the ADGRB1 promoter, and inhibition of EZH2, the catalytic component of the Polycomb Repressive complex 2 (PRC2) that methylates H3K27, switches the gene into an active chromatin status and reactivates BAI1 expression.	human	tumour	High+Lowthroughput	EZH2 targeting reduces medulloblastoma growth through epigenetic reactivation of the BAI1/p53 tumor suppressor pathway	否	无	Medulloblastoma	Medulloblastoma cell	E_01_0243	PCR,Western blot	Histone 3 trimethylated on lysine 27 (H3K27me3), a marker of silent chromatin conformation is present at the ADGRB1 promoter, and inhibition of EZH2, the catalytic component of the Polycomb Repressive complex 2 (PRC2) that methylates H3K27, switches the gene into an active chromatin status and reactivates BAI1 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Histone 3 trimethylated on lysine 27 (H3K27me3), a marker of silent chromatin conformation is present at the ADGRB1 promoter, and inhibition of EZH2, the catalytic component of the Polycomb Repressive complex 2 (PRC2) that methylates H3K27, switches the gene into an active chromatin status and reactivates BAI1 expression.	Immunohistochemical staining	Histone 3 trimethylated on lysine 27 (H3K27me3), a marker of silent chromatin conformation is present at the ADGRB1 promoter, and inhibition of EZH2, the catalytic component of the Polycomb Repressive complex 2 (PRC2) that methylates H3K27, switches the gene into an active chromatin status and reactivates BAI1 expression.	EZH2		PCR,Western blot	Histone 3 trimethylated on lysine 27 (H3K27me3), a marker of silent chromatin conformation is present at the ADGRB1 promoter, and inhibition of EZH2, the catalytic component of the Polycomb Repressive complex 2 (PRC2) that methylates H3K27, switches the gene into an active chromatin status and reactivates BAI1 expression.			
31581708	chr17	39726151	39728151	MIEN1	Migration and invasion enhancer 1 (MIEN1) is a membrane-anchored protein and exists in various cancerous tissues. However, the roles of MIEN1 in prostate cancer have not yet been clearly addressed.	human	prostate	High+Lowthroughput	Migration and Invasion Enhancer 1 Is an NF-?B-Inducing Gene Enhancing the Cell Proliferation and Invasion Ability of Human Prostate Carcinoma Cells In Vitro and In Vivo	否	无	prostatic cancer	prostate cancer cell	E_01_0244	PCR,Western blot,Flow cytometry	Migration and invasion enhancer 1 (MIEN1) is a membrane-anchored protein and exists in various cancerous tissues. However, the roles of MIEN1 in prostate cancer have not yet been clearly addressed.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Migration and invasion enhancer 1 (MIEN1) is a membrane-anchored protein and exists in various cancerous tissues. However, the roles of MIEN1 in prostate cancer have not yet been clearly addressed.		Migration and invasion enhancer 1 (MIEN1) is a membrane-anchored protein and exists in various cancerous tissues. However, the roles of MIEN1 in prostate cancer have not yet been clearly addressed.	Immunohistochemical staining	Migration and invasion enhancer 1 (MIEN1) is a membrane-anchored protein and exists in various cancerous tissues. However, the roles of MIEN1 in prostate cancer have not yet been clearly addressed.			PCR,Western blot,Flow cytometry				MIEN1
31581708	chr8	133234553	133236553	NDRG1	Interleukin-6 (IL-6), a pluripotency cytokine, is involved in the malignant progression of prostate cancer [15,16], while N_x0002_myc downstream regulated 1 (NDRG1) is a tumor suppressor gene in numerous cancer cells [17], including prostate [18,19].	human	Epithelial tissues	High+Lowthroughput	Migration and Invasion Enhancer 1 Is an NF-?B-Inducing Gene Enhancing the Cell Proliferation and Invasion Ability of Human Prostate Carcinoma Cells In Vitro and In Vivo	否	无	prostatic cancer	epithelial cell	E_01_0244	PCR,Western blot,Flow cytometry	Interleukin-6 (IL-6), a pluripotency cytokine, is involved in the malignant progression of prostate cancer [15,16], while N_x0002_myc downstream regulated 1 (NDRG1) is a tumor suppressor gene in numerous cancer cells [17], including prostate [18,19].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Interleukin-6 (IL-6), a pluripotency cytokine, is involved in the malignant progression of prostate cancer [15,16], while N_x0002_myc downstream regulated 1 (NDRG1) is a tumor suppressor gene in numerous cancer cells [17], including prostate [18,19].		Interleukin-6 (IL-6), a pluripotency cytokine, is involved in the malignant progression of prostate cancer [15,16], while N_x0002_myc downstream regulated 1 (NDRG1) is a tumor suppressor gene in numerous cancer cells [17], including prostate [18,19].	Immunohistochemical staining	Interleukin-6 (IL-6), a pluripotency cytokine, is involved in the malignant progression of prostate cancer [15,16], while N_x0002_myc downstream regulated 1 (NDRG1) is a tumor suppressor gene in numerous cancer cells [17], including prostate [18,19].			PCR,Western blot,Flow cytometry				NDRG1
31581661	chr8	127733019	127735019	MYC	Our findings also established that MYC Proto-Oncogene, basic helix-loop-helix (bHLH) Transcription Factor (MYC) signaling was down-regulated in curcumin-treated cell lines.	human	prostate	High+Lowthroughput	Curcumin-Gene Expression Response in Hormone Dependent and Independent Metastatic Prostate Cancer Cells	否	无	prostatic cancer	prostate cancer cell	E_01_0245	PCR 	Our findings also established that MYC Proto-Oncogene, basic helix-loop-helix (bHLH) Transcription Factor (MYC) signaling was down-regulated in curcumin-treated cell lines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our findings also established that MYC Proto-Oncogene, basic helix-loop-helix (bHLH) Transcription Factor (MYC) signaling was down-regulated in curcumin-treated cell lines.	Immunohistochemical staining	Our findings also established that MYC Proto-Oncogene, basic helix-loop-helix (bHLH) Transcription Factor (MYC) signaling was down-regulated in curcumin-treated cell lines.	MYC		PCR 	Our findings also established that MYC Proto-Oncogene, basic helix-loop-helix (bHLH) Transcription Factor (MYC) signaling was down-regulated in curcumin-treated cell lines.			
31579944	chr7	148804427	148806427	EZH2	Dysregulation of histone methyltransferase enhancer of zeste homolog 2 (EZH2) has been implicated in the pathogenesis of many cancers.	human,mouse	Epithelial tissues	High+Lowthroughput	Genetic or pharmacologic blockade of enhancer of zeste homolog 2 inhibits the progression of peritoneal fibrosis	否	无	cancer	peritoneal mesothelial cell	E_02_0197	PCR, Western blot, immunofluorescence staining	Dysregulation of histone methyltransferase enhancer of zeste homolog 2 (EZH2) has been implicated in the pathogenesis of many cancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Dysregulation of histone methyltransferase enhancer of zeste homolog 2 (EZH2) has been implicated in the pathogenesis of many cancers.		Dysregulation of histone methyltransferase enhancer of zeste homolog 2 (EZH2) has been implicated in the pathogenesis of many cancers.	Immunohistochemical staining	Dysregulation of histone methyltransferase enhancer of zeste homolog 2 (EZH2) has been implicated in the pathogenesis of many cancers.			PCR,Western blot,免疫荧光染色				EZH2
31579944	chr17	78850292	78852292	TIMP2	Moreover, delayed administration of 3-DZNeP inhibited peritoneal fibrosis progression, reversed established peritoneal fibrosis and reduced expression of tissue inhibitor of metalloproteinase 2 (TIMP2), and matrix metalloproteinase-2 and -9. 	human,mouse	connective tissue	High+Lowthroughput	Genetic or pharmacologic blockade of enhancer of zeste homolog 2 inhibits the progression of peritoneal fibrosis	否	无	inflammation	Inflammatory cell	E_02_0197	PCR, Western blot, immunofluorescence staining	Moreover, delayed administration of 3-DZNeP inhibited peritoneal fibrosis progression, reversed established peritoneal fibrosis and reduced expression of tissue inhibitor of metalloproteinase 2 (TIMP2), and matrix metalloproteinase-2 and -9. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, delayed administration of 3-DZNeP inhibited peritoneal fibrosis progression, reversed established peritoneal fibrosis and reduced expression of tissue inhibitor of metalloproteinase 2 (TIMP2), and matrix metalloproteinase-2 and -9. 		Moreover, delayed administration of 3-DZNeP inhibited peritoneal fibrosis progression, reversed established peritoneal fibrosis and reduced expression of tissue inhibitor of metalloproteinase 2 (TIMP2), and matrix metalloproteinase-2 and -9. 	Immunohistochemical staining	Moreover, delayed administration of 3-DZNeP inhibited peritoneal fibrosis progression, reversed established peritoneal fibrosis and reduced expression of tissue inhibitor of metalloproteinase 2 (TIMP2), and matrix metalloproteinase-2 and -9. 			PCR,Western blot,免疫荧光染色				TIMP2
31579944	chr17	42310753	42312753	STAT3	Therefore, we speculated that EZH2 blockade suppressed the MMP2 by inhibiting the EZH2- STAT3 signaling axis. In addition, genome wide approaches suggest that EZH2 targets Fosl1 and Klf5, two activators of MMP9 [40].	human,mouse	pancreas	High+Lowthroughput	Genetic or pharmacologic blockade of enhancer of zeste homolog 2 inhibits the progression of peritoneal fibrosis	否	无	pancreatic cancer	pancreatic cancer cell	E_02_0197	PCR, Western blot, immunofluorescence staining	Therefore, we speculated that EZH2 blockade suppressed the MMP2 by inhibiting the EZH2- STAT3 signaling axis. In addition, genome wide approaches suggest that EZH2 targets Fosl1 and Klf5, two activators of MMP9 [40].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, we speculated that EZH2 blockade suppressed the MMP2 by inhibiting the EZH2- STAT3 signaling axis. In addition, genome wide approaches suggest that EZH2 targets Fosl1 and Klf5, two activators of MMP9 [40].		Therefore, we speculated that EZH2 blockade suppressed the MMP2 by inhibiting the EZH2- STAT3 signaling axis. In addition, genome wide approaches suggest that EZH2 targets Fosl1 and Klf5, two activators of MMP9 [40].	Immunohistochemical staining	Therefore, we speculated that EZH2 blockade suppressed the MMP2 by inhibiting the EZH2- STAT3 signaling axis. In addition, genome wide approaches suggest that EZH2 targets Fosl1 and Klf5, two activators of MMP9 [40].			PCR,Western blot,免疫荧光染色				STAT3
31579913	chr20	63192571	63194571	YTHDF1	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	human	colon	High+Lowthroughput	Genetic variants in m6A modification genes are associated with colorectal cancer risk	是	rs118049207	Colon cancer	Human colorectal carcinoma cell	E_01_0246	PCR	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and		After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Immunohistochemical staining	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and			PCR				YTHDF1
31579913	chr8	63165861	63167861	YTHDF3	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	human	colon	High+Lowthroughput	Genetic variants in m6A modification genes are associated with colorectal cancer risk	是	rs118049207	Colon cancer	Human colorectal carcinoma cell	E_01_0246	PCR	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and		After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Immunohistochemical staining	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and			PCR				YTHDF3
31579913	chr1	28734326	28736326	YTHDF2	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	human	colon	High+Lowthroughput	Genetic variants in m6A modification genes are associated with colorectal cancer risk	是	rs118049207	Colon cancer	Human colorectal carcinoma cell	E_01_0246	PCR	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and		After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Immunohistochemical staining	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and			PCR				YTHDF2
31579913	chr10	119031225	119033225	EIF3A	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	human	colon	High+Lowthroughput	Genetic variants in m6A modification genes are associated with colorectal cancer risk	是	rs118049207	Colon cancer	Human colorectal carcinoma cell	E_01_0246	PCR	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and		After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and	Immunohistochemical staining	After excluding genes located on the X chromosome, the resultant twenty related autosomal chromosome genes involved in the m6A modification of methylated RNA were obtained. Briefly, we included seven literatures (14,19,34-38), which described the YTH N6-methyladenosine RNA binding protein 1 (YTHDF1), YTH N6-methyladenosine RNA binding protein 3 (YTHDF3), YTH N6-methyladenosine RNA binding protein 2 (YTHDF2), YTH domain-containing 1 (YTHDC1), heterogeneous nuclear ribonucleoprotein C (HNRNPC), eukaryotic translation initiation factor 3 subunit A (EIF3A), and			PCR				EIF3A
31579098	chr7	148804077	148806077	EZH2	The results demonstrated that different concen_x0002_trations of DZNep could inhibit the expression of enhancer of zeste homolog 2 (EZH2) protein, decrease the RNA and protein expression levels of Hif-1α, total β-catenin and phosphorylated-β-catenin and increase the expression levels of non-phosphorylated-β-catenin to different degrees.	human	tumour	High+Lowthroughput	DZNep inhibits Hif-1α and Wnt signalling molecules to attenuate the proliferation and invasion of BGC-823 gastric cancer cells	否	无	tumour	tumor cell	E_01_0247	PCR,Western blot,Flow cytometry	The results demonstrated that different concen_x0002_trations of DZNep could inhibit the expression of enhancer of zeste homolog 2 (EZH2) protein, decrease the RNA and protein expression levels of Hif-1α, total β-catenin and phosphorylated-β-catenin and increase the expression levels of non-phosphorylated-β-catenin to different degrees.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The results demonstrated that different concen_x0002_trations of DZNep could inhibit the expression of enhancer of zeste homolog 2 (EZH2) protein, decrease the RNA and protein expression levels of Hif-1α, total β-catenin and phosphorylated-β-catenin and increase the expression levels of non-phosphorylated-β-catenin to different degrees.	Immunohistochemical staining	The results demonstrated that different concen_x0002_trations of DZNep could inhibit the expression of enhancer of zeste homolog 2 (EZH2) protein, decrease the RNA and protein expression levels of Hif-1α, total β-catenin and phosphorylated-β-catenin and increase the expression levels of non-phosphorylated-β-catenin to different degrees.	EZH2		PCR,Western blot,Flow cytometry	The results demonstrated that different concen_x0002_trations of DZNep could inhibit the expression of enhancer of zeste homolog 2 (EZH2) protein, decrease the RNA and protein expression levels of Hif-1α, total β-catenin and phosphorylated-β-catenin and increase the expression levels of non-phosphorylated-β-catenin to different degrees.			
31575636	chr22	41830453	41832453	SREBF2	Among the cholesterol biosynthetic genes,we observed upregulation during mid-regeneration (4-7 dpi) of SREBF2, a known cholesterol master-regulatory transcription factor (Madison 2016; Smith et al. 2018).	human,mouse		High+Lowthroughput	Regeneration Rosetta: An Interactive Web Application To Explore Regeneration-Associated Gene Expression and Chromatin Accessibility	否	无			E_02_0198	RNA-seq	Among the cholesterol biosynthetic genes,we observed upregulation during mid-regeneration (4-7 dpi) of SREBF2, a known cholesterol master-regulatory transcription factor (Madison 2016; Smith et al. 2018).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Among the cholesterol biosynthetic genes,we observed upregulation during mid-regeneration (4-7 dpi) of SREBF2, a known cholesterol master-regulatory transcription factor (Madison 2016; Smith et al. 2018).		Among the cholesterol biosynthetic genes,we observed upregulation during mid-regeneration (4-7 dpi) of SREBF2, a known cholesterol master-regulatory transcription factor (Madison 2016; Smith et al. 2018).	Immunohistochemical staining	Among the cholesterol biosynthetic genes,we observed upregulation during mid-regeneration (4-7 dpi) of SREBF2, a known cholesterol master-regulatory transcription factor (Madison 2016; Smith et al. 2018).			RNA-seq				SREBF2
31573688	chr12	16545165	16547165	LMO3	LIM domain only 3 (LMO3), a member of the LIM_x0002_only protein group, enhances adipogenesis of human adipose-derived stromal cells by enhancing peroxisome proliferator-activated receptor γ (PPARG) transcriptional activity, and LMO3 is a specific regulator of human adipogenesis, but not of mouse, whose white adipocytes lack LMO3 expression. Moreover, LMO3 is upregulated in a tissue-specific manner in human obese visceral fat, and is an attractive target for interfering with human visceral obe_x0002_sity (Lindroos et al., 2013).	human	connective tissue	High+Lowthroughput	Resveratrol Inhibits Human Visceral Preadipocyte Proliferation and Differentiation in vitro	否	无	diabetes	3T3-L1 cell	E_01_0248	PCR,Western blot	LIM domain only 3 (LMO3), a member of the LIM_x0002_only protein group, enhances adipogenesis of human adipose-derived stromal cells by enhancing peroxisome proliferator-activated receptor γ (PPARG) transcriptional activity, and LMO3 is a specific regulator of human adipogenesis, but not of mouse, whose white adipocytes lack LMO3 expression. Moreover, LMO3 is upregulated in a tissue-specific manner in human obese visceral fat, and is an attractive target for interfering with human visceral obe_x0002_sity (Lindroos et al., 2013).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	LIM domain only 3 (LMO3), a member of the LIM_x0002_only protein group, enhances adipogenesis of human adipose-derived stromal cells by enhancing peroxisome proliferator-activated receptor γ (PPARG) transcriptional activity, and LMO3 is a specific regulator of human adipogenesis, but not of mouse, whose white adipocytes lack LMO3 expression. Moreover, LMO3 is upregulated in a tissue-specific manner in human obese visceral fat, and is an attractive target for interfering with human visceral obe_x0002_sity (Lindroos et al., 2013).		LIM domain only 3 (LMO3), a member of the LIM_x0002_only protein group, enhances adipogenesis of human adipose-derived stromal cells by enhancing peroxisome proliferator-activated receptor γ (PPARG) transcriptional activity, and LMO3 is a specific regulator of human adipogenesis, but not of mouse, whose white adipocytes lack LMO3 expression. Moreover, LMO3 is upregulated in a tissue-specific manner in human obese visceral fat, and is an attractive target for interfering with human visceral obe_x0002_sity (Lindroos et al., 2013).	Immunohistochemical staining	LIM domain only 3 (LMO3), a member of the LIM_x0002_only protein group, enhances adipogenesis of human adipose-derived stromal cells by enhancing peroxisome proliferator-activated receptor γ (PPARG) transcriptional activity, and LMO3 is a specific regulator of human adipogenesis, but not of mouse, whose white adipocytes lack LMO3 expression. Moreover, LMO3 is upregulated in a tissue-specific manner in human obese visceral fat, and is an attractive target for interfering with human visceral obe_x0002_sity (Lindroos et al., 2013).			PCR,Western blot				LMO3
31572429	chr22	41558440	41560440	CSDC2	Furthermore, the targeting sequences located in E-cadherin, cold-shock domain-containing protein C2 (CSDC2), and PDE4D genes could interact with miR-373 in MCF-7 cells rather than HeLa cells, which is consistent with our data that these three genes can be regulated by miR_x0002_373 in MCF-7 cells while not in HeLa cells.	human	breast	High+Lowthroughput	Purification and Identification of miRNA Target Sites in Genome Using DNA Affinity Precipitation	否	无	mammary cancer	MCF-7 cell	E_01_0249		Furthermore, the targeting sequences located in E-cadherin, cold-shock domain-containing protein C2 (CSDC2), and PDE4D genes could interact with miR-373 in MCF-7 cells rather than HeLa cells, which is consistent with our data that these three genes can be regulated by miR_x0002_373 in MCF-7 cells while not in HeLa cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, the targeting sequences located in E-cadherin, cold-shock domain-containing protein C2 (CSDC2), and PDE4D genes could interact with miR-373 in MCF-7 cells rather than HeLa cells, which is consistent with our data that these three genes can be regulated by miR_x0002_373 in MCF-7 cells while not in HeLa cells.		Furthermore, the targeting sequences located in E-cadherin, cold-shock domain-containing protein C2 (CSDC2), and PDE4D genes could interact with miR-373 in MCF-7 cells rather than HeLa cells, which is consistent with our data that these three genes can be regulated by miR_x0002_373 in MCF-7 cells while not in HeLa cells.	Immunohistochemical staining	Furthermore, the targeting sequences located in E-cadherin, cold-shock domain-containing protein C2 (CSDC2), and PDE4D genes could interact with miR-373 in MCF-7 cells rather than HeLa cells, which is consistent with our data that these three genes can be regulated by miR_x0002_373 in MCF-7 cells while not in HeLa cells.							CSDC2
31571902	chr22	15781801	15783801	DUXAP8	Dysregulated DUXAP8, LINC01116, LINC01138, and PCAT6 are significantly associated with HCC patients' poor outcomes.	human	liver	High+Lowthroughput	Up-regulated long non-coding RNA DUXAP8 promotes cell growth through repressing Krüppel-like factor 2 expression in human hepatocellular carcinoma	否	无	liver cancer	hepatocellular carcinoma cell	E_01_0250	PCR	Dysregulated DUXAP8, LINC01116, LINC01138, and PCAT6 are significantly associated with HCC patients' poor outcomes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Dysregulated DUXAP8, LINC01116, LINC01138, and PCAT6 are significantly associated with HCC patients' poor outcomes.		Dysregulated DUXAP8, LINC01116, LINC01138, and PCAT6 are significantly associated with HCC patients' poor outcomes.	Immunohistochemical staining	Dysregulated DUXAP8, LINC01116, LINC01138, and PCAT6 are significantly associated with HCC patients' poor outcomes.			PCR				DUXAP8
31570750	chr1	10633990	10635990	CASZ1	This study demonstrates that the CASZ1 gene associated C-allele of rs11121615 has a signifcant, reproducible, association with CVD (CEAP C≥2 meta-odds ratio 1.31, 95% CI 1.27–1.34, P=1×10−98, PHet=0.25), but not with non-varicose vein (CEAP C1, telangiectasia or reticular veins) forms of venous disease.	human	kidney	High+Lowthroughput	A variant of the castor zinc finger 1 (CASZ1) gene is differentially associated with the clinical classification of chronic venous disease	是	rs11121615	Chronic venous disease	HEK293 cell	E_01_0251	PCR,Flow cytometry	This study demonstrates that the CASZ1 gene associated C-allele of rs11121615 has a signifcant, reproducible, association with CVD (CEAP C≥2 meta-odds ratio 1.31, 95% CI 1.27–1.34, P=1×10−98, PHet=0.25), but not with non-varicose vein (CEAP C1, telangiectasia or reticular veins) forms of venous disease.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This study demonstrates that the CASZ1 gene associated C-allele of rs11121615 has a signifcant, reproducible, association with CVD (CEAP C≥2 meta-odds ratio 1.31, 95% CI 1.27–1.34, P=1×10−98, PHet=0.25), but not with non-varicose vein (CEAP C1, telangiectasia or reticular veins) forms of venous disease.		This study demonstrates that the CASZ1 gene associated C-allele of rs11121615 has a signifcant, reproducible, association with CVD (CEAP C≥2 meta-odds ratio 1.31, 95% CI 1.27–1.34, P=1×10−98, PHet=0.25), but not with non-varicose vein (CEAP C1, telangiectasia or reticular veins) forms of venous disease.	Immunohistochemical staining	This study demonstrates that the CASZ1 gene associated C-allele of rs11121615 has a signifcant, reproducible, association with CVD (CEAP C≥2 meta-odds ratio 1.31, 95% CI 1.27–1.34, P=1×10−98, PHet=0.25), but not with non-varicose vein (CEAP C1, telangiectasia or reticular veins) forms of venous disease.			PCR,Flow cytometry				CASZ1
31570746	chr13	40553093	40555093	FOXO1	Lastly, point mutations were induced in the binding sites of FOXO1 and HFH-3, enabling the exclusion of all the identifed and selected TFBSs. In this instance, enhancer activity was further downregulated	human	connective tissue	High+Lowthroughput	Characterization of the Long Terminal Repeat of the Endogenous Retrovirus-derived microRNAs in the Olive Flounder	否	无	cancer	cancer cell	E_01_0252	PCR	Lastly, point mutations were induced in the binding sites of FOXO1 and HFH-3, enabling the exclusion of all the identifed and selected TFBSs. In this instance, enhancer activity was further downregulated	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Lastly, point mutations were induced in the binding sites of FOXO1 and HFH-3, enabling the exclusion of all the identifed and selected TFBSs. In this instance, enhancer activity was further downregulated	Immunohistochemical staining	Lastly, point mutations were induced in the binding sites of FOXO1 and HFH-3, enabling the exclusion of all the identifed and selected TFBSs. In this instance, enhancer activity was further downregulated	FOXO1		PCR	Lastly, point mutations were induced in the binding sites of FOXO1 and HFH-3, enabling the exclusion of all the identifed and selected TFBSs. In this instance, enhancer activity was further downregulated			
31570000	chr19	10651535	10653535	ILF3	The presence of multiple additional ILF3 binding interac_x0002_tions with introns, coding exons, noncoding non-AS exons, and SINEs on the transcribed strand probably reflects the extensive functional diversity of the ILF3 gene in addition to an incomplete annotation of the transcriptome.	human,mouse		High+Lowthroughput	The RNA-binding protein ILF3 binds to transposable element sequences in SINEUP lncRNAs	否	无	liver cancer	DH5a cells	E_02_0199	Western blot,Flow cytometry,PCR	The presence of multiple additional ILF3 binding interac_x0002_tions with introns, coding exons, noncoding non-AS exons, and SINEs on the transcribed strand probably reflects the extensive functional diversity of the ILF3 gene in addition to an incomplete annotation of the transcriptome.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The presence of multiple additional ILF3 binding interac_x0002_tions with introns, coding exons, noncoding non-AS exons, and SINEs on the transcribed strand probably reflects the extensive functional diversity of the ILF3 gene in addition to an incomplete annotation of the transcriptome.		The presence of multiple additional ILF3 binding interac_x0002_tions with introns, coding exons, noncoding non-AS exons, and SINEs on the transcribed strand probably reflects the extensive functional diversity of the ILF3 gene in addition to an incomplete annotation of the transcriptome.	Immunohistochemical staining	The presence of multiple additional ILF3 binding interac_x0002_tions with introns, coding exons, noncoding non-AS exons, and SINEs on the transcribed strand probably reflects the extensive functional diversity of the ILF3 gene in addition to an incomplete annotation of the transcriptome.			Western blot,Flow cytometry,PCR				ILF3
31563853	chr3	186840138	186842138	ADIPOQ	Relative to untreated control cells, T-brites had increased mRNA expression of PPARγ target genes (ADIPOQ, FABP3, FABP4, and RXRA) and brite/beige marker genes (PGC1α/β, PRDM16, CEBPβ, CIDEA, and ELOVL3), without expression changes in lipogenic genes (FASN and SCD1) (Figure S4a and S4b)	human	Fat	High+Lowthroughput	CIDEA Transcriptionally Regulates UCP1 for Britening and Thermogenesis in Human Fat Cells	否	无		fat cell	E_01_0253	Western blot, flow cytometry, PCR, immunofluorescence staining	Relative to untreated control cells, T-brites had increased mRNA expression of PPARγ target genes (ADIPOQ, FABP3, FABP4, and RXRA) and brite/beige marker genes (PGC1α/β, PRDM16, CEBPβ, CIDEA, and ELOVL3), without expression changes in lipogenic genes (FASN and SCD1) (Figure S4a and S4b)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Relative to untreated control cells, T-brites had increased mRNA expression of PPARγ target genes (ADIPOQ, FABP3, FABP4, and RXRA) and brite/beige marker genes (PGC1α/β, PRDM16, CEBPβ, CIDEA, and ELOVL3), without expression changes in lipogenic genes (FASN and SCD1) (Figure S4a and S4b)		Relative to untreated control cells, T-brites had increased mRNA expression of PPARγ target genes (ADIPOQ, FABP3, FABP4, and RXRA) and brite/beige marker genes (PGC1α/β, PRDM16, CEBPβ, CIDEA, and ELOVL3), without expression changes in lipogenic genes (FASN and SCD1) (Figure S4a and S4b)	Immunohistochemical staining	Relative to untreated control cells, T-brites had increased mRNA expression of PPARγ target genes (ADIPOQ, FABP3, FABP4, and RXRA) and brite/beige marker genes (PGC1α/β, PRDM16, CEBPβ, CIDEA, and ELOVL3), without expression changes in lipogenic genes (FASN and SCD1) (Figure S4a and S4b)			Western blot,Flow cytometry,PCR,免疫荧光染色				ADIPOQ
31563432	chr4	154747879	154749879	Actrt2	Neither wild-type nor mutant b-catenin factors were found to occupy the typical enhancers of Actrt2 and Fam168b (Fig_x0002_ure S5B).	human	colon	High+Lowthroughput	Mediator Condensates Localize Signaling Factors to Key Cell Identity Genes	否	无	Colon cancer	HCT116 cells	E_01_0254	Immunofluorescence light staining, flow cytometry, PCR	Neither wild-type nor mutant b-catenin factors were found to occupy the typical enhancers of Actrt2 and Fam168b (Fig_x0002_ure S5B).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Neither wild-type nor mutant b-catenin factors were found to occupy the typical enhancers of Actrt2 and Fam168b (Fig_x0002_ure S5B).		Neither wild-type nor mutant b-catenin factors were found to occupy the typical enhancers of Actrt2 and Fam168b (Fig_x0002_ure S5B).	Immunohistochemical staining	Neither wild-type nor mutant b-catenin factors were found to occupy the typical enhancers of Actrt2 and Fam168b (Fig_x0002_ure S5B).			免疫荧光光染色,Flow cytometry,PCR				Actrt2
31563432	chr17	42310179	42312179	STAT3	Recent studies have shown that TFs and Mediator form phase_x0002_separated condensates at super-enhancers (Boija et al., 2018; Cho et al., 2018; Sabari et al., 2018), and the terminal signaling factors of the WNT, JAK/STAT, and TGF-b pathways (b-catenin, STAT3, and SMAD3, respectively) have been shown to preferen_x0002_tially occupy super-enhancers (Hnisz et al., 2015).	human	kidney	High+Lowthroughput	Mediator Condensates Localize Signaling Factors to Key Cell Identity Genes	否	无		HEK293T	E_01_0254	Immunofluorescence light staining, flow cytometry, PCR	Recent studies have shown that TFs and Mediator form phase_x0002_separated condensates at super-enhancers (Boija et al., 2018; Cho et al., 2018; Sabari et al., 2018), and the terminal signaling factors of the WNT, JAK/STAT, and TGF-b pathways (b-catenin, STAT3, and SMAD3, respectively) have been shown to preferen_x0002_tially occupy super-enhancers (Hnisz et al., 2015).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Recent studies have shown that TFs and Mediator form phase_x0002_separated condensates at super-enhancers (Boija et al., 2018; Cho et al., 2018; Sabari et al., 2018), and the terminal signaling factors of the WNT, JAK/STAT, and TGF-b pathways (b-catenin, STAT3, and SMAD3, respectively) have been shown to preferen_x0002_tially occupy super-enhancers (Hnisz et al., 2015).	Immunohistochemical staining	Recent studies have shown that TFs and Mediator form phase_x0002_separated condensates at super-enhancers (Boija et al., 2018; Cho et al., 2018; Sabari et al., 2018), and the terminal signaling factors of the WNT, JAK/STAT, and TGF-b pathways (b-catenin, STAT3, and SMAD3, respectively) have been shown to preferen_x0002_tially occupy super-enhancers (Hnisz et al., 2015).	STAT3		免疫荧光光染色,Flow cytometry,PCR	Recent studies have shown that TFs and Mediator form phase_x0002_separated condensates at super-enhancers (Boija et al., 2018; Cho et al., 2018; Sabari et al., 2018), and the terminal signaling factors of the WNT, JAK/STAT, and TGF-b pathways (b-catenin, STAT3, and SMAD3, respectively) have been shown to preferen_x0002_tially occupy super-enhancers (Hnisz et al., 2015).			
31562697	chr3	69736600	69738600	MITF	MITF, a gene that is mutated in familial melanoma and Waardenburg syndrome, en_x0002_codes multiple isoforms expressed from alternative promoters that share common coding exons but have unique amino termini.	human,mouse	connective tissue	High+Lowthroughput	Delineating the role of MITF isoforms in pigmentation and tissue homeostasis	否	无	Melanoma	Pigment Cell	E_02_0200	PCR, Western blot, immunofluorescence staining	MITF, a gene that is mutated in familial melanoma and Waardenburg syndrome, en_x0002_codes multiple isoforms expressed from alternative promoters that share common coding exons but have unique amino termini.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MITF, a gene that is mutated in familial melanoma and Waardenburg syndrome, en_x0002_codes multiple isoforms expressed from alternative promoters that share common coding exons but have unique amino termini.		MITF, a gene that is mutated in familial melanoma and Waardenburg syndrome, en_x0002_codes multiple isoforms expressed from alternative promoters that share common coding exons but have unique amino termini.	Immunohistochemical staining	MITF, a gene that is mutated in familial melanoma and Waardenburg syndrome, en_x0002_codes multiple isoforms expressed from alternative promoters that share common coding exons but have unique amino termini.			PCR,Western blot,免疫荧光染色				MITF
31562697	chr11	89175705	89177705	TYR	We previously showed that 9‐cis retinoic acid upregulates MITF and TYR expression in cultured melanocytes, stimulating pigment production in melano_x0002_cyte and melanoma cell lines (Paterson, Ho, Kapadia, & Ganesan, 2013).	human,mouse	breast	High+Lowthroughput	Delineating the role of MITF isoforms in pigmentation and tissue homeostasis	否	无	mammary cancer	breast cancer stem cell 	E_02_0200	PCR, Western blot, immunofluorescence staining	We previously showed that 9‐cis retinoic acid upregulates MITF and TYR expression in cultured melanocytes, stimulating pigment production in melano_x0002_cyte and melanoma cell lines (Paterson, Ho, Kapadia, & Ganesan, 2013).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We previously showed that 9‐cis retinoic acid upregulates MITF and TYR expression in cultured melanocytes, stimulating pigment production in melano_x0002_cyte and melanoma cell lines (Paterson, Ho, Kapadia, & Ganesan, 2013).		We previously showed that 9‐cis retinoic acid upregulates MITF and TYR expression in cultured melanocytes, stimulating pigment production in melano_x0002_cyte and melanoma cell lines (Paterson, Ho, Kapadia, & Ganesan, 2013).	Immunohistochemical staining	We previously showed that 9‐cis retinoic acid upregulates MITF and TYR expression in cultured melanocytes, stimulating pigment production in melano_x0002_cyte and melanoma cell lines (Paterson, Ho, Kapadia, & Ganesan, 2013).			PCR,Western blot,免疫荧光染色				TYR
31561451	chr7	55016281	55018281	EGFR	In vitro, we did not find a significant difference in nanoparticle binding to EGFR overexpressing head and neck cancer cells between EGFR-targeted and untargeted FITC-SiO2-NPs.	human	connective tissue	High+Lowthroughput	Fluorescein- and EGFR-Antibody Conjugated Silica Nanoparticles for Enhancement of Real-time Tumor Border Definition Using Confocal Laser Endomicroscopy in Squamous Cell Carcinoma of the Head and Neck	否	无	tumour	squamous cell	E_01_0255	PCR, Western blot, immunofluorescence staining	In vitro, we did not find a significant difference in nanoparticle binding to EGFR overexpressing head and neck cancer cells between EGFR-targeted and untargeted FITC-SiO2-NPs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In vitro, we did not find a significant difference in nanoparticle binding to EGFR overexpressing head and neck cancer cells between EGFR-targeted and untargeted FITC-SiO2-NPs.	Immunohistochemical staining	In vitro, we did not find a significant difference in nanoparticle binding to EGFR overexpressing head and neck cancer cells between EGFR-targeted and untargeted FITC-SiO2-NPs.	EGFR		PCR,Western blot,免疫荧光染色	In vitro, we did not find a significant difference in nanoparticle binding to EGFR overexpressing head and neck cancer cells between EGFR-targeted and untargeted FITC-SiO2-NPs.			
31561366	chr11	47463063	47465063	CELF1	The DASHR overlap analysis found only one sncRNA overlap, where the variant rs4543938 in the CELF1 region overlapped the piRNA piR-56133.	human	blood	High+Lowthroughput	Fluorescein- and EGFR-Antibody Conjugated Silica Nanoparticles for Enhancement of Real-time Tumor Border Definition Using Confocal Laser Endomicroscopy in Squamous Cell Carcinoma of the Head and Neck	是	rs8093731	Chronic myeloid leukemia	K562  cells	E_01_0256	PCR,Flow cytometry	The DASHR overlap analysis found only one sncRNA overlap, where the variant rs4543938 in the CELF1 region overlapped the piRNA piR-56133.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The DASHR overlap analysis found only one sncRNA overlap, where the variant rs4543938 in the CELF1 region overlapped the piRNA piR-56133.		The DASHR overlap analysis found only one sncRNA overlap, where the variant rs4543938 in the CELF1 region overlapped the piRNA piR-56133.	Immunohistochemical staining	The DASHR overlap analysis found only one sncRNA overlap, where the variant rs4543938 in the CELF1 region overlapped the piRNA piR-56133.			PCR,Flow cytometry				CELF1
31561366	chr14	52854332	52856332	FERMT2	Analysis of miRNA seed disruption found that 46 variants across 5 tag regions (CELF1, FERMT2, INPP5D, MS4A6A, and ZCWPW1) overlapped binding sites for 40 miRNAs in 11 target genes (Supplementary Table 2).	human	connective tissue	High+Lowthroughput	Inferring the Molecular Mechanisms of Noncoding Alzheimer's Disease-Associated Genetic Variants	是	rs4543938	Chronic myeloid leukemia	monocyte cells	E_01_0256	PCR,Flow cytometry	Analysis of miRNA seed disruption found that 46 variants across 5 tag regions (CELF1, FERMT2, INPP5D, MS4A6A, and ZCWPW1) overlapped binding sites for 40 miRNAs in 11 target genes (Supplementary Table 2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Analysis of miRNA seed disruption found that 46 variants across 5 tag regions (CELF1, FERMT2, INPP5D, MS4A6A, and ZCWPW1) overlapped binding sites for 40 miRNAs in 11 target genes (Supplementary Table 2).		Analysis of miRNA seed disruption found that 46 variants across 5 tag regions (CELF1, FERMT2, INPP5D, MS4A6A, and ZCWPW1) overlapped binding sites for 40 miRNAs in 11 target genes (Supplementary Table 2).	Immunohistochemical staining	Analysis of miRNA seed disruption found that 46 variants across 5 tag regions (CELF1, FERMT2, INPP5D, MS4A6A, and ZCWPW1) overlapped binding sites for 40 miRNAs in 11 target genes (Supplementary Table 2).			PCR,Flow cytometry				FERMT2
31560287	chr11	116832779	116834779	APOA1	Apolipoprotein A5 (ApoA5) has been shown as a vital regulator of lipid metabolism. Human APOA5 gene is located on the long arm of chromosome 11 adjacent to APOA1/APOC3/APOA4 gene clusters [7].	human	Fat	High+Lowthroughput	New Insights into Apolipoprotein A5 and the Modulation of Human Adipose-derived Mesenchymal Stem Cells Adipogenesis	是	无	Obesity	adipose-derived mesenchymal stem cells	E_01_0257	PCR,Western blot	Apolipoprotein A5 (ApoA5) has been shown as a vital regulator of lipid metabolism. Human APOA5 gene is located on the long arm of chromosome 11 adjacent to APOA1/APOC3/APOA4 gene clusters [7].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Apolipoprotein A5 (ApoA5) has been shown as a vital regulator of lipid metabolism. Human APOA5 gene is located on the long arm of chromosome 11 adjacent to APOA1/APOC3/APOA4 gene clusters [7].		Apolipoprotein A5 (ApoA5) has been shown as a vital regulator of lipid metabolism. Human APOA5 gene is located on the long arm of chromosome 11 adjacent to APOA1/APOC3/APOA4 gene clusters [7].	Immunohistochemical staining	Apolipoprotein A5 (ApoA5) has been shown as a vital regulator of lipid metabolism. Human APOA5 gene is located on the long arm of chromosome 11 adjacent to APOA1/APOC3/APOA4 gene clusters [7].			PCR,Western blot				APOA1
31558567	chrX	47579564	47581564	TIMP1	Among the 40 chemo_x0002_kines/cytokines we analyzed, nine were consistently up_x0002_regulated in Lats1/2 CKO sham hearts, including TIMP1, CXCL1, CXCL12, and CSF1.	human,mouse	bone	High+Lowthroughput	Hippo pathway deletion in adult resting cardiac fibroblasts initiates a cell state transition with spontaneous and self-sustaining fibrosis	否	无	miocardial infarction	myeloid cell	E_02_0201	PCR, flow cytometry, gene knockdown	Among the 40 chemo_x0002_kines/cytokines we analyzed, nine were consistently up_x0002_regulated in Lats1/2 CKO sham hearts, including TIMP1, CXCL1, CXCL12, and CSF1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Among the 40 chemo_x0002_kines/cytokines we analyzed, nine were consistently up_x0002_regulated in Lats1/2 CKO sham hearts, including TIMP1, CXCL1, CXCL12, and CSF1.		Among the 40 chemo_x0002_kines/cytokines we analyzed, nine were consistently up_x0002_regulated in Lats1/2 CKO sham hearts, including TIMP1, CXCL1, CXCL12, and CSF1.	Immunohistochemical staining	Among the 40 chemo_x0002_kines/cytokines we analyzed, nine were consistently up_x0002_regulated in Lats1/2 CKO sham hearts, including TIMP1, CXCL1, CXCL12, and CSF1.			PCR,Flow cytometry,基因敲降				TIMP1
31557715	chr7	25947403	25949403	MIR148A	Physical map of the region showing the position of annotated genes, MIR148A and genetic polymorphisms (SNPs, annotated with their rs identifiers) associated with obesity and other related phenotypes	human	connective tissue	High+Lowthroughput	Detailed Functional Characterization of a Waist-Hip Ratio Locus in 7p15.2 Defines an Enhancer Controlling Adipocyte Differentiation	是	rs1055144	liver cancer	mesenchymal stem cell	E_01_0258	PCR, flow cytometry, immunofluorescence staining	Physical map of the region showing the position of annotated genes, MIR148A and genetic polymorphisms (SNPs, annotated with their rs identifiers) associated with obesity and other related phenotypes	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Physical map of the region showing the position of annotated genes, MIR148A and genetic polymorphisms (SNPs, annotated with their rs identifiers) associated with obesity and other related phenotypes		Physical map of the region showing the position of annotated genes, MIR148A and genetic polymorphisms (SNPs, annotated with their rs identifiers) associated with obesity and other related phenotypes	Immunohistochemical staining	Physical map of the region showing the position of annotated genes, MIR148A and genetic polymorphisms (SNPs, annotated with their rs identifiers) associated with obesity and other related phenotypes			PCR,Flow cytometry,免疫荧光染色				MIR148A
31557715	chr7	26288944	26290944	SNX10	The region is delimited by the distal gene NPVF and the proximal gene SNX10.	human	Fat	High+Lowthroughput	Detailed Functional Characterization of a Waist-Hip Ratio Locus in 7p15.2 Defines an Enhancer Controlling Adipocyte Differentiation	是	rs7798002	liver cancer	SGBS cells	E_01_0258	PCR, flow cytometry, immunofluorescence staining	The region is delimited by the distal gene NPVF and the proximal gene SNX10.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The region is delimited by the distal gene NPVF and the proximal gene SNX10.		The region is delimited by the distal gene NPVF and the proximal gene SNX10.	Immunohistochemical staining	The region is delimited by the distal gene NPVF and the proximal gene SNX10.			PCR,Flow cytometry,免疫荧光染色				SNX10
31557715	chr1	203176161	203178161	CHI3L1	RNA-sequencing of cells with disrupted enhancer showed reduced expression of established adipocyte markers, such as ADIPOQ and LPL, and identified CHI3L1 on chromosome 1 as a potential gene involved in adipocyte differentiation. In conclusion, we identified and characterized an enhancer in the SNX10 locus, outlined its plausible mechanisms of action and downstream targets.	human	liver cancer	High+Lowthroughput	Detailed Functional Characterization of a Waist-Hip Ratio Locus in 7p15.2 Defines an Enhancer Controlling Adipocyte Differentiation	是	rs1451385	liver cancer	HepG2 cell	E_01_0258	PCR, flow cytometry, immunofluorescence staining	RNA-sequencing of cells with disrupted enhancer showed reduced expression of established adipocyte markers, such as ADIPOQ and LPL, and identified CHI3L1 on chromosome 1 as a potential gene involved in adipocyte differentiation. In conclusion, we identified and characterized an enhancer in the SNX10 locus, outlined its plausible mechanisms of action and downstream targets.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RNA-sequencing of cells with disrupted enhancer showed reduced expression of established adipocyte markers, such as ADIPOQ and LPL, and identified CHI3L1 on chromosome 1 as a potential gene involved in adipocyte differentiation. In conclusion, we identified and characterized an enhancer in the SNX10 locus, outlined its plausible mechanisms of action and downstream targets.		RNA-sequencing of cells with disrupted enhancer showed reduced expression of established adipocyte markers, such as ADIPOQ and LPL, and identified CHI3L1 on chromosome 1 as a potential gene involved in adipocyte differentiation. In conclusion, we identified and characterized an enhancer in the SNX10 locus, outlined its plausible mechanisms of action and downstream targets.	Immunohistochemical staining	RNA-sequencing of cells with disrupted enhancer showed reduced expression of established adipocyte markers, such as ADIPOQ and LPL, and identified CHI3L1 on chromosome 1 as a potential gene involved in adipocyte differentiation. In conclusion, we identified and characterized an enhancer in the SNX10 locus, outlined its plausible mechanisms of action and downstream targets.			PCR,Flow cytometry,免疫荧光染色				CHI3L1
31554806	chr1	37806934	37808934	MTF1	PSIONIC-predicted activity for MTF1 in cell line models correlates with sensitivity to MTF1 inhibition, showing the potential of our approach for personalized therapy. Many identified TFs are significantly associated with survival outcome	human	breast	High+Lowthroughput	Chromatin-informed inference of transcriptional programs in gynecologic and basal breast cancers	否	无	mammary cancer	breast cancer cell	E_01_0259	Flow cytometry	PSIONIC-predicted activity for MTF1 in cell line models correlates with sensitivity to MTF1 inhibition, showing the potential of our approach for personalized therapy. Many identified TFs are significantly associated with survival outcome	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	PSIONIC-predicted activity for MTF1 in cell line models correlates with sensitivity to MTF1 inhibition, showing the potential of our approach for personalized therapy. Many identified TFs are significantly associated with survival outcome		PSIONIC-predicted activity for MTF1 in cell line models correlates with sensitivity to MTF1 inhibition, showing the potential of our approach for personalized therapy. Many identified TFs are significantly associated with survival outcome	Immunohistochemical staining	PSIONIC-predicted activity for MTF1 in cell line models correlates with sensitivity to MTF1 inhibition, showing the potential of our approach for personalized therapy. Many identified TFs are significantly associated with survival outcome			Flow cytometry				MTF1
31551362	chr3	181709186	181711186	SOX2	We proposed SOX2 as a lineage_x0002_survival oncogene in squamous cell cancers for its essential role during the development in the specification of the squamous cell lineages by opposing the role of Nkx2-1 in the dividing foregut and its essentiality for LUSC cell survival (9).	human,mouse	lung	High+Lowthroughput	Epigenomic Profiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma	是	无	Lung squamous cell carcinoma	Lung squamous cell	E_02_0202	PCR, Western blot, flow cytometry, immunofluorescence staining	We proposed SOX2 as a lineage_x0002_survival oncogene in squamous cell cancers for its essential role during the development in the specification of the squamous cell lineages by opposing the role of Nkx2-1 in the dividing foregut and its essentiality for LUSC cell survival (9).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We proposed SOX2 as a lineage_x0002_survival oncogene in squamous cell cancers for its essential role during the development in the specification of the squamous cell lineages by opposing the role of Nkx2-1 in the dividing foregut and its essentiality for LUSC cell survival (9).		We proposed SOX2 as a lineage_x0002_survival oncogene in squamous cell cancers for its essential role during the development in the specification of the squamous cell lineages by opposing the role of Nkx2-1 in the dividing foregut and its essentiality for LUSC cell survival (9).	Immunohistochemical staining	We proposed SOX2 as a lineage_x0002_survival oncogene in squamous cell cancers for its essential role during the development in the specification of the squamous cell lineages by opposing the role of Nkx2-1 in the dividing foregut and its essentiality for LUSC cell survival (9).			PCR,Western blot,Flow cytometry,免疫荧光染色				SOX2
31551362	chr6	98831871	98833871	POU3F2	For the TCGA-LUSC RNA-seq data, the 501 LUSC tumor tissues were classified on the basis of the expression level of TP63, SOX2, and POU3F2.	human,mouse	kidney	High+Lowthroughput	Epigenomic Profiling Discovers Trans-lineage SOX2 Partnerships Driving Tumor Heterogeneity in Lung Squamous Cell Carcinoma	是	无		HEK293T	E_02_0202	PCR, Western blot, flow cytometry, immunofluorescence staining	For the TCGA-LUSC RNA-seq data, the 501 LUSC tumor tissues were classified on the basis of the expression level of TP63, SOX2, and POU3F2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	For the TCGA-LUSC RNA-seq data, the 501 LUSC tumor tissues were classified on the basis of the expression level of TP63, SOX2, and POU3F2.		For the TCGA-LUSC RNA-seq data, the 501 LUSC tumor tissues were classified on the basis of the expression level of TP63, SOX2, and POU3F2.	Immunohistochemical staining	For the TCGA-LUSC RNA-seq data, the 501 LUSC tumor tissues were classified on the basis of the expression level of TP63, SOX2, and POU3F2.			PCR,Western blot,Flow cytometry,免疫荧光染色				POU3F2
31551335	chr12	55963742	55965742	CDK2	HEAL-FUS complex binds the HIV promoter and enhances recruit_x0002_ment of the histone acetyltransferase p300, which positively regulates HIV transcrip_x0002_tion by increasing histone H3K27 acetylation and P-TEFb enrichment on the HIV promoter, and (ii) HEAL-FUS complex is enriched at the promoter of the cyclin_x0002_dependent kinase 2 gene, CDK2, to enhance CDK2 expression.	human	blood	High+Lowthroughput	The Long Noncoding RNA HEAL Regulates HIV-1 Replication through Epigenetic Regulation of the HIV-1 Promoter	否	无	AIDS	blood mononuclear cells	E_01_0260	Western blot,PCR	HEAL-FUS complex binds the HIV promoter and enhances recruit_x0002_ment of the histone acetyltransferase p300, which positively regulates HIV transcrip_x0002_tion by increasing histone H3K27 acetylation and P-TEFb enrichment on the HIV promoter, and (ii) HEAL-FUS complex is enriched at the promoter of the cyclin_x0002_dependent kinase 2 gene, CDK2, to enhance CDK2 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HEAL-FUS complex binds the HIV promoter and enhances recruit_x0002_ment of the histone acetyltransferase p300, which positively regulates HIV transcrip_x0002_tion by increasing histone H3K27 acetylation and P-TEFb enrichment on the HIV promoter, and (ii) HEAL-FUS complex is enriched at the promoter of the cyclin_x0002_dependent kinase 2 gene, CDK2, to enhance CDK2 expression.		HEAL-FUS complex binds the HIV promoter and enhances recruit_x0002_ment of the histone acetyltransferase p300, which positively regulates HIV transcrip_x0002_tion by increasing histone H3K27 acetylation and P-TEFb enrichment on the HIV promoter, and (ii) HEAL-FUS complex is enriched at the promoter of the cyclin_x0002_dependent kinase 2 gene, CDK2, to enhance CDK2 expression.	Immunohistochemical staining	HEAL-FUS complex binds the HIV promoter and enhances recruit_x0002_ment of the histone acetyltransferase p300, which positively regulates HIV transcrip_x0002_tion by increasing histone H3K27 acetylation and P-TEFb enrichment on the HIV promoter, and (ii) HEAL-FUS complex is enriched at the promoter of the cyclin_x0002_dependent kinase 2 gene, CDK2, to enhance CDK2 expression.			Western blot,PCR				CDK2
31551335	chr11	65419837	65421837	NEAT1	The first evidence that lncRNAs might be involved in HIV-1 replication came from experiments in the Jurkat T cell line, in which knockdown (KD) of NEAT1 increased viral production by enhancing the nuclear export of Rev-dependent instability element (INS)-containing HIV-1 mRNAs	human	blood	High+Lowthroughput	The Long Noncoding RNA HEAL Regulates HIV-1 Replication through Epigenetic Regulation of the HIV-1 Promoter	否	无	AIDS	T cell	E_01_0260	Western blot,PCR	The first evidence that lncRNAs might be involved in HIV-1 replication came from experiments in the Jurkat T cell line, in which knockdown (KD) of NEAT1 increased viral production by enhancing the nuclear export of Rev-dependent instability element (INS)-containing HIV-1 mRNAs	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The first evidence that lncRNAs might be involved in HIV-1 replication came from experiments in the Jurkat T cell line, in which knockdown (KD) of NEAT1 increased viral production by enhancing the nuclear export of Rev-dependent instability element (INS)-containing HIV-1 mRNAs		The first evidence that lncRNAs might be involved in HIV-1 replication came from experiments in the Jurkat T cell line, in which knockdown (KD) of NEAT1 increased viral production by enhancing the nuclear export of Rev-dependent instability element (INS)-containing HIV-1 mRNAs	Immunohistochemical staining	The first evidence that lncRNAs might be involved in HIV-1 replication came from experiments in the Jurkat T cell line, in which knockdown (KD) of NEAT1 increased viral production by enhancing the nuclear export of Rev-dependent instability element (INS)-containing HIV-1 mRNAs			Western blot,PCR				NEAT1
31551256	chr9	134027777	134029777	BRD3	BRD3 is recruited to and controls the activity of a subset ERa transcriptional enhancers, providing a therapeu_x0002_tic opportunity to target BRD3 with BET inhibitors in ERa_x0002_positive breast cancers.	human	breast	High+Lowthroughput	Distinct Roles for BET Family Members in Estrogen Receptor α Enhancer Function and Gene Regulation in Breast Cancer Cells	否	无	mammary cancer	breast cancer cell	E_01_0261	Western blot,PCR,Flow cytometry	BRD3 is recruited to and controls the activity of a subset ERa transcriptional enhancers, providing a therapeu_x0002_tic opportunity to target BRD3 with BET inhibitors in ERa_x0002_positive breast cancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	BRD3 is recruited to and controls the activity of a subset ERa transcriptional enhancers, providing a therapeu_x0002_tic opportunity to target BRD3 with BET inhibitors in ERa_x0002_positive breast cancers.		BRD3 is recruited to and controls the activity of a subset ERa transcriptional enhancers, providing a therapeu_x0002_tic opportunity to target BRD3 with BET inhibitors in ERa_x0002_positive breast cancers.	Immunohistochemical staining	BRD3 is recruited to and controls the activity of a subset ERa transcriptional enhancers, providing a therapeu_x0002_tic opportunity to target BRD3 with BET inhibitors in ERa_x0002_positive breast cancers.			Western blot,PCR,Flow cytometry				BRD3
31551012	chr7	148804569	148806569	EZH2	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	human	stomach	High+Lowthroughput	HOXD-AS1 confers cisplatin resistance in gastric cancer through epigenetically silencing PDCD4 via recruiting EZH2	否	无	gastric cancer	gastric cancer cell	E_01_0262	Western blot,PCR	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	Immunohistochemical staining	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	EZH2		Western blot,PCR	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells			
31551012	chr10	110869187	110871187	PDCD4	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	human	stomach	High+Lowthroughput	HOXD-AS1 confers cisplatin resistance in gastric cancer through epigenetically silencing PDCD4 via recruiting EZH2	否	无	gastric cancer	gastric cancer cell	E_01_0262	Western blot,PCR	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells		Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells	Immunohistochemical staining	Additionally, HOXD-AS1 epigenetically silenced PDCD4 through binding to the histone methyltransferase enhancer of zeste homologue 2 (EZH2) on the promoter of PDCD4, thus increasing H3K27me3. More importantly, PDCD4 silencing coun_x0002_teracted HOXD-AS1 knockdown-mediated enhancement of DDP sensitivity in DDP-resistant gastric cancer cells			Western blot,PCR				PDCD4
31550664	chr17	13222491	13224491	Sod2	Specifically, we used Mn2+-superoxide dismutase (Sod2) deficient mice, in which oxidative stress is significantly increased even in a heterozygous state [6].	human,mouse	pancreas	High+Lowthroughput	Gestational oxidative stress protects against adult obesity and insulin resistance	否	无	Pancreatic β - cell dysfunction	Beta cell	E_02_0203	PCR	Specifically, we used Mn2+-superoxide dismutase (Sod2) deficient mice, in which oxidative stress is significantly increased even in a heterozygous state [6].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Specifically, we used Mn2+-superoxide dismutase (Sod2) deficient mice, in which oxidative stress is significantly increased even in a heterozygous state [6].		Specifically, we used Mn2+-superoxide dismutase (Sod2) deficient mice, in which oxidative stress is significantly increased even in a heterozygous state [6].	Immunohistochemical staining	Specifically, we used Mn2+-superoxide dismutase (Sod2) deficient mice, in which oxidative stress is significantly increased even in a heterozygous state [6].			PCR				Sod2
31548608	chr9	107481891	107483891	KLF4	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	human,mouse	connective tissue	High+Lowthroughput	KLF4 is involved in the organization and regulation of pluripotency-associated three-dimensional enhancer networks	否	无		pluripotent stem cell	E_02_0204	Western blot,PCR,Flow cytometry	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22		The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	Immunohistochemical staining	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22			Western blot,PCR,Flow cytometry				KLF4
31548608	chr17	35814159	35816159	Pou5f1	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	human,mouse	connective tissue	High+Lowthroughput	KLF4 is involved in the organization and regulation of pluripotency-associated three-dimensional enhancer networks	否	无		pluripotent stem cell	E_02_0204	Western blot,PCR,Flow cytometry	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22		The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	Immunohistochemical staining	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22			Western blot,PCR,Flow cytometry				Pou5f1
31548608	chr4	56645505	56647505	HOPX	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	human,mouse	connective tissue	High+Lowthroughput	KLF4 is involved in the organization and regulation of pluripotency-associated three-dimensional enhancer networks	否	无		pluripotent stem cell	E_02_0204	Western blot,PCR,Flow cytometry	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22		The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22	Immunohistochemical staining	The architectural function of KLF4 is further supported by the observations that KLF4 depletion abrogates long-range chromatin contacts at specific genomic loci, such as the Pou5f1 (Oct4) locus in mouse PSCs18 and the HOPX gene in human epidermal keratinocytes22			Western blot,PCR,Flow cytometry				HOPX
31547883	chr16	67559930	67561930	CTCF	In the lysates from starved cells, the recip_x0002_rocal pull-down of CTCF and CGGBP1 was very weak. In lysates from stimulated cells, however, using CGGBP1 antibody we could pull down a major fraction of CTCF (Fig.  2b).	human	kidney	High+Lowthroughput	CGGBP1 regulates CTCF occupancy at repeats	否	无		HEK293T	E_01_0263	Flow cytometry,PCR	In the lysates from starved cells, the recip_x0002_rocal pull-down of CTCF and CGGBP1 was very weak. In lysates from stimulated cells, however, using CGGBP1 antibody we could pull down a major fraction of CTCF (Fig.  2b).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In the lysates from starved cells, the recip_x0002_rocal pull-down of CTCF and CGGBP1 was very weak. In lysates from stimulated cells, however, using CGGBP1 antibody we could pull down a major fraction of CTCF (Fig.  2b).	Immunohistochemical staining	In the lysates from starved cells, the recip_x0002_rocal pull-down of CTCF and CGGBP1 was very weak. In lysates from stimulated cells, however, using CGGBP1 antibody we could pull down a major fraction of CTCF (Fig.  2b).	CTCF		Flow cytometry,PCR	In the lysates from starved cells, the recip_x0002_rocal pull-down of CTCF and CGGBP1 was very weak. In lysates from stimulated cells, however, using CGGBP1 antibody we could pull down a major fraction of CTCF (Fig.  2b).			
31547433	chr13	40553074	40555074	FOXO1	The forkhead box protein class O type 1 (FOXO1) also participates in adipogenesis, by preventing adipose tissue differentiation through the inhibition of PPAR-γ transcription.	human,mouse	connective tissue	High+Lowthroughput	Transcriptional Analysis of FOXO1, C/EBP-α and PPAR-γ2 Genes and Their Association with Obesity-Related Insulin Resistance	否	无	Obesity	NIH-3T3 fibroblastic cell	E_02_0205	Western blot,PCR	The forkhead box protein class O type 1 (FOXO1) also participates in adipogenesis, by preventing adipose tissue differentiation through the inhibition of PPAR-γ transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The forkhead box protein class O type 1 (FOXO1) also participates in adipogenesis, by preventing adipose tissue differentiation through the inhibition of PPAR-γ transcription.		The forkhead box protein class O type 1 (FOXO1) also participates in adipogenesis, by preventing adipose tissue differentiation through the inhibition of PPAR-γ transcription.	Immunohistochemical staining	The forkhead box protein class O type 1 (FOXO1) also participates in adipogenesis, by preventing adipose tissue differentiation through the inhibition of PPAR-γ transcription.			Western blot,PCR				FOXO1
31546863	chr11	36480909	36482909	TRAF6	sion of the proteins involved in osteoclastogenesis including TRAF6, c-Fos, NFATc1, and cathepsin K. Western blotting indicated that RANKL significantly increased the expression of TRAF6, NFATc1, and cathepsin K. Pre-treatm	mouse	blood	High+Lowthroughput	Egg White Ovotransferrin Attenuates RANKL-Induced Osteoclastogenesis and Bone Resorption	否	无	osteoporosis	B cell	E_02_0206	Western blot,PCR	sion of the proteins involved in osteoclastogenesis including TRAF6, c-Fos, NFATc1, and cathepsin K. Western blotting indicated that RANKL significantly increased the expression of TRAF6, NFATc1, and cathepsin K. Pre-treatm	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	sion of the proteins involved in osteoclastogenesis including TRAF6, c-Fos, NFATc1, and cathepsin K. Western blotting indicated that RANKL significantly increased the expression of TRAF6, NFATc1, and cathepsin K. Pre-treatm		sion of the proteins involved in osteoclastogenesis including TRAF6, c-Fos, NFATc1, and cathepsin K. Western blotting indicated that RANKL significantly increased the expression of TRAF6, NFATc1, and cathepsin K. Pre-treatm	Immunohistochemical staining	sion of the proteins involved in osteoclastogenesis including TRAF6, c-Fos, NFATc1, and cathepsin K. Western blotting indicated that RANKL significantly increased the expression of TRAF6, NFATc1, and cathepsin K. Pre-treatm			Western blot,PCR				TRAF6
31546763	chr4	77508709	77510709	CXCL13	During the disease state, this subset of mDCs displayed heightened toll-like receptors 7 and 9 (TLR 7/9) responses with increased interleukin 10 (IL-10) and C-X-C motif chemokine ligand 13 (CXCL13) expressions.	human,mouse	blood	High+Lowthroughput	Heightened TLR7/9-Induced IL-10 and CXCL13 Production with Dysregulated NF-?B Activation in CD11c(hi)CD11b(+) Dendritic Cells in NZB/W F1 Mice	否	无	Systemic lupus erythematosus	T cell	E_02_0207	Western blot,PCR,Flow cytometry	During the disease state, this subset of mDCs displayed heightened toll-like receptors 7 and 9 (TLR 7/9) responses with increased interleukin 10 (IL-10) and C-X-C motif chemokine ligand 13 (CXCL13) expressions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	During the disease state, this subset of mDCs displayed heightened toll-like receptors 7 and 9 (TLR 7/9) responses with increased interleukin 10 (IL-10) and C-X-C motif chemokine ligand 13 (CXCL13) expressions.		During the disease state, this subset of mDCs displayed heightened toll-like receptors 7 and 9 (TLR 7/9) responses with increased interleukin 10 (IL-10) and C-X-C motif chemokine ligand 13 (CXCL13) expressions.	Immunohistochemical staining	During the disease state, this subset of mDCs displayed heightened toll-like receptors 7 and 9 (TLR 7/9) responses with increased interleukin 10 (IL-10) and C-X-C motif chemokine ligand 13 (CXCL13) expressions.			Western blot,PCR,Flow cytometry				CXCL13
31546150	chr16	68734373	68736373	CDH1	EMT is a process in which epithelial cells lose their cell junctions and polarity characterized by E-cadherin (CDH1) downregulation to gain a motile mesenchymal phenotype, in_x0002_duction of a series of mesenchymal-specific transcription factors, such as Snail1, Snail2, ZEB1, ZEB2 and Twist1.	human,mouse	pancreas	High+Lowthroughput	Menin Coordinates C/EBPβ-Mediated TGF-β Signaling for Epithelial-Mesenchymal Transition and Growth Inhibition in Pancreatic Cancer	否	无	Pancreatic ductal adenocarcinoma	PANC1 cells	E_02_0208	Western blot,PCR,Flow cytometry	EMT is a process in which epithelial cells lose their cell junctions and polarity characterized by E-cadherin (CDH1) downregulation to gain a motile mesenchymal phenotype, in_x0002_duction of a series of mesenchymal-specific transcription factors, such as Snail1, Snail2, ZEB1, ZEB2 and Twist1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EMT is a process in which epithelial cells lose their cell junctions and polarity characterized by E-cadherin (CDH1) downregulation to gain a motile mesenchymal phenotype, in_x0002_duction of a series of mesenchymal-specific transcription factors, such as Snail1, Snail2, ZEB1, ZEB2 and Twist1.		EMT is a process in which epithelial cells lose their cell junctions and polarity characterized by E-cadherin (CDH1) downregulation to gain a motile mesenchymal phenotype, in_x0002_duction of a series of mesenchymal-specific transcription factors, such as Snail1, Snail2, ZEB1, ZEB2 and Twist1.	Immunohistochemical staining	EMT is a process in which epithelial cells lose their cell junctions and polarity characterized by E-cadherin (CDH1) downregulation to gain a motile mesenchymal phenotype, in_x0002_duction of a series of mesenchymal-specific transcription factors, such as Snail1, Snail2, ZEB1, ZEB2 and Twist1.			Western blot,PCR,Flow cytometry				CDH1
31546122	chr11	120694060	120696060	Fasn	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).	mouse	connective tissue	High+Lowthroughput	Promoting differentiation and lipid metabolism are the primary effects for DINP exposure on 3T3-L1 preadipocytes	否	无		3T3-L1 cell	E_02_0209	PCR,Western blot,Flow cytometry	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).		We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).	Immunohistochemical staining	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).			PCR,Western blot,Flow cytometry				Fasn
31546122	chr16	22962769	22964769	Adipoq	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).	mouse	kidney	High+Lowthroughput	Promoting differentiation and lipid metabolism are the primary effects for DINP exposure on 3T3-L1 preadipocytes	否	无		HEK-293T cells	E_02_0209	PCR,Western blot,Flow cytometry	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).		We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).	Immunohistochemical staining	We also measured the expression of adiponectin (Adipoq), li_x0002_poprotein lipase (Lpl), and fatty acid synthase (Fasn), which were reported to be used as adipogenesis markers, and the results showed that the DINP exposure induced the upregulation of Adipoq and Lpl, however, unlike Rosi, the Fasn was not significantly affected with DINP exposure (Fig. S4).			PCR,Western blot,Flow cytometry				Adipoq
31545422	chr7	148804556	148806556	EZH2	In this study, we found that inhibition of enhancer of zeste homolog 2 (EZH2) resulted in suppressed EMT in HNSCC in vitro and in vivo.	human	neck	High+Lowthroughput	Targeting of EZH2 inhibits epithelial?mesenchymal transition in head and neck squamous cell carcinoma via regulating the STAT3/VEGFR2 axis	否	无	cancer	neck squamous cell	E_01_0264	PCR, Western blot, immunofluorescence staining	In this study, we found that inhibition of enhancer of zeste homolog 2 (EZH2) resulted in suppressed EMT in HNSCC in vitro and in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In this study, we found that inhibition of enhancer of zeste homolog 2 (EZH2) resulted in suppressed EMT in HNSCC in vitro and in vivo.	Immunohistochemical staining	In this study, we found that inhibition of enhancer of zeste homolog 2 (EZH2) resulted in suppressed EMT in HNSCC in vitro and in vivo.	EZH2		PCR,Western blot,免疫荧光染色	In this study, we found that inhibition of enhancer of zeste homolog 2 (EZH2) resulted in suppressed EMT in HNSCC in vitro and in vivo.			
31545422	chr17	42310472	42312472	STAT3	We reported that signal transducer and activator of transcription factor 3 (STAT3)/vascular endothelial growth factor receptor 2 (VEGFR2) axis served as the downstream signaling of EZH2 and mediated EMT in HNSCC.	human	Head, neck	High+Lowthroughput	Targeting of EZH2 inhibits epithelial?mesenchymal transition in head and neck squamous cell carcinoma via regulating the STAT3/VEGFR2 axis	否	无	cancer	HNSCC cells	E_01_0264	PCR, Western blot, immunofluorescence staining	We reported that signal transducer and activator of transcription factor 3 (STAT3)/vascular endothelial growth factor receptor 2 (VEGFR2) axis served as the downstream signaling of EZH2 and mediated EMT in HNSCC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We reported that signal transducer and activator of transcription factor 3 (STAT3)/vascular endothelial growth factor receptor 2 (VEGFR2) axis served as the downstream signaling of EZH2 and mediated EMT in HNSCC.	Immunohistochemical staining	We reported that signal transducer and activator of transcription factor 3 (STAT3)/vascular endothelial growth factor receptor 2 (VEGFR2) axis served as the downstream signaling of EZH2 and mediated EMT in HNSCC.	STAT3		PCR,Western blot,免疫荧光染色	We reported that signal transducer and activator of transcription factor 3 (STAT3)/vascular endothelial growth factor receptor 2 (VEGFR2) axis served as the downstream signaling of EZH2 and mediated EMT in HNSCC.			
31544892	chr13	30453885	30455885	HMGB1	In this study, we examined the role of Ig and Ek enhancers in enhancing SHM in the episomal vector pCEP4 that expresses an anti-high mobility group box 1 (HMGB1) full-length antibody.	human,Hamster	ovary	High+Lowthroughput	Enhancers Improve the AID-Induced Hypermutation in Episomal Vector for Antibody Affinity Maturation in Mammalian Cell Display	否	无	cancer	CHO cells	E_02_0210	Flow cytometry	In this study, we examined the role of Ig and Ek enhancers in enhancing SHM in the episomal vector pCEP4 that expresses an anti-high mobility group box 1 (HMGB1) full-length antibody.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we examined the role of Ig and Ek enhancers in enhancing SHM in the episomal vector pCEP4 that expresses an anti-high mobility group box 1 (HMGB1) full-length antibody.		In this study, we examined the role of Ig and Ek enhancers in enhancing SHM in the episomal vector pCEP4 that expresses an anti-high mobility group box 1 (HMGB1) full-length antibody.	Immunohistochemical staining	In this study, we examined the role of Ig and Ek enhancers in enhancing SHM in the episomal vector pCEP4 that expresses an anti-high mobility group box 1 (HMGB1) full-length antibody.			Flow cytometry				HMGB1
31542774	chr19	29809345	29811345	CCNE1	By integrating SVs associated with acetylated chro_x0002_matin identified by paired-end NanoChIP-seq (PeNChIP-seq) with whole-genome sequencing (WGS) analysis of a large GC cohort, we observed enhancer hijacking events in GC targeting CCNE1, IGF2 and CCND1.	human	blood	High+Lowthroughput	Integrated paired-end enhancer profiling and whole-genome sequencing reveals recurrent CCNE1 and IGF2 enhancer hijacking in primary gastric adenocarcinoma	否	无	gastric cancer	B cell	E_01_0265	PCR,Flow cytometry	By integrating SVs associated with acetylated chro_x0002_matin identified by paired-end NanoChIP-seq (PeNChIP-seq) with whole-genome sequencing (WGS) analysis of a large GC cohort, we observed enhancer hijacking events in GC targeting CCNE1, IGF2 and CCND1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			By integrating SVs associated with acetylated chro_x0002_matin identified by paired-end NanoChIP-seq (PeNChIP-seq) with whole-genome sequencing (WGS) analysis of a large GC cohort, we observed enhancer hijacking events in GC targeting CCNE1, IGF2 and CCND1.	Immunohistochemical staining	By integrating SVs associated with acetylated chro_x0002_matin identified by paired-end NanoChIP-seq (PeNChIP-seq) with whole-genome sequencing (WGS) analysis of a large GC cohort, we observed enhancer hijacking events in GC targeting CCNE1, IGF2 and CCND1.	CCNE1		PCR,Flow cytometry	By integrating SVs associated with acetylated chro_x0002_matin identified by paired-end NanoChIP-seq (PeNChIP-seq) with whole-genome sequencing (WGS) analysis of a large GC cohort, we observed enhancer hijacking events in GC targeting CCNE1, IGF2 and CCND1.			
31541592	chr6	35570844	35572844	FKBP5	We then carried out qRT‐PCR using primers of APP and FKBP5, a representative AR target gene, to evaluate their expression at the mRNA level.	human	bone	High+Lowthroughput	Amyloid precursor protein, an androgen-regulated gene, is targeted by RNA-binding protein PSF/SFPQ in neuronal cells	否	无	Osteoma	SH‐SY5Y cells	E_01_0266	PCR,Western blot	We then carried out qRT‐PCR using primers of APP and FKBP5, a representative AR target gene, to evaluate their expression at the mRNA level.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We then carried out qRT‐PCR using primers of APP and FKBP5, a representative AR target gene, to evaluate their expression at the mRNA level.		We then carried out qRT‐PCR using primers of APP and FKBP5, a representative AR target gene, to evaluate their expression at the mRNA level.	Immunohistochemical staining	We then carried out qRT‐PCR using primers of APP and FKBP5, a representative AR target gene, to evaluate their expression at the mRNA level.			PCR,Western blot				FKBP5
31538139	chr3	186839743	186841743	ADIPOQ	The 50,336 ATAC-seq peaks that were more accessible in primary human adipocytes (‘adipocyte accessible’) included the promoters of the ADIPOQ and PPARGC1A genes with known adipocyte-spe_x0002_cific expression (Fig. 1c,d), providing evidence that we successfully differentiated adipocytes in vitro.	human	Fat	High+Lowthroughput	Reverse gene-environment interaction approach to identify variants influencing body-mass index in humans	是	rs10788522		fat cell	E_01_0267	PCR,Flow cytometry	The 50,336 ATAC-seq peaks that were more accessible in primary human adipocytes (‘adipocyte accessible’) included the promoters of the ADIPOQ and PPARGC1A genes with known adipocyte-spe_x0002_cific expression (Fig. 1c,d), providing evidence that we successfully differentiated adipocytes in vitro.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The 50,336 ATAC-seq peaks that were more accessible in primary human adipocytes (‘adipocyte accessible’) included the promoters of the ADIPOQ and PPARGC1A genes with known adipocyte-spe_x0002_cific expression (Fig. 1c,d), providing evidence that we successfully differentiated adipocytes in vitro.		The 50,336 ATAC-seq peaks that were more accessible in primary human adipocytes (‘adipocyte accessible’) included the promoters of the ADIPOQ and PPARGC1A genes with known adipocyte-spe_x0002_cific expression (Fig. 1c,d), providing evidence that we successfully differentiated adipocytes in vitro.	Immunohistochemical staining	The 50,336 ATAC-seq peaks that were more accessible in primary human adipocytes (‘adipocyte accessible’) included the promoters of the ADIPOQ and PPARGC1A genes with known adipocyte-spe_x0002_cific expression (Fig. 1c,d), providing evidence that we successfully differentiated adipocytes in vitro.			PCR,Flow cytometry				ADIPOQ
31536603	chr22	43148768	43150768	TSPO	The 18- kDa translocator protein TSPO is used as an imaging target in positron emission tomogra_x0002_phy to detect neuroinflammation, and its expression is correlated with microglial activation	human,mouse	Nervous tissue	High+Lowthroughput	Lipopolysaccharide induces mouse translocator protein (18 kDa) expression via the AP-1 complex in the microglial cell line, BV-2	否	无	Neuroinflammation	microglial cell	E_02_0211	PCR, Western blot, immunofluorescence staining	The 18- kDa translocator protein TSPO is used as an imaging target in positron emission tomogra_x0002_phy to detect neuroinflammation, and its expression is correlated with microglial activation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The 18- kDa translocator protein TSPO is used as an imaging target in positron emission tomogra_x0002_phy to detect neuroinflammation, and its expression is correlated with microglial activation		The 18- kDa translocator protein TSPO is used as an imaging target in positron emission tomogra_x0002_phy to detect neuroinflammation, and its expression is correlated with microglial activation	Immunohistochemical staining	The 18- kDa translocator protein TSPO is used as an imaging target in positron emission tomogra_x0002_phy to detect neuroinflammation, and its expression is correlated with microglial activation			PCR,Western blot,免疫荧光染色				TSPO
31536603	chr1	32289598	32291598	HDAC1	In addition, the binding of histone deacetylase 1 (HDAC1) to the enhancer region, which contains the AP-1 site, was decreased by LPS treatment, but there were no significant differences in HDAC1 binding to the proximal promoter region with or without LPS.	human,mouse	connective tissue	High+Lowthroughput	Lipopolysaccharide induces mouse translocator protein (18 kDa) expression via the AP-1 complex in the microglial cell line, BV-2	否	无	Neuroinflammation	immune cell	E_02_0211	PCR, Western blot, immunofluorescence staining	In addition, the binding of histone deacetylase 1 (HDAC1) to the enhancer region, which contains the AP-1 site, was decreased by LPS treatment, but there were no significant differences in HDAC1 binding to the proximal promoter region with or without LPS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, the binding of histone deacetylase 1 (HDAC1) to the enhancer region, which contains the AP-1 site, was decreased by LPS treatment, but there were no significant differences in HDAC1 binding to the proximal promoter region with or without LPS.		In addition, the binding of histone deacetylase 1 (HDAC1) to the enhancer region, which contains the AP-1 site, was decreased by LPS treatment, but there were no significant differences in HDAC1 binding to the proximal promoter region with or without LPS.	Immunohistochemical staining	In addition, the binding of histone deacetylase 1 (HDAC1) to the enhancer region, which contains the AP-1 site, was decreased by LPS treatment, but there were no significant differences in HDAC1 binding to the proximal promoter region with or without LPS.			PCR,Western blot,免疫荧光染色				HDAC1
31535083	chr6	90460328	90462328	Aldh1l1	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).	human,mouse	Epithelial tissues	High+Lowthroughput	Genomic and epigenomic mapping of leptin-responsive neuronal populations involved in body weight regulation	是	rs11804091	Obesity	endothelial cell	E_02_0212	Immunofluorescence staining, chip, flow cytometry	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).		We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).	Immunohistochemical staining	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).			免疫荧光染色,CHIP,Flow cytometry				Aldh1l1
31535083	chr9	119727541	119729541	Cx3cr1	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).	human,mouse	tumour	High+Lowthroughput	Genomic and epigenomic mapping of leptin-responsive neuronal populations involved in body weight regulation	是	rs11804091	Obesity	tumor cell	E_02_0212	Immunofluorescence staining, chip, flow cytometry	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).		We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).	Immunohistochemical staining	We performed RNA-seq both on GFP+ and GFP− sorted nuclei in all physiological conditions tested. The specificity of our nuclei isolation protocol was validated by the high level of enrichment of Lepr and by the strong depletion of genes spe_x0002_cifically expressed in oligodendrocytes (Mag), microglia (Cx3cr1) and astrocytes (Aldh1l1) (Fig. 2a).			免疫荧光染色,CHIP,Flow cytometry				Cx3cr1
31534142	chr16	67559649	67561649	CTCF	To evaluate the specificity of epigenome editing systematically, we used ChIP-seq to map H3K9me3 and CTCF genome-wide in HEK293 cells after CTCF disruption by dCas9-KRAB (Fig. 1d, e).	human	kidney	High+Lowthroughput	Epigenome editing strategies for the functional annotation of CTCF insulators	否	无	tumour	HEK293 cell	E_01_0268	PCR,Flow cytometry	To evaluate the specificity of epigenome editing systematically, we used ChIP-seq to map H3K9me3 and CTCF genome-wide in HEK293 cells after CTCF disruption by dCas9-KRAB (Fig. 1d, e).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			To evaluate the specificity of epigenome editing systematically, we used ChIP-seq to map H3K9me3 and CTCF genome-wide in HEK293 cells after CTCF disruption by dCas9-KRAB (Fig. 1d, e).	Immunohistochemical staining	To evaluate the specificity of epigenome editing systematically, we used ChIP-seq to map H3K9me3 and CTCF genome-wide in HEK293 cells after CTCF disruption by dCas9-KRAB (Fig. 1d, e).	CTCF		PCR,Flow cytometry	To evaluate the specificity of epigenome editing systematically, we used ChIP-seq to map H3K9me3 and CTCF genome-wide in HEK293 cells after CTCF disruption by dCas9-KRAB (Fig. 1d, e).			
31534142	chr4	54096948	54098948	GSX2	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	human		High+Lowthroughput	Epigenome editing strategies for the functional annotation of CTCF insulators	否	无	tumour		E_01_0268	PCR,Flow cytometry	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.		We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	Immunohistochemical staining	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.			PCR,Flow cytometry				GSX2
31534142	chr4	54226570	54228570	PDGFRA	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	human		High+Lowthroughput	Epigenome editing strategies for the functional annotation of CTCF insulators	否	无	tumour		E_01_0268	PCR,Flow cytometry	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	Immunohistochemical staining	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.	PDGFRA		PCR,Flow cytometry	We found that the interaction between the GSX2 promoter and the PDGFRA insulator was reduced by disruption of the latter, albeit to a lesser extent than that observed for the PDGFRA promoter viewpoint.			
31533028	chr21	34785012	34787012	RUNX1	The t(8;21) (q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoiet_x0002_ic master regulator RUNX1.	human	blood	High+Lowthroughput	RUNX1-ETO Depletion in t(8;21) AML Leads to C/EBPα- and AP-1-Mediated Alterations in Enhancer-Promoter Interaction	否	无	leukemia	hematopoietic stem cell	E_01_0269	PCR,Flow cytometry	The t(8;21) (q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoiet_x0002_ic master regulator RUNX1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The t(8;21) (q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoiet_x0002_ic master regulator RUNX1.	Immunohistochemical staining	The t(8;21) (q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoiet_x0002_ic master regulator RUNX1.	RUNX1		PCR,Flow cytometry	The t(8;21) (q22;q22) translocation generates the RUNX1-ETO fusion protein, which interferes with the hematopoiet_x0002_ic master regulator RUNX1.			
31533028	chr12	4266618	4268618	CCND2	Figure 2F shows an example of interactions at the upregulated CCND2 gene, which shows changes in interactions between its promoter and two up_x0002_stream distal elements (depicted in red).	human	blood	High+Lowthroughput	RUNX1-ETO Depletion in t(8;21) AML Leads to C/EBPα- and AP-1-Mediated Alterations in Enhancer-Promoter Interaction	否	无	leukemia	Kasumi-1 cells	E_01_0269	PCR,Flow cytometry	Figure 2F shows an example of interactions at the upregulated CCND2 gene, which shows changes in interactions between its promoter and two up_x0002_stream distal elements (depicted in red).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Figure 2F shows an example of interactions at the upregulated CCND2 gene, which shows changes in interactions between its promoter and two up_x0002_stream distal elements (depicted in red).		Figure 2F shows an example of interactions at the upregulated CCND2 gene, which shows changes in interactions between its promoter and two up_x0002_stream distal elements (depicted in red).	Immunohistochemical staining	Figure 2F shows an example of interactions at the upregulated CCND2 gene, which shows changes in interactions between its promoter and two up_x0002_stream distal elements (depicted in red).			PCR,Flow cytometry				CCND2
31531679	chr16	86564387	86566387	FOXC2	FOXC2 is a transcription factor essential for inducing podocyte diferentiation, development and maturation, and is considered to be the earliest podocyte marker.	human	Epithelial tissues	High+Lowthroughput	Evidence for miR-548c-5p regulation of FOXC2 transcription through a distal genomic target site in human podocytes	否	无		epithelial cell	E_01_0270	PCR, Western blot, immunofluorescence staining	FOXC2 is a transcription factor essential for inducing podocyte diferentiation, development and maturation, and is considered to be the earliest podocyte marker.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FOXC2 is a transcription factor essential for inducing podocyte diferentiation, development and maturation, and is considered to be the earliest podocyte marker.	Immunohistochemical staining	FOXC2 is a transcription factor essential for inducing podocyte diferentiation, development and maturation, and is considered to be the earliest podocyte marker.	FOXC2		PCR,Western blot,免疫荧光染色	FOXC2 is a transcription factor essential for inducing podocyte diferentiation, development and maturation, and is considered to be the earliest podocyte marker.			
31531679	chr1	179548051	179550051	NPHS2	As the earliest podocyte marker, it has a prominent role in the diferen_x0002_tiation, development and maturation of podocytes, through the transcriptional regulation of a variety of diferent genes, such as podocin (NPHS2) [20, 22].	human	Epithelial tissues	High+Lowthroughput	Evidence for miR-548c-5p regulation of FOXC2 transcription through a distal genomic target site in human podocytes	否	无		epithelial cell	E_01_0270	PCR, Western blot, immunofluorescence staining	As the earliest podocyte marker, it has a prominent role in the diferen_x0002_tiation, development and maturation of podocytes, through the transcriptional regulation of a variety of diferent genes, such as podocin (NPHS2) [20, 22].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	As the earliest podocyte marker, it has a prominent role in the diferen_x0002_tiation, development and maturation of podocytes, through the transcriptional regulation of a variety of diferent genes, such as podocin (NPHS2) [20, 22].		As the earliest podocyte marker, it has a prominent role in the diferen_x0002_tiation, development and maturation of podocytes, through the transcriptional regulation of a variety of diferent genes, such as podocin (NPHS2) [20, 22].	Immunohistochemical staining	As the earliest podocyte marker, it has a prominent role in the diferen_x0002_tiation, development and maturation of podocytes, through the transcriptional regulation of a variety of diferent genes, such as podocin (NPHS2) [20, 22].			PCR,Western blot,免疫荧光染色				NPHS2
31531679	chr16	86527297	86529297	MTHFSD	Schematic alignment of human vs mouse synteny of the miRNA target region. Head-to-head arrangement of MTHFSD and FOXC2 in mouse chromosome 8 corresponds to (or is syntenic to) human chromosome 16.	human	Epithelial tissues	High+Lowthroughput	Evidence for miR-548c-5p regulation of FOXC2 transcription through a distal genomic target site in human podocytes	否	无		epithelial cell	E_01_0270	PCR, Western blot, immunofluorescence staining	Schematic alignment of human vs mouse synteny of the miRNA target region. Head-to-head arrangement of MTHFSD and FOXC2 in mouse chromosome 8 corresponds to (or is syntenic to) human chromosome 16.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Schematic alignment of human vs mouse synteny of the miRNA target region. Head-to-head arrangement of MTHFSD and FOXC2 in mouse chromosome 8 corresponds to (or is syntenic to) human chromosome 16.		Schematic alignment of human vs mouse synteny of the miRNA target region. Head-to-head arrangement of MTHFSD and FOXC2 in mouse chromosome 8 corresponds to (or is syntenic to) human chromosome 16.	Immunohistochemical staining	Schematic alignment of human vs mouse synteny of the miRNA target region. Head-to-head arrangement of MTHFSD and FOXC2 in mouse chromosome 8 corresponds to (or is syntenic to) human chromosome 16.			PCR,Western blot,免疫荧光染色				MTHFSD
31530818	chr8	127732403	127734403	MYC	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	human	blood	High+Lowthroughput	Identification of significant chromatin contacts from HiChIP data by FitHiChIP	否	无	leukemia	T cell	E_01_0271	Flow cytometry	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	Immunohistochemical staining	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	MYC		Flow cytometry	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.			
31530818	chr17	7659021	7661021	TP53	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	human	blood	High+Lowthroughput	Identification of significant chromatin contacts from HiChIP data by FitHiChIP	否	无	leukemia	K562 cell	E_01_0271	Flow cytometry	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	Immunohistochemical staining	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.	TP53		Flow cytometry	FitHiChIP also captures previously validated enhancer interactions for several genes including MYC, TP53, and NMU.			
31530812	chr2	24200308	24202308	ITSN2	In the PFC, according to the published transcriptome data of 16 PFC layers and the adjacent white matter48, the expression of ITSN2 is significantly lower in humans and chimpanzees than in rhesus macaques, consistent with their reduced H3K27Ac signals (an indication of enhancer activity) owing to the ASSV that disrupts an ADE in ITSN2 (Fig. 5c, d, g).	human	Nervous tissue	High+Lowthroughput	Long-read assembly of the Chinese rhesus macaque genome and identification of ape-specific structural variants	是	无		neuronal cell	E_01_0272	Flow cytometry,Western blot	In the PFC, according to the published transcriptome data of 16 PFC layers and the adjacent white matter48, the expression of ITSN2 is significantly lower in humans and chimpanzees than in rhesus macaques, consistent with their reduced H3K27Ac signals (an indication of enhancer activity) owing to the ASSV that disrupts an ADE in ITSN2 (Fig. 5c, d, g).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the PFC, according to the published transcriptome data of 16 PFC layers and the adjacent white matter48, the expression of ITSN2 is significantly lower in humans and chimpanzees than in rhesus macaques, consistent with their reduced H3K27Ac signals (an indication of enhancer activity) owing to the ASSV that disrupts an ADE in ITSN2 (Fig. 5c, d, g).		In the PFC, according to the published transcriptome data of 16 PFC layers and the adjacent white matter48, the expression of ITSN2 is significantly lower in humans and chimpanzees than in rhesus macaques, consistent with their reduced H3K27Ac signals (an indication of enhancer activity) owing to the ASSV that disrupts an ADE in ITSN2 (Fig. 5c, d, g).	Immunohistochemical staining	In the PFC, according to the published transcriptome data of 16 PFC layers and the adjacent white matter48, the expression of ITSN2 is significantly lower in humans and chimpanzees than in rhesus macaques, consistent with their reduced H3K27Ac signals (an indication of enhancer activity) owing to the ASSV that disrupts an ADE in ITSN2 (Fig. 5c, d, g).			Flow cytometry,Western blot				ITSN2
31530812	chr6	11180134	11182134	NEDD9	Gene expression data of cerebellum in NHPs are not available to check its effect on NEDD9 expression	human	connective tissue	High+Lowthroughput	Long-read assembly of the Chinese rhesus macaque genome and identification of ape-specific structural variants	是	无		male germ cells	E_01_0272	Flow cytometry,Western blot	Gene expression data of cerebellum in NHPs are not available to check its effect on NEDD9 expression	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gene expression data of cerebellum in NHPs are not available to check its effect on NEDD9 expression		Gene expression data of cerebellum in NHPs are not available to check its effect on NEDD9 expression	Immunohistochemical staining	Gene expression data of cerebellum in NHPs are not available to check its effect on NEDD9 expression			Flow cytometry,Western blot				NEDD9
31530225	chr16	53698982	53700982	FTO	FTO encodes an ortholog to the AlkB family of enzymes that demethylate nucleic acids	human	connective tissue	High+Lowthroughput	Functional genomic characterization of the FTO locus in African Americans	是	rs9927317	Obesity	mesenchymal stem cell	E_01_0273	Flow cytometry	FTO encodes an ortholog to the AlkB family of enzymes that demethylate nucleic acids	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	FTO encodes an ortholog to the AlkB family of enzymes that demethylate nucleic acids		FTO encodes an ortholog to the AlkB family of enzymes that demethylate nucleic acids	Immunohistochemical staining	FTO encodes an ortholog to the AlkB family of enzymes that demethylate nucleic acids			Flow cytometry				FTO
31530225	chr16	53595395	53597395	RPGRIP1L	The first intronic region of FTO is less than 100 bp 3’ from the transcriptional start site of the gene Retinitis Pigmentosa GTPase Regulator-Interacting Protein-1 Like (RPGRIP1L), a ciliary gene (24, 56) that is transcribed in the 5’ direction.	human	connective tissue	High+Lowthroughput	Functional genomic characterization of the FTO locus in African Americans	是	rs62033405	Obesity	mesenchymal stem cell	E_01_0273	Flow cytometry	The first intronic region of FTO is less than 100 bp 3’ from the transcriptional start site of the gene Retinitis Pigmentosa GTPase Regulator-Interacting Protein-1 Like (RPGRIP1L), a ciliary gene (24, 56) that is transcribed in the 5’ direction.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The first intronic region of FTO is less than 100 bp 3’ from the transcriptional start site of the gene Retinitis Pigmentosa GTPase Regulator-Interacting Protein-1 Like (RPGRIP1L), a ciliary gene (24, 56) that is transcribed in the 5’ direction.		The first intronic region of FTO is less than 100 bp 3’ from the transcriptional start site of the gene Retinitis Pigmentosa GTPase Regulator-Interacting Protein-1 Like (RPGRIP1L), a ciliary gene (24, 56) that is transcribed in the 5’ direction.	Immunohistochemical staining	The first intronic region of FTO is less than 100 bp 3’ from the transcriptional start site of the gene Retinitis Pigmentosa GTPase Regulator-Interacting Protein-1 Like (RPGRIP1L), a ciliary gene (24, 56) that is transcribed in the 5’ direction.			Flow cytometry				RPGRIP1L
31530225	chr7	101813374	101815374	CUX1	We previously showed that rs8050136 resides within a putative binding site for the transcription factor Cut-like Homeobox 1 (CUX1) (46), which regulates expression of FTO and RPGRIP1L (43, 44).	human	Fat	High+Lowthroughput	Functional genomic characterization of the FTO locus in African Americans	是	rs9939609	Obesity	white adipocytes	E_01_0273	Flow cytometry	We previously showed that rs8050136 resides within a putative binding site for the transcription factor Cut-like Homeobox 1 (CUX1) (46), which regulates expression of FTO and RPGRIP1L (43, 44).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We previously showed that rs8050136 resides within a putative binding site for the transcription factor Cut-like Homeobox 1 (CUX1) (46), which regulates expression of FTO and RPGRIP1L (43, 44).	Immunohistochemical staining	We previously showed that rs8050136 resides within a putative binding site for the transcription factor Cut-like Homeobox 1 (CUX1) (46), which regulates expression of FTO and RPGRIP1L (43, 44).	CUX1		Flow cytometry	We previously showed that rs8050136 resides within a putative binding site for the transcription factor Cut-like Homeobox 1 (CUX1) (46), which regulates expression of FTO and RPGRIP1L (43, 44).			
31530225	chr16	54280685	54282685	IRX3	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.	human	Fat	High+Lowthroughput	Functional genomic characterization of the FTO locus in African Americans	是	rs8050136	Obesity	white adipocytes	E_01_0273	Flow cytometry	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.		Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.	Immunohistochemical staining	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.			Flow cytometry				IRX3
31530225	chr16	54928124	54930124	IRX5	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.	human	Fat	High+Lowthroughput	Functional genomic characterization of the FTO locus in African Americans	是	rs9930506	Obesity	white adipocytes	E_01_0273	Flow cytometry	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.		Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.	Immunohistochemical staining	Other groups have shown that rs9930506 is associated with expression of IRX3 in the brain (39), as well as expression of both IRX3 and IRX5 in adipose tissue (7), with apparent biological relevance conveyed by physical interactions (chromosome conformation) with these genes’ promoters, although the resolution of this chromatin interaction data was not sufficient to detect (or rule out) interactions with RPGRIP1L.			Flow cytometry				IRX5
31530015	chr16	23577727	23579727	NDUFAB1	A dramatic decrease of NDUFAB1 protein was detected in the skeletal muscle of both db/db diabetic mice (Fig. 2A) and HFD-induced insulin resistance mice (Fig. 2B), amid myriads of other changes, such as elevated serum glucose levels, and altered insulin signaling and gene expression (22, 23).	human,mouse	connective tissue	High+Lowthroughput	NDUFAB1 protects against obesity and insulin resistance by enhancing mitochondrial metabolism	否	无	insulin resistance 	murine embryonic stem (ES) cell	E_02_0213	PCR,Western blot	A dramatic decrease of NDUFAB1 protein was detected in the skeletal muscle of both db/db diabetic mice (Fig. 2A) and HFD-induced insulin resistance mice (Fig. 2B), amid myriads of other changes, such as elevated serum glucose levels, and altered insulin signaling and gene expression (22, 23).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A dramatic decrease of NDUFAB1 protein was detected in the skeletal muscle of both db/db diabetic mice (Fig. 2A) and HFD-induced insulin resistance mice (Fig. 2B), amid myriads of other changes, such as elevated serum glucose levels, and altered insulin signaling and gene expression (22, 23).		A dramatic decrease of NDUFAB1 protein was detected in the skeletal muscle of both db/db diabetic mice (Fig. 2A) and HFD-induced insulin resistance mice (Fig. 2B), amid myriads of other changes, such as elevated serum glucose levels, and altered insulin signaling and gene expression (22, 23).	Immunohistochemical staining	A dramatic decrease of NDUFAB1 protein was detected in the skeletal muscle of both db/db diabetic mice (Fig. 2A) and HFD-induced insulin resistance mice (Fig. 2B), amid myriads of other changes, such as elevated serum glucose levels, and altered insulin signaling and gene expression (22, 23).			PCR,Western blot				NDUFAB1
31529763	chr17	43041465	43043465	BRCA1	Here we study how the N-terminal plastic region of Myc folds in complex with Max in the absence and presence of an E_x0002_box DNA fragment, and another intrinsically disordered binding partner, BRCA1.	human		High+Lowthroughput	(19) F?NMR Spectroscopy Tagging and Paramagnetic Relaxation Enhancement-Based Conformation Analysis of Intrinsically Disordered Protein Complexes	否	无	tumour	E-coli cell	E_01_0274	Flow cytometry	Here we study how the N-terminal plastic region of Myc folds in complex with Max in the absence and presence of an E_x0002_box DNA fragment, and another intrinsically disordered binding partner, BRCA1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here we study how the N-terminal plastic region of Myc folds in complex with Max in the absence and presence of an E_x0002_box DNA fragment, and another intrinsically disordered binding partner, BRCA1.	Immunohistochemical staining	Here we study how the N-terminal plastic region of Myc folds in complex with Max in the absence and presence of an E_x0002_box DNA fragment, and another intrinsically disordered binding partner, BRCA1.	BRCA1		Flow cytometry	Here we study how the N-terminal plastic region of Myc folds in complex with Max in the absence and presence of an E_x0002_box DNA fragment, and another intrinsically disordered binding partner, BRCA1.			
31525599	chr11	10302280	10304280	ADM	ADMs were cut into disks with different diameters (4 mm and 8 mm) using a puncher, placed in a 24-well plate (Corning Costar) and ster_x0002_ilized with water (Millipore) containing 0.1 (v/v) peracetic acid and 4% (v/v) ethanol and incubated for 2 h at room temperature.	human		High+Lowthroughput	Tracing upconversion nanoparticle penetration in human skin	否	无			E_01_0275	PCR, immunofluorescence staining	ADMs were cut into disks with different diameters (4 mm and 8 mm) using a puncher, placed in a 24-well plate (Corning Costar) and ster_x0002_ilized with water (Millipore) containing 0.1 (v/v) peracetic acid and 4% (v/v) ethanol and incubated for 2 h at room temperature.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ADMs were cut into disks with different diameters (4 mm and 8 mm) using a puncher, placed in a 24-well plate (Corning Costar) and ster_x0002_ilized with water (Millipore) containing 0.1 (v/v) peracetic acid and 4% (v/v) ethanol and incubated for 2 h at room temperature.		ADMs were cut into disks with different diameters (4 mm and 8 mm) using a puncher, placed in a 24-well plate (Corning Costar) and ster_x0002_ilized with water (Millipore) containing 0.1 (v/v) peracetic acid and 4% (v/v) ethanol and incubated for 2 h at room temperature.	Immunohistochemical staining	ADMs were cut into disks with different diameters (4 mm and 8 mm) using a puncher, placed in a 24-well plate (Corning Costar) and ster_x0002_ilized with water (Millipore) containing 0.1 (v/v) peracetic acid and 4% (v/v) ethanol and incubated for 2 h at room temperature.			PCR,免疫荧光染色				ADM
31521883	chr18	63120882	63122882	BCL2	In experiment 4, the effect of trehalose treatment on the mRNA expression of lysosome-associated membrane protein 2 (LAMP2), porcine autophagy-related 5 (pATG5), LC3, BCL2 antagonist/ killer (Bak), BCL2 associated X (Bax), and B-cell lymphoma 2 (Bcl2) in cumulus cells and blastocysts were analyzed.	human	blood	High+Lowthroughput	Trehalose supplementation during porcine oocytes in?vitro maturation improves the developmental capacity of parthenotes	否	无		B cell	E_01_0276	PCR, immunofluorescence staining	In experiment 4, the effect of trehalose treatment on the mRNA expression of lysosome-associated membrane protein 2 (LAMP2), porcine autophagy-related 5 (pATG5), LC3, BCL2 antagonist/ killer (Bak), BCL2 associated X (Bax), and B-cell lymphoma 2 (Bcl2) in cumulus cells and blastocysts were analyzed.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In experiment 4, the effect of trehalose treatment on the mRNA expression of lysosome-associated membrane protein 2 (LAMP2), porcine autophagy-related 5 (pATG5), LC3, BCL2 antagonist/ killer (Bak), BCL2 associated X (Bax), and B-cell lymphoma 2 (Bcl2) in cumulus cells and blastocysts were analyzed.	Immunohistochemical staining	In experiment 4, the effect of trehalose treatment on the mRNA expression of lysosome-associated membrane protein 2 (LAMP2), porcine autophagy-related 5 (pATG5), LC3, BCL2 antagonist/ killer (Bak), BCL2 associated X (Bax), and B-cell lymphoma 2 (Bcl2) in cumulus cells and blastocysts were analyzed.	BCL2		PCR,免疫荧光染色	In experiment 4, the effect of trehalose treatment on the mRNA expression of lysosome-associated membrane protein 2 (LAMP2), porcine autophagy-related 5 (pATG5), LC3, BCL2 antagonist/ killer (Bak), BCL2 associated X (Bax), and B-cell lymphoma 2 (Bcl2) in cumulus cells and blastocysts were analyzed.			
31521109	chr11	58037956	58039956	VN2R9P	For the human genome, cluster34 (chr11:54591480– 59,749,574) is the richest cluster of the olfactome 1 Mb cutoff list; it harbors a single VR pseudogene (VN2R9P) in between OR genes. Cluster15 (chr6:131700469–132, 646,003) of the same list is the TAAR locus, which starts with a single, otherwise remarkably isolated (39 Mb) OR gene: OR2A4 [25]	human,mouse	blood	High+Lowthroughput	A purely bioinformatic pipeline for the prediction of mammalian odorant receptor gene enhancers	否	无		T cell	E_02_0214	PCR	For the human genome, cluster34 (chr11:54591480– 59,749,574) is the richest cluster of the olfactome 1 Mb cutoff list; it harbors a single VR pseudogene (VN2R9P) in between OR genes. Cluster15 (chr6:131700469–132, 646,003) of the same list is the TAAR locus, which starts with a single, otherwise remarkably isolated (39 Mb) OR gene: OR2A4 [25]	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	For the human genome, cluster34 (chr11:54591480– 59,749,574) is the richest cluster of the olfactome 1 Mb cutoff list; it harbors a single VR pseudogene (VN2R9P) in between OR genes. Cluster15 (chr6:131700469–132, 646,003) of the same list is the TAAR locus, which starts with a single, otherwise remarkably isolated (39 Mb) OR gene: OR2A4 [25]		For the human genome, cluster34 (chr11:54591480– 59,749,574) is the richest cluster of the olfactome 1 Mb cutoff list; it harbors a single VR pseudogene (VN2R9P) in between OR genes. Cluster15 (chr6:131700469–132, 646,003) of the same list is the TAAR locus, which starts with a single, otherwise remarkably isolated (39 Mb) OR gene: OR2A4 [25]	Immunohistochemical staining	For the human genome, cluster34 (chr11:54591480– 59,749,574) is the richest cluster of the olfactome 1 Mb cutoff list; it harbors a single VR pseudogene (VN2R9P) in between OR genes. Cluster15 (chr6:131700469–132, 646,003) of the same list is the TAAR locus, which starts with a single, otherwise remarkably isolated (39 Mb) OR gene: OR2A4 [25]			PCR				VN2R9P
31520529	chr1	156461014	156463014	MEF2D	Mt2Ddn bound strongly to the ND6-MEF2 site and disrupted the function of normal mitochondrial MEF2D without affecting the expression of the nuclear MEF2 reporter (She et al. 2011).	mouse	Nervous tissue	High+Lowthroughput	Salidroside protects dopaminergic neurons by regulating the mitochondrial MEF2D-ND6 pathway in the MPTP/MPP(+) -induced model of Parkinson's disease	是	无	Parkinson	SN4741 cells	E_02_0215	PCR, immunofluorescence staining, Western blot	Mt2Ddn bound strongly to the ND6-MEF2 site and disrupted the function of normal mitochondrial MEF2D without affecting the expression of the nuclear MEF2 reporter (She et al. 2011).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mt2Ddn bound strongly to the ND6-MEF2 site and disrupted the function of normal mitochondrial MEF2D without affecting the expression of the nuclear MEF2 reporter (She et al. 2011).		Mt2Ddn bound strongly to the ND6-MEF2 site and disrupted the function of normal mitochondrial MEF2D without affecting the expression of the nuclear MEF2 reporter (She et al. 2011).	Immunohistochemical staining	Mt2Ddn bound strongly to the ND6-MEF2 site and disrupted the function of normal mitochondrial MEF2D without affecting the expression of the nuclear MEF2 reporter (She et al. 2011).			PCR,免疫荧光染色,Western blot				MEF2D
31519749	chr3	142303842	142305842	XRN1	Insect-borne flaviviruses produce a 300- 500 base long noncoding RNA, termed subgenomic flavivirus RNA (sfRNA), by stalling the cellular 5’-3’ exoribonuclease 1 (XRN1) via structures located in their 3’ UTRs.	human		High+Lowthroughput	Zika virus noncoding sfRNAs sequester multiple host-derived RNA-binding proteins and modulate mRNA decay and splicing during infection	否	无	Villous carcinoma	choriocarcinoma cells	E_01_0277	PCR,Western blot	Insect-borne flaviviruses produce a 300- 500 base long noncoding RNA, termed subgenomic flavivirus RNA (sfRNA), by stalling the cellular 5’-3’ exoribonuclease 1 (XRN1) via structures located in their 3’ UTRs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Insect-borne flaviviruses produce a 300- 500 base long noncoding RNA, termed subgenomic flavivirus RNA (sfRNA), by stalling the cellular 5’-3’ exoribonuclease 1 (XRN1) via structures located in their 3’ UTRs.		Insect-borne flaviviruses produce a 300- 500 base long noncoding RNA, termed subgenomic flavivirus RNA (sfRNA), by stalling the cellular 5’-3’ exoribonuclease 1 (XRN1) via structures located in their 3’ UTRs.	Immunohistochemical staining	Insect-borne flaviviruses produce a 300- 500 base long noncoding RNA, termed subgenomic flavivirus RNA (sfRNA), by stalling the cellular 5’-3’ exoribonuclease 1 (XRN1) via structures located in their 3’ UTRs.			PCR,Western blot				XRN1
31519704	chr9	136491964	136493964	NOTCH1	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.	human,mouse	blood	High+Lowthroughput	GATA3-Controlled Nucleosome Eviction Drives MYC Enhancer Activity in T-cell Development and Leukemia	否	无	leukemia	T cell	E_02_0216	PCR,Flow cytometry	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.		MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.	Immunohistochemical staining	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.			PCR,Flow cytometry				NOTCH1
31519704	chr8	127732540	127734540	MYC	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.	human,mouse	blood	High+Lowthroughput	GATA3-Controlled Nucleosome Eviction Drives MYC Enhancer Activity in T-cell Development and Leukemia	否	无	leukemia	T cell	E_02_0216	PCR,Flow cytometry	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.		MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.	Immunohistochemical staining	MYC is a major effector of NOTCH1 oncogenic programs in T-ALL.			PCR,Flow cytometry				MYC
31519520	chr16	67560000	67562000	CTCF	Sequence constraint was even higher when considering DI bins either bound by CTCF (DI_CTCF) or MYOD (DI_MYOD) or co-bound by these two TFs (DI_MYOD_CTCF) (Figure S5A).	human,mouse	connective tissue	High+Lowthroughput	Transcription Factor-Directed Re-wiring of Chromatin Architecture for Somatic Cell Nuclear Reprogramming toward trans-Differentiation	否	无		somatic cell	E_02_0217	PCR, Western blot, flow cytometry, immunofluorescence staining	Sequence constraint was even higher when considering DI bins either bound by CTCF (DI_CTCF) or MYOD (DI_MYOD) or co-bound by these two TFs (DI_MYOD_CTCF) (Figure S5A).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Sequence constraint was even higher when considering DI bins either bound by CTCF (DI_CTCF) or MYOD (DI_MYOD) or co-bound by these two TFs (DI_MYOD_CTCF) (Figure S5A).		Sequence constraint was even higher when considering DI bins either bound by CTCF (DI_CTCF) or MYOD (DI_MYOD) or co-bound by these two TFs (DI_MYOD_CTCF) (Figure S5A).	Immunohistochemical staining	Sequence constraint was even higher when considering DI bins either bound by CTCF (DI_CTCF) or MYOD (DI_MYOD) or co-bound by these two TFs (DI_MYOD_CTCF) (Figure S5A).			PCR,Western blot,Flow cytometry,免疫荧光染色				CTCF
31519520	chr12	55681811	55683811	ITGA7	Upon ectopic expression, MYOD bound the promoter of ITGA7 and RDH5 at CTCF-bound elements in IMR90 (Figure 4L) and this coincided with increased interaction between the two CTCF-bound re_x0002_gions, as measured by Hi-C (Figures 4K and 4L) and validated by 3C (Figure 4L, bottom right). Importantly, these events corre_x0002_lated with an increased expression of both ITGA7 and RDH5 (Figure 4L, bottom left).	human,mouse	bone	High+Lowthroughput	Transcription Factor-Directed Re-wiring of Chromatin Architecture for Somatic Cell Nuclear Reprogramming toward trans-Differentiation	否	无		mouse cell of skeletal muscle	E_02_0217	PCR, Western blot, flow cytometry, immunofluorescence staining	Upon ectopic expression, MYOD bound the promoter of ITGA7 and RDH5 at CTCF-bound elements in IMR90 (Figure 4L) and this coincided with increased interaction between the two CTCF-bound re_x0002_gions, as measured by Hi-C (Figures 4K and 4L) and validated by 3C (Figure 4L, bottom right). Importantly, these events corre_x0002_lated with an increased expression of both ITGA7 and RDH5 (Figure 4L, bottom left).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Upon ectopic expression, MYOD bound the promoter of ITGA7 and RDH5 at CTCF-bound elements in IMR90 (Figure 4L) and this coincided with increased interaction between the two CTCF-bound re_x0002_gions, as measured by Hi-C (Figures 4K and 4L) and validated by 3C (Figure 4L, bottom right). Importantly, these events corre_x0002_lated with an increased expression of both ITGA7 and RDH5 (Figure 4L, bottom left).		Upon ectopic expression, MYOD bound the promoter of ITGA7 and RDH5 at CTCF-bound elements in IMR90 (Figure 4L) and this coincided with increased interaction between the two CTCF-bound re_x0002_gions, as measured by Hi-C (Figures 4K and 4L) and validated by 3C (Figure 4L, bottom right). Importantly, these events corre_x0002_lated with an increased expression of both ITGA7 and RDH5 (Figure 4L, bottom left).	Immunohistochemical staining	Upon ectopic expression, MYOD bound the promoter of ITGA7 and RDH5 at CTCF-bound elements in IMR90 (Figure 4L) and this coincided with increased interaction between the two CTCF-bound re_x0002_gions, as measured by Hi-C (Figures 4K and 4L) and validated by 3C (Figure 4L, bottom right). Importantly, these events corre_x0002_lated with an increased expression of both ITGA7 and RDH5 (Figure 4L, bottom left).			PCR,Western blot,Flow cytometry,免疫荧光染色				ITGA7
31519520	chr1	201356451	201358451	TNNT2	Upon MYOD induction in fibroblasts and its binding to TNNT2 promoter, we observed an increase in TNNT2 pro_x0002_moter-enhancer interaction together with an increase in TNNT2 expression (Figures 5D–5F).	human,mouse	lung	High+Lowthroughput	Transcription Factor-Directed Re-wiring of Chromatin Architecture for Somatic Cell Nuclear Reprogramming toward trans-Differentiation	否	无		IMR90 cell	E_02_0217	PCR, Western blot, flow cytometry, immunofluorescence staining	Upon MYOD induction in fibroblasts and its binding to TNNT2 promoter, we observed an increase in TNNT2 pro_x0002_moter-enhancer interaction together with an increase in TNNT2 expression (Figures 5D–5F).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Upon MYOD induction in fibroblasts and its binding to TNNT2 promoter, we observed an increase in TNNT2 pro_x0002_moter-enhancer interaction together with an increase in TNNT2 expression (Figures 5D–5F).		Upon MYOD induction in fibroblasts and its binding to TNNT2 promoter, we observed an increase in TNNT2 pro_x0002_moter-enhancer interaction together with an increase in TNNT2 expression (Figures 5D–5F).	Immunohistochemical staining	Upon MYOD induction in fibroblasts and its binding to TNNT2 promoter, we observed an increase in TNNT2 pro_x0002_moter-enhancer interaction together with an increase in TNNT2 expression (Figures 5D–5F).			PCR,Western blot,Flow cytometry,免疫荧光染色				TNNT2
31518916	chr7	148804819	148806819	EZH2	The function of histone methyltransferase enhancer of zeste homolog 2 (EZH2) in sepsis remains unknown.	human,mouse	connective tissue	High+Lowthroughput	Novel pharmacological inhibition of EZH2 attenuates septic shock by altering innate inflammatory responses to sepsis	否	无	Sepsis	Inflammatory cell	E_02_0218	PCR, Western blot, flow cytometry, immunofluorescence staining	The function of histone methyltransferase enhancer of zeste homolog 2 (EZH2) in sepsis remains unknown.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The function of histone methyltransferase enhancer of zeste homolog 2 (EZH2) in sepsis remains unknown.		The function of histone methyltransferase enhancer of zeste homolog 2 (EZH2) in sepsis remains unknown.	Immunohistochemical staining	The function of histone methyltransferase enhancer of zeste homolog 2 (EZH2) in sepsis remains unknown.			PCR,Western blot,Flow cytometry,免疫荧光染色				EZH2
31518916	chr17	42310415	42312415	STAT3	Blockage of EZH2 also suppressed the progression of lung injury and alleviated in_x0002_flammation by decreasing the pulmonary cell apoptosis, reducing inflammatory cells infiltration and cytokines release through inhibition of the STAT3 signaling pathway and recovery of PPARγ activation. I	human,mouse	lung	High+Lowthroughput	Novel pharmacological inhibition of EZH2 attenuates septic shock by altering innate inflammatory responses to sepsis	否	无	Sepsis	pneumocyte	E_02_0218	PCR, Western blot, flow cytometry, immunofluorescence staining	Blockage of EZH2 also suppressed the progression of lung injury and alleviated in_x0002_flammation by decreasing the pulmonary cell apoptosis, reducing inflammatory cells infiltration and cytokines release through inhibition of the STAT3 signaling pathway and recovery of PPARγ activation. I	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Blockage of EZH2 also suppressed the progression of lung injury and alleviated in_x0002_flammation by decreasing the pulmonary cell apoptosis, reducing inflammatory cells infiltration and cytokines release through inhibition of the STAT3 signaling pathway and recovery of PPARγ activation. I		Blockage of EZH2 also suppressed the progression of lung injury and alleviated in_x0002_flammation by decreasing the pulmonary cell apoptosis, reducing inflammatory cells infiltration and cytokines release through inhibition of the STAT3 signaling pathway and recovery of PPARγ activation. I	Immunohistochemical staining	Blockage of EZH2 also suppressed the progression of lung injury and alleviated in_x0002_flammation by decreasing the pulmonary cell apoptosis, reducing inflammatory cells infiltration and cytokines release through inhibition of the STAT3 signaling pathway and recovery of PPARγ activation. I			PCR,Western blot,Flow cytometry,免疫荧光染色				STAT3
31518916	chr17	78354497	78356497	SOCS3	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.	human,mouse	Epithelial tissues	High+Lowthroughput	Novel pharmacological inhibition of EZH2 attenuates septic shock by altering innate inflammatory responses to sepsis	否	无	Sepsis	epithelial cell	E_02_0218	PCR, Western blot, flow cytometry, immunofluorescence staining	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.		In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.	Immunohistochemical staining	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.			PCR,Western blot,Flow cytometry,免疫荧光染色				SOCS3
31518916	chr2	190905505	190907505	STAT1	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.	human,mouse	Epithelial tissues	High+Lowthroughput	Novel pharmacological inhibition of EZH2 attenuates septic shock by altering innate inflammatory responses to sepsis	否	无	Sepsis	epithelial cell	E_02_0218	PCR, Western blot, flow cytometry, immunofluorescence staining	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.		In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.	Immunohistochemical staining	In addition, EZH2 inhibitor blunted macrophage M1 polarization by SOCS3/STAT1 pathway. Overall, these data suggest that EZH2 could be a potential biomarker predicting clinical outcome and a new target for therapeutic interference in sepsis.			PCR,Western blot,Flow cytometry,免疫荧光染色				STAT1
31517633	chr19	2246854	2248854	AMH	Hormonal disturbances, including increased level of androgens, estradiol, AMH and lower level of progesterone, also are one of etiologies related to PCOS (Patel 2018).	human,mouse	stomach	High+Lowthroughput	Ulmus minor bark hydro-alcoholic extract ameliorates histological parameters and testosterone level in an experimental model of PCOS rats	否	无	Gastric adenocarcinoma, polycystic ovary syndrome	gastric adenocarcinoma cell	E_02_0219	PCR 	Hormonal disturbances, including increased level of androgens, estradiol, AMH and lower level of progesterone, also are one of etiologies related to PCOS (Patel 2018).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hormonal disturbances, including increased level of androgens, estradiol, AMH and lower level of progesterone, also are one of etiologies related to PCOS (Patel 2018).		Hormonal disturbances, including increased level of androgens, estradiol, AMH and lower level of progesterone, also are one of etiologies related to PCOS (Patel 2018).	Immunohistochemical staining	Hormonal disturbances, including increased level of androgens, estradiol, AMH and lower level of progesterone, also are one of etiologies related to PCOS (Patel 2018).			PCR 				AMH
31515577	chr19	4966088	4968088	KDM4B	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.	human,mouse	bone	High+Lowthroughput	Histone demethylase KDM4A regulates adipogenic and osteogenic differentiation via epigenetic regulation of C/EBPα and canonical Wnt signaling	否	无	osteoporosis	Bone marrow stromal cell	E_02_0220	PCR,Western blot 	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.		Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.	Immunohistochemical staining	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.			PCR,Western blot 				KDM4B
31515577	chr17	7831872	7833872	KDM6B	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.	human,mouse	bone	High+Lowthroughput	Histone demethylase KDM4A regulates adipogenic and osteogenic differentiation via epigenetic regulation of C/EBPα and canonical Wnt signaling	否	无	osteoporosis	Bone marrow stromal cell	E_02_0220	PCR,Western blot 	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.		Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.	Immunohistochemical staining	Depletion of KDM4B or KDM6B favored adipogenic dif_x0002_ferentiation at the expense of osteogenic differentiation.			PCR,Western blot 				KDM6B
31515577	chr17	72118259	72120259	SOX9	KDM4B also promotes chondrogenic differentiation of human MSCs due to its recruitment to the chondrogenic gene SOX9 promoter, removing the silencing H3K9me3 marks, and thus activat_x0002_ing the transcription of SOX9 [14].	human,mouse	bone	High+Lowthroughput	Histone demethylase KDM4A regulates adipogenic and osteogenic differentiation via epigenetic regulation of C/EBPα and canonical Wnt signaling	否	无	osteoporosis	ST2 cell	E_02_0220	PCR,Western blot 	KDM4B also promotes chondrogenic differentiation of human MSCs due to its recruitment to the chondrogenic gene SOX9 promoter, removing the silencing H3K9me3 marks, and thus activat_x0002_ing the transcription of SOX9 [14].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	KDM4B also promotes chondrogenic differentiation of human MSCs due to its recruitment to the chondrogenic gene SOX9 promoter, removing the silencing H3K9me3 marks, and thus activat_x0002_ing the transcription of SOX9 [14].		KDM4B also promotes chondrogenic differentiation of human MSCs due to its recruitment to the chondrogenic gene SOX9 promoter, removing the silencing H3K9me3 marks, and thus activat_x0002_ing the transcription of SOX9 [14].	Immunohistochemical staining	KDM4B also promotes chondrogenic differentiation of human MSCs due to its recruitment to the chondrogenic gene SOX9 promoter, removing the silencing H3K9me3 marks, and thus activat_x0002_ing the transcription of SOX9 [14].			PCR,Western blot 				SOX9
31515496	chr16	67559926	67561926	CTCF	By combining the in situ Hi-C data with active and repressive histone marks, CTCF binding sites, nucleosome-depleted regions, and tran_x0002_scriptome profiling, we identify topologically associating domains (TADs) that change in size and epigenetic states between normal and prostate cancer cells.	human	prostate	High+Lowthroughput	A high-resolution 3D epigenomic map reveals insights into the creation of the prostate cancer transcriptome	是	无	prostatic cancer	prostate cancer cell	E_01_0278	PCR,Flow cytometry	By combining the in situ Hi-C data with active and repressive histone marks, CTCF binding sites, nucleosome-depleted regions, and tran_x0002_scriptome profiling, we identify topologically associating domains (TADs) that change in size and epigenetic states between normal and prostate cancer cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			By combining the in situ Hi-C data with active and repressive histone marks, CTCF binding sites, nucleosome-depleted regions, and tran_x0002_scriptome profiling, we identify topologically associating domains (TADs) that change in size and epigenetic states between normal and prostate cancer cells.	Immunohistochemical staining	By combining the in situ Hi-C data with active and repressive histone marks, CTCF binding sites, nucleosome-depleted regions, and tran_x0002_scriptome profiling, we identify topologically associating domains (TADs) that change in size and epigenetic states between normal and prostate cancer cells.	CTCF		PCR,Flow cytometry	By combining the in situ Hi-C data with active and repressive histone marks, CTCF binding sites, nucleosome-depleted regions, and tran_x0002_scriptome profiling, we identify topologically associating domains (TADs) that change in size and epigenetic states between normal and prostate cancer cells.			
31515496	chr14	37586728	37588728	FOXA1	Moreover, we identify normal and prostate cancer-specific enhancer-promoter loops and involved transcription factors. For example, we show that FOXA1 is enriched in prostate cancer-specific enhancer_x0002_promoter loop anchors.	human	prostate	High+Lowthroughput	A high-resolution 3D epigenomic map reveals insights into the creation of the prostate cancer transcriptome	是	无	prostatic cancer	RWPE1 cell	E_01_0278	PCR,Flow cytometry	Moreover, we identify normal and prostate cancer-specific enhancer-promoter loops and involved transcription factors. For example, we show that FOXA1 is enriched in prostate cancer-specific enhancer_x0002_promoter loop anchors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Moreover, we identify normal and prostate cancer-specific enhancer-promoter loops and involved transcription factors. For example, we show that FOXA1 is enriched in prostate cancer-specific enhancer_x0002_promoter loop anchors.	Immunohistochemical staining	Moreover, we identify normal and prostate cancer-specific enhancer-promoter loops and involved transcription factors. For example, we show that FOXA1 is enriched in prostate cancer-specific enhancer_x0002_promoter loop anchors.	FOXA1		PCR,Flow cytometry	Moreover, we identify normal and prostate cancer-specific enhancer-promoter loops and involved transcription factors. For example, we show that FOXA1 is enriched in prostate cancer-specific enhancer_x0002_promoter loop anchors.			
31515496	chr12	114667426	114669426	TBX3	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	human	connective tissue	High+Lowthroughput	A high-resolution 3D epigenomic map reveals insights into the creation of the prostate cancer transcriptome	是	无	prostatic cancer	cancer cell	E_01_0278	PCR,Flow cytometry	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	Immunohistochemical staining	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	TBX3		PCR,Flow cytometry	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.			
31515496	chr1	107053881	107055881	PRMT6	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	human	connective tissue	High+Lowthroughput	A high-resolution 3D epigenomic map reveals insights into the creation of the prostate cancer transcriptome	是	无	prostatic cancer	cancer cell	E_01_0278	PCR,Flow cytometry	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.		Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.	Immunohistochemical staining	Examples of genes that belong to this cate_x0002_gory are TBX3 and PRMT6, which are known to be involved in prostate cancers23,24.			PCR,Flow cytometry				PRMT6
31515496	chr15	26540728	26542728	GABRB3	Moreover, we found that the size change of a TAD can be related to gene expression changes. For example, in normal cells, there is one large TAD at chromosome 15q12 containing the GABRB3 gene, which is not expressed in RWPE1.	human	Prostate A.H	High+Lowthroughput	A high-resolution 3D epigenomic map reveals insights into the creation of the prostate cancer transcriptome	是	无	prostatic cancer	22Rv1 cell	E_01_0278	PCR,Flow cytometry	Moreover, we found that the size change of a TAD can be related to gene expression changes. For example, in normal cells, there is one large TAD at chromosome 15q12 containing the GABRB3 gene, which is not expressed in RWPE1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, we found that the size change of a TAD can be related to gene expression changes. For example, in normal cells, there is one large TAD at chromosome 15q12 containing the GABRB3 gene, which is not expressed in RWPE1.		Moreover, we found that the size change of a TAD can be related to gene expression changes. For example, in normal cells, there is one large TAD at chromosome 15q12 containing the GABRB3 gene, which is not expressed in RWPE1.	Immunohistochemical staining	Moreover, we found that the size change of a TAD can be related to gene expression changes. For example, in normal cells, there is one large TAD at chromosome 15q12 containing the GABRB3 gene, which is not expressed in RWPE1.			PCR,Flow cytometry				GABRB3
31514731	chr16	67559877	67561877	CTCF	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	human	blood	High+Lowthroughput	The first enhancer in an enhancer chain safeguards subsequent enhancer-promoter contacts from a distance	是	无	leukemia	K562 cell	E_01_0279	PCR	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	Immunohistochemical staining	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.	CTCF		PCR	These first en_x0002_hancers maintain more Hi-C interactions with other en_x0002_hancers and promoters, are more enriched for the loop factors CCCTC-binding factor (CTCF) and cohesin, and commonly overlap with the boundaries of chromatin loops.			
31513772	chr9	21074265	21076265	IFNB1	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	human	uterus	High+Lowthroughput	The Nuclear Matrix Protein SAFA Surveils Viral RNA and Facilitates Immunity by Activating Antiviral Enhancers and Super-enhancers	否	无	cervical carcinoma	HeLa cell	E_01_0280	PCR, Western blot, flow cytometry, immunofluorescence staining	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	Immunohistochemical staining	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).	IFNB1		PCR,Western blot,Flow cytometry,免疫荧光染色	We constructed IFNB1 luciferase reporter plasmids composed of IFNB1 immediate promoter followed by these enhancers (Figure S6D).			
31513343	chr17	42310771	42312771	STAT3	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.	human,mouse	connective tissue	High+Lowthroughput	Generation of Nanog reporter mice that distinguish pluripotent stem cells from unipotent primordial germ cells	否	无		pluripotent stem cell	E_02_0221	PCR, flow cytometry, immunofluorescence staining	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.		Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.	Immunohistochemical staining	Nanog is also regulated by the binding of STAT3 (Suzuki et al., 2006a), T (also known as Brachyury) (Suzuki et al., 2006a), and Sall4/ Nanog complex (Wu et al., 2006) at −4.9 kb region. Although the reg_x0002_ulation of Nanog expression by these transcription factors has been elucidated using the reporter assays in vitro, in vivo tissue specificity has not been demonstrated by using the standard Nanog reporter Tg mouse lines.			PCR,Flow cytometry,免疫荧光染色				STAT3
31511694	chr21	45491095	45493095	SLC19A1	SLC19A1 was one of the most significant hits in both screens. SLC19A1 is a folate–organic phosphate antiporter that transports folates, structurally similar antifolates and a variety of organic phos_x0002_phates encompassing (among others) thiamine derivatives and nucle_x0002_otides15,16.	human,mouse	blood	High+Lowthroughput	SLC19A1 transports immunoreactive cyclic dinucleotides	否	无	leukemia	B cell	E_02_0222	Western blot,PCR,Flow cytometry	SLC19A1 was one of the most significant hits in both screens. SLC19A1 is a folate–organic phosphate antiporter that transports folates, structurally similar antifolates and a variety of organic phos_x0002_phates encompassing (among others) thiamine derivatives and nucle_x0002_otides15,16.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SLC19A1 was one of the most significant hits in both screens. SLC19A1 is a folate–organic phosphate antiporter that transports folates, structurally similar antifolates and a variety of organic phos_x0002_phates encompassing (among others) thiamine derivatives and nucle_x0002_otides15,16.		SLC19A1 was one of the most significant hits in both screens. SLC19A1 is a folate–organic phosphate antiporter that transports folates, structurally similar antifolates and a variety of organic phos_x0002_phates encompassing (among others) thiamine derivatives and nucle_x0002_otides15,16.	Immunohistochemical staining	SLC19A1 was one of the most significant hits in both screens. SLC19A1 is a folate–organic phosphate antiporter that transports folates, structurally similar antifolates and a variety of organic phos_x0002_phates encompassing (among others) thiamine derivatives and nucle_x0002_otides15,16.			Western blot,PCR,Flow cytometry				SLC19A1
31511694	chr17	35868537	35870537	CCL5	SLC19A1 depletion—similar to depletion of IRF3 or STING—also inhibited CDN-induced expression of direct downstream target genes in the STING pathway, including IFNB1 and the chemokine genes CCL5 and CXCL1021,22 (Fig. 2c, Extended Data Fig. 3g–i).	human,mouse	blood	High+Lowthroughput	SLC19A1 transports immunoreactive cyclic dinucleotides	否	无	leukemia	THP-1 cells	E_02_0222	Western blot,PCR,Flow cytometry	SLC19A1 depletion—similar to depletion of IRF3 or STING—also inhibited CDN-induced expression of direct downstream target genes in the STING pathway, including IFNB1 and the chemokine genes CCL5 and CXCL1021,22 (Fig. 2c, Extended Data Fig. 3g–i).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SLC19A1 depletion—similar to depletion of IRF3 or STING—also inhibited CDN-induced expression of direct downstream target genes in the STING pathway, including IFNB1 and the chemokine genes CCL5 and CXCL1021,22 (Fig. 2c, Extended Data Fig. 3g–i).		SLC19A1 depletion—similar to depletion of IRF3 or STING—also inhibited CDN-induced expression of direct downstream target genes in the STING pathway, including IFNB1 and the chemokine genes CCL5 and CXCL1021,22 (Fig. 2c, Extended Data Fig. 3g–i).	Immunohistochemical staining	SLC19A1 depletion—similar to depletion of IRF3 or STING—also inhibited CDN-induced expression of direct downstream target genes in the STING pathway, including IFNB1 and the chemokine genes CCL5 and CXCL1021,22 (Fig. 2c, Extended Data Fig. 3g–i).			Western blot,PCR,Flow cytometry				CCL5
31511694	chr19	49656530	49658530	IRF3	Protein levels of STING, TBK1 and IRF3 were unaltered in SLC19A1- depleted cells	human,mouse	blood	High+Lowthroughput	SLC19A1 transports immunoreactive cyclic dinucleotides	否	无	leukemia	L1210 cell	E_02_0222	Western blot,PCR,Flow cytometry	Protein levels of STING, TBK1 and IRF3 were unaltered in SLC19A1- depleted cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Protein levels of STING, TBK1 and IRF3 were unaltered in SLC19A1- depleted cells		Protein levels of STING, TBK1 and IRF3 were unaltered in SLC19A1- depleted cells	Immunohistochemical staining	Protein levels of STING, TBK1 and IRF3 were unaltered in SLC19A1- depleted cells			Western blot,PCR,Flow cytometry				IRF3
31511524	chr20	43664495	43666495	MYBL2	Strikingly, targeting this GGAA-microsatellite by clustered regularly interspaced short palindromic repeats inter_x0002_ference (CRISPRi)26–28 in highly MYBL2 expressing RDES cells strongly suppressed MYBL2 transcription (Fig. 1f) and induced a potentially counter-regulatory upregulation of EWSR1-FLI1 (Sup_x0002_plementary Fig. 1i). I	human,mouse	connective tissue	High+Lowthroughput	Cooperation of cancer drivers with regulatory germline variants shapes clinical outcomes	否	无	Malignancy		E_02_0223	Flow cytometry,Western blot	Strikingly, targeting this GGAA-microsatellite by clustered regularly interspaced short palindromic repeats inter_x0002_ference (CRISPRi)26–28 in highly MYBL2 expressing RDES cells strongly suppressed MYBL2 transcription (Fig. 1f) and induced a potentially counter-regulatory upregulation of EWSR1-FLI1 (Sup_x0002_plementary Fig. 1i). I	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Strikingly, targeting this GGAA-microsatellite by clustered regularly interspaced short palindromic repeats inter_x0002_ference (CRISPRi)26–28 in highly MYBL2 expressing RDES cells strongly suppressed MYBL2 transcription (Fig. 1f) and induced a potentially counter-regulatory upregulation of EWSR1-FLI1 (Sup_x0002_plementary Fig. 1i). I		Strikingly, targeting this GGAA-microsatellite by clustered regularly interspaced short palindromic repeats inter_x0002_ference (CRISPRi)26–28 in highly MYBL2 expressing RDES cells strongly suppressed MYBL2 transcription (Fig. 1f) and induced a potentially counter-regulatory upregulation of EWSR1-FLI1 (Sup_x0002_plementary Fig. 1i). I	Immunohistochemical staining	Strikingly, targeting this GGAA-microsatellite by clustered regularly interspaced short palindromic repeats inter_x0002_ference (CRISPRi)26–28 in highly MYBL2 expressing RDES cells strongly suppressed MYBL2 transcription (Fig. 1f) and induced a potentially counter-regulatory upregulation of EWSR1-FLI1 (Sup_x0002_plementary Fig. 1i). I			Flow cytometry,Western blot				MYBL2
31511524	chr12	55964008	55966008	CDK2	High MYBL2 levels sensitize EwS cells for inhibition of its upstream activating kinase CDK2 in vitro and in vivo, suggesting MYBL2 as a putative biomarker for anti-CDK2-therapy.	human,mouse	kidney	High+Lowthroughput	Cooperation of cancer drivers with regulatory germline variants shapes clinical outcomes	否	无	Malignancy	HEK293T	E_02_0223	Flow cytometry,Western blot	High MYBL2 levels sensitize EwS cells for inhibition of its upstream activating kinase CDK2 in vitro and in vivo, suggesting MYBL2 as a putative biomarker for anti-CDK2-therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	High MYBL2 levels sensitize EwS cells for inhibition of its upstream activating kinase CDK2 in vitro and in vivo, suggesting MYBL2 as a putative biomarker for anti-CDK2-therapy.		High MYBL2 levels sensitize EwS cells for inhibition of its upstream activating kinase CDK2 in vitro and in vivo, suggesting MYBL2 as a putative biomarker for anti-CDK2-therapy.	Immunohistochemical staining	High MYBL2 levels sensitize EwS cells for inhibition of its upstream activating kinase CDK2 in vitro and in vivo, suggesting MYBL2 as a putative biomarker for anti-CDK2-therapy.			Flow cytometry,Western blot				CDK2
31511494	chr7	148804549	148806549	EZH2	Here we found that Pb exposure diminished H3K27me3 levels in vivo by suppressing EZH2 (enhancer of zeste homolog 2) expression at an early stage.	mouse	connective tissue	High+Lowthroughput	Interplay of miR-137 and EZH2 contributes to the genome-wide redistribution of H3K27me3 underlying the Pb-induced memory impairment	否	无	Multiple neurodegenerative diseases	PC 12 cell	E_02_0224	PCR, Western blot, immunofluorescence staining	Here we found that Pb exposure diminished H3K27me3 levels in vivo by suppressing EZH2 (enhancer of zeste homolog 2) expression at an early stage.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we found that Pb exposure diminished H3K27me3 levels in vivo by suppressing EZH2 (enhancer of zeste homolog 2) expression at an early stage.		Here we found that Pb exposure diminished H3K27me3 levels in vivo by suppressing EZH2 (enhancer of zeste homolog 2) expression at an early stage.	Immunohistochemical staining	Here we found that Pb exposure diminished H3K27me3 levels in vivo by suppressing EZH2 (enhancer of zeste homolog 2) expression at an early stage.			PCR,Western blot,免疫荧光染色				EZH2
31511252	chr5	29675484	29677484	Mnx1	Our data suggest that these substantial alterations in TAD structure have no readily detectable effect on Shh expression patterns or levels of Shh expression during development – except where enhancers are deleted – and result in no detectable phenotypes. Only in the case of a larger deletion at one TAD boundary could ectopic influence of the Shh limb enhancer be detected on a gene (Mnx1) in the neighbouring TAD.	mouse	connective tissue	High+Lowthroughput	Developmentally regulated Shh expression is robust to TAD perturbations	否	无		embryonic stem cell	E_02_0225	PCR,Flow cytometry	Our data suggest that these substantial alterations in TAD structure have no readily detectable effect on Shh expression patterns or levels of Shh expression during development – except where enhancers are deleted – and result in no detectable phenotypes. Only in the case of a larger deletion at one TAD boundary could ectopic influence of the Shh limb enhancer be detected on a gene (Mnx1) in the neighbouring TAD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data suggest that these substantial alterations in TAD structure have no readily detectable effect on Shh expression patterns or levels of Shh expression during development – except where enhancers are deleted – and result in no detectable phenotypes. Only in the case of a larger deletion at one TAD boundary could ectopic influence of the Shh limb enhancer be detected on a gene (Mnx1) in the neighbouring TAD.		Our data suggest that these substantial alterations in TAD structure have no readily detectable effect on Shh expression patterns or levels of Shh expression during development – except where enhancers are deleted – and result in no detectable phenotypes. Only in the case of a larger deletion at one TAD boundary could ectopic influence of the Shh limb enhancer be detected on a gene (Mnx1) in the neighbouring TAD.	Immunohistochemical staining	Our data suggest that these substantial alterations in TAD structure have no readily detectable effect on Shh expression patterns or levels of Shh expression during development – except where enhancers are deleted – and result in no detectable phenotypes. Only in the case of a larger deletion at one TAD boundary could ectopic influence of the Shh limb enhancer be detected on a gene (Mnx1) in the neighbouring TAD.			PCR,Flow cytometry				Mnx1
31511252	chr16	67559977	67561977	CTCF	Interprobe distances between all three probe pairs were significantly increased in CTCF deletion cells compared with wild-type ESCs (Fig. 3E; Table S2), consistent with the reduced interactions between Shh and	mouse	connective tissue	High+Lowthroughput	Developmentally regulated Shh expression is robust to TAD perturbations	否	无		posterior limb bud cell	E_02_0225	PCR,Flow cytometry	Interprobe distances between all three probe pairs were significantly increased in CTCF deletion cells compared with wild-type ESCs (Fig. 3E; Table S2), consistent with the reduced interactions between Shh and	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Interprobe distances between all three probe pairs were significantly increased in CTCF deletion cells compared with wild-type ESCs (Fig. 3E; Table S2), consistent with the reduced interactions between Shh and		Interprobe distances between all three probe pairs were significantly increased in CTCF deletion cells compared with wild-type ESCs (Fig. 3E; Table S2), consistent with the reduced interactions between Shh and	Immunohistochemical staining	Interprobe distances between all three probe pairs were significantly increased in CTCF deletion cells compared with wild-type ESCs (Fig. 3E; Table S2), consistent with the reduced interactions between Shh and			PCR,Flow cytometry				CTCF
31509720	chr10	121475640	121477640	FGFR2	Fibroblast growth factor receptor 2 (FGFR2) in craniofacial bones mediates osteoprogenitor proliferation, differentiation, and apoptosis.	human	bone	High+Lowthroughput	Genetic Polymorphisms in FGFR2 Underlie Skeletal Malocclusion	是	rs2162540	Osteosarcoma	MG-63 cell	E_01_0281	Western blot,PCR,Flow cytometry	Fibroblast growth factor receptor 2 (FGFR2) in craniofacial bones mediates osteoprogenitor proliferation, differentiation, and apoptosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Fibroblast growth factor receptor 2 (FGFR2) in craniofacial bones mediates osteoprogenitor proliferation, differentiation, and apoptosis.	Immunohistochemical staining	Fibroblast growth factor receptor 2 (FGFR2) in craniofacial bones mediates osteoprogenitor proliferation, differentiation, and apoptosis.	FGFR2		Western blot,PCR,Flow cytometry	Fibroblast growth factor receptor 2 (FGFR2) in craniofacial bones mediates osteoprogenitor proliferation, differentiation, and apoptosis.			
31509720	chr6	45325598	45327598	RUNX2	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	human	bone	High+Lowthroughput	Genetic Polymorphisms in FGFR2 Underlie Skeletal Malocclusion	是	rs11200014	Osteosarcoma	cementoblast	E_01_0281	Western blot,PCR,Flow cytometry	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	Immunohistochemical staining	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	RUNX2		Western blot,PCR,Flow cytometry	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.			
31509720	chr18	51025518	51027518	SMAD4	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	human	lung	High+Lowthroughput	Genetic Polymorphisms in FGFR2 Underlie Skeletal Malocclusion	是	rs2981578	asthma	NHLF cell	E_01_0281	Western blot,PCR,Flow cytometry	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	Immunohistochemical staining	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.	SMAD4		Western blot,PCR,Flow cytometry	That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4.			
31509011	chr12	9617434	9619434	Osr1	Other transcription factors such as Osr1, Eya1, Sall1 and Cited1 also play critical roles in nephron progenitors during kidney development (39, 66, 74, 91, 92).	mouse	kidney	High+Lowthroughput	In utero exposure to maternal diabetes impairs nephron progenitor differentiation	否	无	diabetes	nephron progenitor cell	E_02_0226	Western blot, immunofluorescence staining, flow cytometry	Other transcription factors such as Osr1, Eya1, Sall1 and Cited1 also play critical roles in nephron progenitors during kidney development (39, 66, 74, 91, 92).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Other transcription factors such as Osr1, Eya1, Sall1 and Cited1 also play critical roles in nephron progenitors during kidney development (39, 66, 74, 91, 92).		Other transcription factors such as Osr1, Eya1, Sall1 and Cited1 also play critical roles in nephron progenitors during kidney development (39, 66, 74, 91, 92).	Immunohistochemical staining	Other transcription factors such as Osr1, Eya1, Sall1 and Cited1 also play critical roles in nephron progenitors during kidney development (39, 66, 74, 91, 92).			Western blot,免疫荧光染色, Flow cytometry				Osr1
31507631	chr11	65877171	65879171	CTSW	This paper presents evidence that the breast_x0002_cancer-associated variant rs3903072 may regulate the expression of CTSW in tumor_x0002_infiltrating lymphocytes.	human	connective tissue	High+Lowthroughput	The Cancer-Associated Genetic Variant Rs3903072 Modulates Immune Cells in the Tumor Microenvironment	是	rs3903072	cancer	immune cell	E_01_0282	Flow cytometry,PCR	This paper presents evidence that the breast_x0002_cancer-associated variant rs3903072 may regulate the expression of CTSW in tumor_x0002_infiltrating lymphocytes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This paper presents evidence that the breast_x0002_cancer-associated variant rs3903072 may regulate the expression of CTSW in tumor_x0002_infiltrating lymphocytes.		This paper presents evidence that the breast_x0002_cancer-associated variant rs3903072 may regulate the expression of CTSW in tumor_x0002_infiltrating lymphocytes.	Immunohistochemical staining	This paper presents evidence that the breast_x0002_cancer-associated variant rs3903072 may regulate the expression of CTSW in tumor_x0002_infiltrating lymphocytes.			Flow cytometry,PCR				CTSW
31504407	chr6	151653980	151655980	ESR1	We observed ESR1 mRNA and ER protein down_x0002_regulation in BC cells treated with conditioned media (CM) from patient-derived, cancer-activated bone marrow stromal cells (BMSCs) and the BMSC cell line HS5.	human	breast	High+Lowthroughput	Bone Marrow Stromal Cells Transcriptionally Repress ESR1 but Cannot Overcome Constitutive ESR1 Mutant Activity	否	无	mammary cancer	MCF7 cell	E_01_0283	PCR, Western blot, immunofluorescence staining	We observed ESR1 mRNA and ER protein down_x0002_regulation in BC cells treated with conditioned media (CM) from patient-derived, cancer-activated bone marrow stromal cells (BMSCs) and the BMSC cell line HS5.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We observed ESR1 mRNA and ER protein down_x0002_regulation in BC cells treated with conditioned media (CM) from patient-derived, cancer-activated bone marrow stromal cells (BMSCs) and the BMSC cell line HS5.	Immunohistochemical staining	We observed ESR1 mRNA and ER protein down_x0002_regulation in BC cells treated with conditioned media (CM) from patient-derived, cancer-activated bone marrow stromal cells (BMSCs) and the BMSC cell line HS5.	ESR1		PCR,Western blot,免疫荧光染色	We observed ESR1 mRNA and ER protein down_x0002_regulation in BC cells treated with conditioned media (CM) from patient-derived, cancer-activated bone marrow stromal cells (BMSCs) and the BMSC cell line HS5.			
31503357	chrX	119233203	119235203	PGRMC1	Expression of PGRMC1 and HSD17B4 was knocked down and subsequent studies were performed to analyze cell proliferation, migration, invasion, and apoptosis. Mechanistic studies that explored the epidermal growth factor receptor (EGFR) pathway were performed by Western blot	human	prostate	High+Lowthroughput	Functional validation of metabolic genes that distinguish Gleason 3 from Gleason 4 prostate cancer foci	否	无	prostatic cancer	prostate cancer cell	E_01_0284	PCR,Western blot 	Expression of PGRMC1 and HSD17B4 was knocked down and subsequent studies were performed to analyze cell proliferation, migration, invasion, and apoptosis. Mechanistic studies that explored the epidermal growth factor receptor (EGFR) pathway were performed by Western blot	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Expression of PGRMC1 and HSD17B4 was knocked down and subsequent studies were performed to analyze cell proliferation, migration, invasion, and apoptosis. Mechanistic studies that explored the epidermal growth factor receptor (EGFR) pathway were performed by Western blot		Expression of PGRMC1 and HSD17B4 was knocked down and subsequent studies were performed to analyze cell proliferation, migration, invasion, and apoptosis. Mechanistic studies that explored the epidermal growth factor receptor (EGFR) pathway were performed by Western blot	Immunohistochemical staining	Expression of PGRMC1 and HSD17B4 was knocked down and subsequent studies were performed to analyze cell proliferation, migration, invasion, and apoptosis. Mechanistic studies that explored the epidermal growth factor receptor (EGFR) pathway were performed by Western blot			PCR,Western blot 				PGRMC1
31501538	chr8	95534429	95536429	Ccl17	We observed robust upregulation of immune marker genes associated with myeloid-derived suppressor cells (MDSCs) (Il10, Ifng, Csf1, Il6, Ptgs2 and Nfkb1), tumour-associ_x0002_ated macrophages (TAMs) (Ccl17, Ccl22, Il1r1, Il1a, Cxcl10 and Tnf) and tumour-associated neutrophils (TANs) (Cxcl1, Cxcl2, Cxcl5, Tnf and Il17a) (Supplementary Table 4) in colonic tumours from P. anaerobius-treated ApcMin/+.	human	colon	High+Lowthroughput	Peptostreptococcus anaerobius promotes colorectal carcinogenesis and modulates tumour immunity	否	无	Colon cancer		E_01_0285	Western blot,PCR	We observed robust upregulation of immune marker genes associated with myeloid-derived suppressor cells (MDSCs) (Il10, Ifng, Csf1, Il6, Ptgs2 and Nfkb1), tumour-associ_x0002_ated macrophages (TAMs) (Ccl17, Ccl22, Il1r1, Il1a, Cxcl10 and Tnf) and tumour-associated neutrophils (TANs) (Cxcl1, Cxcl2, Cxcl5, Tnf and Il17a) (Supplementary Table 4) in colonic tumours from P. anaerobius-treated ApcMin/+.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We observed robust upregulation of immune marker genes associated with myeloid-derived suppressor cells (MDSCs) (Il10, Ifng, Csf1, Il6, Ptgs2 and Nfkb1), tumour-associ_x0002_ated macrophages (TAMs) (Ccl17, Ccl22, Il1r1, Il1a, Cxcl10 and Tnf) and tumour-associated neutrophils (TANs) (Cxcl1, Cxcl2, Cxcl5, Tnf and Il17a) (Supplementary Table 4) in colonic tumours from P. anaerobius-treated ApcMin/+.		We observed robust upregulation of immune marker genes associated with myeloid-derived suppressor cells (MDSCs) (Il10, Ifng, Csf1, Il6, Ptgs2 and Nfkb1), tumour-associ_x0002_ated macrophages (TAMs) (Ccl17, Ccl22, Il1r1, Il1a, Cxcl10 and Tnf) and tumour-associated neutrophils (TANs) (Cxcl1, Cxcl2, Cxcl5, Tnf and Il17a) (Supplementary Table 4) in colonic tumours from P. anaerobius-treated ApcMin/+.	Immunohistochemical staining	We observed robust upregulation of immune marker genes associated with myeloid-derived suppressor cells (MDSCs) (Il10, Ifng, Csf1, Il6, Ptgs2 and Nfkb1), tumour-associ_x0002_ated macrophages (TAMs) (Ccl17, Ccl22, Il1r1, Il1a, Cxcl10 and Tnf) and tumour-associated neutrophils (TANs) (Cxcl1, Cxcl2, Cxcl5, Tnf and Il17a) (Supplementary Table 4) in colonic tumours from P. anaerobius-treated ApcMin/+.			Western blot,PCR				Ccl17
31501517	chr19	46644863	46646863	DACT3	For instance, strong chromatin interactions were found between the DACT3 and AP2S1 promoter regions, and one significant eQTL, rs78730097 (NC_000019) for DACT3 was located in the AP2S1 promoter in the dorsolateral prefrontal cortex (Supplementary Fig. 10a)	human	connective tissue	High+Lowthroughput	A compendium of promoter-centered long-range chromatin interactions in the human genome	是	无		embryonic cell 	E_01_0286	Flow cytometry,PCR	For instance, strong chromatin interactions were found between the DACT3 and AP2S1 promoter regions, and one significant eQTL, rs78730097 (NC_000019) for DACT3 was located in the AP2S1 promoter in the dorsolateral prefrontal cortex (Supplementary Fig. 10a)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	For instance, strong chromatin interactions were found between the DACT3 and AP2S1 promoter regions, and one significant eQTL, rs78730097 (NC_000019) for DACT3 was located in the AP2S1 promoter in the dorsolateral prefrontal cortex (Supplementary Fig. 10a)		For instance, strong chromatin interactions were found between the DACT3 and AP2S1 promoter regions, and one significant eQTL, rs78730097 (NC_000019) for DACT3 was located in the AP2S1 promoter in the dorsolateral prefrontal cortex (Supplementary Fig. 10a)	Immunohistochemical staining	For instance, strong chromatin interactions were found between the DACT3 and AP2S1 promoter regions, and one significant eQTL, rs78730097 (NC_000019) for DACT3 was located in the AP2S1 promoter in the dorsolateral prefrontal cortex (Supplementary Fig. 10a)			Flow cytometry,PCR				DACT3
31500558	chr7	18084316	18086316	HDAC9	Targeted resequencing of the HDAC9 locus in patients with atherosclerotic stroke and controls supported candidacy of rs2107595 as the causative single nucleotide polymorphism. A proteomic search for nuclear binding partners revealed preferential binding of the E2F3/TFDP1/Rb1 complex (E2F transcription factor 3/transcription factor Dp-1/Retinoblastoma 1) to the rs2107595 common allele, consistent with the disruption of an E2F3 consensus site by the risk allele.	human	connective tissue	High+Lowthroughput	The Atherosclerosis Risk Variant rs2107595 Mediates Allele-Specific Transcriptional Regulation of HDAC9 via E2F3 and Rb1	是	rs2107595	atherosclerosis	immune cell	E_01_0287	Flow cytometry,PCR	Targeted resequencing of the HDAC9 locus in patients with atherosclerotic stroke and controls supported candidacy of rs2107595 as the causative single nucleotide polymorphism. A proteomic search for nuclear binding partners revealed preferential binding of the E2F3/TFDP1/Rb1 complex (E2F transcription factor 3/transcription factor Dp-1/Retinoblastoma 1) to the rs2107595 common allele, consistent with the disruption of an E2F3 consensus site by the risk allele.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Targeted resequencing of the HDAC9 locus in patients with atherosclerotic stroke and controls supported candidacy of rs2107595 as the causative single nucleotide polymorphism. A proteomic search for nuclear binding partners revealed preferential binding of the E2F3/TFDP1/Rb1 complex (E2F transcription factor 3/transcription factor Dp-1/Retinoblastoma 1) to the rs2107595 common allele, consistent with the disruption of an E2F3 consensus site by the risk allele.		Targeted resequencing of the HDAC9 locus in patients with atherosclerotic stroke and controls supported candidacy of rs2107595 as the causative single nucleotide polymorphism. A proteomic search for nuclear binding partners revealed preferential binding of the E2F3/TFDP1/Rb1 complex (E2F transcription factor 3/transcription factor Dp-1/Retinoblastoma 1) to the rs2107595 common allele, consistent with the disruption of an E2F3 consensus site by the risk allele.	Immunohistochemical staining	Targeted resequencing of the HDAC9 locus in patients with atherosclerotic stroke and controls supported candidacy of rs2107595 as the causative single nucleotide polymorphism. A proteomic search for nuclear binding partners revealed preferential binding of the E2F3/TFDP1/Rb1 complex (E2F transcription factor 3/transcription factor Dp-1/Retinoblastoma 1) to the rs2107595 common allele, consistent with the disruption of an E2F3 consensus site by the risk allele.			Flow cytometry,PCR				HDAC9
31491956	chr7	55015564	55017564	EGFR	ROS are known to activate the epidermal growth factor receptor (EGFR), which causes the activation of the Ras/mitogen-activated protein kinases (MAPKs)pathway.	human	stomach	High+Lowthroughput	Lycopene Inhibits Activation of Epidermal Growth Factor Receptor and Expression of Cyclooxygenase-2 in Gastric Cancer Cells	否	无	gastric cancer	gastric cancer cell	E_01_0288	PCR,Western blot,Flow cytometry	ROS are known to activate the epidermal growth factor receptor (EGFR), which causes the activation of the Ras/mitogen-activated protein kinases (MAPKs)pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			ROS are known to activate the epidermal growth factor receptor (EGFR), which causes the activation of the Ras/mitogen-activated protein kinases (MAPKs)pathway.	Immunohistochemical staining	ROS are known to activate the epidermal growth factor receptor (EGFR), which causes the activation of the Ras/mitogen-activated protein kinases (MAPKs)pathway.	EGFR		PCR,Western blot,Flow cytometry	ROS are known to activate the epidermal growth factor receptor (EGFR), which causes the activation of the Ras/mitogen-activated protein kinases (MAPKs)pathway.			
31489250	chr7	142201541	142203541	Igf2	gf2, H19, and Nctc1 are linked co-regulated genes on distal mouse chromosome 7.	mouse	Musculature	High+Lowthroughput	Paternal bias expression of Igf2as is enhancer-dependent on the imprinting cluster of Igf2, H19 and Nctc1 in muscle cells	是	无		muscle cell	E_02_0227	Western blot, PCR, immunofluorescence staining	gf2, H19, and Nctc1 are linked co-regulated genes on distal mouse chromosome 7.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	gf2, H19, and Nctc1 are linked co-regulated genes on distal mouse chromosome 7.		gf2, H19, and Nctc1 are linked co-regulated genes on distal mouse chromosome 7.	Immunohistochemical staining	gf2, H19, and Nctc1 are linked co-regulated genes on distal mouse chromosome 7.			Western blot,PCR,免疫荧光染色				Igf2
31487061	chr7	148803986	148805986	EZH2	EZH2 plays an important role in bone homeostasis and the use of the small molecule inhibitor GSK126 (a potent and highly selective EZH2 methyltransferase inhibitor(22)) exhibited promising bone protecting effects in several osteoporotic/inflam_x0002_matory and malignant osteolytic bone pathologies.(23–27)	mouse	connective tissue	High+Lowthroughput	EZH2 Supports Osteoclast Differentiation and Bone Resorption Via Epigenetic and Cytoplasmic Targets	否	无		stem cell	E_02_0228	Western blot, PCR, immunofluorescence staining	EZH2 plays an important role in bone homeostasis and the use of the small molecule inhibitor GSK126 (a potent and highly selective EZH2 methyltransferase inhibitor(22)) exhibited promising bone protecting effects in several osteoporotic/inflam_x0002_matory and malignant osteolytic bone pathologies.(23–27)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EZH2 plays an important role in bone homeostasis and the use of the small molecule inhibitor GSK126 (a potent and highly selective EZH2 methyltransferase inhibitor(22)) exhibited promising bone protecting effects in several osteoporotic/inflam_x0002_matory and malignant osteolytic bone pathologies.(23–27)		EZH2 plays an important role in bone homeostasis and the use of the small molecule inhibitor GSK126 (a potent and highly selective EZH2 methyltransferase inhibitor(22)) exhibited promising bone protecting effects in several osteoporotic/inflam_x0002_matory and malignant osteolytic bone pathologies.(23–27)	Immunohistochemical staining	EZH2 plays an important role in bone homeostasis and the use of the small molecule inhibitor GSK126 (a potent and highly selective EZH2 methyltransferase inhibitor(22)) exhibited promising bone protecting effects in several osteoporotic/inflam_x0002_matory and malignant osteolytic bone pathologies.(23–27)			Western blot,PCR,免疫荧光染色				EZH2
31481796	chr7	148804478	148806478	EZH2	Typical genomic dis_x0002_tributions of Pol II, EZH2 and H3K27me3 were also identified in our data (Supplementary Fig. 3d,h; Fig. 2h).	human,mouse	Epithelial tissues	High+Lowthroughput	Profiling chromatin states using single-cell itChIP-seq	否	无		endothelial cell	E_02_0229	Flow cytometry	Typical genomic dis_x0002_tributions of Pol II, EZH2 and H3K27me3 were also identified in our data (Supplementary Fig. 3d,h; Fig. 2h).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Typical genomic dis_x0002_tributions of Pol II, EZH2 and H3K27me3 were also identified in our data (Supplementary Fig. 3d,h; Fig. 2h).		Typical genomic dis_x0002_tributions of Pol II, EZH2 and H3K27me3 were also identified in our data (Supplementary Fig. 3d,h; Fig. 2h).	Immunohistochemical staining	Typical genomic dis_x0002_tributions of Pol II, EZH2 and H3K27me3 were also identified in our data (Supplementary Fig. 3d,h; Fig. 2h).			Flow cytometry				EZH2
31481496	chr17	42310597	42312597	STAT3	Deregulated activation of the latent oncogenic transcription factor STAT3 in many human epithelial malignancies, includ_x0002_ing gastric cancer, has invariably been associated with its canonical tyrosine phosphorylation and enhanced transcrip_x0002_tional activity.	human,mouse	stomach	High+Lowthroughput	Serine-Phosphorylated STAT3 Promotes Tumorigenesis via Modulation of RNA Polymerase Transcriptional Activity	否	无	gastric cancer	gastric cancer cell	E_02_0230	Western blot,PCR	Deregulated activation of the latent oncogenic transcription factor STAT3 in many human epithelial malignancies, includ_x0002_ing gastric cancer, has invariably been associated with its canonical tyrosine phosphorylation and enhanced transcrip_x0002_tional activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Deregulated activation of the latent oncogenic transcription factor STAT3 in many human epithelial malignancies, includ_x0002_ing gastric cancer, has invariably been associated with its canonical tyrosine phosphorylation and enhanced transcrip_x0002_tional activity.		Deregulated activation of the latent oncogenic transcription factor STAT3 in many human epithelial malignancies, includ_x0002_ing gastric cancer, has invariably been associated with its canonical tyrosine phosphorylation and enhanced transcrip_x0002_tional activity.	Immunohistochemical staining	Deregulated activation of the latent oncogenic transcription factor STAT3 in many human epithelial malignancies, includ_x0002_ing gastric cancer, has invariably been associated with its canonical tyrosine phosphorylation and enhanced transcrip_x0002_tional activity.			Western blot,PCR				STAT3
31481468	chr9	6410546	6412546	UHRF2	In mammals, SRA domains are found in only two proteins (15), the DNA methylation maintenance factor UHRF1 and the structurally related, but functionally distinct, UHRF2 (16, 17).	human	colon	High+Lowthroughput	The finger loop of the SRA domain in the E3 ligase UHRF1 is a regulator of ubiquitin targeting and is required for the maintenance of DNA methylation	否	无	Colon cancer	colon cancer cell	E_01_0289	Western blot	In mammals, SRA domains are found in only two proteins (15), the DNA methylation maintenance factor UHRF1 and the structurally related, but functionally distinct, UHRF2 (16, 17).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In mammals, SRA domains are found in only two proteins (15), the DNA methylation maintenance factor UHRF1 and the structurally related, but functionally distinct, UHRF2 (16, 17).	Immunohistochemical staining	In mammals, SRA domains are found in only two proteins (15), the DNA methylation maintenance factor UHRF1 and the structurally related, but functionally distinct, UHRF2 (16, 17).	UHRF2		Western blot	In mammals, SRA domains are found in only two proteins (15), the DNA methylation maintenance factor UHRF1 and the structurally related, but functionally distinct, UHRF2 (16, 17).			
31478258	chr7	148803962	148805962	EZH2	In addition, PCAT‐1 epigenetically silenced PTEN through binding to the histone methyltransferase enhancer of zeste homolog 2 (EZH2), thus increasing H3K27me3.	human	stomach	High+Lowthroughput	PCAT-1 contributes to cisplatin resistance in gastric cancer through epigenetically silencing PTEN via recruiting EZH2	否	无	gastric cancer	gastric cancer cell	E_01_0290	Western blot, PCR,Flow cytometry	In addition, PCAT‐1 epigenetically silenced PTEN through binding to the histone methyltransferase enhancer of zeste homolog 2 (EZH2), thus increasing H3K27me3.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, PCAT‐1 epigenetically silenced PTEN through binding to the histone methyltransferase enhancer of zeste homolog 2 (EZH2), thus increasing H3K27me3.	Immunohistochemical staining	In addition, PCAT‐1 epigenetically silenced PTEN through binding to the histone methyltransferase enhancer of zeste homolog 2 (EZH2), thus increasing H3K27me3.	EZH2		Western blot, PCR,Flow cytometry	In addition, PCAT‐1 epigenetically silenced PTEN through binding to the histone methyltransferase enhancer of zeste homolog 2 (EZH2), thus increasing H3K27me3.			
31477927	chr3	101825274	101827274	NFKBIZ	We checked typical examples of the short- and long-lived mRNAs NFKBIZ35 and GAPDH, respectively, in MCF-7 cells. The signal from NFKBIZ (Figs. 2a and 3a,b) was higher in NET_x0002_CAGE than in CAGE, whereas the opposite was true for GAPDH (Figs. 2a and 3b).	human,mouse	breast	High+Lowthroughput	NET-CAGE characterizes the dynamics and topology of human transcribed cis-regulatory elements	否	无	mammary cancer	breast cancer cell	E_02_0231	PCR,Flow cytometry	We checked typical examples of the short- and long-lived mRNAs NFKBIZ35 and GAPDH, respectively, in MCF-7 cells. The signal from NFKBIZ (Figs. 2a and 3a,b) was higher in NET_x0002_CAGE than in CAGE, whereas the opposite was true for GAPDH (Figs. 2a and 3b).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We checked typical examples of the short- and long-lived mRNAs NFKBIZ35 and GAPDH, respectively, in MCF-7 cells. The signal from NFKBIZ (Figs. 2a and 3a,b) was higher in NET_x0002_CAGE than in CAGE, whereas the opposite was true for GAPDH (Figs. 2a and 3b).		We checked typical examples of the short- and long-lived mRNAs NFKBIZ35 and GAPDH, respectively, in MCF-7 cells. The signal from NFKBIZ (Figs. 2a and 3a,b) was higher in NET_x0002_CAGE than in CAGE, whereas the opposite was true for GAPDH (Figs. 2a and 3b).	Immunohistochemical staining	We checked typical examples of the short- and long-lived mRNAs NFKBIZ35 and GAPDH, respectively, in MCF-7 cells. The signal from NFKBIZ (Figs. 2a and 3a,b) was higher in NET_x0002_CAGE than in CAGE, whereas the opposite was true for GAPDH (Figs. 2a and 3b).			PCR,Flow cytometry				NFKBIZ
31477927	chr12	6532002	6534002	GAPDH	We checked typical examples of the short- and long-lived mRNAs NFKBIZ35 and GAPDH, respectively, in MCF-7 cells. The signal from NFKBIZ (Figs. 2a and 3a,b) was higher in NET_x0002_CAGE than in CAGE, whereas the opposite was true for GAPDH (Figs. 2a and 3b).	human,mouse	uterus	High+Lowthroughput	NET-CAGE characterizes the dynamics and topology of human transcribed cis-regulatory elements	否	无	cervical carcinoma	HeLa-S3 cell	E_02_0231	PCR,Flow cytometry	We checked typical examples of the short- and long-lived mRNAs NFKBIZ35 and GAPDH, respectively, in MCF-7 cells. The signal from NFKBIZ (Figs. 2a and 3a,b) was higher in NET_x0002_CAGE than in CAGE, whereas the opposite was true for GAPDH (Figs. 2a and 3b).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We checked typical examples of the short- and long-lived mRNAs NFKBIZ35 and GAPDH, respectively, in MCF-7 cells. The signal from NFKBIZ (Figs. 2a and 3a,b) was higher in NET_x0002_CAGE than in CAGE, whereas the opposite was true for GAPDH (Figs. 2a and 3b).		We checked typical examples of the short- and long-lived mRNAs NFKBIZ35 and GAPDH, respectively, in MCF-7 cells. The signal from NFKBIZ (Figs. 2a and 3a,b) was higher in NET_x0002_CAGE than in CAGE, whereas the opposite was true for GAPDH (Figs. 2a and 3b).	Immunohistochemical staining	We checked typical examples of the short- and long-lived mRNAs NFKBIZ35 and GAPDH, respectively, in MCF-7 cells. The signal from NFKBIZ (Figs. 2a and 3a,b) was higher in NET_x0002_CAGE than in CAGE, whereas the opposite was true for GAPDH (Figs. 2a and 3b).			PCR,Flow cytometry				GAPDH
30700785	chr17	31933934	31935934	SUZ12	PRC2 is composed of four main subunits; Suppressor of Zeste 12 (SUZ12), Retinoblastoma-Associated Protein 46/48 (RbAp46/48)	human		High+Lowthroughput	The EZH2 SANT1 domain is a histone reader providing sensitivity to the modification state of the H4 tail	否			eukaryotic,HeLa,E. coli Rosetta2 (DE3) pLysS cell	E_01_0291	ChIP-seq,Gateway Recombination cloning,EMSAs,HADDOCK Modeling	PRC2 is composed of four main subunits; Suppressor of Zeste 12 (SUZ12), Retinoblastoma-Associated Protein 46/48 (RbAp46/48)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			PRC2 is composed of four main subunits; Suppressor of Zeste 12 (SUZ12), Retinoblastoma-Associated Protein 46/48 (RbAp46/48)	Immunohistochemical staining	PRC2 is composed of four main subunits; Suppressor of Zeste 12 (SUZ12), Retinoblastoma-Associated Protein 46/48 (RbAp46/48)	SUZ12		ChIP-seq,Gateway Recombination cloning,EMSAs,HADDOCK Modeling	PRC2 is composed of four main subunits; Suppressor of Zeste 12 (SUZ12), Retinoblastoma-Associated Protein 46/48 (RbAp46/48)			
30700527	chr4	109910195	109912195	EGF	Genetic screens in the nematode Caenorhabditis elegans identified the EGF/Ras and Notch pathways as central for vulval precursor cell fate patterning.	mouse	epithelial	High+Lowthroughput	Necessity and Contingency in Developmental Genetic Screens: EGF, Wnt, and Semaphorin Pathways in Vulval Induction of the Nematode Oscheius tipulae	否			precursor cell	E_02_0232	PCR, sequencing technology, neighbor joining method	Genetic screens in the nematode Caenorhabditis elegans identified the EGF/Ras and Notch pathways as central for vulval precursor cell fate patterning.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genetic screens in the nematode Caenorhabditis elegans identified the EGF/Ras and Notch pathways as central for vulval precursor cell fate patterning.		Genetic screens in the nematode Caenorhabditis elegans identified the EGF/Ras and Notch pathways as central for vulval precursor cell fate patterning.	Immunohistochemical staining	Genetic screens in the nematode Caenorhabditis elegans identified the EGF/Ras and Notch pathways as central for vulval precursor cell fate patterning.			PCR,测序技术,neighbor-joining method				EGF
30700190	chr9	117701691	117703691	TLR4	Expression of nuclear factor kappa-light-chain-enhancer of activated B cells p65 (NF-κB p65), Toll-like receptor 4 (TLR4), and zonula occludens-1 (ZO-1) in the small intestinal mucosa was also assessed.	mouse	pancreas	High+Lowthroughput	Qingyi decoction attenuates severe acute pancreatitis in rats via inhibition of inflammation and protection of the intestinal barrier	否		Acute severe pancreatitis	pancreatic acinar cells	E_02_0233	Western blotting,	Expression of nuclear factor kappa-light-chain-enhancer of activated B cells p65 (NF-κB p65), Toll-like receptor 4 (TLR4), and zonula occludens-1 (ZO-1) in the small intestinal mucosa was also assessed.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Expression of nuclear factor kappa-light-chain-enhancer of activated B cells p65 (NF-κB p65), Toll-like receptor 4 (TLR4), and zonula occludens-1 (ZO-1) in the small intestinal mucosa was also assessed.		Expression of nuclear factor kappa-light-chain-enhancer of activated B cells p65 (NF-κB p65), Toll-like receptor 4 (TLR4), and zonula occludens-1 (ZO-1) in the small intestinal mucosa was also assessed.	Immunohistochemical staining	Expression of nuclear factor kappa-light-chain-enhancer of activated B cells p65 (NF-κB p65), Toll-like receptor 4 (TLR4), and zonula occludens-1 (ZO-1) in the small intestinal mucosa was also assessed.			Western blotting,				TLR4
30699347	chrX	72326894	72328894	HDAC8	By contrast, our results indicate that recruiting dCas9-HDAC8 (-ac) to Fos Enh2 predominantly reduces the ON rate relative to control-transfected neurons.	mouse	nerve	High+Lowthroughput	Enhancer Histone Acetylation Modulates Transcriptional Bursting Dynamics of Neuronal Activity-Inducible Genes	否				E_02_0234	FISH	By contrast, our results indicate that recruiting dCas9-HDAC8 (-ac) to Fos Enh2 predominantly reduces the ON rate relative to control-transfected neurons.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	By contrast, our results indicate that recruiting dCas9-HDAC8 (-ac) to Fos Enh2 predominantly reduces the ON rate relative to control-transfected neurons.		By contrast, our results indicate that recruiting dCas9-HDAC8 (-ac) to Fos Enh2 predominantly reduces the ON rate relative to control-transfected neurons.	Immunohistochemical staining	By contrast, our results indicate that recruiting dCas9-HDAC8 (-ac) to Fos Enh2 predominantly reduces the ON rate relative to control-transfected neurons.			FISH				HDAC8
30699336	chr17	80098759	80100759	GAA	The surface decoration of CPNL was performed by adding Transcutol which act as a nonionic penetration enhancer. Accurately weighed 100 mg of Capecitabine and 0.4% w/v of Chitosan were dissolved in 1% v/v aqueous glacial acetic acid (GAA) solution.	human,mouse	skin	High+Lowthroughput	pH triggered and charge attracted nanogel for simultaneous evaluation of penetration and toxicity against skin cancer: In-vitro and ex-vivo study	否		Skin cancer		E_02_0235	Ionotropic gelation technique,	The surface decoration of CPNL was performed by adding Transcutol which act as a nonionic penetration enhancer. Accurately weighed 100 mg of Capecitabine and 0.4% w/v of Chitosan were dissolved in 1% v/v aqueous glacial acetic acid (GAA) solution.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The surface decoration of CPNL was performed by adding Transcutol which act as a nonionic penetration enhancer. Accurately weighed 100 mg of Capecitabine and 0.4% w/v of Chitosan were dissolved in 1% v/v aqueous glacial acetic acid (GAA) solution.		The surface decoration of CPNL was performed by adding Transcutol which act as a nonionic penetration enhancer. Accurately weighed 100 mg of Capecitabine and 0.4% w/v of Chitosan were dissolved in 1% v/v aqueous glacial acetic acid (GAA) solution.	Immunohistochemical staining	The surface decoration of CPNL was performed by adding Transcutol which act as a nonionic penetration enhancer. Accurately weighed 100 mg of Capecitabine and 0.4% w/v of Chitosan were dissolved in 1% v/v aqueous glacial acetic acid (GAA) solution.			Ionotropic gelation technique,				GAA
30696717	chr4	71738822	71740822	GC	Our classifiers also indicate that there are functionally relevant differences in enhancer and promoter GC content beyond the influence of CpG islands	human	Liver	High+Lowthroughput	Sequence Characteristics Distinguish Transcribed Enhancers from Promoters and Predict Their Breadth of Activity	否		common metabolic disorders		E_01_0292	Western blot,Immunostaining,RT-PCR	Our classifiers also indicate that there are functionally relevant differences in enhancer and promoter GC content beyond the influence of CpG islands	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our classifiers also indicate that there are functionally relevant differences in enhancer and promoter GC content beyond the influence of CpG islands		Our classifiers also indicate that there are functionally relevant differences in enhancer and promoter GC content beyond the influence of CpG islands	Immunohistochemical staining	Our classifiers also indicate that there are functionally relevant differences in enhancer and promoter GC content beyond the influence of CpG islands			Western blot,Immunostaining,RT-PCR				GC
30696265	chr2	136111778	136113778	CXCR4	These data confirm CXCR4 blockade as a promising treatment strategy after MI. We identify dendritic cell-primed splenic Treg cells as the central arbiters of these therapeutic effects and thereby delineate a pharmacological strategy to promote infarct repair by augmenting Treg cell function in vivo.	mouse	lymph	High+Lowthroughput	C-X-C Motif Chemokine Receptor 4 Blockade Promotes Tissue Repair After Myocardial Infarction by Enhancing Regulatory T Cell Mobilization and Immune-Regulatory Function	否		miocardial infarction	T cell	E_02_0236	FISH	These data confirm CXCR4 blockade as a promising treatment strategy after MI. We identify dendritic cell-primed splenic Treg cells as the central arbiters of these therapeutic effects and thereby delineate a pharmacological strategy to promote infarct repair by augmenting Treg cell function in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These data confirm CXCR4 blockade as a promising treatment strategy after MI. We identify dendritic cell-primed splenic Treg cells as the central arbiters of these therapeutic effects and thereby delineate a pharmacological strategy to promote infarct repair by augmenting Treg cell function in vivo.		These data confirm CXCR4 blockade as a promising treatment strategy after MI. We identify dendritic cell-primed splenic Treg cells as the central arbiters of these therapeutic effects and thereby delineate a pharmacological strategy to promote infarct repair by augmenting Treg cell function in vivo.	Immunohistochemical staining	These data confirm CXCR4 blockade as a promising treatment strategy after MI. We identify dendritic cell-primed splenic Treg cells as the central arbiters of these therapeutic effects and thereby delineate a pharmacological strategy to promote infarct repair by augmenting Treg cell function in vivo.			FISH				CXCR4
30692641	chrX	44870388	44872388	KDM6A	We exploit the loss of function mutations in KDM6A and SWI/SNF complex to make bladder cancer cells susceptible to EZH2-based epigenetic therapy that activates an immune response to drive tumor cell differentiation and death.	human,mouse	muscle	High+Lowthroughput	Inhibition of EZH2 induces NK cell-mediated differentiation and death in?muscle-invasive bladder cancer	否		Muscle invasive bladder cancer		E_02_0237	PCR, Western blots, sequencing technology	We exploit the loss of function mutations in KDM6A and SWI/SNF complex to make bladder cancer cells susceptible to EZH2-based epigenetic therapy that activates an immune response to drive tumor cell differentiation and death.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We exploit the loss of function mutations in KDM6A and SWI/SNF complex to make bladder cancer cells susceptible to EZH2-based epigenetic therapy that activates an immune response to drive tumor cell differentiation and death.		We exploit the loss of function mutations in KDM6A and SWI/SNF complex to make bladder cancer cells susceptible to EZH2-based epigenetic therapy that activates an immune response to drive tumor cell differentiation and death.	Immunohistochemical staining	We exploit the loss of function mutations in KDM6A and SWI/SNF complex to make bladder cancer cells susceptible to EZH2-based epigenetic therapy that activates an immune response to drive tumor cell differentiation and death.			PCR，Western blots,测序技术				KDM6A
30692044	chr10	100732827	100734827	PAX2	To generate the recombinant lentivirus, lentiviral pLKO-shAR/pLKO-Scr with pMD2.G packaging and psPAX2 envelope plasmids	human	prostate	High+Lowthroughput	Preclinical study using androgen receptor (AR) degradation enhancer to increase radiotherapy efficacy via targeting radiation-increased AR to better suppress prostate cancer progression			Prostate cancer		E_01_0293	PCR,Western blot	To generate the recombinant lentivirus, lentiviral pLKO-shAR/pLKO-Scr with pMD2.G packaging and psPAX2 envelope plasmids	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			To generate the recombinant lentivirus, lentiviral pLKO-shAR/pLKO-Scr with pMD2.G packaging and psPAX2 envelope plasmids	Immunohistochemical staining	To generate the recombinant lentivirus, lentiviral pLKO-shAR/pLKO-Scr with pMD2.G packaging and psPAX2 envelope plasmids	PAX2		PCR,Western blot	To generate the recombinant lentivirus, lentiviral pLKO-shAR/pLKO-Scr with pMD2.G packaging and psPAX2 envelope plasmids			
33147208	chr9	21074558	21076558	IFNB1	This variant prevents binding of the C/EBP-β transcription factor, and is associated with decreased expression of IFNB1 in activated monocytes.	human	Epithelial	High+Lowthroughput	A genetic variant controls interferon-尾 gene expression in human myeloid cells by preventing C/EBP-尾 binding on a conserved enhancer	是	12553564		monocyte cells	E_01_0294	Flow cytometry	This variant prevents binding of the C/EBP-β transcription factor, and is associated with decreased expression of IFNB1 in activated monocytes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			This variant prevents binding of the C/EBP-β transcription factor, and is associated with decreased expression of IFNB1 in activated monocytes.	Immunohistochemical staining	This variant prevents binding of the C/EBP-β transcription factor, and is associated with decreased expression of IFNB1 in activated monocytes.	IFNB1		流式细胞术	This variant prevents binding of the C/EBP-β transcription factor, and is associated with decreased expression of IFNB1 in activated monocytes.			
30691060	chr4	74742012	74744012	BTC	The dried powders of CIVT and CIEE were stored at 4 °C until use. CIVT was provided from BTC corporation	mouse	fat	High+Lowthroughput	Effect of Enzymatic Treatment of Chrysanthemum indicum Linné Extracts on Lipid Accumulation and Adipogenesis in High-Fat-Diet-Induced Obese Male Mice	否		Hyperostosis	mesenchymal precursor cell	E_02_0238	Western Blot,ELISA,HPLC,Micro-CT	The dried powders of CIVT and CIEE were stored at 4 °C until use. CIVT was provided from BTC corporation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The dried powders of CIVT and CIEE were stored at 4 °C until use. CIVT was provided from BTC corporation		The dried powders of CIVT and CIEE were stored at 4 °C until use. CIVT was provided from BTC corporation	Immunohistochemical staining	The dried powders of CIVT and CIEE were stored at 4 °C until use. CIVT was provided from BTC corporation			Western Blot,ELISA,HPLC,Micro-CT				BTC
30688289	chr4	73737463	73739463	CXCL8	Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were performed to determine the expressions of inflammatory cytokines including interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), apoptosis-related genes, and the downstream target genes of NF-κB signaling pathway, including NFKBIA, CXCL8, and cyclin D1.	human	Kidney	High+Lowthroughput	The Effect of Overexpression of the Enhancer of Zeste Homolog 1 (EZH1) Gene on Aristolochic Acid-Induced Injury in HK-2 Human Kidney Proximal Tubule Cells In Vitro			Acute kidney injury	Human Kidney Proximal Tubule cell	E_01_0295	PCR, Western blots, sequencing technology	Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were performed to determine the expressions of inflammatory cytokines including interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), apoptosis-related genes, and the downstream target genes of NF-κB signaling pathway, including NFKBIA, CXCL8, and cyclin D1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were performed to determine the expressions of inflammatory cytokines including interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), apoptosis-related genes, and the downstream target genes of NF-κB signaling pathway, including NFKBIA, CXCL8, and cyclin D1.	Immunohistochemical staining	Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were performed to determine the expressions of inflammatory cytokines including interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), apoptosis-related genes, and the downstream target genes of NF-κB signaling pathway, including NFKBIA, CXCL8, and cyclin D1.	CXCL8		PCR，Western blots,测序技术	Quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot were performed to determine the expressions of inflammatory cytokines including interleukin (IL)-1β, IL-6, tumor necrosis factor-α (TNF-α), apoptosis-related genes, and the downstream target genes of NF-κB signaling pathway, including NFKBIA, CXCL8, and cyclin D1.			
30687302	chr16	67559454	67561454	CTCF	RNA sequencing on the lungs of infected hosts yielded reads mapping to 74,964 non-coding RNAs, 206 and 277 of which were determined to be significantly up- and down-regulated, respectively, in comparison to uninfected controls. Following removal of short non-coding RNAs and ambiguous transcripts, remaining transcripts underwent in-depth analysis of mouse lung epigenetic signatures H3K4Me1 and H3K4Me3, active transcript markers (POLR2A, p300, CTCF)	mouse	lung	High+Lowthroughput	Enhancer Associated Long Non-coding RNA Transcription and Gene Regulation in Experimental Models of Rickettsial Infection			Human spotted fever rickettsial disease	endothelial cell	E_02_0239	PCR，ChIP-Seq	RNA sequencing on the lungs of infected hosts yielded reads mapping to 74,964 non-coding RNAs, 206 and 277 of which were determined to be significantly up- and down-regulated, respectively, in comparison to uninfected controls. Following removal of short non-coding RNAs and ambiguous transcripts, remaining transcripts underwent in-depth analysis of mouse lung epigenetic signatures H3K4Me1 and H3K4Me3, active transcript markers (POLR2A, p300, CTCF)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RNA sequencing on the lungs of infected hosts yielded reads mapping to 74,964 non-coding RNAs, 206 and 277 of which were determined to be significantly up- and down-regulated, respectively, in comparison to uninfected controls. Following removal of short non-coding RNAs and ambiguous transcripts, remaining transcripts underwent in-depth analysis of mouse lung epigenetic signatures H3K4Me1 and H3K4Me3, active transcript markers (POLR2A, p300, CTCF)		RNA sequencing on the lungs of infected hosts yielded reads mapping to 74,964 non-coding RNAs, 206 and 277 of which were determined to be significantly up- and down-regulated, respectively, in comparison to uninfected controls. Following removal of short non-coding RNAs and ambiguous transcripts, remaining transcripts underwent in-depth analysis of mouse lung epigenetic signatures H3K4Me1 and H3K4Me3, active transcript markers (POLR2A, p300, CTCF)	Immunohistochemical staining	RNA sequencing on the lungs of infected hosts yielded reads mapping to 74,964 non-coding RNAs, 206 and 277 of which were determined to be significantly up- and down-regulated, respectively, in comparison to uninfected controls. Following removal of short non-coding RNAs and ambiguous transcripts, remaining transcripts underwent in-depth analysis of mouse lung epigenetic signatures H3K4Me1 and H3K4Me3, active transcript markers (POLR2A, p300, CTCF)			PCR，ChIP-Seq				CTCF
30686579	chr3	133743493	133745493	TF	Relating transcription factor (TF) expression to the genome-wide accessibility of their binding motifs classifies them as predominantly openers or closers of local chromatin accessibility	mouse	lymph	High+Lowthroughput	The cis-Regulatory Atlas of the Mouse Immune System				immune cell	E_02_0240	PCR，ChIP-seq	Relating transcription factor (TF) expression to the genome-wide accessibility of their binding motifs classifies them as predominantly openers or closers of local chromatin accessibility	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Relating transcription factor (TF) expression to the genome-wide accessibility of their binding motifs classifies them as predominantly openers or closers of local chromatin accessibility		Relating transcription factor (TF) expression to the genome-wide accessibility of their binding motifs classifies them as predominantly openers or closers of local chromatin accessibility	Immunohistochemical staining	Relating transcription factor (TF) expression to the genome-wide accessibility of their binding motifs classifies them as predominantly openers or closers of local chromatin accessibility			PCR，ChIP-seq				TF
30683753	chr3	133743339	133745339	TF	This higher tissue specificity is strongly associated with having less complex transcription factor (TF) motif profiles at the core promoter.	human	Liver	High+Lowthroughput	High-throughput functional analysis of lncRNA core promoters elucidates rules governing tissue specificity			common metabolic disorders		E_01_0296	Western blot,Immunostaining,RT-PCR	This higher tissue specificity is strongly associated with having less complex transcription factor (TF) motif profiles at the core promoter.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This higher tissue specificity is strongly associated with having less complex transcription factor (TF) motif profiles at the core promoter.		This higher tissue specificity is strongly associated with having less complex transcription factor (TF) motif profiles at the core promoter.	Immunohistochemical staining	This higher tissue specificity is strongly associated with having less complex transcription factor (TF) motif profiles at the core promoter.			Western blot,Immunostaining,RT-PCR				TF
30683142	chr17	43041963	43043963	BRCA1	o provide insights into alternative classification and potential therapeutic targeting strategies of BRCA1-like hormone-receptor-positive tumors we developed and applied a novel copy number classifier to identify BRCA1-like hormone-receptor-positive tumors and their characteristic somatic alteration profiles.	human	Breast	High+Lowthroughput	Molecular and epigenetic profiles of BRCA1-like hormone-receptor-positive breast tumors identified with development and application of a copy-number-based classifier			mammary cancer	breast cancer cell	E_01_0297	PCR, sequencing technology	o provide insights into alternative classification and potential therapeutic targeting strategies of BRCA1-like hormone-receptor-positive tumors we developed and applied a novel copy number classifier to identify BRCA1-like hormone-receptor-positive tumors and their characteristic somatic alteration profiles.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			o provide insights into alternative classification and potential therapeutic targeting strategies of BRCA1-like hormone-receptor-positive tumors we developed and applied a novel copy number classifier to identify BRCA1-like hormone-receptor-positive tumors and their characteristic somatic alteration profiles.	Immunohistochemical staining	o provide insights into alternative classification and potential therapeutic targeting strategies of BRCA1-like hormone-receptor-positive tumors we developed and applied a novel copy number classifier to identify BRCA1-like hormone-receptor-positive tumors and their characteristic somatic alteration profiles.	BRCA1		PCR，测序技术	o provide insights into alternative classification and potential therapeutic targeting strategies of BRCA1-like hormone-receptor-positive tumors we developed and applied a novel copy number classifier to identify BRCA1-like hormone-receptor-positive tumors and their characteristic somatic alteration profiles.			
30682089	chr15	72964799	72966799	Ago2	One strand then incorporates with Argonaute (Ago2) proteins into the RNA Inducing Silencing Complex (RISC)	human	lymph	High+Lowthroughput	HIV-1 infection increases microRNAs that inhibit Dicer1, HRB and HIV-EP2, thereby reducing viral replication			AIDS	Sup-T1 cell，HeLa-MAGI cell	E_01_0298	PCR, Western blot, sequencing technology	One strand then incorporates with Argonaute (Ago2) proteins into the RNA Inducing Silencing Complex (RISC)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	One strand then incorporates with Argonaute (Ago2) proteins into the RNA Inducing Silencing Complex (RISC)		One strand then incorporates with Argonaute (Ago2) proteins into the RNA Inducing Silencing Complex (RISC)	Immunohistochemical staining	One strand then incorporates with Argonaute (Ago2) proteins into the RNA Inducing Silencing Complex (RISC)			PCR，Western blot，测序技术				Ago2
30680334	chr12	109416349	109418349	Dlk1	The highest level of Dlk1 transcript was found at 7 days of age, followed by significant and steady drops of the transcript level until 44 days of age	mouse	epididymis	High+Lowthroughput	Expressional Patterns of Adipocyte-Associated Molecules in the Rat Epididymal Fat during Postnatal Development Period				fat cell	E_02_0241	PCR, Western blot, sequencing technology	The highest level of Dlk1 transcript was found at 7 days of age, followed by significant and steady drops of the transcript level until 44 days of age	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The highest level of Dlk1 transcript was found at 7 days of age, followed by significant and steady drops of the transcript level until 44 days of age		The highest level of Dlk1 transcript was found at 7 days of age, followed by significant and steady drops of the transcript level until 44 days of age	Immunohistochemical staining	The highest level of Dlk1 transcript was found at 7 days of age, followed by significant and steady drops of the transcript level until 44 days of age			PCR，Western blot，测序技术				Dlk1
30678091	chr15	99562775	99564775	MEF2A	The strongest effect visible in three distinct cell types was observed for rs12946510 that is predicted to alter MEF2A/C and FOXO1 binding sites.	human	lymph	High+Lowthroughput	Functional SNPs in the Human Autoimmunity-Associated Locus 17q12-21		12946510	mammary cancer	immune cell	E_01_0299	PCR，Western blot，ChIP-seq	The strongest effect visible in three distinct cell types was observed for rs12946510 that is predicted to alter MEF2A/C and FOXO1 binding sites.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The strongest effect visible in three distinct cell types was observed for rs12946510 that is predicted to alter MEF2A/C and FOXO1 binding sites.	Immunohistochemical staining	The strongest effect visible in three distinct cell types was observed for rs12946510 that is predicted to alter MEF2A/C and FOXO1 binding sites.	MEF2A		PCR，Western blot，ChIP-seq	The strongest effect visible in three distinct cell types was observed for rs12946510 that is predicted to alter MEF2A/C and FOXO1 binding sites.			
30676242	chr14	64081786	64083786	ESR2	They were also more likely to be in ARNT and ESR2 transcription factor binding sites	human	lymph	High+Lowthroughput	Exposure to polybrominated biphenyl (PBB) associates with genome-wide DNA methylation differences in peripheral blood			Autoimmune diseases	B cell	E_01_0300	ChIP-seq	They were also more likely to be in ARNT and ESR2 transcription factor binding sites	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			They were also more likely to be in ARNT and ESR2 transcription factor binding sites	Immunohistochemical staining	They were also more likely to be in ARNT and ESR2 transcription factor binding sites	ESR2		ChIP-seq	They were also more likely to be in ARNT and ESR2 transcription factor binding sites			
30675263	chr13	73052370	73054370	KLF5	In addition, the expression levels of tumor invasion-associated proteins, including Kruppel-like factor 5 (KLF5), matrix metallopeptidase (MMP)-2, MMP-9, and E-cadherin (ECD) were detected subsequent to transfection.	human	lymph	High+Lowthroughput	Association of the invasiveness of colon cancer with the expression of C/EBPα			Colon cancer	SW480 cell，CC cell	E_01_0301	PCR，ChIP-Seq	In addition, the expression levels of tumor invasion-associated proteins, including Kruppel-like factor 5 (KLF5), matrix metallopeptidase (MMP)-2, MMP-9, and E-cadherin (ECD) were detected subsequent to transfection.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, the expression levels of tumor invasion-associated proteins, including Kruppel-like factor 5 (KLF5), matrix metallopeptidase (MMP)-2, MMP-9, and E-cadherin (ECD) were detected subsequent to transfection.		In addition, the expression levels of tumor invasion-associated proteins, including Kruppel-like factor 5 (KLF5), matrix metallopeptidase (MMP)-2, MMP-9, and E-cadherin (ECD) were detected subsequent to transfection.	Immunohistochemical staining	In addition, the expression levels of tumor invasion-associated proteins, including Kruppel-like factor 5 (KLF5), matrix metallopeptidase (MMP)-2, MMP-9, and E-cadherin (ECD) were detected subsequent to transfection.			PCR，ChIP-Seq				KLF5
30672466	chr11	114255412	114257412	NNMT	Subsequently, PLZF was recruited to osteogenic enhancers, influencing H3K27 acetylation and expression of nearby genes important for osteogenic function. Furthermore, we identified a latent enhancer within the ZBTB16/PLZF locus itself that became active, gained PLZF, p300 and Mediator binding and looped to the promoter of the nicotinamide N-methyltransferase (NNMT) gene.	human	bone	High+Lowthroughput	PLZF targets developmental enhancers for activation during osteogenic differentiation of human mesenchymal stem cells					E_01_0302	PCR，Western blot，ChIP-seq	Subsequently, PLZF was recruited to osteogenic enhancers, influencing H3K27 acetylation and expression of nearby genes important for osteogenic function. Furthermore, we identified a latent enhancer within the ZBTB16/PLZF locus itself that became active, gained PLZF, p300 and Mediator binding and looped to the promoter of the nicotinamide N-methyltransferase (NNMT) gene.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Subsequently, PLZF was recruited to osteogenic enhancers, influencing H3K27 acetylation and expression of nearby genes important for osteogenic function. Furthermore, we identified a latent enhancer within the ZBTB16/PLZF locus itself that became active, gained PLZF, p300 and Mediator binding and looped to the promoter of the nicotinamide N-methyltransferase (NNMT) gene.		Subsequently, PLZF was recruited to osteogenic enhancers, influencing H3K27 acetylation and expression of nearby genes important for osteogenic function. Furthermore, we identified a latent enhancer within the ZBTB16/PLZF locus itself that became active, gained PLZF, p300 and Mediator binding and looped to the promoter of the nicotinamide N-methyltransferase (NNMT) gene.	Immunohistochemical staining	Subsequently, PLZF was recruited to osteogenic enhancers, influencing H3K27 acetylation and expression of nearby genes important for osteogenic function. Furthermore, we identified a latent enhancer within the ZBTB16/PLZF locus itself that became active, gained PLZF, p300 and Mediator binding and looped to the promoter of the nicotinamide N-methyltransferase (NNMT) gene.			PCR，Western blot，ChIP-seq				NNMT
34529725	chr7	128935299	128937299	IRF5	Here, we performed a comprehensive integrated post-GWAS analysis of T1D to identify functional regulatory variants in enhancers and their cognate target genes. Starting with 1,817 candidate T1D SNPs defined from the GWAS catalog and LDlink databases	human	Renal	High+Lowthroughput	"A comprehensive integrated post-GWAS
analysis of Type 1 diabetes reveals enhancer_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_based immune dysregulation"	有	886424	Type 1 diabetes		E_01_0303	Gel electrophoresis Western blot flow cytometry chip	Here, we performed a comprehensive integrated post-GWAS analysis of T1D to identify functional regulatory variants in enhancers and their cognate target genes. Starting with 1,817 candidate T1D SNPs defined from the GWAS catalog and LDlink databases	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we performed a comprehensive integrated post-GWAS analysis of T1D to identify functional regulatory variants in enhancers and their cognate target genes. Starting with 1,817 candidate T1D SNPs defined from the GWAS catalog and LDlink databases	Immunohistochemical staining	Here, we performed a comprehensive integrated post-GWAS analysis of T1D to identify functional regulatory variants in enhancers and their cognate target genes. Starting with 1,817 candidate T1D SNPs defined from the GWAS catalog and LDlink databases	IRF5		凝胶电泳 Western blot 流式细胞术 CHIP	Here, we performed a comprehensive integrated post-GWAS analysis of T1D to identify functional regulatory variants in enhancers and their cognate target genes. Starting with 1,817 candidate T1D SNPs defined from the GWAS catalog and LDlink databases			
30671485	chr3	194133166	194135166	HES1	The effects of polarized BMDMs on the expression of hepatic progenitor cell- (HPC-) specific markers and hairy and enhancer of split-1 (HES1) in HPCs in coculture were also analyzed.	mouse	liver	High+Lowthroughput	M1-Polarized Macrophages Promote Self-Renewing Phenotype of Hepatic Progenitor Cells with Jagged1-Notch Signalling Involved: Relevance in Primary Sclerosing Cholangitis			Primary sclerosing cholangitis	macrophage	E_02_0242	PCR，Western blot	The effects of polarized BMDMs on the expression of hepatic progenitor cell- (HPC-) specific markers and hairy and enhancer of split-1 (HES1) in HPCs in coculture were also analyzed.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The effects of polarized BMDMs on the expression of hepatic progenitor cell- (HPC-) specific markers and hairy and enhancer of split-1 (HES1) in HPCs in coculture were also analyzed.		The effects of polarized BMDMs on the expression of hepatic progenitor cell- (HPC-) specific markers and hairy and enhancer of split-1 (HES1) in HPCs in coculture were also analyzed.	Immunohistochemical staining	The effects of polarized BMDMs on the expression of hepatic progenitor cell- (HPC-) specific markers and hairy and enhancer of split-1 (HES1) in HPCs in coculture were also analyzed.			PCR，Western blot				HES1
30670628	chr6	43767278	43769278	VEGFA	Integration of gene expression, dynamic enhancer, and transcription factor occupancy changes induced by VEGFA yielded a VEGFA-regulated transcriptional regulatory network	human	endothelial	High+Lowthroughput	A dynamic and integrated epigenetic program at distal regions orchestrates transcriptional responses to VEGFA				endothelial cell	E_01_0304	PCR，Western blot，ChIP-seq	Integration of gene expression, dynamic enhancer, and transcription factor occupancy changes induced by VEGFA yielded a VEGFA-regulated transcriptional regulatory network	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Integration of gene expression, dynamic enhancer, and transcription factor occupancy changes induced by VEGFA yielded a VEGFA-regulated transcriptional regulatory network	Immunohistochemical staining	Integration of gene expression, dynamic enhancer, and transcription factor occupancy changes induced by VEGFA yielded a VEGFA-regulated transcriptional regulatory network	VEGFA		PCR，Western blot，ChIP-seq	Integration of gene expression, dynamic enhancer, and transcription factor occupancy changes induced by VEGFA yielded a VEGFA-regulated transcriptional regulatory network			
30670569	chrX	55006658	55008658	ALAS2	we first generated mutant mice by disrupting the GATA-1 binding motif at the intron 1 enhancer of the ALAS2 gene	human	blood	High+Lowthroughput	Generation and Molecular Characterization of Human Ring Sideroblasts: a Key Role of Ferrous Iron in Terminal Erythroid Differentiation and Ring Sideroblast Formation			anemia		E_01_0305	PCR，Western blot，ChIP-seq	we first generated mutant mice by disrupting the GATA-1 binding motif at the intron 1 enhancer of the ALAS2 gene	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	we first generated mutant mice by disrupting the GATA-1 binding motif at the intron 1 enhancer of the ALAS2 gene		we first generated mutant mice by disrupting the GATA-1 binding motif at the intron 1 enhancer of the ALAS2 gene	Immunohistochemical staining	we first generated mutant mice by disrupting the GATA-1 binding motif at the intron 1 enhancer of the ALAS2 gene			PCR，Western blot，ChIP-seq				ALAS2
30669987	chr11	83550448	83552448	Ccl4	Our data suggest that enhancers might drive macrophage response via transcriptional activation of key immune genes, such as Tnf, Tnfrsf1b, Irg1, Hilpda, Ccl3, and Ccl4.	mouse	lymph	High+Lowthroughput	Transcriptionally induced enhancers in the macrophage immune response to Mycobacterium tuberculosis infection			Tuberculosis	macrophage	E_02_0243	ChIP-seq	Our data suggest that enhancers might drive macrophage response via transcriptional activation of key immune genes, such as Tnf, Tnfrsf1b, Irg1, Hilpda, Ccl3, and Ccl4.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data suggest that enhancers might drive macrophage response via transcriptional activation of key immune genes, such as Tnf, Tnfrsf1b, Irg1, Hilpda, Ccl3, and Ccl4.		Our data suggest that enhancers might drive macrophage response via transcriptional activation of key immune genes, such as Tnf, Tnfrsf1b, Irg1, Hilpda, Ccl3, and Ccl4.	Immunohistochemical staining	Our data suggest that enhancers might drive macrophage response via transcriptional activation of key immune genes, such as Tnf, Tnfrsf1b, Irg1, Hilpda, Ccl3, and Ccl4.			ChIP-seq				Ccl4
30664779	chr5	69231799	69233799	CDK7	These systematic approaches reveal that the developmental transcription factor T (brachyury; TBXT) is the top selectively essential gene in chordoma, and that transcriptional cyclin-dependent kinase (CDK) inhibitors targeting CDK7/12/13 and CDK9 potently suppress chordoma cell proliferation.	human	bone	High+Lowthroughput	Small-molecule targeting of brachyury transcription factor addiction in chordoma			chordoma	chordoma cell	E_01_0306	PCR，ChIP-seq	These systematic approaches reveal that the developmental transcription factor T (brachyury; TBXT) is the top selectively essential gene in chordoma, and that transcriptional cyclin-dependent kinase (CDK) inhibitors targeting CDK7/12/13 and CDK9 potently suppress chordoma cell proliferation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These systematic approaches reveal that the developmental transcription factor T (brachyury; TBXT) is the top selectively essential gene in chordoma, and that transcriptional cyclin-dependent kinase (CDK) inhibitors targeting CDK7/12/13 and CDK9 potently suppress chordoma cell proliferation.		These systematic approaches reveal that the developmental transcription factor T (brachyury; TBXT) is the top selectively essential gene in chordoma, and that transcriptional cyclin-dependent kinase (CDK) inhibitors targeting CDK7/12/13 and CDK9 potently suppress chordoma cell proliferation.	Immunohistochemical staining	These systematic approaches reveal that the developmental transcription factor T (brachyury; TBXT) is the top selectively essential gene in chordoma, and that transcriptional cyclin-dependent kinase (CDK) inhibitors targeting CDK7/12/13 and CDK9 potently suppress chordoma cell proliferation.			PCR，ChIP-seq				CDK7
30664630	chr9	99819018	99821018	NR4A3	Here we report on recurrent rearrangements [t(4;9)(q13;q31)] in AciCC that translocate active enhancer regions from the SCPP gene cluster to the region upstream of Nuclear Receptor Subfamily 4 Group A Member 3 (NR4A3) at 9q31.	mouse	sialaden	High+Lowthroughput	Enhancer hijacking activates oncogenic transcription factor NR4A3 in acinic cell carcinomas of the salivary glands			Salivary gland acinar cell carcinoma	Acinar cell of salivary gland	E_02_0244	PCR，Western blot，ChIP-seq	Here we report on recurrent rearrangements [t(4;9)(q13;q31)] in AciCC that translocate active enhancer regions from the SCPP gene cluster to the region upstream of Nuclear Receptor Subfamily 4 Group A Member 3 (NR4A3) at 9q31.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we report on recurrent rearrangements [t(4;9)(q13;q31)] in AciCC that translocate active enhancer regions from the SCPP gene cluster to the region upstream of Nuclear Receptor Subfamily 4 Group A Member 3 (NR4A3) at 9q31.		Here we report on recurrent rearrangements [t(4;9)(q13;q31)] in AciCC that translocate active enhancer regions from the SCPP gene cluster to the region upstream of Nuclear Receptor Subfamily 4 Group A Member 3 (NR4A3) at 9q31.	Immunohistochemical staining	Here we report on recurrent rearrangements [t(4;9)(q13;q31)] in AciCC that translocate active enhancer regions from the SCPP gene cluster to the region upstream of Nuclear Receptor Subfamily 4 Group A Member 3 (NR4A3) at 9q31.			PCR，Western blot，ChIP-seq				NR4A3
30664211	chr1	153387368	153389368	S100A8	The reporter assay demonstrated that the upregulatory effect of S100A8 induced by IL‑1α was dependent on the S100A8 promoter specific region	human	epithelial	High+Lowthroughput	Expression of S100A8 is induced by interleukin?1α in TR146 epithelial cells through a mechanism involving CCAAT/enhancer binding protein β			Infection of mucosal epithelial cells	TR146 epithelial cell	E_01_0307	PCR, Western blot, chip SEQ bioinformatic prediction	The reporter assay demonstrated that the upregulatory effect of S100A8 induced by IL‑1α was dependent on the S100A8 promoter specific region	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The reporter assay demonstrated that the upregulatory effect of S100A8 induced by IL‑1α was dependent on the S100A8 promoter specific region		The reporter assay demonstrated that the upregulatory effect of S100A8 induced by IL‑1α was dependent on the S100A8 promoter specific region	Immunohistochemical staining	The reporter assay demonstrated that the upregulatory effect of S100A8 induced by IL‑1α was dependent on the S100A8 promoter specific region			PCR，Western blot，ChIP-seq生物信息预测				S100A8
30664173	chr9	117701433	117703433	TLR4	The cell proliferation rate and inflammatory cytokine expression of PBMCs treated with the FimA fusion protein with or without transfection with toll‑like receptor 4 (TLR4) small interfering (si)RNA were detected by CCK‑8 assays and ELISAs, respectively.	human	blood	High+Lowthroughput	Recombinant fimbriae protein of Porphyromonas gingivalis induces an inflammatory response via the TLR4/NF?κB signaling pathway in human peripheral blood mononuclear cells			Periodontal disease	peripheral blood mononuclear cell	E_01_0308	PCR, Western blot, sequencing technology	The cell proliferation rate and inflammatory cytokine expression of PBMCs treated with the FimA fusion protein with or without transfection with toll‑like receptor 4 (TLR4) small interfering (si)RNA were detected by CCK‑8 assays and ELISAs, respectively.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The cell proliferation rate and inflammatory cytokine expression of PBMCs treated with the FimA fusion protein with or without transfection with toll‑like receptor 4 (TLR4) small interfering (si)RNA were detected by CCK‑8 assays and ELISAs, respectively.	Immunohistochemical staining	The cell proliferation rate and inflammatory cytokine expression of PBMCs treated with the FimA fusion protein with or without transfection with toll‑like receptor 4 (TLR4) small interfering (si)RNA were detected by CCK‑8 assays and ELISAs, respectively.	TLR4		PCR，Western blot，测序技术	The cell proliferation rate and inflammatory cytokine expression of PBMCs treated with the FimA fusion protein with or without transfection with toll‑like receptor 4 (TLR4) small interfering (si)RNA were detected by CCK‑8 assays and ELISAs, respectively.			
30662920	chr6	137864227	137866227	TNFAIP3	The TNFAIP3 gene encodes the A20 protein essential for the development and functional performance of dendritic, B and T cells and macrophages as well as an important negative feedback regulator of the NF-κB pathway	human	lymph	High+Lowthroughput	TNFAIP3 F127C Coding Variation in Greek Primary Sjogren's Syndrome Patients		2230926	Periodontal disease	peripheral blood mononuclear cell	E_01_0309	PCR	The TNFAIP3 gene encodes the A20 protein essential for the development and functional performance of dendritic, B and T cells and macrophages as well as an important negative feedback regulator of the NF-κB pathway	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The TNFAIP3 gene encodes the A20 protein essential for the development and functional performance of dendritic, B and T cells and macrophages as well as an important negative feedback regulator of the NF-κB pathway	Immunohistochemical staining	The TNFAIP3 gene encodes the A20 protein essential for the development and functional performance of dendritic, B and T cells and macrophages as well as an important negative feedback regulator of the NF-κB pathway	TNFAIP3		PCR	The TNFAIP3 gene encodes the A20 protein essential for the development and functional performance of dendritic, B and T cells and macrophages as well as an important negative feedback regulator of the NF-κB pathway			
30662804	chr6	11180709	11182709	NEDD9	Human enhancer of filamentation 1 (HEF1, also known as CasL and NEDD9) is a non-catalytic scaffolding protein belonging to CAS (Crk-associated substrate) protein family that interacts with multiple signaling cascades.	human	bladder	High+Lowthroughput	SPAG9 regulates HEF1 expression and drives EMT in bladder transitional cell carcinoma via rac1 signaling pathway			Transitional cell carcinoma of the urinary bladder	bladder cancer cell	E_01_0310	PCR, Western blot, sequencing technology	Human enhancer of filamentation 1 (HEF1, also known as CasL and NEDD9) is a non-catalytic scaffolding protein belonging to CAS (Crk-associated substrate) protein family that interacts with multiple signaling cascades.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Human enhancer of filamentation 1 (HEF1, also known as CasL and NEDD9) is a non-catalytic scaffolding protein belonging to CAS (Crk-associated substrate) protein family that interacts with multiple signaling cascades.		Human enhancer of filamentation 1 (HEF1, also known as CasL and NEDD9) is a non-catalytic scaffolding protein belonging to CAS (Crk-associated substrate) protein family that interacts with multiple signaling cascades.	Immunohistochemical staining	Human enhancer of filamentation 1 (HEF1, also known as CasL and NEDD9) is a non-catalytic scaffolding protein belonging to CAS (Crk-associated substrate) protein family that interacts with multiple signaling cascades.			PCR，Western blot，测序技术				NEDD9
30662285	chr11	102517572	102519572	MMP7	Notch3 may affect the invasiveness and metastasis of osteosarcoma cells by regulating the downstream target gene Hes1 and its effector protein, MMP7.	human	bone	High+Lowthroughput	Overexpression of Notch3 is associated with metastasis and poor prognosis in osteosarcoma patients			Osteosarcoma	osteosarcoma cell	E_01_0311	Lentiviral transfection, gene knockdown, PCR, Western blot	Notch3 may affect the invasiveness and metastasis of osteosarcoma cells by regulating the downstream target gene Hes1 and its effector protein, MMP7.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Notch3 may affect the invasiveness and metastasis of osteosarcoma cells by regulating the downstream target gene Hes1 and its effector protein, MMP7.	Immunohistochemical staining	Notch3 may affect the invasiveness and metastasis of osteosarcoma cells by regulating the downstream target gene Hes1 and its effector protein, MMP7.	MMP7		慢病毒转染，基因敲除，PCR，Western blot	Notch3 may affect the invasiveness and metastasis of osteosarcoma cells by regulating the downstream target gene Hes1 and its effector protein, MMP7.			
30660454	chr3	38135367	38137367	MYD88	Arthritis index, C-reactive protein (CRP), rheumatoid factor (RF) and myeloperoxidase (MPO) in serum and protein level of TLR-4, myeloid differentiation factor 88 (MYD88), NF-κB, TNF-α, IL-1β	mouse	lymph	High+Lowthroughput	Scientific validation of anti-arthritic effect of Kashayams - A polyherbal formulation in collagen induced arthritic rats			arthritis	B cell	E_02_0245	PCR	Arthritis index, C-reactive protein (CRP), rheumatoid factor (RF) and myeloperoxidase (MPO) in serum and protein level of TLR-4, myeloid differentiation factor 88 (MYD88), NF-κB, TNF-α, IL-1β	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Arthritis index, C-reactive protein (CRP), rheumatoid factor (RF) and myeloperoxidase (MPO) in serum and protein level of TLR-4, myeloid differentiation factor 88 (MYD88), NF-κB, TNF-α, IL-1β		Arthritis index, C-reactive protein (CRP), rheumatoid factor (RF) and myeloperoxidase (MPO) in serum and protein level of TLR-4, myeloid differentiation factor 88 (MYD88), NF-κB, TNF-α, IL-1β	Immunohistochemical staining	Arthritis index, C-reactive protein (CRP), rheumatoid factor (RF) and myeloperoxidase (MPO) in serum and protein level of TLR-4, myeloid differentiation factor 88 (MYD88), NF-κB, TNF-α, IL-1β			PCR				MYD88
30659980	chrX	154538337	154540337	IKBKG	IKBKG loss-of-function mutation causes incontinentia pigmenti (IP), a rare X-linked disease featuring linear hypopigmentation, alopecia, hypodontia, and immunodeficiency.	human	bone	High+Lowthroughput	Absence of an osteopetrosis phenotype in IKBKG (NEMO) mutation-positive women: A case-control study			Osteosclerosis	B cell， Oc precursor cell	E_01_0312	PCR，Bone marrow aspiration，Histomorphometry	IKBKG loss-of-function mutation causes incontinentia pigmenti (IP), a rare X-linked disease featuring linear hypopigmentation, alopecia, hypodontia, and immunodeficiency.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	IKBKG loss-of-function mutation causes incontinentia pigmenti (IP), a rare X-linked disease featuring linear hypopigmentation, alopecia, hypodontia, and immunodeficiency.		IKBKG loss-of-function mutation causes incontinentia pigmenti (IP), a rare X-linked disease featuring linear hypopigmentation, alopecia, hypodontia, and immunodeficiency.	Immunohistochemical staining	IKBKG loss-of-function mutation causes incontinentia pigmenti (IP), a rare X-linked disease featuring linear hypopigmentation, alopecia, hypodontia, and immunodeficiency.			PCR，Bone marrow aspiration，Histomorphometry				IKBKG
30659195	chr19	15232704	15234704	BRD4	Conversely, deletion of this enhancer via CRISPR/Cas9 reduces C/EBPβ expression and its genome-wide co-occupancy with BRD4 at H3K27ac-marked enhancers and super-enhancers	human	liver	High+Lowthroughput	Aberrant enhancer hypomethylation contributes to hepatic carcinogenesis through global transcriptional reprogramming			liver cancer	HCC cell	E_01_0313	PCR，Western blot，ChIP-seq	Conversely, deletion of this enhancer via CRISPR/Cas9 reduces C/EBPβ expression and its genome-wide co-occupancy with BRD4 at H3K27ac-marked enhancers and super-enhancers	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Conversely, deletion of this enhancer via CRISPR/Cas9 reduces C/EBPβ expression and its genome-wide co-occupancy with BRD4 at H3K27ac-marked enhancers and super-enhancers	Immunohistochemical staining	Conversely, deletion of this enhancer via CRISPR/Cas9 reduces C/EBPβ expression and its genome-wide co-occupancy with BRD4 at H3K27ac-marked enhancers and super-enhancers	BRD4		PCR，Western blot，ChIP-seq	Conversely, deletion of this enhancer via CRISPR/Cas9 reduces C/EBPβ expression and its genome-wide co-occupancy with BRD4 at H3K27ac-marked enhancers and super-enhancers			
30659184	chr4	108044594	108046594	LEF1	Mechanistically, HPIP promotes the transcription of Wnt targets by interacting with lymphoid enhancer binding factor 1 (LEF1).	mouse	bone	High+Lowthroughput	Hematopoietic PBX-interacting protein mediates cartilage degeneration during the pathogenesis of osteoarthritis			Osteoarthritis	hematopoietic pre-B cell	E_02_0246	PCR，Western blot，ChIP-seq	Mechanistically, HPIP promotes the transcription of Wnt targets by interacting with lymphoid enhancer binding factor 1 (LEF1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mechanistically, HPIP promotes the transcription of Wnt targets by interacting with lymphoid enhancer binding factor 1 (LEF1).		Mechanistically, HPIP promotes the transcription of Wnt targets by interacting with lymphoid enhancer binding factor 1 (LEF1).	Immunohistochemical staining	Mechanistically, HPIP promotes the transcription of Wnt targets by interacting with lymphoid enhancer binding factor 1 (LEF1).			PCR，Western blot，ChIP-seq				LEF1
30659153	chr16	67560054	67562054	CTCF	chromHMM chromatin states from Roadmap (32), cross-tissue gene expression for TSSs from GTEx (33), TAD boundaries from high-resolution Hi-C data, called using an arrowhead score (34), and binding clusters for the insulator protein CTCF from ENCODE	human		High+Lowthroughput	Chromatin features constrain structural variation across evolutionary timescales					E_01_0314	Western blot，ChIP-seq	chromHMM chromatin states from Roadmap (32), cross-tissue gene expression for TSSs from GTEx (33), TAD boundaries from high-resolution Hi-C data, called using an arrowhead score (34), and binding clusters for the insulator protein CTCF from ENCODE	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			chromHMM chromatin states from Roadmap (32), cross-tissue gene expression for TSSs from GTEx (33), TAD boundaries from high-resolution Hi-C data, called using an arrowhead score (34), and binding clusters for the insulator protein CTCF from ENCODE	Immunohistochemical staining	chromHMM chromatin states from Roadmap (32), cross-tissue gene expression for TSSs from GTEx (33), TAD boundaries from high-resolution Hi-C data, called using an arrowhead score (34), and binding clusters for the insulator protein CTCF from ENCODE	CTCF		Western blot，ChIP-seq	chromHMM chromatin states from Roadmap (32), cross-tissue gene expression for TSSs from GTEx (33), TAD boundaries from high-resolution Hi-C data, called using an arrowhead score (34), and binding clusters for the insulator protein CTCF from ENCODE			
30657937	chr16	85896547	85898547	IRF8	We analyze binding of PU.1/SPI1 and IRF8 from human monocytes, delineate DNA-sequence determinants for their cooperativity	human		High+Lowthroughput	NextPBM: a platform to study cell-specific transcription factor binding and cooperativity					E_01_0315	HT nextPBM	We analyze binding of PU.1/SPI1 and IRF8 from human monocytes, delineate DNA-sequence determinants for their cooperativity	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We analyze binding of PU.1/SPI1 and IRF8 from human monocytes, delineate DNA-sequence determinants for their cooperativity	Immunohistochemical staining	We analyze binding of PU.1/SPI1 and IRF8 from human monocytes, delineate DNA-sequence determinants for their cooperativity	IRF8		HT nextPBM	We analyze binding of PU.1/SPI1 and IRF8 from human monocytes, delineate DNA-sequence determinants for their cooperativity			
30655737	chr7	44101607	44103607	AEBP1	The present study aimed to analyze adipocyte enhancer-binding protein 1 (AEBP1) expression in colorectal cancer (CRC)	human,mouse	lymph	High+Lowthroughput	MicroRNA 214 inhibits adipocyte enhancer-binding protein 1 activity and increases the sensitivity of chemotherapy in colorectal cancer			Colorectal cancer	HT-29 cell	E_02_0247	Western blot, flow cytometry	The present study aimed to analyze adipocyte enhancer-binding protein 1 (AEBP1) expression in colorectal cancer (CRC)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present study aimed to analyze adipocyte enhancer-binding protein 1 (AEBP1) expression in colorectal cancer (CRC)		The present study aimed to analyze adipocyte enhancer-binding protein 1 (AEBP1) expression in colorectal cancer (CRC)	Immunohistochemical staining	The present study aimed to analyze adipocyte enhancer-binding protein 1 (AEBP1) expression in colorectal cancer (CRC)			Western blot,流式细胞术				AEBP1
30655550	chr19	17400341	17402341	BST2	CBX6 induced significant downregulation of bone marrow stromal cell antigen-2 (BST2), a potential therapeutic target, via interactions with its promoter region. Our collective findings support a tumor suppressor role of CBX6 in breast cancer.	human	breast	High+Lowthroughput	CBX6 is negatively regulated by EZH2 and plays a potential tumor suppressor role in breast cancer			mammary cancer	breast cancer cell	E_01_0316	PCR，Western blot，ChIP-seq	CBX6 induced significant downregulation of bone marrow stromal cell antigen-2 (BST2), a potential therapeutic target, via interactions with its promoter region. Our collective findings support a tumor suppressor role of CBX6 in breast cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CBX6 induced significant downregulation of bone marrow stromal cell antigen-2 (BST2), a potential therapeutic target, via interactions with its promoter region. Our collective findings support a tumor suppressor role of CBX6 in breast cancer.		CBX6 induced significant downregulation of bone marrow stromal cell antigen-2 (BST2), a potential therapeutic target, via interactions with its promoter region. Our collective findings support a tumor suppressor role of CBX6 in breast cancer.	Immunohistochemical staining	CBX6 induced significant downregulation of bone marrow stromal cell antigen-2 (BST2), a potential therapeutic target, via interactions with its promoter region. Our collective findings support a tumor suppressor role of CBX6 in breast cancer.			PCR，Western blot，ChIP-seq				BST2
30655376	chr14	68785051	68787051	ZFP36L1	In vitro reporter assay and 5'-azacitidine treatment confirmed the functional relevance of hyper-methylation of ZFP36L1 enhancer.	human	bone	High+Lowthroughput	Epigenomic profiling of myelofibrosis reveals widespread DNA methylation changes in enhancer elements and ZFP36L1 as a potential tumor suppressor gene that is epigenetically regulated			Myelofibrosis	bone marrow cell	E_01_0317	PCR，Western blot	In vitro reporter assay and 5'-azacitidine treatment confirmed the functional relevance of hyper-methylation of ZFP36L1 enhancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In vitro reporter assay and 5'-azacitidine treatment confirmed the functional relevance of hyper-methylation of ZFP36L1 enhancer.		In vitro reporter assay and 5'-azacitidine treatment confirmed the functional relevance of hyper-methylation of ZFP36L1 enhancer.	Immunohistochemical staining	In vitro reporter assay and 5'-azacitidine treatment confirmed the functional relevance of hyper-methylation of ZFP36L1 enhancer.			PCR，Western blot				ZFP36L1
30654703	chr12	57092847	57094847	STAT6	The overexpression vectors of NEAT1 and ITCH, and siRNA targeting NEAT1, EZH2 (enhancer of zeste homolog 2) and STAT6 (signal transducer and activator of transcription 6) were transfected into CD4+T cells.	human	lymph	High+Lowthroughput	NEAT1 regulates Th2 cell development by targeting STAT6 for degradation				Th2 cell	E_01_0318	PCR, Western blot, chip SEQ, RNA immunoprecipitation, cell transfection	The overexpression vectors of NEAT1 and ITCH, and siRNA targeting NEAT1, EZH2 (enhancer of zeste homolog 2) and STAT6 (signal transducer and activator of transcription 6) were transfected into CD4+T cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The overexpression vectors of NEAT1 and ITCH, and siRNA targeting NEAT1, EZH2 (enhancer of zeste homolog 2) and STAT6 (signal transducer and activator of transcription 6) were transfected into CD4+T cells.	Immunohistochemical staining	The overexpression vectors of NEAT1 and ITCH, and siRNA targeting NEAT1, EZH2 (enhancer of zeste homolog 2) and STAT6 (signal transducer and activator of transcription 6) were transfected into CD4+T cells.	STAT6		PCR，Western blot，ChIP-seq，RNA免疫沉淀，细胞转染	The overexpression vectors of NEAT1 and ITCH, and siRNA targeting NEAT1, EZH2 (enhancer of zeste homolog 2) and STAT6 (signal transducer and activator of transcription 6) were transfected into CD4+T cells.			
30653446	chr3	11269697	11271697	ATG7	Specifically, deletion of ATG7 in retinal vascular ECs of db/db mice and cultured HUVECs indicated a detrimental role of autophagy in hyperglycemia-induced endothelial dysfunction. Pretreatment with GANT61, a Hh pathway inhibitor, abolished the metformin-mediated downregulation of autophagy and endothelial protective action	human	kidney	High+Lowthroughput	Metformin alleviates hyperglycemia-induced endothelial impairment by downregulating autophagy via the Hedgehog pathway			diabetes	endothelial cell	E_01_0319	PCR	Specifically, deletion of ATG7 in retinal vascular ECs of db/db mice and cultured HUVECs indicated a detrimental role of autophagy in hyperglycemia-induced endothelial dysfunction. Pretreatment with GANT61, a Hh pathway inhibitor, abolished the metformin-mediated downregulation of autophagy and endothelial protective action	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Specifically, deletion of ATG7 in retinal vascular ECs of db/db mice and cultured HUVECs indicated a detrimental role of autophagy in hyperglycemia-induced endothelial dysfunction. Pretreatment with GANT61, a Hh pathway inhibitor, abolished the metformin-mediated downregulation of autophagy and endothelial protective action		Specifically, deletion of ATG7 in retinal vascular ECs of db/db mice and cultured HUVECs indicated a detrimental role of autophagy in hyperglycemia-induced endothelial dysfunction. Pretreatment with GANT61, a Hh pathway inhibitor, abolished the metformin-mediated downregulation of autophagy and endothelial protective action	Immunohistochemical staining	Specifically, deletion of ATG7 in retinal vascular ECs of db/db mice and cultured HUVECs indicated a detrimental role of autophagy in hyperglycemia-induced endothelial dysfunction. Pretreatment with GANT61, a Hh pathway inhibitor, abolished the metformin-mediated downregulation of autophagy and endothelial protective action			PCR				ATG7
30653446	chr10	131965299	131967299	BNIP3	Mechanistically, GLI1 knockdown-triggered autophagy was related to upregulation of BNIP3, which subsequently disrupted the association of BECN1/Beclin 1 and BCL2.	human	kidney	High+Lowthroughput	Metformin alleviates hyperglycemia-induced endothelial impairment by downregulating autophagy via the Hedgehog pathway			diabetes	endothelial cell	E_01_0319	PCR	Mechanistically, GLI1 knockdown-triggered autophagy was related to upregulation of BNIP3, which subsequently disrupted the association of BECN1/Beclin 1 and BCL2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mechanistically, GLI1 knockdown-triggered autophagy was related to upregulation of BNIP3, which subsequently disrupted the association of BECN1/Beclin 1 and BCL2.		Mechanistically, GLI1 knockdown-triggered autophagy was related to upregulation of BNIP3, which subsequently disrupted the association of BECN1/Beclin 1 and BCL2.	Immunohistochemical staining	Mechanistically, GLI1 knockdown-triggered autophagy was related to upregulation of BNIP3, which subsequently disrupted the association of BECN1/Beclin 1 and BCL2.			PCR				BNIP3
30652078	chr11	73122225	73124225	Trpv1	Trpv1 altered the cell signaling events that increase myogenic transcription factors in myoblast cells in response to heat. Trpv1 plays important roles in the process of differentiation.	mouse	bone	High+Lowthroughput	Heat induces myogenic transcription factors of myoblast cells via transient receptor potential vanilloid 1 (Trpv1)				myoblast cell	E_02_0248	PCR，Western blot	Trpv1 altered the cell signaling events that increase myogenic transcription factors in myoblast cells in response to heat. Trpv1 plays important roles in the process of differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Trpv1 altered the cell signaling events that increase myogenic transcription factors in myoblast cells in response to heat. Trpv1 plays important roles in the process of differentiation.		Trpv1 altered the cell signaling events that increase myogenic transcription factors in myoblast cells in response to heat. Trpv1 plays important roles in the process of differentiation.	Immunohistochemical staining	Trpv1 altered the cell signaling events that increase myogenic transcription factors in myoblast cells in response to heat. Trpv1 plays important roles in the process of differentiation.			PCR，Western blot				Trpv1
30651971	chr9	117701165	117703165	TLR4	Furthermore, defciency of TLR4 receptor resulted in disappeared of the autophagy activation by treatment with IL-33 or EBSS (Fig.  6).	human	lymph	High+Lowthroughput	IL-33 ameliorates experimental colitis involving regulation of autophagy of macrophages in mice			colitis	macrophage	E_01_0320	Western blot, immunofluorescence staining	Furthermore, defciency of TLR4 receptor resulted in disappeared of the autophagy activation by treatment with IL-33 or EBSS (Fig.  6).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Furthermore, defciency of TLR4 receptor resulted in disappeared of the autophagy activation by treatment with IL-33 or EBSS (Fig.  6).	Immunohistochemical staining	Furthermore, defciency of TLR4 receptor resulted in disappeared of the autophagy activation by treatment with IL-33 or EBSS (Fig.  6).	TLR4		Western blot，免疫荧光染色法	Furthermore, defciency of TLR4 receptor resulted in disappeared of the autophagy activation by treatment with IL-33 or EBSS (Fig.  6).			
30651760	chr13	30454192	30456192	HMGB1	The results of the RT-qPCR demonstrated that hypoxia stimulation increased the expression of HMGB1, PPAR, RAGE and TNF-α mRNA, and decreased the expression of SIRT1 mRNA in kidney tissues (P<0.05).	mouse	kidney	High+Lowthroughput	The HMGB1-RAGE/TLR-TNF-α signaling pathway may contribute to kidney injury induced by hypoxia			Renal impairment	B cell	E_02_0249	PCR, sequencing technology	The results of the RT-qPCR demonstrated that hypoxia stimulation increased the expression of HMGB1, PPAR, RAGE and TNF-α mRNA, and decreased the expression of SIRT1 mRNA in kidney tissues (P<0.05).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The results of the RT-qPCR demonstrated that hypoxia stimulation increased the expression of HMGB1, PPAR, RAGE and TNF-α mRNA, and decreased the expression of SIRT1 mRNA in kidney tissues (P<0.05).		The results of the RT-qPCR demonstrated that hypoxia stimulation increased the expression of HMGB1, PPAR, RAGE and TNF-α mRNA, and decreased the expression of SIRT1 mRNA in kidney tissues (P<0.05).	Immunohistochemical staining	The results of the RT-qPCR demonstrated that hypoxia stimulation increased the expression of HMGB1, PPAR, RAGE and TNF-α mRNA, and decreased the expression of SIRT1 mRNA in kidney tissues (P<0.05).			PCR，测序技术				HMGB1
30651597	chr3	69736856	69738856	MITF	Thus, MITF ensures the rapid resumption of transcription after completion of strand repair and maintains transcriptional output, which is indispensable for survival of the melanocytic lineage including melanoma in vitro and in vivo.	human	kidney	High+Lowthroughput	Lineage-specific control of TFIIH by MITF determines transcriptional homeostasis and DNA repair				Renal cell	E_01_0321	PCR, Western blot, chip SEQ, lentiviral infection, Clontech	Thus, MITF ensures the rapid resumption of transcription after completion of strand repair and maintains transcriptional output, which is indispensable for survival of the melanocytic lineage including melanoma in vitro and in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, MITF ensures the rapid resumption of transcription after completion of strand repair and maintains transcriptional output, which is indispensable for survival of the melanocytic lineage including melanoma in vitro and in vivo.	Immunohistochemical staining	Thus, MITF ensures the rapid resumption of transcription after completion of strand repair and maintains transcriptional output, which is indispensable for survival of the melanocytic lineage including melanoma in vitro and in vivo.	MITF		PCR，Western blot，ChIP-seq，慢病毒感染，克隆技术	Thus, MITF ensures the rapid resumption of transcription after completion of strand repair and maintains transcriptional output, which is indispensable for survival of the melanocytic lineage including melanoma in vitro and in vivo.			
30651597	chr5	69232092	69234092	CDK7	Moreover, MITF controls cMYC implicated in general transcription by transactivation of far upstream binding protein 2 (FUBP2/KSHRP), which induces c-MYC pulse regulation through TFIIH, and experimental depletion of MITF results in consecutive loss of CDK7 in the TFIIH-CAK subcomplex	human	kidney	High+Lowthroughput	Lineage-specific control of TFIIH by MITF determines transcriptional homeostasis and DNA repair				Renal cell	E_01_0321	PCR, Western blot, chip SEQ, lentiviral infection, Clontech	Moreover, MITF controls cMYC implicated in general transcription by transactivation of far upstream binding protein 2 (FUBP2/KSHRP), which induces c-MYC pulse regulation through TFIIH, and experimental depletion of MITF results in consecutive loss of CDK7 in the TFIIH-CAK subcomplex	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, MITF controls cMYC implicated in general transcription by transactivation of far upstream binding protein 2 (FUBP2/KSHRP), which induces c-MYC pulse regulation through TFIIH, and experimental depletion of MITF results in consecutive loss of CDK7 in the TFIIH-CAK subcomplex		Moreover, MITF controls cMYC implicated in general transcription by transactivation of far upstream binding protein 2 (FUBP2/KSHRP), which induces c-MYC pulse regulation through TFIIH, and experimental depletion of MITF results in consecutive loss of CDK7 in the TFIIH-CAK subcomplex	Immunohistochemical staining	Moreover, MITF controls cMYC implicated in general transcription by transactivation of far upstream binding protein 2 (FUBP2/KSHRP), which induces c-MYC pulse regulation through TFIIH, and experimental depletion of MITF results in consecutive loss of CDK7 in the TFIIH-CAK subcomplex			PCR，Western blot，ChIP-seq，慢病毒感染，克隆技术				CDK7
30651597	chr8	127732959	127734959	MYC	Moreover, MITF controls cMYC implicated in general transcription by transactivation of far upstream binding protein 2 (FUBP2/KSHRP), which induces c-MYC pulse regulation through TFIIH, and experimental depletion of MITF results in consecutive loss of CDK7 in the TFIIH-CAK subcomplex	human	kidney	High+Lowthroughput	Lineage-specific control of TFIIH by MITF determines transcriptional homeostasis and DNA repair				Renal cell	E_01_0321	PCR, Western blot, chip SEQ, lentiviral infection, Clontech	Moreover, MITF controls cMYC implicated in general transcription by transactivation of far upstream binding protein 2 (FUBP2/KSHRP), which induces c-MYC pulse regulation through TFIIH, and experimental depletion of MITF results in consecutive loss of CDK7 in the TFIIH-CAK subcomplex	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Moreover, MITF controls cMYC implicated in general transcription by transactivation of far upstream binding protein 2 (FUBP2/KSHRP), which induces c-MYC pulse regulation through TFIIH, and experimental depletion of MITF results in consecutive loss of CDK7 in the TFIIH-CAK subcomplex	Immunohistochemical staining	Moreover, MITF controls cMYC implicated in general transcription by transactivation of far upstream binding protein 2 (FUBP2/KSHRP), which induces c-MYC pulse regulation through TFIIH, and experimental depletion of MITF results in consecutive loss of CDK7 in the TFIIH-CAK subcomplex	MYC		PCR，Western blot，ChIP-seq，慢病毒感染，克隆技术	Moreover, MITF controls cMYC implicated in general transcription by transactivation of far upstream binding protein 2 (FUBP2/KSHRP), which induces c-MYC pulse regulation through TFIIH, and experimental depletion of MITF results in consecutive loss of CDK7 in the TFIIH-CAK subcomplex			
30651277	chr15	45089423	45091423	DUOX2	This mutation, located within an exonic splicing enhancer motif, caused aberrant splicing of DUOX2 transcripts and resulted in lower H2O2 production, which might cause a severe defect in thyroid hormone production.	mouse	internal secretion	High+Lowthroughput	An exonic splicing enhancer mutation in DUOX2 causes aberrant alternative splicing and severe congenital hypothyroidism in Bama pigs			Congenital hypothyroidism	HeLa cell	E_02_0250	PCR, Western blot, sequencing technology	This mutation, located within an exonic splicing enhancer motif, caused aberrant splicing of DUOX2 transcripts and resulted in lower H2O2 production, which might cause a severe defect in thyroid hormone production.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This mutation, located within an exonic splicing enhancer motif, caused aberrant splicing of DUOX2 transcripts and resulted in lower H2O2 production, which might cause a severe defect in thyroid hormone production.		This mutation, located within an exonic splicing enhancer motif, caused aberrant splicing of DUOX2 transcripts and resulted in lower H2O2 production, which might cause a severe defect in thyroid hormone production.	Immunohistochemical staining	This mutation, located within an exonic splicing enhancer motif, caused aberrant splicing of DUOX2 transcripts and resulted in lower H2O2 production, which might cause a severe defect in thyroid hormone production.			PCR，Western blot，测序技术				DUOX2
30649550	chr2	86437792	86439792	KDM3A	In the current study, using a FBSinducing model following serum starvation, we identified KDM3A, a demethylase of histone H3K9me1/2, as a positive regulator for hippo target genes.	human	lymph	High+Lowthroughput	Histone demethylase KDM3A is required for enhancer activation of hippo target genes in colorectal cancer			colorectal cancer 	HCT116 cell	E_01_0322	PCR，Western blot，ChIP-seq	In the current study, using a FBSinducing model following serum starvation, we identified KDM3A, a demethylase of histone H3K9me1/2, as a positive regulator for hippo target genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the current study, using a FBSinducing model following serum starvation, we identified KDM3A, a demethylase of histone H3K9me1/2, as a positive regulator for hippo target genes.		In the current study, using a FBSinducing model following serum starvation, we identified KDM3A, a demethylase of histone H3K9me1/2, as a positive regulator for hippo target genes.	Immunohistochemical staining	In the current study, using a FBSinducing model following serum starvation, we identified KDM3A, a demethylase of histone H3K9me1/2, as a positive regulator for hippo target genes.			PCR，Western blot，ChIP-seq				KDM3A
30647808	chr20	5112515	5114515	PCNA	The vetsin experimental group in this study exhibited hepatocyte deterioration, significant necrosis, and scattered growth of Kupffer cells among certain hepatocytes and around the portal area, significant blockage of blood sinusoids, and elevated hepatic expression of PCNA and P53.	mouse	Liver	High+Lowthroughput	Roles of Moringa oleifera Leaf Extract in Improving the Impact of High Dietary Intake of Monosodium Glutamate-Induced Liver Toxicity, Oxidative Stress, Genotoxicity, DNA Damage, and PCNA Alterations in Male Rats				hepatocyte	E_02_0251	Immunohistochemical detection	The vetsin experimental group in this study exhibited hepatocyte deterioration, significant necrosis, and scattered growth of Kupffer cells among certain hepatocytes and around the portal area, significant blockage of blood sinusoids, and elevated hepatic expression of PCNA and P53.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The vetsin experimental group in this study exhibited hepatocyte deterioration, significant necrosis, and scattered growth of Kupffer cells among certain hepatocytes and around the portal area, significant blockage of blood sinusoids, and elevated hepatic expression of PCNA and P53.		The vetsin experimental group in this study exhibited hepatocyte deterioration, significant necrosis, and scattered growth of Kupffer cells among certain hepatocytes and around the portal area, significant blockage of blood sinusoids, and elevated hepatic expression of PCNA and P53.	Immunohistochemical staining	The vetsin experimental group in this study exhibited hepatocyte deterioration, significant necrosis, and scattered growth of Kupffer cells among certain hepatocytes and around the portal area, significant blockage of blood sinusoids, and elevated hepatic expression of PCNA and P53.			免疫组化检测				PCNA
30644437	chr22	30922640	30924640	MORC2	Here, we found that MORC2 interacted with TE-III domain of C/EBPα, and the overexpression of MORC2 promoted wild-type C/EBPα sumoylation and its subsequent degradation, which didn’t significantly observe in mutant C/EBPα-K161R.	human	lymph	High+Lowthroughput	MORC2 regulates C/EBPα-mediated cell differentiation via sumoylation				C2C12 cell	E_01_0323	PCR，Western blot	Here, we found that MORC2 interacted with TE-III domain of C/EBPα, and the overexpression of MORC2 promoted wild-type C/EBPα sumoylation and its subsequent degradation, which didn’t significantly observe in mutant C/EBPα-K161R.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we found that MORC2 interacted with TE-III domain of C/EBPα, and the overexpression of MORC2 promoted wild-type C/EBPα sumoylation and its subsequent degradation, which didn’t significantly observe in mutant C/EBPα-K161R.		Here, we found that MORC2 interacted with TE-III domain of C/EBPα, and the overexpression of MORC2 promoted wild-type C/EBPα sumoylation and its subsequent degradation, which didn’t significantly observe in mutant C/EBPα-K161R.	Immunohistochemical staining	Here, we found that MORC2 interacted with TE-III domain of C/EBPα, and the overexpression of MORC2 promoted wild-type C/EBPα sumoylation and its subsequent degradation, which didn’t significantly observe in mutant C/EBPα-K161R.			PCR，Western blot				MORC2
30643696	chr2	239045624	239047624	HDAC4	These findings are consistent with observations of precocious cartilage ossification in Hdac4 mutant mice, demonstrating that the function of Hdac4 in skeletal development is conserved among vertebrates.	mouse	bone	High+Lowthroughput	hdac4 mediates perichondral ossification and pharyngeal skeleton development in the zebrafish				chondroblast	E_02_0252	PCR，Western blot	These findings are consistent with observations of precocious cartilage ossification in Hdac4 mutant mice, demonstrating that the function of Hdac4 in skeletal development is conserved among vertebrates.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings are consistent with observations of precocious cartilage ossification in Hdac4 mutant mice, demonstrating that the function of Hdac4 in skeletal development is conserved among vertebrates.		These findings are consistent with observations of precocious cartilage ossification in Hdac4 mutant mice, demonstrating that the function of Hdac4 in skeletal development is conserved among vertebrates.	Immunohistochemical staining	These findings are consistent with observations of precocious cartilage ossification in Hdac4 mutant mice, demonstrating that the function of Hdac4 in skeletal development is conserved among vertebrates.			PCR，Western blot				HDAC4
30643424	chr17	42310283	42312283	STAT3	Zhang et al’s29 research showed that pancreatic cancer stem cells developed chemoresistance toward GEM through the NAPDH oxidase/ROS (Nox/ROS)/NF-κB/STAT 3 signaling pathway (STAT3).	human	tongue	High+Lowthroughput	Evodiamine inactivates NF-κB and potentiates the antitumor effects of gemcitabine on tongue cancer both in vitro and in vivo			tongue cancer	tongue cancer cell，Tca8113 cell	E_01_0324	PCR, sequencing technology	Zhang et al’s29 research showed that pancreatic cancer stem cells developed chemoresistance toward GEM through the NAPDH oxidase/ROS (Nox/ROS)/NF-κB/STAT 3 signaling pathway (STAT3).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Zhang et al’s29 research showed that pancreatic cancer stem cells developed chemoresistance toward GEM through the NAPDH oxidase/ROS (Nox/ROS)/NF-κB/STAT 3 signaling pathway (STAT3).	Immunohistochemical staining	Zhang et al’s29 research showed that pancreatic cancer stem cells developed chemoresistance toward GEM through the NAPDH oxidase/ROS (Nox/ROS)/NF-κB/STAT 3 signaling pathway (STAT3).	STAT3		PCR，测序技术	Zhang et al’s29 research showed that pancreatic cancer stem cells developed chemoresistance toward GEM through the NAPDH oxidase/ROS (Nox/ROS)/NF-κB/STAT 3 signaling pathway (STAT3).			
30642336	chr18	76976527	76978527	MBP	ScFv antibody proteins without any tag and with different fusion tags such as 6xHis, GST and MBP, were expressed in E. coli in diferent growth condition.	human	lymph	High+Lowthroughput	Evaluation of scFv protein recovery from E. coli by in vitro refolding and mild solubilization process					E_01_0325	In vitro refolding and gentle lysis method	ScFv antibody proteins without any tag and with different fusion tags such as 6xHis, GST and MBP, were expressed in E. coli in diferent growth condition.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ScFv antibody proteins without any tag and with different fusion tags such as 6xHis, GST and MBP, were expressed in E. coli in diferent growth condition.		ScFv antibody proteins without any tag and with different fusion tags such as 6xHis, GST and MBP, were expressed in E. coli in diferent growth condition.	Immunohistochemical staining	ScFv antibody proteins without any tag and with different fusion tags such as 6xHis, GST and MBP, were expressed in E. coli in diferent growth condition.			体外重折叠和温和溶解法				MBP
30642251	chr17	7658541	7660541	TP53	If gene symbols are used that do not occur in the downloaded annotation data, as can be the case if an invalid or outdated symbol is used (e.g., P53 instead of the official gene symbol TP53), GOPHER will issue a warning and report a list of unmappable symbols that can be used to search for the current correct symbols.	human	adipose	High+Lowthroughput	GOPHER: Generator Of Probes for capture Hi-C Experiments at high Resolution				IWAT cell	E_01_0326	Hi-C，PCR，Western blot，ChIP-seq	If gene symbols are used that do not occur in the downloaded annotation data, as can be the case if an invalid or outdated symbol is used (e.g., P53 instead of the official gene symbol TP53), GOPHER will issue a warning and report a list of unmappable symbols that can be used to search for the current correct symbols.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			If gene symbols are used that do not occur in the downloaded annotation data, as can be the case if an invalid or outdated symbol is used (e.g., P53 instead of the official gene symbol TP53), GOPHER will issue a warning and report a list of unmappable symbols that can be used to search for the current correct symbols.	Immunohistochemical staining	If gene symbols are used that do not occur in the downloaded annotation data, as can be the case if an invalid or outdated symbol is used (e.g., P53 instead of the official gene symbol TP53), GOPHER will issue a warning and report a list of unmappable symbols that can be used to search for the current correct symbols.	TP53		Hi-C，PCR，Western blot，ChIP-seq	If gene symbols are used that do not occur in the downloaded annotation data, as can be the case if an invalid or outdated symbol is used (e.g., P53 instead of the official gene symbol TP53), GOPHER will issue a warning and report a list of unmappable symbols that can be used to search for the current correct symbols.			
30641938	chr8	84014018	84016018	Ucp1	Here, we show that the expression of uncoupling protein 1 (Ucp1) involved in thermoregulation is severely suppressed under ER stress conditions (afflicted by tunicamycin) in inguinal white adipose tissue (IWAT) both in vitro and in vivo.	mouse	adipose	High+Lowthroughput	Endoplasmic Reticulum Stress Impaired Uncoupling Protein 1 Expression via the Suppression of Peroxisome Proliferator-Activated Receptor γ Binding Activity in Mice Beige Adipocytes			tongue cancer	IWAT cell	E_02_0253	PCR，Western blot，ChIP-seq	Here, we show that the expression of uncoupling protein 1 (Ucp1) involved in thermoregulation is severely suppressed under ER stress conditions (afflicted by tunicamycin) in inguinal white adipose tissue (IWAT) both in vitro and in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we show that the expression of uncoupling protein 1 (Ucp1) involved in thermoregulation is severely suppressed under ER stress conditions (afflicted by tunicamycin) in inguinal white adipose tissue (IWAT) both in vitro and in vivo.		Here, we show that the expression of uncoupling protein 1 (Ucp1) involved in thermoregulation is severely suppressed under ER stress conditions (afflicted by tunicamycin) in inguinal white adipose tissue (IWAT) both in vitro and in vivo.	Immunohistochemical staining	Here, we show that the expression of uncoupling protein 1 (Ucp1) involved in thermoregulation is severely suppressed under ER stress conditions (afflicted by tunicamycin) in inguinal white adipose tissue (IWAT) both in vitro and in vivo.			PCR，Western blot，ChIP-seq				Ucp1
30639323	chr16	86507633	86509633	FOXF1	In contrast to ACDMPV caused by loss-of-function (LoF) of FOXF1 (MIM: 601089),20,21 the molecular etiology of AcDys and CAD is largely unknown.	human	Lung	High+Lowthroughput	Complex Compound Inheritance of Lethal Lung Developmental Disorders Due to Disruption of the TBX-FGF Pathway			Pulmonary hypoplasia	IMR-90 ，NHLF cell	E_01_0327	PCR, chip SEQ, variant enrichment analysis, bioinformatics prediction	In contrast to ACDMPV caused by loss-of-function (LoF) of FOXF1 (MIM: 601089),20,21 the molecular etiology of AcDys and CAD is largely unknown.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In contrast to ACDMPV caused by loss-of-function (LoF) of FOXF1 (MIM: 601089),20,21 the molecular etiology of AcDys and CAD is largely unknown.	Immunohistochemical staining	In contrast to ACDMPV caused by loss-of-function (LoF) of FOXF1 (MIM: 601089),20,21 the molecular etiology of AcDys and CAD is largely unknown.	FOXF1		PCR，ChIP-seq，变体富集分析，生物信息学预测	In contrast to ACDMPV caused by loss-of-function (LoF) of FOXF1 (MIM: 601089),20,21 the molecular etiology of AcDys and CAD is largely unknown.			
30632221	chr8	127732390	127734390	MYC	MYC is known to cause increased expression of EZH2 in prostate cancer, both directly and through downregulation of miR-26a and miR-26b, which are known to inhibit EZH2.5	human	brain	High+Lowthroughput	Inhibition of enhancer of zest homologue 2 is a potential therapeutic target for high-MYC medulloblastoma			Medulloblastoma		E_01_0328	PCR，Western blot	MYC is known to cause increased expression of EZH2 in prostate cancer, both directly and through downregulation of miR-26a and miR-26b, which are known to inhibit EZH2.5	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MYC is known to cause increased expression of EZH2 in prostate cancer, both directly and through downregulation of miR-26a and miR-26b, which are known to inhibit EZH2.5	Immunohistochemical staining	MYC is known to cause increased expression of EZH2 in prostate cancer, both directly and through downregulation of miR-26a and miR-26b, which are known to inhibit EZH2.5	MYC		PCR，Western blot	MYC is known to cause increased expression of EZH2 in prostate cancer, both directly and through downregulation of miR-26a and miR-26b, which are known to inhibit EZH2.5			
30632221	chr7	148804528	148806528	EZH2	MYC is known to cause increased expression of EZH2 in prostate cancer, both directly and through downregulation of miR-26a and miR-26b, which are known to inhibit EZH2.5	human	brain	High+Lowthroughput	Inhibition of enhancer of zest homologue 2 is a potential therapeutic target for high-MYC medulloblastoma			Medulloblastoma		E_01_0328	PCR，Western blot	MYC is known to cause increased expression of EZH2 in prostate cancer, both directly and through downregulation of miR-26a and miR-26b, which are known to inhibit EZH2.5	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MYC is known to cause increased expression of EZH2 in prostate cancer, both directly and through downregulation of miR-26a and miR-26b, which are known to inhibit EZH2.5	Immunohistochemical staining	MYC is known to cause increased expression of EZH2 in prostate cancer, both directly and through downregulation of miR-26a and miR-26b, which are known to inhibit EZH2.5	EZH2		PCR，Western blot	MYC is known to cause increased expression of EZH2 in prostate cancer, both directly and through downregulation of miR-26a and miR-26b, which are known to inhibit EZH2.5			
30631044	chr13	27957842	27959842	CDX2	Caudal-related homeobox transcription factor 2 (CDX2), an intestine-specific nuclear transcription factor, has been strongly implicated in the tumourigenesis of various human cancers.	human	lymph	High+Lowthroughput	CDX2 inhibits the proliferation and tumor formation of colon cancer cells by suppressing Wnt/β-catenin signaling via transactivation of GSK-3β and Axin2 expression			Colon cancer	colon cancer cell	E_01_0329	Immunohistochemistry, PCR, Western blot, chip seq	Caudal-related homeobox transcription factor 2 (CDX2), an intestine-specific nuclear transcription factor, has been strongly implicated in the tumourigenesis of various human cancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Caudal-related homeobox transcription factor 2 (CDX2), an intestine-specific nuclear transcription factor, has been strongly implicated in the tumourigenesis of various human cancers.	Immunohistochemical staining	Caudal-related homeobox transcription factor 2 (CDX2), an intestine-specific nuclear transcription factor, has been strongly implicated in the tumourigenesis of various human cancers.	CDX2		免疫组化检测，PCR，Western blot，ChIP-seq	Caudal-related homeobox transcription factor 2 (CDX2), an intestine-specific nuclear transcription factor, has been strongly implicated in the tumourigenesis of various human cancers.			
30630822	chr4	54654587	54656587	KIT	In this study, we identify regulatory regions of the KIT enhancer essential for KIT gene expression and GIST cell viability.	human,mouse	stomach	High+Lowthroughput	Enhancer Domains in Gastrointestinal Stromal Tumor Regulate KIT Expression and Are Targetable by BET Bromodomain Inhibition			Gastrointestinal stromal tumors	GIST cell	E_02_0254	Chip SEQ, RNA SEQ, immunoblotting, cloning, CRISPR assays, PCR	In this study, we identify regulatory regions of the KIT enhancer essential for KIT gene expression and GIST cell viability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we identify regulatory regions of the KIT enhancer essential for KIT gene expression and GIST cell viability.		In this study, we identify regulatory regions of the KIT enhancer essential for KIT gene expression and GIST cell viability.	Immunohistochemical staining	In this study, we identify regulatory regions of the KIT enhancer essential for KIT gene expression and GIST cell viability.			ChIP-seq，RNA-seq，免疫印迹法，Cloning ，CRISPR assays，PCR				KIT
30630179	chr17	42310249	42312249	STAT3	The expression vectors for wild type (WT) STAT3 (Stat3 Flag pRC/CMV, #8707, Addgene, Cambridge), dominant negative (DN) STAT3 (Stat3 Y705F Flag pRC/CMV, #8704,  Addgene, Cambridge), constitutively active (CA) STAT3 (Stat3-C Flag pRC/CMV,  #8722, Addgene, Cambridge), and luciferase reporter containing STAT3 response  element (SBR, 4xM67 pTATA TK-Luc, #8688, Addgene, Cambridge, MA) were  purchased from Addgene and have previously been described [74].	mouse	blood	High+Lowthroughput	Leukemia Inhibitory Factor Represses GnRH Gene Expression via cFOS during Inflammation in Male Mice			leukemia	GT1–7 cell	E_02_0255	Immunohistochemistry, cell transfection, PCR, Western blot	The expression vectors for wild type (WT) STAT3 (Stat3 Flag pRC/CMV, #8707, Addgene, Cambridge), dominant negative (DN) STAT3 (Stat3 Y705F Flag pRC/CMV, #8704,  Addgene, Cambridge), constitutively active (CA) STAT3 (Stat3-C Flag pRC/CMV,  #8722, Addgene, Cambridge), and luciferase reporter containing STAT3 response  element (SBR, 4xM67 pTATA TK-Luc, #8688, Addgene, Cambridge, MA) were  purchased from Addgene and have previously been described [74].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression vectors for wild type (WT) STAT3 (Stat3 Flag pRC/CMV, #8707, Addgene, Cambridge), dominant negative (DN) STAT3 (Stat3 Y705F Flag pRC/CMV, #8704,  Addgene, Cambridge), constitutively active (CA) STAT3 (Stat3-C Flag pRC/CMV,  #8722, Addgene, Cambridge), and luciferase reporter containing STAT3 response  element (SBR, 4xM67 pTATA TK-Luc, #8688, Addgene, Cambridge, MA) were  purchased from Addgene and have previously been described [74].		The expression vectors for wild type (WT) STAT3 (Stat3 Flag pRC/CMV, #8707, Addgene, Cambridge), dominant negative (DN) STAT3 (Stat3 Y705F Flag pRC/CMV, #8704,  Addgene, Cambridge), constitutively active (CA) STAT3 (Stat3-C Flag pRC/CMV,  #8722, Addgene, Cambridge), and luciferase reporter containing STAT3 response  element (SBR, 4xM67 pTATA TK-Luc, #8688, Addgene, Cambridge, MA) were  purchased from Addgene and have previously been described [74].	Immunohistochemical staining	The expression vectors for wild type (WT) STAT3 (Stat3 Flag pRC/CMV, #8707, Addgene, Cambridge), dominant negative (DN) STAT3 (Stat3 Y705F Flag pRC/CMV, #8704,  Addgene, Cambridge), constitutively active (CA) STAT3 (Stat3-C Flag pRC/CMV,  #8722, Addgene, Cambridge), and luciferase reporter containing STAT3 response  element (SBR, 4xM67 pTATA TK-Luc, #8688, Addgene, Cambridge, MA) were  purchased from Addgene and have previously been described [74].			免疫组化，细胞转染，PCR，Western blot				STAT3
30628724	chr7	148804584	148806584	EZH2	Polycomb group proteins are important epigenetic regulators for cell proliferation and differentiation, organ development, as well as initiation and progression of lethal diseases, including cancer. Upregulated Polycomb group proteins, including Enhancer of zeste homolog 2 (EZH2), promote proliferation, migration, invasion and metastasis of cancer cells, as well as self-renewal of cancer stem cells.	human	prostate	High+Lowthroughput	Polycomb group proteins EZH2 and EED directly regulate androgen receptor in advanced prostate cancer			prostatic cancer	Cancer Stem Cell	E_01_0330	Immunoprecipitation, RNA SEQ, PCR, Western blot	Polycomb group proteins are important epigenetic regulators for cell proliferation and differentiation, organ development, as well as initiation and progression of lethal diseases, including cancer. Upregulated Polycomb group proteins, including Enhancer of zeste homolog 2 (EZH2), promote proliferation, migration, invasion and metastasis of cancer cells, as well as self-renewal of cancer stem cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Polycomb group proteins are important epigenetic regulators for cell proliferation and differentiation, organ development, as well as initiation and progression of lethal diseases, including cancer. Upregulated Polycomb group proteins, including Enhancer of zeste homolog 2 (EZH2), promote proliferation, migration, invasion and metastasis of cancer cells, as well as self-renewal of cancer stem cells.	Immunohistochemical staining	Polycomb group proteins are important epigenetic regulators for cell proliferation and differentiation, organ development, as well as initiation and progression of lethal diseases, including cancer. Upregulated Polycomb group proteins, including Enhancer of zeste homolog 2 (EZH2), promote proliferation, migration, invasion and metastasis of cancer cells, as well as self-renewal of cancer stem cells.	EZH2		免疫沉淀法，RNA-seq，PCR，Western blot	Polycomb group proteins are important epigenetic regulators for cell proliferation and differentiation, organ development, as well as initiation and progression of lethal diseases, including cancer. Upregulated Polycomb group proteins, including Enhancer of zeste homolog 2 (EZH2), promote proliferation, migration, invasion and metastasis of cancer cells, as well as self-renewal of cancer stem cells.			
30628655	chr11	1155242	1157242	MUC5AC	P300 decreases the protein expression level of MUC5AC. The empty vector, untransfected control, the P300 expression plasmid and P300 siRNA, together with their control plasmids, were transfected into A549 cells. Immunofluorescence was then performed to detect the protein expression of MUC5AC in each group.	human	Lung	High+Lowthroughput	Characterization of the human mucin 5AC promoter and its regulation by the histone acetyltransferase P300			asthma	A549 cell	E_01_0331	Transient transfection, luciferase assay, immunoprecipitation, PCR, Western blot	P300 decreases the protein expression level of MUC5AC. The empty vector, untransfected control, the P300 expression plasmid and P300 siRNA, together with their control plasmids, were transfected into A549 cells. Immunofluorescence was then performed to detect the protein expression of MUC5AC in each group.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	P300 decreases the protein expression level of MUC5AC. The empty vector, untransfected control, the P300 expression plasmid and P300 siRNA, together with their control plasmids, were transfected into A549 cells. Immunofluorescence was then performed to detect the protein expression of MUC5AC in each group.		P300 decreases the protein expression level of MUC5AC. The empty vector, untransfected control, the P300 expression plasmid and P300 siRNA, together with their control plasmids, were transfected into A549 cells. Immunofluorescence was then performed to detect the protein expression of MUC5AC in each group.	Immunohistochemical staining	P300 decreases the protein expression level of MUC5AC. The empty vector, untransfected control, the P300 expression plasmid and P300 siRNA, together with their control plasmids, were transfected into A549 cells. Immunofluorescence was then performed to detect the protein expression of MUC5AC in each group.			瞬时转染，荧光素酶检测，免疫沉淀法，PCR，Western blot				MUC5AC
30627958	chr9	104778131	104780131	ABCA1	In detail, PGA1 activated the peroxisome proliferator-activated receptor-gamma (PPARγ) and ATP-binding cassette subfamily A member 1 (ABCA1) signalling pathways, promoting the efflux of cholesterol and decreasing the intracellular cholesterol levels.	mouse	nerve	High+Lowthroughput	Prostaglandin A1 Inhibits the Cognitive Decline of APP/PS1 Transgenic Mice via PPARγ/ABCA1-dependent Cholesterol Efflux Mechanisms			Chronic neurodegenerative diseases	microglial cell	E_02_0256	Immunohistochemistry staining, PCR, Western blot, immunofluorescence	In detail, PGA1 activated the peroxisome proliferator-activated receptor-gamma (PPARγ) and ATP-binding cassette subfamily A member 1 (ABCA1) signalling pathways, promoting the efflux of cholesterol and decreasing the intracellular cholesterol levels.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In detail, PGA1 activated the peroxisome proliferator-activated receptor-gamma (PPARγ) and ATP-binding cassette subfamily A member 1 (ABCA1) signalling pathways, promoting the efflux of cholesterol and decreasing the intracellular cholesterol levels.		In detail, PGA1 activated the peroxisome proliferator-activated receptor-gamma (PPARγ) and ATP-binding cassette subfamily A member 1 (ABCA1) signalling pathways, promoting the efflux of cholesterol and decreasing the intracellular cholesterol levels.	Immunohistochemical staining	In detail, PGA1 activated the peroxisome proliferator-activated receptor-gamma (PPARγ) and ATP-binding cassette subfamily A member 1 (ABCA1) signalling pathways, promoting the efflux of cholesterol and decreasing the intracellular cholesterol levels.			免疫组织化学染色法，PCR，Western blot，免疫荧光法				ABCA1
30626972	chr9	123999195	124001195	LHX2	The Greek-island-bound transcription factor LHX2 and adaptor protein LDB1 regulate the assembly and maintenance of olfactory receptor compartments, Greek island hubs and olfactory receptor transcription, providing mechanistic insights into and functional support for the role of trans interactions in gene expression.	mouse	nerve	High+Lowthroughput	LHX2- and LDB1-mediated trans interactions regulate olfactory receptor choice					E_02_0257	Hi-C，PCR，Western blot	The Greek-island-bound transcription factor LHX2 and adaptor protein LDB1 regulate the assembly and maintenance of olfactory receptor compartments, Greek island hubs and olfactory receptor transcription, providing mechanistic insights into and functional support for the role of trans interactions in gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The Greek-island-bound transcription factor LHX2 and adaptor protein LDB1 regulate the assembly and maintenance of olfactory receptor compartments, Greek island hubs and olfactory receptor transcription, providing mechanistic insights into and functional support for the role of trans interactions in gene expression.		The Greek-island-bound transcription factor LHX2 and adaptor protein LDB1 regulate the assembly and maintenance of olfactory receptor compartments, Greek island hubs and olfactory receptor transcription, providing mechanistic insights into and functional support for the role of trans interactions in gene expression.	Immunohistochemical staining	The Greek-island-bound transcription factor LHX2 and adaptor protein LDB1 regulate the assembly and maintenance of olfactory receptor compartments, Greek island hubs and olfactory receptor transcription, providing mechanistic insights into and functional support for the role of trans interactions in gene expression.			Hi-C，PCR，Western blot				LHX2
30626694	chr5	141617717	141619717	HDAC3	We demonstrate that HDAC3 is required to repress expression of the purinergic receptor P2X7 to prevent DP cell death. HDAC3-deficient DP thymocytes upregulate the P2X7 receptor, increasing sensitivity to ATP-induced cell death.	mouse	thymic	High+Lowthroughput	Cutting Edge: HDAC3 Protects Double-Positive Thymocytes from P2X7 Receptor-Induced Cell Death				T cell	E_02_0258	Flow cytometry, PCR, chip seq	We demonstrate that HDAC3 is required to repress expression of the purinergic receptor P2X7 to prevent DP cell death. HDAC3-deficient DP thymocytes upregulate the P2X7 receptor, increasing sensitivity to ATP-induced cell death.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We demonstrate that HDAC3 is required to repress expression of the purinergic receptor P2X7 to prevent DP cell death. HDAC3-deficient DP thymocytes upregulate the P2X7 receptor, increasing sensitivity to ATP-induced cell death.		We demonstrate that HDAC3 is required to repress expression of the purinergic receptor P2X7 to prevent DP cell death. HDAC3-deficient DP thymocytes upregulate the P2X7 receptor, increasing sensitivity to ATP-induced cell death.	Immunohistochemical staining	We demonstrate that HDAC3 is required to repress expression of the purinergic receptor P2X7 to prevent DP cell death. HDAC3-deficient DP thymocytes upregulate the P2X7 receptor, increasing sensitivity to ATP-induced cell death.			流式细胞术，PCR，ChIP-seq				HDAC3
30626398	chr17	48604528	48606528	HOXB7	Finally, we performed both technical and experimental bisulfte pyrosequencing validations of three of the CpGs found at the HOXB7 (cg07547765), SOCS3 (cg11047325) and ZFPM2 (cg03830443) genes (Fig.  5, see Additional fle  13: Table  S7 for full data).	human	blood	High+Lowthroughput	Longitudinal genome-wide DNA methylation analysis uncovers persistent early-life DNA methylation changes					E_01_0332	Bisulfite pyrosequencing	Finally, we performed both technical and experimental bisulfte pyrosequencing validations of three of the CpGs found at the HOXB7 (cg07547765), SOCS3 (cg11047325) and ZFPM2 (cg03830443) genes (Fig.  5, see Additional fle  13: Table  S7 for full data).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Finally, we performed both technical and experimental bisulfte pyrosequencing validations of three of the CpGs found at the HOXB7 (cg07547765), SOCS3 (cg11047325) and ZFPM2 (cg03830443) genes (Fig.  5, see Additional fle  13: Table  S7 for full data).	Immunohistochemical staining	Finally, we performed both technical and experimental bisulfte pyrosequencing validations of three of the CpGs found at the HOXB7 (cg07547765), SOCS3 (cg11047325) and ZFPM2 (cg03830443) genes (Fig.  5, see Additional fle  13: Table  S7 for full data).	HOXB7		亚硫酸氢盐焦磷酸测序	Finally, we performed both technical and experimental bisulfte pyrosequencing validations of three of the CpGs found at the HOXB7 (cg07547765), SOCS3 (cg11047325) and ZFPM2 (cg03830443) genes (Fig.  5, see Additional fle  13: Table  S7 for full data).			
30622230	chr12	95513693	95515693	USP44	Here, we found that enhancer of zeste homolog 2 (EZH2), a histone H3 lysine 27 methyltransferase, is regulated by USP44.	human	prostate	High+Lowthroughput	USP44 Promotes the Tumorigenesis of Prostate Cancer Cells through EZH2 Protein Stabilization			prostatic cancer	prostate cancer cell	E_01_0333	PCR, immunofluorescence staining	Here, we found that enhancer of zeste homolog 2 (EZH2), a histone H3 lysine 27 methyltransferase, is regulated by USP44.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we found that enhancer of zeste homolog 2 (EZH2), a histone H3 lysine 27 methyltransferase, is regulated by USP44.		Here, we found that enhancer of zeste homolog 2 (EZH2), a histone H3 lysine 27 methyltransferase, is regulated by USP44.	Immunohistochemical staining	Here, we found that enhancer of zeste homolog 2 (EZH2), a histone H3 lysine 27 methyltransferase, is regulated by USP44.			PCR，免疫荧光染色法				USP44
30622137	chr12	106060956	106062956	NUAK1	We here report that NUAK family kinase 1 (NUAK1) and NUAK2 are two TGF target genes. NUAK1/2 belong to the AMPactivated protein kinase (AMPK) family, whose members control central and protein metabolism, polarity and overall cellular homeostasis.	mouse	myofibroblast	High+Lowthroughput	Transforming growth factor β (TGFβ) induces NUAK kinase expression to fine-tune its signaling output					E_02_0259	Luciferase assay, fluorescence immunomicroscopy, PCR, Western blot	We here report that NUAK family kinase 1 (NUAK1) and NUAK2 are two TGF target genes. NUAK1/2 belong to the AMPactivated protein kinase (AMPK) family, whose members control central and protein metabolism, polarity and overall cellular homeostasis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We here report that NUAK family kinase 1 (NUAK1) and NUAK2 are two TGF target genes. NUAK1/2 belong to the AMPactivated protein kinase (AMPK) family, whose members control central and protein metabolism, polarity and overall cellular homeostasis.		We here report that NUAK family kinase 1 (NUAK1) and NUAK2 are two TGF target genes. NUAK1/2 belong to the AMPactivated protein kinase (AMPK) family, whose members control central and protein metabolism, polarity and overall cellular homeostasis.	Immunohistochemical staining	We here report that NUAK family kinase 1 (NUAK1) and NUAK2 are two TGF target genes. NUAK1/2 belong to the AMPactivated protein kinase (AMPK) family, whose members control central and protein metabolism, polarity and overall cellular homeostasis.			荧光素酶检测，荧光免疫显微技术，PCR，Western blot				NUAK1
30621608	chr3	190319460	190321460	CLDN16	This rare disease is caused by mutations in CLDN16 that encodes claudin-16, a tight-junction protein involved in paracellular reabsorption of magnesium and calcium in the renal tubule. Most of these variants are located in exons and have been classified as missense mutations.	human	kidney	High+Lowthroughput	Exonic CLDN16 mutations associated with familial hypomagnesemia with hypercalciuria and nephrocalcinosis can induce deleterious mRNA alterations			Familial hypomagnesemia, hypercalciuria, and nephrocalcinosis	COS7 cells	E_01_0334	PCR	This rare disease is caused by mutations in CLDN16 that encodes claudin-16, a tight-junction protein involved in paracellular reabsorption of magnesium and calcium in the renal tubule. Most of these variants are located in exons and have been classified as missense mutations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This rare disease is caused by mutations in CLDN16 that encodes claudin-16, a tight-junction protein involved in paracellular reabsorption of magnesium and calcium in the renal tubule. Most of these variants are located in exons and have been classified as missense mutations.		This rare disease is caused by mutations in CLDN16 that encodes claudin-16, a tight-junction protein involved in paracellular reabsorption of magnesium and calcium in the renal tubule. Most of these variants are located in exons and have been classified as missense mutations.	Immunohistochemical staining	This rare disease is caused by mutations in CLDN16 that encodes claudin-16, a tight-junction protein involved in paracellular reabsorption of magnesium and calcium in the renal tubule. Most of these variants are located in exons and have been classified as missense mutations.			PCR				CLDN16
30620726	chr3	128476298	128478298	GATA2	GATA-binding protein 2 (GATA2) mutations cause GATA-2 deficiency syndrome involving immunodeficiency, myelodysplastic syndrome, and acute myeloid leukemia.	human	blood	High+Lowthroughput	Single-nucleotide human disease mutation inactivates a blood-regenerative GATA2 enhancer			Acute myeloid leukemia	progenitor cell	E_01_0335	PCR，ChIP-seq	GATA-binding protein 2 (GATA2) mutations cause GATA-2 deficiency syndrome involving immunodeficiency, myelodysplastic syndrome, and acute myeloid leukemia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			GATA-binding protein 2 (GATA2) mutations cause GATA-2 deficiency syndrome involving immunodeficiency, myelodysplastic syndrome, and acute myeloid leukemia.	Immunohistochemical staining	GATA-binding protein 2 (GATA2) mutations cause GATA-2 deficiency syndrome involving immunodeficiency, myelodysplastic syndrome, and acute myeloid leukemia.	GATA2		PCR，ChIP-seq	GATA-binding protein 2 (GATA2) mutations cause GATA-2 deficiency syndrome involving immunodeficiency, myelodysplastic syndrome, and acute myeloid leukemia.			
30619879	chrX	147909131	147911131	FMR1	The FMR1 gene encodes the Fragile X Mental Retardation Protein, that harbors three canonical RNA-binding domains (KH1, KH2 and RGGBox) in addition to a Nuclear Localization Signal (NLS) and a Nuclear Export Signal (NES; Bardoni et al., 1997).	mouse	nerve	High+Lowthroughput	Fragile X Mental Retardation Protein: To Be or Not to Be a Translational Enhancer			Fragile X syndrome		E_02_0260	PCR	The FMR1 gene encodes the Fragile X Mental Retardation Protein, that harbors three canonical RNA-binding domains (KH1, KH2 and RGGBox) in addition to a Nuclear Localization Signal (NLS) and a Nuclear Export Signal (NES; Bardoni et al., 1997).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The FMR1 gene encodes the Fragile X Mental Retardation Protein, that harbors three canonical RNA-binding domains (KH1, KH2 and RGGBox) in addition to a Nuclear Localization Signal (NLS) and a Nuclear Export Signal (NES; Bardoni et al., 1997).		The FMR1 gene encodes the Fragile X Mental Retardation Protein, that harbors three canonical RNA-binding domains (KH1, KH2 and RGGBox) in addition to a Nuclear Localization Signal (NLS) and a Nuclear Export Signal (NES; Bardoni et al., 1997).	Immunohistochemical staining	The FMR1 gene encodes the Fragile X Mental Retardation Protein, that harbors three canonical RNA-binding domains (KH1, KH2 and RGGBox) in addition to a Nuclear Localization Signal (NLS) and a Nuclear Export Signal (NES; Bardoni et al., 1997).			PCR				FMR1
30619471	chr17	42310619	42312619	STAT3	As a proof of concept of a possible functional relevance of this observation, we experimentally verified that the expression levels of a circRNA derived from an MS-associated locus, i.e., hsa_circ_0043813 from the STAT3 gene, can be modulated by the three genotypes at the disease-associated SNP.	human	nerve	High+Lowthroughput	Interpreting Non-coding Genetic Variation in Multiple Sclerosis Genome-Wide Associated Regions			Multiple sclerosis	SH-SY5Y， Jurkat cell	E_01_0336	RNA sequencing, PCR	As a proof of concept of a possible functional relevance of this observation, we experimentally verified that the expression levels of a circRNA derived from an MS-associated locus, i.e., hsa_circ_0043813 from the STAT3 gene, can be modulated by the three genotypes at the disease-associated SNP.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			As a proof of concept of a possible functional relevance of this observation, we experimentally verified that the expression levels of a circRNA derived from an MS-associated locus, i.e., hsa_circ_0043813 from the STAT3 gene, can be modulated by the three genotypes at the disease-associated SNP.	Immunohistochemical staining	As a proof of concept of a possible functional relevance of this observation, we experimentally verified that the expression levels of a circRNA derived from an MS-associated locus, i.e., hsa_circ_0043813 from the STAT3 gene, can be modulated by the three genotypes at the disease-associated SNP.	STAT3		RNA测序，PCR	As a proof of concept of a possible functional relevance of this observation, we experimentally verified that the expression levels of a circRNA derived from an MS-associated locus, i.e., hsa_circ_0043813 from the STAT3 gene, can be modulated by the three genotypes at the disease-associated SNP.			
30618413	chr4	153681347	153683347	TLR2	Lipopolysaccharide-stimulated RWPE-1 cells expressed higher levels of TLR2, TLR10, high mobility group box 1 (HMGB1), phospho-nuclear factor kappa-light-chain-enhancer of activated B-cells P65 (phospho-NF-κB P65)	human	prostate	High+Lowthroughput	Toll-like receptor 10 (TLR10) exhibits suppressive effects on inflammation of prostate epithelial cells			prostatitis	prostate epithelial cell	E_01_0337	PCR，Western blot，ChIP-seq	Lipopolysaccharide-stimulated RWPE-1 cells expressed higher levels of TLR2, TLR10, high mobility group box 1 (HMGB1), phospho-nuclear factor kappa-light-chain-enhancer of activated B-cells P65 (phospho-NF-κB P65)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Lipopolysaccharide-stimulated RWPE-1 cells expressed higher levels of TLR2, TLR10, high mobility group box 1 (HMGB1), phospho-nuclear factor kappa-light-chain-enhancer of activated B-cells P65 (phospho-NF-κB P65)	Immunohistochemical staining	Lipopolysaccharide-stimulated RWPE-1 cells expressed higher levels of TLR2, TLR10, high mobility group box 1 (HMGB1), phospho-nuclear factor kappa-light-chain-enhancer of activated B-cells P65 (phospho-NF-κB P65)	TLR2		PCR，Western blot，ChIP-seq	Lipopolysaccharide-stimulated RWPE-1 cells expressed higher levels of TLR2, TLR10, high mobility group box 1 (HMGB1), phospho-nuclear factor kappa-light-chain-enhancer of activated B-cells P65 (phospho-NF-κB P65)			
30610059	chr10	70594223	70596223	PRF1	H3K9me3 was enriched in the promoters of GZMB, PRF1, FASLG, and IFNG in quiescent T cells.	human	colorectum	High+Lowthroughput	SUV39H1 Represses the Expression of Cytotoxic T-Lymphocyte Effector Genes to Promote Colon Tumor Immune Evasion			Colon neoplasms	T cell	E_01_0338	Immunohistochemical staining, flow cytometry, PCR, Western blot, chip seq	H3K9me3 was enriched in the promoters of GZMB, PRF1, FASLG, and IFNG in quiescent T cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			H3K9me3 was enriched in the promoters of GZMB, PRF1, FASLG, and IFNG in quiescent T cells.	Immunohistochemical staining	H3K9me3 was enriched in the promoters of GZMB, PRF1, FASLG, and IFNG in quiescent T cells.	ZNF395		免疫组织化学染色法，流式细胞术，PCR，Western blot，ChIP-seq	H3K9me3 was enriched in the promoters of GZMB, PRF1, FASLG, and IFNG in quiescent T cells.			
30606720	chr3	181709342	181711342	SOX2	In several triple-negative breast cancer (TNBC) models, Six2 enhanced the expression of genes associated with embryonic stem cell programs. Six2 directly bound the Sox2 Srr2 enhancer	human	breast	High+Lowthroughput	SIX2 Mediates Late-Stage Metastasis via Direct Regulation of SOX2 and Induction of a Cancer Stem Cell Program			mammary cancer	Cancer Stem Cell	E_01_0339	PCR，Western blot，RNA-seq	In several triple-negative breast cancer (TNBC) models, Six2 enhanced the expression of genes associated with embryonic stem cell programs. Six2 directly bound the Sox2 Srr2 enhancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In several triple-negative breast cancer (TNBC) models, Six2 enhanced the expression of genes associated with embryonic stem cell programs. Six2 directly bound the Sox2 Srr2 enhancer	Immunohistochemical staining	In several triple-negative breast cancer (TNBC) models, Six2 enhanced the expression of genes associated with embryonic stem cell programs. Six2 directly bound the Sox2 Srr2 enhancer	SOX2		PCR，Western blot，RNA-seq	In several triple-negative breast cancer (TNBC) models, Six2 enhanced the expression of genes associated with embryonic stem cell programs. Six2 directly bound the Sox2 Srr2 enhancer			
30605688	chr2	69455371	69457371	AAK1	Here, using a gain-of-function screen of the human kinome, we report that the AP2 associated kinase 1 (AAK1), a known CME enhancer	human		High+Lowthroughput	WNT Activates the AAK1 Kinase to Promote Clathrin-Mediated Endocytosis of LRP6 and Establish a Negative Feedback Loop				HEK293T	E_01_0340	PCR，Western blot	Here, using a gain-of-function screen of the human kinome, we report that the AP2 associated kinase 1 (AAK1), a known CME enhancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, using a gain-of-function screen of the human kinome, we report that the AP2 associated kinase 1 (AAK1), a known CME enhancer		Here, using a gain-of-function screen of the human kinome, we report that the AP2 associated kinase 1 (AAK1), a known CME enhancer	Immunohistochemical staining	Here, using a gain-of-function screen of the human kinome, we report that the AP2 associated kinase 1 (AAK1), a known CME enhancer			PCR，Western blot				AAK1
30603559	chr7	148804645	148806645	EZH2	Western blot determined the expression levels of enhancer of zeste homolog 2 (EZH2)	human	Hair	High+Lowthroughput	MiR-214 Regulates the Human Hair Follicle Stem Cell Proliferation and Differentiation by Targeting EZH2 and Wnt/β-Catenin Signaling Way In Vitro				Hair Follicle Stem Cell	E_01_0341	Immunofluorescence, DAPI staining, PCR	Western blot determined the expression levels of enhancer of zeste homolog 2 (EZH2)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Western blot determined the expression levels of enhancer of zeste homolog 2 (EZH2)	Immunohistochemical staining	Western blot determined the expression levels of enhancer of zeste homolog 2 (EZH2)	EZH2		免疫荧光法，DAPI染色，PCR	Western blot determined the expression levels of enhancer of zeste homolog 2 (EZH2)			
30596070	chr19	10130616	10132616	DNMT1	Our previous studies showed that HOTAIR modulated HOXA1 DNA methylation by reducing DNMT1 and DNMT3b expression in drug-resistant small cell lung cancer (SCLC).	human	Lung	High+Lowthroughput	H3K27me3 induces multidrug resistance in small cell lung cancer by affecting HOXA1 DNA methylation via regulation of the lncRNA HOTAIR			lung cancer	NSCLC cell	E_01_0342	Flow cytometry, cell transfection techniques, immunohistochemical staining, PCR, Western blot, chip seq	Our previous studies showed that HOTAIR modulated HOXA1 DNA methylation by reducing DNMT1 and DNMT3b expression in drug-resistant small cell lung cancer (SCLC).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our previous studies showed that HOTAIR modulated HOXA1 DNA methylation by reducing DNMT1 and DNMT3b expression in drug-resistant small cell lung cancer (SCLC).	Immunohistochemical staining	Our previous studies showed that HOTAIR modulated HOXA1 DNA methylation by reducing DNMT1 and DNMT3b expression in drug-resistant small cell lung cancer (SCLC).	DNMT1		流式细胞术，细胞转染技术，免疫组织化学染色，PCR，Western blot，ChIP-seq	Our previous studies showed that HOTAIR modulated HOXA1 DNA methylation by reducing DNMT1 and DNMT3b expression in drug-resistant small cell lung cancer (SCLC).			
30594152	chr22	37967907	37969907	SOX10	Two inhibitory activity regions were found in the - 1409 bp to - 1381 bp and - 1196 bp to - 1124 bp fragments, which might be bound to the GATA or SOX10 transcription factors as predicted by the JASPAR software.	human	nerve	High+Lowthroughput	Characterization and functional analyses of the human HTR1A gene: 5' regulatory region modulates gene expression in vitro			Schizophrenia	SK-N-SH cell	E_01_0343	Cell transfection	Two inhibitory activity regions were found in the - 1409 bp to - 1381 bp and - 1196 bp to - 1124 bp fragments, which might be bound to the GATA or SOX10 transcription factors as predicted by the JASPAR software.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Two inhibitory activity regions were found in the - 1409 bp to - 1381 bp and - 1196 bp to - 1124 bp fragments, which might be bound to the GATA or SOX10 transcription factors as predicted by the JASPAR software.	Immunohistochemical staining	Two inhibitory activity regions were found in the - 1409 bp to - 1381 bp and - 1196 bp to - 1124 bp fragments, which might be bound to the GATA or SOX10 transcription factors as predicted by the JASPAR software.	SOX10		细胞转染	Two inhibitory activity regions were found in the - 1409 bp to - 1381 bp and - 1196 bp to - 1124 bp fragments, which might be bound to the GATA or SOX10 transcription factors as predicted by the JASPAR software.			
30590588	chr2	144361789	144363789	ZEB2	The spatiotemporal regulation of ZEB2 is complex and involves various regulatory elements, including alternative promoters and specific enhancers that contribute to the multifactorial function of this transcription factor	human	nerve	High+Lowthroughput	Functional characterization of the ZEB2 regulatory landscape				neural crest cell	E_01_0344	Hi-C，PCR，Western blot，ChIP-seq	The spatiotemporal regulation of ZEB2 is complex and involves various regulatory elements, including alternative promoters and specific enhancers that contribute to the multifactorial function of this transcription factor	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The spatiotemporal regulation of ZEB2 is complex and involves various regulatory elements, including alternative promoters and specific enhancers that contribute to the multifactorial function of this transcription factor	Immunohistochemical staining	The spatiotemporal regulation of ZEB2 is complex and involves various regulatory elements, including alternative promoters and specific enhancers that contribute to the multifactorial function of this transcription factor	ZEB2		Hi-C，PCR，Western blot，ChIP-seq	The spatiotemporal regulation of ZEB2 is complex and involves various regulatory elements, including alternative promoters and specific enhancers that contribute to the multifactorial function of this transcription factor			
30590042	chr20	33672756	33674756	E2F1	We found that the transcription factor E2F1 and its heterodimerization partner DP1 represent a dependency in multiple myeloma cells.	human	bone	High+Lowthroughput	Non-overlapping Control of Transcriptome by Promoter- and Super-Enhancer-Associated Dependencies in Multiple Myeloma			Multiple myeloma	multiple myeloma cell	E_01_0345	PCR，Western blot，ChIP-seq	We found that the transcription factor E2F1 and its heterodimerization partner DP1 represent a dependency in multiple myeloma cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found that the transcription factor E2F1 and its heterodimerization partner DP1 represent a dependency in multiple myeloma cells.	Immunohistochemical staining	We found that the transcription factor E2F1 and its heterodimerization partner DP1 represent a dependency in multiple myeloma cells.	E2F1		PCR，Western blot，ChIP-seq	We found that the transcription factor E2F1 and its heterodimerization partner DP1 represent a dependency in multiple myeloma cells.			
30563971	chr3	189628751	189630751	TP63	We further identified that the TP63 gene was repressed by this precision-guided machinery of TRPS1-CHD4/NuRD(MTA2) complex, which decommissions its enhancer leading to a decrease in ΔNp63 and enhancing the metastatic ability of breast cancer cells.	human	breast	High+Lowthroughput	Atypical GATA transcription factor TRPS1 represses gene expression by recruiting CHD4/NuRD(MTA2) and suppresses cell migration and invasion by repressing TP63 expression			mammary cancer	T47D cell	E_01_0346	PCR，Western blot，ChIP-seq	We further identified that the TP63 gene was repressed by this precision-guided machinery of TRPS1-CHD4/NuRD(MTA2) complex, which decommissions its enhancer leading to a decrease in ΔNp63 and enhancing the metastatic ability of breast cancer cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We further identified that the TP63 gene was repressed by this precision-guided machinery of TRPS1-CHD4/NuRD(MTA2) complex, which decommissions its enhancer leading to a decrease in ΔNp63 and enhancing the metastatic ability of breast cancer cells.	Immunohistochemical staining	We further identified that the TP63 gene was repressed by this precision-guided machinery of TRPS1-CHD4/NuRD(MTA2) complex, which decommissions its enhancer leading to a decrease in ΔNp63 and enhancing the metastatic ability of breast cancer cells.	TP63		PCR，Western blot，ChIP-seq	We further identified that the TP63 gene was repressed by this precision-guided machinery of TRPS1-CHD4/NuRD(MTA2) complex, which decommissions its enhancer leading to a decrease in ΔNp63 and enhancing the metastatic ability of breast cancer cells.			
30559760	chr7	151553558	151555558	PRKAG2	we analyzed a whole genome case-control expression profiles in human CKD to investigate whether the susceptibility gene PRKAG2 is differently expressed in CKD cases compared with control samples.	human	kidney	High+Lowthroughput	Functional Prediction of Chronic Kidney Disease Susceptibility Gene PRKAG2 by Comprehensively Bioinformatics Analysis			Chronic kidney disease	Caco2 cell	E_01_0347	ChIP-seq	we analyzed a whole genome case-control expression profiles in human CKD to investigate whether the susceptibility gene PRKAG2 is differently expressed in CKD cases compared with control samples.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	we analyzed a whole genome case-control expression profiles in human CKD to investigate whether the susceptibility gene PRKAG2 is differently expressed in CKD cases compared with control samples.		we analyzed a whole genome case-control expression profiles in human CKD to investigate whether the susceptibility gene PRKAG2 is differently expressed in CKD cases compared with control samples.	Immunohistochemical staining	we analyzed a whole genome case-control expression profiles in human CKD to investigate whether the susceptibility gene PRKAG2 is differently expressed in CKD cases compared with control samples.			ChIP-seq				PRKAG2
30552336	chr17	72118256	72120256	SOX9	In a recent independent but complementary study on Sox9 regulation in the mouse by Gonen and colleagues, an orthologous mouse enhancer (Enh13) showing 80% sequence conservation with eSR-A was identified13 .	human	epithelial	High+Lowthroughput	Human sex reversal is caused by duplication or deletion of core enhancers upstream of SOX9				COS7 cells	E_01_0348	PCR，ChIP-seq	In a recent independent but complementary study on Sox9 regulation in the mouse by Gonen and colleagues, an orthologous mouse enhancer (Enh13) showing 80% sequence conservation with eSR-A was identified13 .	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In a recent independent but complementary study on Sox9 regulation in the mouse by Gonen and colleagues, an orthologous mouse enhancer (Enh13) showing 80% sequence conservation with eSR-A was identified13 .	Immunohistochemical staining	In a recent independent but complementary study on Sox9 regulation in the mouse by Gonen and colleagues, an orthologous mouse enhancer (Enh13) showing 80% sequence conservation with eSR-A was identified13 .	SOX9		PCR，ChIP-seq	In a recent independent but complementary study on Sox9 regulation in the mouse by Gonen and colleagues, an orthologous mouse enhancer (Enh13) showing 80% sequence conservation with eSR-A was identified13 .			
30544251	chr12	35939690	35990427	GLIS1	The combination of the two approaches identified aryl hydrocarbon receptor (AHR) and Glis family zinc finger 1 (GLIS1) as mesenchymal key TFs controlled by dynamic cell type-specific super-enhancers that become repressed in both lineages.	mouse	bone	Low+High throughput	Temporal enhancer profiling of parallel lineages identifies AHR and GLIS1 as regulators of mesenchymal multipotency		--	--		E_02_0261	ChIP-seq	The four adjacent merged SEs (SE283,SE284,SE285,and SE286) at the Ahr locus together cover a continuous region over 300 kb of active enhancer signal downstream of the Ahr gene in the ST2 cells.Moreover, all four SEs showed a very high correlation (r ≥ 0.95) with Ahr mRNA levels as measured by RNA-seq (Figure 5C and D, upper panels) and validated by RT-qPCR.	Super-Enhancer	--	RT-qPCR,ChIP,RNA-seq	Ahr is regulated by multiple SEs with lineage-specific dynamics The Ahr mRNA level was measured across the differentiation by RNA-seq and RT-qPCR in both adipocyte and osteoblast differentiation and is indicated astheintactline.	Ah,Ahhe,In,bHLHe76,Ahr	--	--	--	Ahr,Glis1	Ah, Ahhe, In, bHLHe76, Ahr,Gli5, Gli6, GliH1	RT-qPCR	To confirm the observed differentiation defects in the presence of high AHR and GLIS1 levels, RT-qPCR analysis of the known adipocyte marker gene Lpl was performed. In ST2-TetOn-GFP cells Lpl was upregulated by D5 of differentiation and remained elevated in D9 cells both in presence and absence of doxycycline.	--	--	Ahr
30544224	chr14	73133812	73135812	PSEN1	Thirty-four unique mutations in patients with HS have been found in three genes encoding the γ-secretase complex: nicastrin (NCSTN), presenilin 1 (PSEN1), presenilin enhancer 2 (PSENEN) and in POGLUT1, an endoplasmic reticulum O-glucosyltransferase involved in Notch signaling.	human	lymph	High+Lowthroughput	Analysis of hidradenitis suppurativa-linked mutations in four genes and the effects of PSEN1-P242LfsX11 on cytokine and chemokine expression in macrophages			Hidradenitis suppurativa	THP-1 cells	E_01_0349	PCR，Western blot	Thirty-four unique mutations in patients with HS have been found in three genes encoding the γ-secretase complex: nicastrin (NCSTN), presenilin 1 (PSEN1), presenilin enhancer 2 (PSENEN) and in POGLUT1, an endoplasmic reticulum O-glucosyltransferase involved in Notch signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thirty-four unique mutations in patients with HS have been found in three genes encoding the γ-secretase complex: nicastrin (NCSTN), presenilin 1 (PSEN1), presenilin enhancer 2 (PSENEN) and in POGLUT1, an endoplasmic reticulum O-glucosyltransferase involved in Notch signaling.	Immunohistochemical staining	Thirty-four unique mutations in patients with HS have been found in three genes encoding the γ-secretase complex: nicastrin (NCSTN), presenilin 1 (PSEN1), presenilin enhancer 2 (PSENEN) and in POGLUT1, an endoplasmic reticulum O-glucosyltransferase involved in Notch signaling.	PSEN1		PCR，Western blot	Thirty-four unique mutations in patients with HS have been found in three genes encoding the γ-secretase complex: nicastrin (NCSTN), presenilin 1 (PSEN1), presenilin enhancer 2 (PSENEN) and in POGLUT1, an endoplasmic reticulum O-glucosyltransferase involved in Notch signaling.			
30540553	chr7	148804397	148806397	EZH2	Enhancer of zeste homolog 2 (EZH2) was expressed differentially, showing significant up-regulation in HSCs activated with TGF-β but not with PDGF-BB.	mouse	epithelial	High+Lowthroughput	Chemical Activation of the Ethylene Signaling Pathway Promotes Fusarium graminearum Resistance in Detached Wheat Heads			Alternaria	eukaryotic cell	E_02_0262	Isolated head method for FHB resistance assessment	Enhancer of zeste homolog 2 (EZH2) was expressed differentially, showing significant up-regulation in HSCs activated with TGF-β but not with PDGF-BB.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of zeste homolog 2 (EZH2) was expressed differentially, showing significant up-regulation in HSCs activated with TGF-β but not with PDGF-BB.		Enhancer of zeste homolog 2 (EZH2) was expressed differentially, showing significant up-regulation in HSCs activated with TGF-β but not with PDGF-BB.	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2) was expressed differentially, showing significant up-regulation in HSCs activated with TGF-β but not with PDGF-BB.			FHB抗性评估的分离头法				EZH2
30538561	chr7	100799729	100801729	EPHB4	We also found that Notch signaling pathway was abnormally activated and treatment of Notch signaling ligand human Jagged1 peptide downregulated EPHB2 and upregulated EPHB4 in the SW620 cells, as well as promoted the chromatin modification protein Jumonji domain-containing protein-3 (JMJD3) cytonuclear trans-localization with the NICD, which indicated that NICD brought JMJD3 to the EPHB4 enhancer region to decrease the H3K27me3 level.	human	colorectum	High+Lowthroughput	Notch signaling promotes serrated neoplasia pathway in colorectal cancer through epigenetic modification of EPHB2 and EPHB4			colorectal cancer 	SW620 cell	E_01_0350	PCR, Western blot, chip SEQ, immunoblotting	We also found that Notch signaling pathway was abnormally activated and treatment of Notch signaling ligand human Jagged1 peptide downregulated EPHB2 and upregulated EPHB4 in the SW620 cells, as well as promoted the chromatin modification protein Jumonji domain-containing protein-3 (JMJD3) cytonuclear trans-localization with the NICD, which indicated that NICD brought JMJD3 to the EPHB4 enhancer region to decrease the H3K27me3 level.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We also found that Notch signaling pathway was abnormally activated and treatment of Notch signaling ligand human Jagged1 peptide downregulated EPHB2 and upregulated EPHB4 in the SW620 cells, as well as promoted the chromatin modification protein Jumonji domain-containing protein-3 (JMJD3) cytonuclear trans-localization with the NICD, which indicated that NICD brought JMJD3 to the EPHB4 enhancer region to decrease the H3K27me3 level.		We also found that Notch signaling pathway was abnormally activated and treatment of Notch signaling ligand human Jagged1 peptide downregulated EPHB2 and upregulated EPHB4 in the SW620 cells, as well as promoted the chromatin modification protein Jumonji domain-containing protein-3 (JMJD3) cytonuclear trans-localization with the NICD, which indicated that NICD brought JMJD3 to the EPHB4 enhancer region to decrease the H3K27me3 level.	Immunohistochemical staining	We also found that Notch signaling pathway was abnormally activated and treatment of Notch signaling ligand human Jagged1 peptide downregulated EPHB2 and upregulated EPHB4 in the SW620 cells, as well as promoted the chromatin modification protein Jumonji domain-containing protein-3 (JMJD3) cytonuclear trans-localization with the NICD, which indicated that NICD brought JMJD3 to the EPHB4 enhancer region to decrease the H3K27me3 level.			PCR，Western blot，ChIP-seq，免疫印迹法				EPHB4
30531963	chrX	48519108	48521108	EBP	However, the mechanisms underlying the induction of this phenomenon are not fully understood. Here we report that a CCAAT-Enhancer-Binding Protein (C/EBP), Xrp1	mouse		High+Lowthroughput	Xrp1 is a transcription factor required for cell competition-driven elimination of loser cells					E_02_0263	PCR，ChIP-seq	However, the mechanisms underlying the induction of this phenomenon are not fully understood. Here we report that a CCAAT-Enhancer-Binding Protein (C/EBP), Xrp1	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, the mechanisms underlying the induction of this phenomenon are not fully understood. Here we report that a CCAAT-Enhancer-Binding Protein (C/EBP), Xrp1		However, the mechanisms underlying the induction of this phenomenon are not fully understood. Here we report that a CCAAT-Enhancer-Binding Protein (C/EBP), Xrp1	Immunohistochemical staining	However, the mechanisms underlying the induction of this phenomenon are not fully understood. Here we report that a CCAAT-Enhancer-Binding Protein (C/EBP), Xrp1			PCR，ChIP-seq				EBP
30531861	chr4	121814031	121816031	CCNA2	Here, we identify a hepatocellular carcinoma (HCC) subgroup exhibiting cyclin activation through various mechanisms including hepatitis B virus (HBV) and adeno-associated virus type 2 (AAV2) insertions, enhancer hijacking and recurrent CCNA2 fusions.	human	liver	High+Lowthroughput	Cyclin A2/E1 activation defines a hepatocellular carcinoma subclass with a rearrangement signature of replication stress			Hepatocellular carcinoma		E_01_0351	PCR，Western blot，ChIP-seq	Here, we identify a hepatocellular carcinoma (HCC) subgroup exhibiting cyclin activation through various mechanisms including hepatitis B virus (HBV) and adeno-associated virus type 2 (AAV2) insertions, enhancer hijacking and recurrent CCNA2 fusions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we identify a hepatocellular carcinoma (HCC) subgroup exhibiting cyclin activation through various mechanisms including hepatitis B virus (HBV) and adeno-associated virus type 2 (AAV2) insertions, enhancer hijacking and recurrent CCNA2 fusions.		Here, we identify a hepatocellular carcinoma (HCC) subgroup exhibiting cyclin activation through various mechanisms including hepatitis B virus (HBV) and adeno-associated virus type 2 (AAV2) insertions, enhancer hijacking and recurrent CCNA2 fusions.	Immunohistochemical staining	Here, we identify a hepatocellular carcinoma (HCC) subgroup exhibiting cyclin activation through various mechanisms including hepatitis B virus (HBV) and adeno-associated virus type 2 (AAV2) insertions, enhancer hijacking and recurrent CCNA2 fusions.			PCR，Western blot，ChIP-seq				CCNA2
30529831	chr6	84684707	84686707	TBX18	Our analyses also suggest a role in atherosclerosis for developmental transcription factor genes having little or no previous association with atherosclerosis, such as NR2F2 (COUP-TFII) and TBX18.	human	blood	High+Lowthroughput	Atherosclerosis-associated differentially methylated regions can reflect the disease phenotype and are often at enhancers			atherosclerosis		E_01_0352	Differentially methylated region method	Our analyses also suggest a role in atherosclerosis for developmental transcription factor genes having little or no previous association with atherosclerosis, such as NR2F2 (COUP-TFII) and TBX18.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our analyses also suggest a role in atherosclerosis for developmental transcription factor genes having little or no previous association with atherosclerosis, such as NR2F2 (COUP-TFII) and TBX18.	Immunohistochemical staining	Our analyses also suggest a role in atherosclerosis for developmental transcription factor genes having little or no previous association with atherosclerosis, such as NR2F2 (COUP-TFII) and TBX18.	TBX18		差异甲基化区域法	Our analyses also suggest a role in atherosclerosis for developmental transcription factor genes having little or no previous association with atherosclerosis, such as NR2F2 (COUP-TFII) and TBX18.			
30979734	chr7	148804362	148806362	EZH2	Both gain-of-function EZH2 mutations and inactivating histone acetyltransferases mutations, such as CREBBP and EP300, have been implicated in the pathogenesis of germinal center (GC) derived lymphomas. 	mouse	lymphoid tissue	High+Lowthroughput	Precision Targeting with EZH2 and HDAC Inhibitors in Epigenetically Dysregulated Lymphomas	否		lymphomas		E_02_0264	Flow cytometry, Western blot, RNA seq	Both gain-of-function EZH2 mutations and inactivating histone acetyltransferases mutations, such as CREBBP and EP300, have been implicated in the pathogenesis of germinal center (GC) derived lymphomas. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Both gain-of-function EZH2 mutations and inactivating histone acetyltransferases mutations, such as CREBBP and EP300, have been implicated in the pathogenesis of germinal center (GC) derived lymphomas. 		Both gain-of-function EZH2 mutations and inactivating histone acetyltransferases mutations, such as CREBBP and EP300, have been implicated in the pathogenesis of germinal center (GC) derived lymphomas. 	Immunohistochemical staining	Both gain-of-function EZH2 mutations and inactivating histone acetyltransferases mutations, such as CREBBP and EP300, have been implicated in the pathogenesis of germinal center (GC) derived lymphomas. 			流式细胞术、Western blot、RNA-seq				EZH2
30976167	chr1	247412836	247414836	NLRP3	SF containing ginsenosides attenuates cytokine secretion by inhibiting the priming and activation steps of inflammasome activation, whereas NS induces upregulation of IL-1β precursor and nucleotide-binding and oligomerization domain (NOD)2–like receptor protein 3 (NLRP3), which are key inflammasome components, via interaction with TLR4 [4], [10]. In addition, a high dose of RGE presents a more SF predominant effect (antiinflammasome), whereas low concentration of RGE shows NS-like efficacy (proinflammasome) in macrophages [10].	mouse	epithelial cells	High+Lowthroughput	Nonsaponin fraction of Korean Red Ginseng attenuates cytokine production via inhibition of TLR4 expression	否		peritonitis		E_02_0265	RT-PCR、qPCR	SF containing ginsenosides attenuates cytokine secretion by inhibiting the priming and activation steps of inflammasome activation, whereas NS induces upregulation of IL-1β precursor and nucleotide-binding and oligomerization domain (NOD)2–like receptor protein 3 (NLRP3), which are key inflammasome components, via interaction with TLR4 [4], [10]. In addition, a high dose of RGE presents a more SF predominant effect (antiinflammasome), whereas low concentration of RGE shows NS-like efficacy (proinflammasome) in macrophages [10].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SF containing ginsenosides attenuates cytokine secretion by inhibiting the priming and activation steps of inflammasome activation, whereas NS induces upregulation of IL-1β precursor and nucleotide-binding and oligomerization domain (NOD)2–like receptor protein 3 (NLRP3), which are key inflammasome components, via interaction with TLR4 [4], [10]. In addition, a high dose of RGE presents a more SF predominant effect (antiinflammasome), whereas low concentration of RGE shows NS-like efficacy (proinflammasome) in macrophages [10].		SF containing ginsenosides attenuates cytokine secretion by inhibiting the priming and activation steps of inflammasome activation, whereas NS induces upregulation of IL-1β precursor and nucleotide-binding and oligomerization domain (NOD)2–like receptor protein 3 (NLRP3), which are key inflammasome components, via interaction with TLR4 [4], [10]. In addition, a high dose of RGE presents a more SF predominant effect (antiinflammasome), whereas low concentration of RGE shows NS-like efficacy (proinflammasome) in macrophages [10].	Immunohistochemical staining	SF containing ginsenosides attenuates cytokine secretion by inhibiting the priming and activation steps of inflammasome activation, whereas NS induces upregulation of IL-1β precursor and nucleotide-binding and oligomerization domain (NOD)2–like receptor protein 3 (NLRP3), which are key inflammasome components, via interaction with TLR4 [4], [10]. In addition, a high dose of RGE presents a more SF predominant effect (antiinflammasome), whereas low concentration of RGE shows NS-like efficacy (proinflammasome) in macrophages [10].			RT-PCR、qPCR				NLRP3
30976167	chr19	55833935	55835935	NLRP4	SF containing ginsenosides attenuates cytokine secretion by inhibiting the priming and activation steps of inflammasome activation, whereas NS induces upregulation of IL-1β precursor and nucleotide-binding and oligomerization domain (NOD)3–like receptor p	mouse	connective tissue	High+Lowthroughput	Nonsaponin fraction of Korean Red Ginseng attenuates cytokine production via inhibition of TLR5 expression	否		peritonitis		E_02_0265	RT-PCR、qPCR	SF containing ginsenosides attenuates cytokine secretion by inhibiting the priming and activation steps of inflammasome activation, whereas NS induces upregulation of IL-1β precursor and nucleotide-binding and oligomerization domain (NOD)3–like receptor p	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SF containing ginsenosides attenuates cytokine secretion by inhibiting the priming and activation steps of inflammasome activation, whereas NS induces upregulation of IL-1β precursor and nucleotide-binding and oligomerization domain (NOD)3–like receptor p		SF containing ginsenosides attenuates cytokine secretion by inhibiting the priming and activation steps of inflammasome activation, whereas NS induces upregulation of IL-1β precursor and nucleotide-binding and oligomerization domain (NOD)3–like receptor p	Immunohistochemical staining	SF containing ginsenosides attenuates cytokine secretion by inhibiting the priming and activation steps of inflammasome activation, whereas NS induces upregulation of IL-1β precursor and nucleotide-binding and oligomerization domain (NOD)3–like receptor p			RT-PCR、qPCR				NLRP4
30975980	chr7	19018300	19020300	TWIST1	SC66 also attenuated expression of TWIST1 and Mcl-1, factors important in cell invasiveness and anti-apoptosis, respectively. 	human	Epithelial tissues	High+Lowthroughput	Akt inhibitor SC66 promotes cell sensitivity to cisplatin in chemoresistant ovarian cancer cells through inhibition of COL11A1 expression	否		Epithelial ovarian carcinoma 		E_01_0353	Gene knockdown, cell transfection techniques, Western blot	SC66 also attenuated expression of TWIST1 and Mcl-1, factors important in cell invasiveness and anti-apoptosis, respectively. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			SC66 also attenuated expression of TWIST1 and Mcl-1, factors important in cell invasiveness and anti-apoptosis, respectively. 	Immunohistochemical staining	SC66 also attenuated expression of TWIST1 and Mcl-1, factors important in cell invasiveness and anti-apoptosis, respectively. 	TWIST1		基因敲降、细胞转染技术、Western blot	SC66 also attenuated expression of TWIST1 and Mcl-1, factors important in cell invasiveness and anti-apoptosis, respectively. 			
30975980	chr2	238844912	238846912	TWIST2	SC66 also attenuated expression of TWIST1 and Mcl-2, factors important in cell invasiveness and anti-apoptosis, respectively. 	human	Tumor tissues	High+Lowthroughput	Akt inhibitor SC66 promotes cell sensitivity to cisplatin in chemoresistant ovarian cancer cells through inhibition of COL11A2 expression	否		Epithelial ovarian carcinoma 		E_01_0353	Gene knockdown, cell transfection techniques, Western blot	SC66 also attenuated expression of TWIST1 and Mcl-2, factors important in cell invasiveness and anti-apoptosis, respectively. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SC66 also attenuated expression of TWIST1 and Mcl-2, factors important in cell invasiveness and anti-apoptosis, respectively. 		SC66 also attenuated expression of TWIST1 and Mcl-2, factors important in cell invasiveness and anti-apoptosis, respectively. 	Immunohistochemical staining	SC66 also attenuated expression of TWIST1 and Mcl-2, factors important in cell invasiveness and anti-apoptosis, respectively. 			基因敲降、细胞转染技术、Western blot				TWIST2
30971697	chr6	45325473	45327473	RUNX2	RUNX2 ensures the expression of pDC-signature genes in leukemic cells, but also confers survival and proliferative properties in BPDCN cells.	mouse	lymphoid tissue	High+Lowthroughput	Lineage-specific RUNX2 super-enhancer activates MYC and promotes the development of blastic plasmacytoid dendritic cell neoplasm	否		acute leukemia		E_02_0266	Immunohistochemistry, flow cytometry, DNA SEQ, RNA SEQ, RT-PCR, Western blot	RUNX2 ensures the expression of pDC-signature genes in leukemic cells, but also confers survival and proliferative properties in BPDCN cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RUNX2 ensures the expression of pDC-signature genes in leukemic cells, but also confers survival and proliferative properties in BPDCN cells.		RUNX2 ensures the expression of pDC-signature genes in leukemic cells, but also confers survival and proliferative properties in BPDCN cells.	Immunohistochemical staining	RUNX2 ensures the expression of pDC-signature genes in leukemic cells, but also confers survival and proliferative properties in BPDCN cells.			免疫组化、流式细胞术、DNA-seq、RNA-seq、RT-PCR、western blot				RUNX2
30971429	chr7	148804676	148806676	EZH2	Enhancer of zeste homolog 2 (EZH2), an epigenetic regulator that plays a key role in cell differentiation and oncogenesis, was reported to promote adipogenic differentiation in vitro by catalyzing trimethylation of histone 3 lysine 27.	mouse	adipose tissue	High+Lowthroughput	Enhancer of zeste homolog 2 (EZH2) regulates adipocyte lipid metabolism independent of adipogenic differentiation: Role of apolipoprotein E	否		prostate and breast cancer		E_02_0267	qPCR、Western blot	Enhancer of zeste homolog 2 (EZH2), an epigenetic regulator that plays a key role in cell differentiation and oncogenesis, was reported to promote adipogenic differentiation in vitro by catalyzing trimethylation of histone 3 lysine 27.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of zeste homolog 2 (EZH2), an epigenetic regulator that plays a key role in cell differentiation and oncogenesis, was reported to promote adipogenic differentiation in vitro by catalyzing trimethylation of histone 3 lysine 27.		Enhancer of zeste homolog 2 (EZH2), an epigenetic regulator that plays a key role in cell differentiation and oncogenesis, was reported to promote adipogenic differentiation in vitro by catalyzing trimethylation of histone 3 lysine 27.	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2), an epigenetic regulator that plays a key role in cell differentiation and oncogenesis, was reported to promote adipogenic differentiation in vitro by catalyzing trimethylation of histone 3 lysine 27.			qPCR、Western blot				EZH2
30970615	chr4	41253337	41255337	UCHL1	UCHL1 was associated with growth breast cancer [61]. The loss of tumor suppressor UCHL1 was responsible for the inactivation of apoptosis, as well as cisplatin resistance, in EOC 	human		High+Lowthroughput	Mining Featured Biomarkers Linked with Epithelial Ovarian CancerBased on Bioinformatics	否		Epithelial Ovarian CancerBased	ovarian cell	E_01_0354	Immunofluorescence staining	UCHL1 was associated with growth breast cancer [61]. The loss of tumor suppressor UCHL1 was responsible for the inactivation of apoptosis, as well as cisplatin resistance, in EOC 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	UCHL1 was associated with growth breast cancer [61]. The loss of tumor suppressor UCHL1 was responsible for the inactivation of apoptosis, as well as cisplatin resistance, in EOC 		UCHL1 was associated with growth breast cancer [61]. The loss of tumor suppressor UCHL1 was responsible for the inactivation of apoptosis, as well as cisplatin resistance, in EOC 	Immunohistochemical staining	UCHL1 was associated with growth breast cancer [61]. The loss of tumor suppressor UCHL1 was responsible for the inactivation of apoptosis, as well as cisplatin resistance, in EOC 			免疫荧光染色				UCHL1
30967505	chr7	148804534	148806534	EZH2	Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb Repressor Complex 2 (PRC2), the enzyme that catalyzes monomethylation, dimethylation, and trimethylation of lysine 27 on histone H3 (H3K27).	human	Ovarian tissue	High+Lowthroughput	Histone H3 tail binds a unique sensing pocket in EZH2 to activate the PRC2 methyltransferase	否		cancer		E_01_0355	gel electrophoresis	Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb Repressor Complex 2 (PRC2), the enzyme that catalyzes monomethylation, dimethylation, and trimethylation of lysine 27 on histone H3 (H3K27).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb Repressor Complex 2 (PRC2), the enzyme that catalyzes monomethylation, dimethylation, and trimethylation of lysine 27 on histone H3 (H3K27).	Immunohistochemical staining	Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb Repressor Complex 2 (PRC2), the enzyme that catalyzes monomethylation, dimethylation, and trimethylation of lysine 27 on histone H3 (H3K27).	EZH2		凝胶电泳	Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb Repressor Complex 2 (PRC2), the enzyme that catalyzes monomethylation, dimethylation, and trimethylation of lysine 27 on histone H3 (H3K27).			
30957628	chr12	131892244	131894244	ULK1	Intriguingly, RAB2 appears to modulate ULK1 kinase activity to propagate signals for autophagosome formation.	mouse		High+Lowthroughput	RAB2 regulates the formation of autophagosome and autolysosome in mammalian cells	否				E_02_0268	Immunofluorescence staining, gel electrophoresis	Intriguingly, RAB2 appears to modulate ULK1 kinase activity to propagate signals for autophagosome formation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Intriguingly, RAB2 appears to modulate ULK1 kinase activity to propagate signals for autophagosome formation.		Intriguingly, RAB2 appears to modulate ULK1 kinase activity to propagate signals for autophagosome formation.	Immunohistochemical staining	Intriguingly, RAB2 appears to modulate ULK1 kinase activity to propagate signals for autophagosome formation.			免疫荧光染色、凝胶电泳				ULK1
30955885	chr16	67559978	67561978	CTCF	Uncoupling DNA demethylation from antisense transcription by Tet3 overexpression in mouse olfactory neurons promotes CTCF binding to all Pcdhα promoters, resulting in proximity-biased DNA looping of the HS5-1 enhancer. 	human	epithelial cells	High+Lowthroughput	Antisense lncRNA Transcription Mediates DNA Demethylation to Drive Stochastic Protocadherin α Promoter Choice	否				E_01_0356	Immunofluorescence staining	Uncoupling DNA demethylation from antisense transcription by Tet3 overexpression in mouse olfactory neurons promotes CTCF binding to all Pcdhα promoters, resulting in proximity-biased DNA looping of the HS5-1 enhancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Uncoupling DNA demethylation from antisense transcription by Tet3 overexpression in mouse olfactory neurons promotes CTCF binding to all Pcdhα promoters, resulting in proximity-biased DNA looping of the HS5-1 enhancer. 	Immunohistochemical staining	Uncoupling DNA demethylation from antisense transcription by Tet3 overexpression in mouse olfactory neurons promotes CTCF binding to all Pcdhα promoters, resulting in proximity-biased DNA looping of the HS5-1 enhancer. 	CTCF		免疫荧光染色	Uncoupling DNA demethylation from antisense transcription by Tet3 overexpression in mouse olfactory neurons promotes CTCF binding to all Pcdhα promoters, resulting in proximity-biased DNA looping of the HS5-1 enhancer. 			
30952976	chr3	194133551	194135551	HES1	We identify transcriptional repressor - hairy and enhancer of split-1 (HES1) - as a mediator of the OGT inhibition response in the TNBC cells. 	human		High+Lowthroughput	O-GlcNAc Transferase Inhibition Differentially Affects Breast Cancer Subtypes	否		Affects Breast Cancer		E_01_0357	Western blot, gene knockdown	We identify transcriptional repressor - hairy and enhancer of split-1 (HES1) - as a mediator of the OGT inhibition response in the TNBC cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We identify transcriptional repressor - hairy and enhancer of split-1 (HES1) - as a mediator of the OGT inhibition response in the TNBC cells. 	Immunohistochemical staining	We identify transcriptional repressor - hairy and enhancer of split-1 (HES1) - as a mediator of the OGT inhibition response in the TNBC cells. 	HES1		Western blot、基因敲降	We identify transcriptional repressor - hairy and enhancer of split-1 (HES1) - as a mediator of the OGT inhibition response in the TNBC cells. 			
30952632	chr3	181709362	181711362	SOX2	The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,2) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generation AR antagonist enzalutamide (Enz), or the androgen-biosynthesis inhibitor abiraterone acetate (3–7). Further, elevated expression of the glucocorticoid receptor can bypass dependence on the AR by promiscuously activating AR target genes (8) or through lineage plasticity driven by SOX2	mouse		High+Lowthroughput	Activation of MAPK Signaling by CXCR7 Leads to Enzalutamide Resistance in Prostate Cancer	否		Prostate Cancer		E_02_0269	Immunofluorescence staining, immunohistochemistry	The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,2) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generation AR antagonist enzalutamide (Enz), or the androgen-biosynthesis inhibitor abiraterone acetate (3–7). Further, elevated expression of the glucocorticoid receptor can bypass dependence on the AR by promiscuously activating AR target genes (8) or through lineage plasticity driven by SOX2	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,2) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generation AR antagonist enzalutamide (Enz), or the androgen-biosynthesis inhibitor abiraterone acetate (3–7). Further, elevated expression of the glucocorticoid receptor can bypass dependence on the AR by promiscuously activating AR target genes (8) or through lineage plasticity driven by SOX2		The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,2) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generation AR antagonist enzalutamide (Enz), or the androgen-biosynthesis inhibitor abiraterone acetate (3–7). Further, elevated expression of the glucocorticoid receptor can bypass dependence on the AR by promiscuously activating AR target genes (8) or through lineage plasticity driven by SOX2	Immunohistochemical staining	The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,2) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generation AR antagonist enzalutamide (Enz), or the androgen-biosynthesis inhibitor abiraterone acetate (3–7). Further, elevated expression of the glucocorticoid receptor can bypass dependence on the AR by promiscuously activating AR target genes (8) or through lineage plasticity driven by SOX2			免疫荧光染色、免疫组化				SOX2
30952632	chrX	140500580	140502580	SOX3	The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,3) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat	mouse		High+Lowthroughput	Activation of MAPK Signaling by CXCR8 Leads to Enzalutamide Resistance in Prostate Cancer	否		Prostate Cancer		E_02_0269	Immunofluorescence staining, immunohistochemistry	The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,3) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,3) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat		The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,3) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat	Immunohistochemical staining	The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,3) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat			免疫荧光染色、免疫组化				SOX3
30952632	chr6	21591137	21593137	SOX4	The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,4) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat&	mouse		High+Lowthroughput	Activation of MAPK Signaling by CXCR9 Leads to Enzalutamide Resistance in Prostate Cancer	否		Prostate Cancer		E_02_0269	Immunofluorescence staining, immunohistochemistry	The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,4) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat&	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,4) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat&		The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,4) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat&	Immunohistochemical staining	The androgen receptor (AR) is a major driver of the growth of prostate cancer (PCa) (1,4) and aberrant AR signaling remains to play major roles in final-stage castration-resistant prostate cancer (CRPC) that have developed resistance to the second-generat&			免疫荧光染色、免疫组化				SOX4
30948729	chr1	27662995	27664995	IFI6	Taken together, this study reveals a non-canonical function for CTCF-s that antagonizes the genomic binding of canonical CTCF and cohesin, and that modulates chromatin looping and causes apoptosis by stimulating IFI6 expression.	human	Epithelial tissues	High+Lowthroughput	An alternative CTCF isoform antagonizes canonical CTCF occupancy and changes chromatin architecture to promote apoptosis	否				E_01_0358	QRT PCR, Western blot, immunofluorescence staining, gel electrophoresis, chip SEQ, RNA seq	Taken together, this study reveals a non-canonical function for CTCF-s that antagonizes the genomic binding of canonical CTCF and cohesin, and that modulates chromatin looping and causes apoptosis by stimulating IFI6 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, this study reveals a non-canonical function for CTCF-s that antagonizes the genomic binding of canonical CTCF and cohesin, and that modulates chromatin looping and causes apoptosis by stimulating IFI6 expression.		Taken together, this study reveals a non-canonical function for CTCF-s that antagonizes the genomic binding of canonical CTCF and cohesin, and that modulates chromatin looping and causes apoptosis by stimulating IFI6 expression.	Immunohistochemical staining	Taken together, this study reveals a non-canonical function for CTCF-s that antagonizes the genomic binding of canonical CTCF and cohesin, and that modulates chromatin looping and causes apoptosis by stimulating IFI6 expression.			qRT-PCR、Western blot、免疫荧光染色、凝胶电泳、ChIP-seq、RNA-seq 				IFI6
30947238	chr7	22723017	22725017	IL6	 The α7 nAChR partial agonist GTS-21 reduces secretion of pro-inflammatory cytokines including interleukin-6 (IL6) and tumor-necrosis factor (TNF) in models of endotoxemia and sepsis, and its anti-inflammatory effects are widely ascribed to α7 nAChR activation. 	mouse		High+Lowthroughput	GTS-21 has cell-specific anti-inflammatory effects independent of α7 nicotinic acetylcholine receptors	否		inflammatory		E_02_0270	Western blot、	 The α7 nAChR partial agonist GTS-21 reduces secretion of pro-inflammatory cytokines including interleukin-6 (IL6) and tumor-necrosis factor (TNF) in models of endotoxemia and sepsis, and its anti-inflammatory effects are widely ascribed to α7 nAChR activation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 The α7 nAChR partial agonist GTS-21 reduces secretion of pro-inflammatory cytokines including interleukin-6 (IL6) and tumor-necrosis factor (TNF) in models of endotoxemia and sepsis, and its anti-inflammatory effects are widely ascribed to α7 nAChR activation. 		 The α7 nAChR partial agonist GTS-21 reduces secretion of pro-inflammatory cytokines including interleukin-6 (IL6) and tumor-necrosis factor (TNF) in models of endotoxemia and sepsis, and its anti-inflammatory effects are widely ascribed to α7 nAChR activation. 	Immunohistochemical staining	 The α7 nAChR partial agonist GTS-21 reduces secretion of pro-inflammatory cytokines including interleukin-6 (IL6) and tumor-necrosis factor (TNF) in models of endotoxemia and sepsis, and its anti-inflammatory effects are widely ascribed to α7 nAChR activation. 			Western blot、				IL6
30945396	chr20	50187983	50189983	CEBPB	Mechanically, PGC1α binds to CCAAT/enhancer binding protein β (CEBPB), a member of the transcription factor family of CEBP, to promote CPT1A transcription, resulting in activation of FAO. 	human	epithelial cells	High+Lowthroughput	PGC1α/CEBPB/CPT1A axis promotes radiation resistance of nasopharyngeal carcinoma through activating fatty acid oxidation	否		nasopharyngeal carcinoma		E_01_0359	Western blot, immunohistochemistry	Mechanically, PGC1α binds to CCAAT/enhancer binding protein β (CEBPB), a member of the transcription factor family of CEBP, to promote CPT1A transcription, resulting in activation of FAO. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mechanically, PGC1α binds to CCAAT/enhancer binding protein β (CEBPB), a member of the transcription factor family of CEBP, to promote CPT1A transcription, resulting in activation of FAO. 	Immunohistochemical staining	Mechanically, PGC1α binds to CCAAT/enhancer binding protein β (CEBPB), a member of the transcription factor family of CEBP, to promote CPT1A transcription, resulting in activation of FAO. 	CEBPB		Western blot、免疫组化	Mechanically, PGC1α binds to CCAAT/enhancer binding protein β (CEBPB), a member of the transcription factor family of CEBP, to promote CPT1A transcription, resulting in activation of FAO. 			
30910956	chr17	40306219	40308219	RARA	Among them, rs10772119 and rs883868 disrupt the binding of retinoic acid receptor α (RARA) and Yin and Yang 1 (YY1), respectively.	human		High+Lowthroughput	Risk variants disrupting enhancers of T(H)1 and T(REG) cells in type 2 diabetes	是	10772120	type 2 diabetes	islet cell	E_01_0360	ChIP-Seq	Among them, rs10772119 and rs883868 disrupt the binding of retinoic acid receptor α (RARA) and Yin and Yang 1 (YY1), respectively.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Among them, rs10772119 and rs883868 disrupt the binding of retinoic acid receptor α (RARA) and Yin and Yang 1 (YY1), respectively.	Immunohistochemical staining	Among them, rs10772119 and rs883868 disrupt the binding of retinoic acid receptor α (RARA) and Yin and Yang 1 (YY1), respectively.	RARA		ChIP-Seq	Among them, rs10772119 and rs883868 disrupt the binding of retinoic acid receptor α (RARA) and Yin and Yang 1 (YY1), respectively.			
30910956	chr14	100235453	100237453	YY1	Among them, rs10772119 and rs883868 disrupt the binding of retinoic acid receptor α (RARA) and Yin and Yang 1 (YY1), respectively.	human		High+Lowthroughput	Risk variants disrupting enhancers of T(H)1 and T(REG) cells in type 2 diabetes	是	10772120	type 2 diabetes	islet cell	E_01_0360	ChIP-Seq	Among them, rs10772119 and rs883868 disrupt the binding of retinoic acid receptor α (RARA) and Yin and Yang 1 (YY1), respectively.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Among them, rs10772119 and rs883868 disrupt the binding of retinoic acid receptor α (RARA) and Yin and Yang 1 (YY1), respectively.	Immunohistochemical staining	Among them, rs10772119 and rs883868 disrupt the binding of retinoic acid receptor α (RARA) and Yin and Yang 1 (YY1), respectively.	YY1		ChIP-Seq	Among them, rs10772119 and rs883868 disrupt the binding of retinoic acid receptor α (RARA) and Yin and Yang 1 (YY1), respectively.			
30905509	chr3	133743290	133745290	TF	"This process is important
to understand because induced pluripotency in somatic cells
represents reversal of ontogeny and transcription factor (TF)-
based reprogramming can leave vestiges of the original cell
lineage."	human	Epithelial tissues	High+Lowthroughput	Extensive Recovery of Embryonic Enhancer and Gene Memory Stored in Hypomethylated Enhancer DNA	否			enterocyte of epithelium of intestinal vi	E_01_0361	ChIP-seq	"This process is important
to understand because induced pluripotency in somatic cells
represents reversal of ontogeny and transcription factor (TF)-
based reprogramming can leave vestiges of the original cell
lineage."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"This process is important
to understand because induced pluripotency in somatic cells
represents reversal of ontogeny and transcription factor (TF)-
based reprogramming can leave vestiges of the original cell
lineage."		"This process is important
to understand because induced pluripotency in somatic cells
represents reversal of ontogeny and transcription factor (TF)-
based reprogramming can leave vestiges of the original cell
lineage."	Immunohistochemical staining	"This process is important
to understand because induced pluripotency in somatic cells
represents reversal of ontogeny and transcription factor (TF)-
based reprogramming can leave vestiges of the original cell
lineage."			ChIP-seq				TF
30903020	chr7	148804044	148806044	EZH2	Robust expression of EZH2 in endocervical neoplastic lesions.	human		High+Lowthroughput	Bromodomain and extraterminal proteins foster the core transcriptional regulatory programs and confer vulnerability in liposarcoma	否			fat cell	E_01_0362	Chip SEQ, QRT PCR, Western blot test	Robust expression of EZH2 in endocervical neoplastic lesions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Robust expression of EZH2 in endocervical neoplastic lesions.	Immunohistochemical staining	Robust expression of EZH2 in endocervical neoplastic lesions.	EZH2		ChIP-seq、qRT-PCR、免疫印迹测试	Robust expression of EZH2 in endocervical neoplastic lesions.			
30901906	chr2	28389918	28391918	FOSL2	We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.	human	connective tissue	High+Lowthroughput	WNT3a and WNT5a Transported by Exosomes Activate WNT Signaling Pathways in Human Cardiac Fibroblasts	否				E_01_0363	Immunofluorescence staining, Western blot RT PCR	We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.	Immunohistochemical staining	We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.	FOSL2		免疫荧光染色、Western blotRT-PCR	We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.			
30901906	chr8	127732441	127734441	MYC	We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.	human	connective tissue	High+Lowthroughput	WNT3a and WNT5a Transported by Exosomes Activate WNT Signaling Pathways in Human Cardiac Fibroblasts	否				E_01_0363	Immunofluorescence staining, Western blot RT PCR	We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.	Immunohistochemical staining	We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.	MYC		免疫荧光染色、Western blotRT-PCR	We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.			
30901906	chr21	34784734	34786734	RUNX1	We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.	human	connective tissue	High+Lowthroughput	WNT3a and WNT5a Transported by Exosomes Activate WNT Signaling Pathways in Human Cardiac Fibroblasts	否				E_01_0363	Immunofluorescence staining, Western blot RT PCR	We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.	Immunohistochemical staining	We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.	RUNX1		免疫荧光染色、Western blotRT-PCR	We identify a bromodomain and extraterminal (BET) protein-cooperated FUS-DDIT3 function in myxoid LPS and a BET protein-dependent core transcriptional regulatory circuitry consisting of FOSL2, MYC, and RUNX1 in de-differentiated LPS.			
30899425	chr12	55722375	55724375	CD63	Obtained exosomes showed size ranging between 20⁻150 nm and expressed exosomal markers ALG-2-interacting protein X (ALIX) and CD63.	human		High+Lowthroughput	Super-enhancers: novel target for pancreatic ductal adenocarcinoma	否		pancreatic ductal adenocarcinoma		E_01_0364	Chip SEQ, Western blot, PCR, immunohistochemistry, immunofluorescence staining	Obtained exosomes showed size ranging between 20⁻150 nm and expressed exosomal markers ALG-2-interacting protein X (ALIX) and CD63.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Obtained exosomes showed size ranging between 20⁻150 nm and expressed exosomal markers ALG-2-interacting protein X (ALIX) and CD63.		Obtained exosomes showed size ranging between 20⁻150 nm and expressed exosomal markers ALG-2-interacting protein X (ALIX) and CD63.	Immunohistochemical staining	Obtained exosomes showed size ranging between 20⁻150 nm and expressed exosomal markers ALG-2-interacting protein X (ALIX) and CD63.			ChIP-Seq、Western blot、PCR、免疫组化、免疫荧光染色				CD63
30898391	chr17	39401325	39403325	MED1	Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.	human	Kidney tissue	High+Lowthroughput	Genome-wide association studies identify susceptibility loci for epithelial ovarian cancer in east Asian women	是	7748275	epithelial ovarian cancer		E_01_0365	Bioinformatic prediction	Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.	Immunohistochemical staining	Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.	MED1		生物信息学预测	Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.			
30898391	chr12	7785014	7787014	NANOG	Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.	human	Kidney tissue	High+Lowthroughput	Genome-wide association studies identify susceptibility loci for epithelial ovarian cancer in east Asian women	是	7748275	epithelial ovarian cancer		E_01_0365	Bioinformatic prediction	Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.		Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.	Immunohistochemical staining	Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.			生物信息学预测				NANOG
30898391	chr3	181709439	181711439	SOX2	Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.	human	Kidney tissue	High+Lowthroughput	Genome-wide association studies identify susceptibility loci for epithelial ovarian cancer in east Asian women	是	7748275	epithelial ovarian cancer		E_01_0365	Bioinformatic prediction	Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.	Immunohistochemical staining	Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.	SOX2		生物信息学预测	Differential H3K27AC marks were identified at enhancer regions of genes including c-MYC, MED1, OCT-4, NANOG, and SOX2 that can act as SE in non-cancerous, cancerous and metastatic PDAC cell lines.			
30898391	chr2	238097903	238099903	ESPNL	At 2q37.3, expression quantitative trait locus analysis in 404 HGSOC tissues identified ESPNL as a putative candidate susceptibility gene .	human	Epithelial tissues	High+Lowthroughput	Genome-wide association studies identify susceptibility loci for epithelial ovarian cancer in east Asian women	是	6902488	epithelial ovarian cancer	ovarian cell	E_01_0365	Bioinformatic prediction	At 2q37.3, expression quantitative trait locus analysis in 404 HGSOC tissues identified ESPNL as a putative candidate susceptibility gene .	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	At 2q37.3, expression quantitative trait locus analysis in 404 HGSOC tissues identified ESPNL as a putative candidate susceptibility gene .		At 2q37.3, expression quantitative trait locus analysis in 404 HGSOC tissues identified ESPNL as a putative candidate susceptibility gene .	Immunohistochemical staining	At 2q37.3, expression quantitative trait locus analysis in 404 HGSOC tissues identified ESPNL as a putative candidate susceptibility gene .			生物信息学预测				ESPNL
30894209	chr12	52484679	52486679	KRT6A	This study aimed to study the mechanisms of ectopic keratin 6A (KRT6A) in NPC.	human		High+Lowthroughput	Hypoxia-induced miR-191-C/EBPβ signaling regulates cell proliferation and apoptosis of fibroblast-like synoviocytes from patients with rheumatoid arthritis	否		rheumatoid arthritis		E_01_0366	RT-PCR, cell transfection techniques, Western blot	This study aimed to study the mechanisms of ectopic keratin 6A (KRT6A) in NPC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This study aimed to study the mechanisms of ectopic keratin 6A (KRT6A) in NPC.		This study aimed to study the mechanisms of ectopic keratin 6A (KRT6A) in NPC.	Immunohistochemical staining	This study aimed to study the mechanisms of ectopic keratin 6A (KRT6A) in NPC.			RT-PCR、细胞转染技术、Western blot				KRT6A
30892634	chr19	16322108	16324108	KLF2	KLF2 (kruppel-like factor 2 [lung]) regulates osteoclastogenesis by modulating autophagy.	human		High+Lowthroughput	PLZF limits enhancer activity during hematopoietic progenitor aging	否				E_01_0367	RT qPCR, immunofluorescence staining, Western blot, ATAC seq	KLF2 (kruppel-like factor 2 [lung]) regulates osteoclastogenesis by modulating autophagy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			KLF2 (kruppel-like factor 2 [lung]) regulates osteoclastogenesis by modulating autophagy.	Immunohistochemical staining	KLF2 (kruppel-like factor 2 [lung]) regulates osteoclastogenesis by modulating autophagy.	KLF2		RT-qPCR、免疫荧光染色、Western blot、ATAC-seq	KLF2 (kruppel-like factor 2 [lung]) regulates osteoclastogenesis by modulating autophagy.			
30892142	chr3	108040340	108042340	CD47	CD47 enhancer-FIREFLY vec_x0002_tor was generated from the previously described construct CD47-E5.	human		High+Lowthroughput	The Transcription Factor ERG Regulates Super-Enhancers Associated With an Endothelial-Specific Gene Expression Program	是				E_01_0368	ChIP-seq	CD47 enhancer-FIREFLY vec_x0002_tor was generated from the previously described construct CD47-E5.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			CD47 enhancer-FIREFLY vec_x0002_tor was generated from the previously described construct CD47-E5.	Immunohistochemical staining	CD47 enhancer-FIREFLY vec_x0002_tor was generated from the previously described construct CD47-E5.	CD47		ChIP-seq	CD47 enhancer-FIREFLY vec_x0002_tor was generated from the previously described construct CD47-E5.			
30891136	chr21	38377346	38379346	ERG	The Transcription Factor ERG Regulates Super-Enhancers Associated With an Endothelial-Specific Gene Expression Program.	mouse	Cancer tissues	High+Lowthroughput	(18)F-Labeled PET Probe Targeting Enhancer of Zeste Homologue 2 (EZH2) for Cancer Imaging	否				E_02_0271	gel electrophoresis	The Transcription Factor ERG Regulates Super-Enhancers Associated With an Endothelial-Specific Gene Expression Program.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The Transcription Factor ERG Regulates Super-Enhancers Associated With an Endothelial-Specific Gene Expression Program.		The Transcription Factor ERG Regulates Super-Enhancers Associated With an Endothelial-Specific Gene Expression Program.	Immunohistochemical staining	The Transcription Factor ERG Regulates Super-Enhancers Associated With an Endothelial-Specific Gene Expression Program.			凝胶电泳				ERG
30891136	chr7	148804816	148806816	EZH2	(18)F-Labeled PET Probe Targeting Enhancer of Zeste Homologue 2 (EZH2) for Cancer Imaging	mouse	Cancer tissues	High+Lowthroughput	(18)F-Labeled PET Probe Targeting Enhancer of Zeste Homologue 2 (EZH3) for Cancer Imaging	否				E_02_0271	gel electrophoresis	(18)F-Labeled PET Probe Targeting Enhancer of Zeste Homologue 2 (EZH2) for Cancer Imaging	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	(18)F-Labeled PET Probe Targeting Enhancer of Zeste Homologue 2 (EZH2) for Cancer Imaging		(18)F-Labeled PET Probe Targeting Enhancer of Zeste Homologue 2 (EZH2) for Cancer Imaging	Immunohistochemical staining	(18)F-Labeled PET Probe Targeting Enhancer of Zeste Homologue 2 (EZH2) for Cancer Imaging			凝胶电泳				EZH2
30888859	chr3	10139527	10141527	VHL	Renal cell carcinoma (RCC) is the major cause of death among patients with von Hippel-Lindau (VHL) disease.	human		High+Lowthroughput	AMPK and PPARβ positive feedback loop regulates endurance exercise training-mediated GLUT4 expression in skeletal muscle	否				E_01_0369	Western blot, immunofluorescence staining	Renal cell carcinoma (RCC) is the major cause of death among patients with von Hippel-Lindau (VHL) disease.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Renal cell carcinoma (RCC) is the major cause of death among patients with von Hippel-Lindau (VHL) disease.	Immunohistochemical staining	Renal cell carcinoma (RCC) is the major cause of death among patients with von Hippel-Lindau (VHL) disease.	VHL		Western blot、免疫荧光染色	Renal cell carcinoma (RCC) is the major cause of death among patients with von Hippel-Lindau (VHL) disease.			
30886108	chr15	99562658	99564658	MEF2A	We discovered that AMPK activation increases PPARβ via myocyte enhancer factor 2A (MEF2A), which acted as a transcription factor for PPARβ.	human		High+Lowthroughput	Gene activation precedes DNA demethylation in response to infection in human dendritic cells	否				E_01_0370	Gene knockdown	We discovered that AMPK activation increases PPARβ via myocyte enhancer factor 2A (MEF2A), which acted as a transcription factor for PPARβ.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We discovered that AMPK activation increases PPARβ via myocyte enhancer factor 2A (MEF2A), which acted as a transcription factor for PPARβ.	Immunohistochemical staining	We discovered that AMPK activation increases PPARβ via myocyte enhancer factor 2A (MEF2A), which acted as a transcription factor for PPARβ.	MEF2A		基因敲降	We discovered that AMPK activation increases PPARβ via myocyte enhancer factor 2A (MEF2A), which acted as a transcription factor for PPARβ.			
30884312	chr15	99563063	99565063	MEF2A	MEF2A alters the proliferation, inflammation-related gene expression profiles and its silencing induces cellular senescence in human coronary endothelial cells.	human	Cancer tissues	High+Lowthroughput	PRISMA: Protein Interaction Screen on Peptide Matrix Reveals Interaction Footprints and Modifications- Dependent Interactome of Intrinsically Disordered C/EBPβ	否		preeclampsia		E_01_0371	Bioinformatic predictions	MEF2A alters the proliferation, inflammation-related gene expression profiles and its silencing induces cellular senescence in human coronary endothelial cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MEF2A alters the proliferation, inflammation-related gene expression profiles and its silencing induces cellular senescence in human coronary endothelial cells.	Immunohistochemical staining	MEF2A alters the proliferation, inflammation-related gene expression profiles and its silencing induces cellular senescence in human coronary endothelial cells.	MEF2A		生物药信息学预测	MEF2A alters the proliferation, inflammation-related gene expression profiles and its silencing induces cellular senescence in human coronary endothelial cells.			
30881868	chr16	56426207	56428207	NUDT21	The role of NUDT21 in microRNA-binging sites of EZH2 gene increases the of risk preeclampsia.	human		High+Lowthroughput	ILF2 Directly Binds and Stabilizes CREB to Stimulate Malignant Phenotypes of Liver Cancer Cells	否				E_01_0372	Immunohistochemistry, immunofluorescence staining, Western blot	The role of NUDT21 in microRNA-binging sites of EZH2 gene increases the of risk preeclampsia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The role of NUDT21 in microRNA-binging sites of EZH2 gene increases the of risk preeclampsia.		The role of NUDT21 in microRNA-binging sites of EZH2 gene increases the of risk preeclampsia.	Immunohistochemical staining	The role of NUDT21 in microRNA-binging sites of EZH2 gene increases the of risk preeclampsia.			免疫组化、免疫荧光染色、Western blot				NUDT21
30881868	chr7	148804780	148806780	EZH2	The role of NUDT21 in microRNA-binging sites of EZH2 gene increases the of risk preeclampsia.	human		High+Lowthroughput	ILF2 Directly Binds and Stabilizes CREB to Stimulate Malignant Phenotypes of Liver Cancer Cells	否				E_01_0372	Immunohistochemistry, immunofluorescence staining, Western blot	The role of NUDT21 in microRNA-binging sites of EZH2 gene increases the of risk preeclampsia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The role of NUDT21 in microRNA-binging sites of EZH2 gene increases the of risk preeclampsia.	Immunohistochemical staining	The role of NUDT21 in microRNA-binging sites of EZH2 gene increases the of risk preeclampsia.	EZH2		免疫组化、免疫荧光染色、Western blot	The role of NUDT21 in microRNA-binging sites of EZH2 gene increases the of risk preeclampsia.			
30881490	chr1	153658951	153660951	ILF2	ILF2 Directly Binds and Stabilizes CREB to Stimulate Malignant Phenotypes of Liver Cancer Cells.	human		High+Lowthroughput	The oncogenic role of Wnt10a in colorectal cancer through activation of canonical Wnt/β-catenin signaling	否		CRC		E_01_0373	RT qPCR, Western blot / cell transfection	ILF2 Directly Binds and Stabilizes CREB to Stimulate Malignant Phenotypes of Liver Cancer Cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ILF2 Directly Binds and Stabilizes CREB to Stimulate Malignant Phenotypes of Liver Cancer Cells.		ILF2 Directly Binds and Stabilizes CREB to Stimulate Malignant Phenotypes of Liver Cancer Cells.	Immunohistochemical staining	ILF2 Directly Binds and Stabilizes CREB to Stimulate Malignant Phenotypes of Liver Cancer Cells.			RT-qPCR、Western blot/细胞转染技术				ILF2
30879360	chr7	148804532	148806532	EZH2	EZH2 Inhibition in Ewing Sarcoma Upregulates G(D2) Expression for Targeting with Gene-Modified T Cells.	human		High+Lowthroughput	Retinoic Acid Is a Negative Regulator of sFLT1 Expression in Decidual Stromal Cells, and Its Levels Are Reduced in Preeclamptic Decidua	否				E_01_0374	PCR, Western blot, immunofluorescence staining	EZH2 Inhibition in Ewing Sarcoma Upregulates G(D2) Expression for Targeting with Gene-Modified T Cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2 Inhibition in Ewing Sarcoma Upregulates G(D2) Expression for Targeting with Gene-Modified T Cells.	Immunohistochemical staining	EZH2 Inhibition in Ewing Sarcoma Upregulates G(D2) Expression for Targeting with Gene-Modified T Cells.	EZH2		PCR、Western blot、免疫荧光染色	EZH2 Inhibition in Ewing Sarcoma Upregulates G(D2) Expression for Targeting with Gene-Modified T Cells.			
33411777	chr7	50301051	50303051	IKZF1	Enhancer polymorphisms at the IKZF1 susceptibility locus for acute lymphoblastic leukemia impact B-cell proliferation and differentiation in both Down syndrome and non-Down syndrome genetic backgrounds.	mouse	lymphoid tissue	High+Lowthroughput	Enhancer polymorphisms at the IKZF2 susceptibility locus for acute lymphoblastic leukemia impact B-cell proliferation and differentiation in both Down syndrome and non-Down syndrome genetic backgrounds	是	6964969	lymphoblastic leukemia	hematopoietic stem cell	E_02_0272	PCR, gel electrophoresis, SNP sequencing technology, statistical analysis	Enhancer polymorphisms at the IKZF1 susceptibility locus for acute lymphoblastic leukemia impact B-cell proliferation and differentiation in both Down syndrome and non-Down syndrome genetic backgrounds.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer polymorphisms at the IKZF1 susceptibility locus for acute lymphoblastic leukemia impact B-cell proliferation and differentiation in both Down syndrome and non-Down syndrome genetic backgrounds.		Enhancer polymorphisms at the IKZF1 susceptibility locus for acute lymphoblastic leukemia impact B-cell proliferation and differentiation in both Down syndrome and non-Down syndrome genetic backgrounds.	Immunohistochemical staining	Enhancer polymorphisms at the IKZF1 susceptibility locus for acute lymphoblastic leukemia impact B-cell proliferation and differentiation in both Down syndrome and non-Down syndrome genetic backgrounds.			PCR、凝胶电泳、SNP测序技术、统计分析				IKZF1
33124415	chr9	70381888	70383888	KLF9	Genomic determinants implicated in the glucocorticoid-mediated induction of KLF9 in pulmonary epithelial cells.	human		High+Lowthroughput	Mass Spectrometry-Based Metabolic Fingerprinting Contributes to Unveil the Role of RSUME in Renal Cell Carcinoma Cell Metabolism.	否		Clear cell renal cell carcinoma	Renal cell	E_01_0375	Cell transfection techniques, PCR	Genomic determinants implicated in the glucocorticoid-mediated induction of KLF9 in pulmonary epithelial cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Genomic determinants implicated in the glucocorticoid-mediated induction of KLF9 in pulmonary epithelial cells.	Immunohistochemical staining	Genomic determinants implicated in the glucocorticoid-mediated induction of KLF9 in pulmonary epithelial cells.	KLF9		细胞转染技术、PCR	Genomic determinants implicated in the glucocorticoid-mediated induction of KLF9 in pulmonary epithelial cells.			
32602275	chr3	10138986	10140986	VHL	Clear cell renal cell carcinoma (ccRCC) is a heterogeneous disease with 50-80% patients exhibiting mutations in the von Hippel-Lindau (VHL) gene.	human	Epithelial tissues	High+Lowthroughput	Enhancer-Gene Interaction Analyses Identified the Epidermal Growth Factor Receptor as a Susceptibility Gene for Type 2 Diabetes Mellitus.	是	4947941	type 2 diabetes	islet cell	E_01_0376	Bioinformatic prediction	Clear cell renal cell carcinoma (ccRCC) is a heterogeneous disease with 50-80% patients exhibiting mutations in the von Hippel-Lindau (VHL) gene.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Clear cell renal cell carcinoma (ccRCC) is a heterogeneous disease with 50-80% patients exhibiting mutations in the von Hippel-Lindau (VHL) gene.	Immunohistochemical staining	Clear cell renal cell carcinoma (ccRCC) is a heterogeneous disease with 50-80% patients exhibiting mutations in the von Hippel-Lindau (VHL) gene.	VHL		生物信息学预测	Clear cell renal cell carcinoma (ccRCC) is a heterogeneous disease with 50-80% patients exhibiting mutations in the von Hippel-Lindau (VHL) gene.			
32602275	chr7	55016309	55018309	EGFR	The SNP rs4947941 was annotated as an enhancer, and rs7785013 was located in the epidermal growth factor receptor (EGFR) gene.	human	Epithelial tissues	High+Lowthroughput		是	7785013	type 3 diabetes	islet cell	E_01_0376	Bioinformatic prediction	The SNP rs4947941 was annotated as an enhancer, and rs7785013 was located in the epidermal growth factor receptor (EGFR) gene.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The SNP rs4947941 was annotated as an enhancer, and rs7785013 was located in the epidermal growth factor receptor (EGFR) gene.	Immunohistochemical staining	The SNP rs4947941 was annotated as an enhancer, and rs7785013 was located in the epidermal growth factor receptor (EGFR) gene.	EGFR		生物信息学预测	The SNP rs4947941 was annotated as an enhancer, and rs7785013 was located in the epidermal growth factor receptor (EGFR) gene.			
31733305	chr4	152317572	152319572	FBXW7	FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.	human	Endothelial tissue	High+Lowthroughput	The novel axis of YAP1, transcription enhancer factor 3 and Down Syndrome Candidate Region 1 isoform 1L is a common signaling pathway downstream of several angiogenic factors.	否			endothelial cell	E_01_0377	PCR, gel electrophoresis, gene knockdown, immunofluorescence staining	FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.	Immunohistochemical staining	FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.	FBXW7		PCR、凝胶电泳、基因敲降、免疫荧光染色	FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.			
31733305	chr7	148804425	148806425	EZH2	FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.	human	Endothelial tissue	High+Lowthroughput	The novel axis of YAP1, transcription enhancer factor 3 and Down Syndrome Candidate Region 1 isoform 1L is a common signaling pathway downstream of several angiogenic factors.	否			endothelial cell	E_01_0377	PCR, gel electrophoresis, gene knockdown, immunofluorescence staining	FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.	Immunohistochemical staining	FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.	EZH2		PCR、凝胶电泳、基因敲降、免疫荧光染色	FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.			
31733305	chr14	60641305	60643305	SIX1	FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.	human	Endothelial tissue	High+Lowthroughput	The novel axis of YAP1, transcription enhancer factor 3 and Down Syndrome Candidate Region 1 isoform 1L is a common signaling pathway downstream of several angiogenic factors.	否			endothelial cell	E_01_0377	PCR, gel electrophoresis, gene knockdown, immunofluorescence staining	FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.		FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.	Immunohistochemical staining	FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling.			PCR、凝胶电泳、基因敲降、免疫荧光染色				SIX1
31076403	chr11	102107558	102109558	YAP1	The novel axis of YAP1, transcription enhancer factor 3 and Down Syndrome Candidate Region 1 isoform 1L is a common signaling pathway downstream of several angiogenic factors.	mouse	Immunohistochem	High+Lowthroughput	Targeting monocyte-intrinsic enhancer reprogramming improves immunotherapy efficacy in hepatocellular carcinoma.	否		 hepatocellular carcinoma	Myeloid-derived suppressor cell	E_02_0273	Flow cytometry, immunofluorescence staining	The novel axis of YAP1, transcription enhancer factor 3 and Down Syndrome Candidate Region 1 isoform 1L is a common signaling pathway downstream of several angiogenic factors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The novel axis of YAP1, transcription enhancer factor 3 and Down Syndrome Candidate Region 1 isoform 1L is a common signaling pathway downstream of several angiogenic factors.		The novel axis of YAP1, transcription enhancer factor 3 and Down Syndrome Candidate Region 1 isoform 1L is a common signaling pathway downstream of several angiogenic factors.	Immunohistochemical staining	The novel axis of YAP1, transcription enhancer factor 3 and Down Syndrome Candidate Region 1 isoform 1L is a common signaling pathway downstream of several angiogenic factors.			流式细胞术、免疫荧光染色				YAP1
32408759	chr15	99562918	99564918	MEF2A	MEF2A alters the proliferation, inflammation-related gene expression profiles and its silencing induces cellular senescence in human coronary endothelial cells.	human	Embryonic tissues	High+Lowthroughput	Variants in miRNA regulome and their association with the risk of nonsyndromi corofacial clefts	否		nonsyndromic orofacial clefts	embryonic cell 	E_01_0378	PCR	MEF2A alters the proliferation, inflammation-related gene expression profiles and its silencing induces cellular senescence in human coronary endothelial cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MEF2A alters the proliferation, inflammation-related gene expression profiles and its silencing induces cellular senescence in human coronary endothelial cells.	Immunohistochemical staining	MEF2A alters the proliferation, inflammation-related gene expression profiles and its silencing induces cellular senescence in human coronary endothelial cells.	MEF2A		PCR	MEF2A alters the proliferation, inflammation-related gene expression profiles and its silencing induces cellular senescence in human coronary endothelial cells.			
33009960	chr17	76373734	76375734	SPHK1	Transcription of the proto-oncogene SPHK1 is regulated by KHPS1, an antisense RNA that activates SPHK1 expression by forming a triple-helical RNA-DNA-DNA structure at the SPHK1 enhancer.	human	Immunohistochem	High+Lowthroughput	Cereblon Promotes the Ubiquitination and Proteasomal Degradation of Interleukin Enhancer-Binding Factor 2	否			leukocyte	E_01_0379	gel electrophoresis	Transcription of the proto-oncogene SPHK1 is regulated by KHPS1, an antisense RNA that activates SPHK1 expression by forming a triple-helical RNA-DNA-DNA structure at the SPHK1 enhancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Transcription of the proto-oncogene SPHK1 is regulated by KHPS1, an antisense RNA that activates SPHK1 expression by forming a triple-helical RNA-DNA-DNA structure at the SPHK1 enhancer.		Transcription of the proto-oncogene SPHK1 is regulated by KHPS1, an antisense RNA that activates SPHK1 expression by forming a triple-helical RNA-DNA-DNA structure at the SPHK1 enhancer.	Immunohistochemical staining	Transcription of the proto-oncogene SPHK1 is regulated by KHPS1, an antisense RNA that activates SPHK1 expression by forming a triple-helical RNA-DNA-DNA structure at the SPHK1 enhancer.			凝胶电泳				SPHK1
32094355	chr1	153658363	153660363	ILF2	Interleukin enhancer-binding factor 2 (ILF2) forms a heterodimer with interleukin enhancer-binding factor 3 (ILF3) via double-stranded RNA-binding motif and zinc finger associated domain and thus regulates gene expression and cancer cell growth.	human	Epithelial tissues	High+Lowthroughput	Altered chromatin landscape and enhancer engagement underlie transcriptional dysregulation in MED12 mutant uterine leiomyomas	否		uterine leiomyomas	uterine smooth muscle cell	E_01_0380	PCR	Interleukin enhancer-binding factor 2 (ILF2) forms a heterodimer with interleukin enhancer-binding factor 3 (ILF3) via double-stranded RNA-binding motif and zinc finger associated domain and thus regulates gene expression and cancer cell growth.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Interleukin enhancer-binding factor 2 (ILF2) forms a heterodimer with interleukin enhancer-binding factor 3 (ILF3) via double-stranded RNA-binding motif and zinc finger associated domain and thus regulates gene expression and cancer cell growth.		Interleukin enhancer-binding factor 2 (ILF2) forms a heterodimer with interleukin enhancer-binding factor 3 (ILF3) via double-stranded RNA-binding motif and zinc finger associated domain and thus regulates gene expression and cancer cell growth.	Immunohistochemical staining	Interleukin enhancer-binding factor 2 (ILF2) forms a heterodimer with interleukin enhancer-binding factor 3 (ILF3) via double-stranded RNA-binding motif and zinc finger associated domain and thus regulates gene expression and cancer cell growth.			PCR				ILF2
32736380	chrX	71115647	71117647	MED12	Altered chromatin landscape and enhancer engagement underlie transcriptional dysregulation in MED12 mutant uterine leiomyomas.	human		High+Lowthroughput	Constructing and deconstructing GATA2-regulated cell fate programs to establish developmental trajectories	否			stem cell	E_01_0381	PCR	Altered chromatin landscape and enhancer engagement underlie transcriptional dysregulation in MED12 mutant uterine leiomyomas.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Altered chromatin landscape and enhancer engagement underlie transcriptional dysregulation in MED12 mutant uterine leiomyomas.		Altered chromatin landscape and enhancer engagement underlie transcriptional dysregulation in MED12 mutant uterine leiomyomas.	Immunohistochemical staining	Altered chromatin landscape and enhancer engagement underlie transcriptional dysregulation in MED12 mutant uterine leiomyomas.			PCR				MED12
33203992	chr3	128476653	128478653	GATA2	Constructing and deconstructing GATA2-regulated cell fate programs to establish developmental trajectories.	human	Thyroid tissue	High+Lowthroughput	Characterizing the function of EPB41L4A in the predisposition to papillary thyroid carcinoma	是	73227498	papillary thyroid carcinoma	thyroid gland cell	E_01_0382	PCR	Constructing and deconstructing GATA2-regulated cell fate programs to establish developmental trajectories.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Constructing and deconstructing GATA2-regulated cell fate programs to establish developmental trajectories.	Immunohistochemical staining	Constructing and deconstructing GATA2-regulated cell fate programs to establish developmental trajectories.	GATA2		PCR	Constructing and deconstructing GATA2-regulated cell fate programs to establish developmental trajectories.			
33203992	chr5	112139859	112141859	EPB41L4A	Characterizing the function of EPB41L4A in the predisposition to papillary thyroid carcinoma.	human	Thyroid tissue	High+Lowthroughput	Characterizing the function of EPB41L5A in the predisposition to papillary thyroid carcinoma	是	17134155	papillary thyroid carcinoma	thyroid gland cell	E_01_0382	PCR	Characterizing the function of EPB41L4A in the predisposition to papillary thyroid carcinoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Characterizing the function of EPB41L4A in the predisposition to papillary thyroid carcinoma.		Characterizing the function of EPB41L4A in the predisposition to papillary thyroid carcinoma.	Immunohistochemical staining	Characterizing the function of EPB41L4A in the predisposition to papillary thyroid carcinoma.			PCR				EPB41L4A
31411680	chr7	148804636	148806636	EZH2	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy .	human	Brain tissue	High+Lowthroughput	[Noncoding Polymorphism rs6832152 Is an Attractive Candidate for Genome Editing Aimed at Finding New Molecular Mechanisms of Autoimmune Diseases].	否			brain cell 	E_01_0383	Single cell sequencing	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy .	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy .	Immunohistochemical staining	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy .	EZH2		单细胞测序	A systems approach identifies Enhancer of Zeste Homolog 2 (EZH2) as a protective factor in epilepsy .			
30896882	chr1	95231641	95233641	RWDD3	Previously we have described that RWDD3 or RSUME (RWD domain-containing protein SUMO Enhancer) sumoylates and binds VHL protein and negatively regulates HIF degradation, leading to xenograft RCC tumor growth in mice.	human		High+Lowthroughput		否		 nasopharyngeal carcinoma		E_01_0384	RT qPCR, Western blot, cell transfection	Previously we have described that RWDD3 or RSUME (RWD domain-containing protein SUMO Enhancer) sumoylates and binds VHL protein and negatively regulates HIF degradation, leading to xenograft RCC tumor growth in mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Previously we have described that RWDD3 or RSUME (RWD domain-containing protein SUMO Enhancer) sumoylates and binds VHL protein and negatively regulates HIF degradation, leading to xenograft RCC tumor growth in mice.		Previously we have described that RWDD3 or RSUME (RWD domain-containing protein SUMO Enhancer) sumoylates and binds VHL protein and negatively regulates HIF degradation, leading to xenograft RCC tumor growth in mice.	Immunohistochemical staining	Previously we have described that RWDD3 or RSUME (RWD domain-containing protein SUMO Enhancer) sumoylates and binds VHL protein and negatively regulates HIF degradation, leading to xenograft RCC tumor growth in mice.			RT-qPCR、Western blot、细胞转染技术				RWDD3
30886108	chr12	52484460	52486460	KRT6A	KRT6A levels, metastasis‑associated factors and the Wnt/β‑catenin pathway were measured using RT‑qPCR and western blotting.	human		High+Lowthroughput	von Hippel-Lindau mutants in renal cell carcinoma are regulated by increased expression of RSUME.	否			dendritic cell	E_01_0370	RNA-seq	KRT6A levels, metastasis‑associated factors and the Wnt/β‑catenin pathway were measured using RT‑qPCR and western blotting.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	KRT6A levels, metastasis‑associated factors and the Wnt/β‑catenin pathway were measured using RT‑qPCR and western blotting.		KRT6A levels, metastasis‑associated factors and the Wnt/β‑catenin pathway were measured using RT‑qPCR and western blotting.	Immunohistochemical staining	KRT6A levels, metastasis‑associated factors and the Wnt/β‑catenin pathway were measured using RT‑qPCR and western blotting.			RNA-seq				KRT6A
34531368	chrX	67540972	67542972	AR	The androgen receptor (AR) is commonly known as a key transcription factor in prostate cancer development, progression and therapy resistance.	human	Immune cells	High+Lowthroughput	Androgen receptor enhancer usage and the chromatin regulatory landscape in human prostate cancers.	否		genomically silent childhood cancer	EwS cell	E_01_0385	PCR	The androgen receptor (AR) is commonly known as a key transcription factor in prostate cancer development, progression and therapy resistance.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The androgen receptor (AR) is commonly known as a key transcription factor in prostate cancer development, progression and therapy resistance.	Immunohistochemical staining	The androgen receptor (AR) is commonly known as a key transcription factor in prostate cancer development, progression and therapy resistance.	AR		PCR	The androgen receptor (AR) is commonly known as a key transcription factor in prostate cancer development, progression and therapy resistance.			
34294917	chr16	23675330	23677330	PLK1	Therapeutic targeting of the PLK1-PRC1-axis triggers cell death in genomically silent childhood cancer .	human		High+Lowthroughput	Therapeutic targeting of the PLK1-PRC1-axis triggers cell death in genomically silent childhood cancer.	否			brain cell 	E_01_0386	RNA SEQ, gel electrophoresis	Therapeutic targeting of the PLK1-PRC1-axis triggers cell death in genomically silent childhood cancer .	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therapeutic targeting of the PLK1-PRC1-axis triggers cell death in genomically silent childhood cancer .		Therapeutic targeting of the PLK1-PRC1-axis triggers cell death in genomically silent childhood cancer .	Immunohistochemical staining	Therapeutic targeting of the PLK1-PRC1-axis triggers cell death in genomically silent childhood cancer .			RNA-seq、凝胶电泳				PLK1
33704060	chr6	1607232	1609232	FOXC1	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	human	Epithelial tissues	High+Lowthroughput	Super-Enhancer-Associated Transcription Factors Maintain Transcriptional Regulation in Mature Podocytes.	否			epithelial cell	E_01_0387	Gel electrophoresis, PCR	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	Immunohistochemical staining	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	FOXC1		凝胶电泳、PCR	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.			
33704060	chr16	86564288	86566288	FOXC2	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	human	Epithelial tissues	High+Lowthroughput	Super-Enhancer-Associated Transcription Factors Maintain Transcriptional Regulation in Mature Podocytes.	否			epithelial cell	E_01_0387	Gel electrophoresis, PCR	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	Immunohistochemical staining	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	FOXC2		凝胶电泳、PCR	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.			
33704060	chr11	32384718	32386718	WT1	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	human	Epithelial tissues	High+Lowthroughput	Super-Enhancer-Associated Transcription Factors Maintain Transcriptional Regulation in Mature Podocytes.	否			epithelial cell	E_01_0387	Gel electrophoresis, PCR	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.		Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	Immunohistochemical staining	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.			凝胶电泳、PCR				WT1
33704060	chr9	126611267	126613267	LMX1B	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	human	Epithelial tissues	High+Lowthroughput	Super-Enhancer-Associated Transcription Factors Maintain Transcriptional Regulation in Mature Podocytes.	否			epithelial cell	E_01_0387	Gel electrophoresis, PCR	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.		Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.	Immunohistochemical staining	Superenhancer distribution revealed a group of potential TFs in core regulatory circuits in human glomerulus cells, including FOXC1/2, WT1, and LMX1B.			凝胶电泳、PCR				LMX1B
29941091	chr16	67559331	67561331	CTCF	The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.	human	lymphoid tissue	High+Lowthroughput	The human leukemia virus HTLV-1 alters the structure and transcription of host chromatin in cis	是	无	leukemia	T lymphocyte	E_01_0388	q4C,CRISPR/Cas9,RNA-seq,ChIP-seq,WGS,	The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.	Immunohistochemical staining	The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.	CTCF		q4C,CRISPR/Cas9,RNA-seq,ChIP-seq,WGS,	The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.			
29941091	chr14	100235422	100237422	YY1	The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.	human	lymphoid tissue	High+Lowthroughput	The human leukemia virus HTLV-1 alters the structure and transcription of host chromatin in cis	是	无	leukemia	T lymphocyte	E_01_0388	q4C,CRISPR/Cas9,RNA-seq,ChIP-seq,WGS,	The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.	Immunohistochemical staining	The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.	YY1		q4C,CRISPR/Cas9,RNA-seq,ChIP-seq,WGS,	The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.			
29941091	chr15	90963243	90965243	PRC1	The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.	human	lymphoid tissue	High+Lowthroughput	The human leukemia virus HTLV-1 alters the structure and transcription of host chromatin in cis	是	无	leukemia	T lymphocyte	E_01_0388	q4C,CRISPR/Cas9,RNA-seq,ChIP-seq,WGS,	The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.		The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.	Immunohistochemical staining	The altered chromosomal looping and consequent effects on host genome transcription depend on the proviral integration site and the presence of nearby CTCF-BS, and so differ in each infected T-cell clone. The changes in chromatin structure caused by HTLV-1 might not only create novel loops but also destroy pre-existing CTCF-dependent loops that are present in uninfected cells. Further work is needed to investigate the impact of altered looping and transcription on the persistence, infectivity and oncogenic potential of the infected T-cell clones.			q4C,CRISPR/Cas9,RNA-seq,ChIP-seq,WGS,				PRC1
29940916	chr7	148804605	148806605	EZH2	"We found a negative correlation between estrogen-related receptors and Enhancer of Zeste Homolog 2, aglobal repressor gene. Immunohistochemistry in primary breast tumors of different grades showed a correlated
expression of estrogen-related receptors and EZH2. Their correlated expression was further validated using online MERAV expression dataset where a negative correlation of variable strengths was observed in breast cancer. Ectopic expression of EZH2 in low EZH2-expressing normal breast epithelial cells abrogated their expression and at the same time, its silencing enhanced the expression of estrogen-related receptors in cancerous cells. Global occupancy of EZH2 on ERRα and ERRβ was observed in-vivo."	human	Mammary tissue	High+Lowthroughput	Estrogen-related receptors alpha, beta and gamma expression and function is associated with transcriptional repressor EZH2 in breast carcinoma	否	无	mammary cancer	epithelial cell	E_01_0389	Immunohistochemistry,transfection,Western blot,CHIP,qRT-PCR,CHIP-qPCR,	"We found a negative correlation between estrogen-related receptors and Enhancer of Zeste Homolog 2, aglobal repressor gene. Immunohistochemistry in primary breast tumors of different grades showed a correlated
expression of estrogen-related receptors and EZH2. Their correlated expression was further validated using online MERAV expression dataset where a negative correlation of variable strengths was observed in breast cancer. Ectopic expression of EZH2 in low EZH2-expressing normal breast epithelial cells abrogated their expression and at the same time, its silencing enhanced the expression of estrogen-related receptors in cancerous cells. Global occupancy of EZH2 on ERRα and ERRβ was observed in-vivo."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"We found a negative correlation between estrogen-related receptors and Enhancer of Zeste Homolog 2, aglobal repressor gene. Immunohistochemistry in primary breast tumors of different grades showed a correlated
expression of estrogen-related receptors and EZH2. Their correlated expression was further validated using online MERAV expression dataset where a negative correlation of variable strengths was observed in breast cancer. Ectopic expression of EZH2 in low EZH2-expressing normal breast epithelial cells abrogated their expression and at the same time, its silencing enhanced the expression of estrogen-related receptors in cancerous cells. Global occupancy of EZH2 on ERRα and ERRβ was observed in-vivo."	Immunohistochemical staining	"We found a negative correlation between estrogen-related receptors and Enhancer of Zeste Homolog 2, aglobal repressor gene. Immunohistochemistry in primary breast tumors of different grades showed a correlated
expression of estrogen-related receptors and EZH2. Their correlated expression was further validated using online MERAV expression dataset where a negative correlation of variable strengths was observed in breast cancer. Ectopic expression of EZH2 in low EZH2-expressing normal breast epithelial cells abrogated their expression and at the same time, its silencing enhanced the expression of estrogen-related receptors in cancerous cells. Global occupancy of EZH2 on ERRα and ERRβ was observed in-vivo."	EZH2		Immunohistochemistry,transfection,Western blot,CHIP,qRT-PCR,CHIP-qPCR,	"We found a negative correlation between estrogen-related receptors and Enhancer of Zeste Homolog 2, aglobal repressor gene. Immunohistochemistry in primary breast tumors of different grades showed a correlated
expression of estrogen-related receptors and EZH2. Their correlated expression was further validated using online MERAV expression dataset where a negative correlation of variable strengths was observed in breast cancer. Ectopic expression of EZH2 in low EZH2-expressing normal breast epithelial cells abrogated their expression and at the same time, its silencing enhanced the expression of estrogen-related receptors in cancerous cells. Global occupancy of EZH2 on ERRα and ERRβ was observed in-vivo."			
29940792	chr16	87381402	87383402	MAP1LC3B	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	human	Liver tissue	High+Lowthroughput	Peritumoral monocytes induce cancer cell autophagy to facilitate the progression of human hepatocellular carcinoma	否	无	Hepatocellular carcinoma	monocyte cells	E_01_0390	Immunofluorescence,Immunohistochemical Staining,qRT-PCR,Immunoblotting,Transmission electron microscopy,ELISA,RNA interference,	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.		These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	Immunohistochemical staining	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.			Immunofluorescence,Immunohistochemical Staining,qRT-PCR,Immunoblotting,Transmission electron microscopy,ELISA,RNA interference,				MAP1LC3B
29940792	chr6	31573024	31575024	TNF	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	human	Liver tissue	High+Lowthroughput	Peritumoral monocytes induce cancer cell autophagy to facilitate the progression of human hepatocellular carcinoma	否	无	Hepatocellular carcinoma	monocyte cells	E_01_0390	Immunofluorescence,Immunohistochemical Staining,qRT-PCR,Immunoblotting,Transmission electron microscopy,ELISA,RNA interference,	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	Immunohistochemical staining	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	TNF		Immunofluorescence,Immunohistochemical Staining,qRT-PCR,Immunoblotting,Transmission electron microscopy,ELISA,RNA interference,	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.			
29940792	chr2	112827014	112829014	IL1B	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	human	Liver tissue	High+Lowthroughput	Peritumoral monocytes induce cancer cell autophagy to facilitate the progression of human hepatocellular carcinoma	否	无	Hepatocellular carcinoma	monocyte cells	E_01_0390	Immunofluorescence,Immunohistochemical Staining,qRT-PCR,Immunoblotting,Transmission electron microscopy,ELISA,RNA interference,	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	Immunohistochemical staining	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	IL1B		Immunofluorescence,Immunohistochemical Staining,qRT-PCR,Immunoblotting,Transmission electron microscopy,ELISA,RNA interference,	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.			
29940792	chr20	49979941	49981941	SNAI1	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	human	Liver tissue	High+Lowthroughput	Peritumoral monocytes induce cancer cell autophagy to facilitate the progression of human hepatocellular carcinoma	否	无	Hepatocellular carcinoma	monocyte cells	E_01_0390	Immunofluorescence,Immunohistochemical Staining,qRT-PCR,Immunoblotting,Transmission electron microscopy,ELISA,RNA interference,	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	Immunohistochemical staining	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.	SNAI1		Immunofluorescence,Immunohistochemical Staining,qRT-PCR,Immunoblotting,Transmission electron microscopy,ELISA,RNA interference,	These findings indicated that cancer cell autophagy is regulated by a collaborative interaction between tumor and immune cell components in distinct HCC microenvironments, thus allowing the inflammatory monocytes to be rerouted in a tumor-promoting direction.			
29939784	chr2	216669369	216671369	IGFBP5	We found that, at relatively high doses, Meth exposure increased C/EBPβ protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBPβ expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBPβ in vitro. Further studies are needed to elucidate the role of C/EBPβ in low-dose Meth-induced neurotoxicity.	mouse	Adrenal medulla	High+Lowthroughput	Methamphetamine exposure triggers apoptosis and autophagy in neuronal cells by activating the C/EBPβ-related signaling pathway	否	无	Dopaminergic neuron apoptosis	chromaffin cell	E_02_0274	Luciferase Reporter assay,Western blot,Annexin V apoptosis staining,shRNA and stereotaxic injection,siRNA and transient transfection,TUNEL staining,Electron microscopy,Immunofluorescence labeling,	We found that, at relatively high doses, Meth exposure increased C/EBPβ protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBPβ expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBPβ in vitro. Further studies are needed to elucidate the role of C/EBPβ in low-dose Meth-induced neurotoxicity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found that, at relatively high doses, Meth exposure increased C/EBPβ protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBPβ expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBPβ in vitro. Further studies are needed to elucidate the role of C/EBPβ in low-dose Meth-induced neurotoxicity.		We found that, at relatively high doses, Meth exposure increased C/EBPβ protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBPβ expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBPβ in vitro. Further studies are needed to elucidate the role of C/EBPβ in low-dose Meth-induced neurotoxicity.	Immunohistochemical staining	We found that, at relatively high doses, Meth exposure increased C/EBPβ protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBPβ expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBPβ in vitro. Further studies are needed to elucidate the role of C/EBPβ in low-dose Meth-induced neurotoxicity.			Luciferase Reporter assay,Western blot,Annexin V apoptosis staining,shRNA and stereotaxic injection,siRNA and transient transfection,TUNEL staining,Electron microscopy,Immunofluorescence labeling,				IGFBP5
29939784	chr2	152177349	152179349	Trib3	We found that, at relatively high doses, Meth exposure increased C/EBPβ protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBPβ expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBPβ in vitro. Further studies are needed to elucidate the role of C/EBPβ in low-dose Meth-induced neurotoxicity.	mouse	Adrenal medulla	High+Lowthroughput	Methamphetamine exposure triggers apoptosis and autophagy in neuronal cells by activating the C/EBPβ-related signaling pathway	否	无	Dopaminergic neuron apoptosis	chromaffin cell	E_02_0274	Luciferase Reporter assay,Western blot,Annexin V apoptosis staining,shRNA and stereotaxic injection,siRNA and transient transfection,TUNEL staining,Electron microscopy,Immunofluorescence labeling,	We found that, at relatively high doses, Meth exposure increased C/EBPβ protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBPβ expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBPβ in vitro. Further studies are needed to elucidate the role of C/EBPβ in low-dose Meth-induced neurotoxicity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found that, at relatively high doses, Meth exposure increased C/EBPβ protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBPβ expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBPβ in vitro. Further studies are needed to elucidate the role of C/EBPβ in low-dose Meth-induced neurotoxicity.		We found that, at relatively high doses, Meth exposure increased C/EBPβ protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBPβ expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBPβ in vitro. Further studies are needed to elucidate the role of C/EBPβ in low-dose Meth-induced neurotoxicity.	Immunohistochemical staining	We found that, at relatively high doses, Meth exposure increased C/EBPβ protein expression, which was accompanied by increased neuronal apoptosis and autophagy; triggered the IGFBP5-mediated, p53-up-regulated modulator of apoptosis (PUMA)-related mitochondrial apoptotic signaling pathway; and stimulated the Trib3-mediated ER stress signaling pathway through the Akt-mTOR signaling axis. We also found that autophagy is an early response to Meth-induced stress upstream of apoptosis and plays a detrimental role in Meth-induced neuronal cell death. These results suggest that Meth exposure induces C/EBPβ expression, which plays an essential role in the neuronal apoptosis and autophagy induced by relatively high doses of Meth; however, relatively low concentrations of Meth did not change the expression of C/EBPβ in vitro. Further studies are needed to elucidate the role of C/EBPβ in low-dose Meth-induced neurotoxicity.			Luciferase Reporter assay,Western blot,Annexin V apoptosis staining,shRNA and stereotaxic injection,siRNA and transient transfection,TUNEL staining,Electron microscopy,Immunofluorescence labeling,				Trib3
29939173	chr14	6031195	6033195	Top2b	In this study, we report a method for the induction of CRISPR-mediated somatic mutations in the cerebellum. Specifically, we utilized conditional knock-in mice, in which Cas9 and GFP are chronically activated by the CAG (CMV enhancer/chicken ß-actin) promoter after Cre-mediated recombination of the genome. The self-designed single-guide RNAs (sgRNAs) and the Cre recombinase sequence, both encoded in a single plasmid construct, were delivered into cerebellar stem/progenitor cells at an embryonic stage using in utero electroporation. Consequently, transfected cells and their daughter cells were labeled with green fluorescent protein (GFP), thus facilitating further phenotypic analyses. Hence, this method is not only showing electroporation-based gene delivery into embryonic cerebellar cells but also proposing a novel quantitative approach to assess CRISPR-mediated loss-of-function phenotypes.	mouse	Kidney tissue	High+Lowthroughput	CRISPR-mediated Loss of Function Analysis in Cerebellar Granule Cells Using In Utero Electroporation-based Gene Transfer	否	无	Brain malformations	epithelial cell	E_02_0275	Immunostaining,CRISPR/Cas9,transfection,PCR,	In this study, we report a method for the induction of CRISPR-mediated somatic mutations in the cerebellum. Specifically, we utilized conditional knock-in mice, in which Cas9 and GFP are chronically activated by the CAG (CMV enhancer/chicken ß-actin) promoter after Cre-mediated recombination of the genome. The self-designed single-guide RNAs (sgRNAs) and the Cre recombinase sequence, both encoded in a single plasmid construct, were delivered into cerebellar stem/progenitor cells at an embryonic stage using in utero electroporation. Consequently, transfected cells and their daughter cells were labeled with green fluorescent protein (GFP), thus facilitating further phenotypic analyses. Hence, this method is not only showing electroporation-based gene delivery into embryonic cerebellar cells but also proposing a novel quantitative approach to assess CRISPR-mediated loss-of-function phenotypes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we report a method for the induction of CRISPR-mediated somatic mutations in the cerebellum. Specifically, we utilized conditional knock-in mice, in which Cas9 and GFP are chronically activated by the CAG (CMV enhancer/chicken ß-actin) promoter after Cre-mediated recombination of the genome. The self-designed single-guide RNAs (sgRNAs) and the Cre recombinase sequence, both encoded in a single plasmid construct, were delivered into cerebellar stem/progenitor cells at an embryonic stage using in utero electroporation. Consequently, transfected cells and their daughter cells were labeled with green fluorescent protein (GFP), thus facilitating further phenotypic analyses. Hence, this method is not only showing electroporation-based gene delivery into embryonic cerebellar cells but also proposing a novel quantitative approach to assess CRISPR-mediated loss-of-function phenotypes.		In this study, we report a method for the induction of CRISPR-mediated somatic mutations in the cerebellum. Specifically, we utilized conditional knock-in mice, in which Cas9 and GFP are chronically activated by the CAG (CMV enhancer/chicken ß-actin) promoter after Cre-mediated recombination of the genome. The self-designed single-guide RNAs (sgRNAs) and the Cre recombinase sequence, both encoded in a single plasmid construct, were delivered into cerebellar stem/progenitor cells at an embryonic stage using in utero electroporation. Consequently, transfected cells and their daughter cells were labeled with green fluorescent protein (GFP), thus facilitating further phenotypic analyses. Hence, this method is not only showing electroporation-based gene delivery into embryonic cerebellar cells but also proposing a novel quantitative approach to assess CRISPR-mediated loss-of-function phenotypes.	Immunohistochemical staining	In this study, we report a method for the induction of CRISPR-mediated somatic mutations in the cerebellum. Specifically, we utilized conditional knock-in mice, in which Cas9 and GFP are chronically activated by the CAG (CMV enhancer/chicken ß-actin) promoter after Cre-mediated recombination of the genome. The self-designed single-guide RNAs (sgRNAs) and the Cre recombinase sequence, both encoded in a single plasmid construct, were delivered into cerebellar stem/progenitor cells at an embryonic stage using in utero electroporation. Consequently, transfected cells and their daughter cells were labeled with green fluorescent protein (GFP), thus facilitating further phenotypic analyses. Hence, this method is not only showing electroporation-based gene delivery into embryonic cerebellar cells but also proposing a novel quantitative approach to assess CRISPR-mediated loss-of-function phenotypes.			Immunostaining,CRISPR/Cas9,transfection,PCR,				Top2b
29938678	chr7	45107986	45109986	Bax	Inhibition of PI3K/Akt signaling pathway abolished protective effect of curcumin in MSG-induced toxicity in rat thymocytes. Obtained findings suggest that curcumin may attenuate the MSG-induced apoptosis through PI3K/Akt signaling pathway which could be useful in preventing the potential deficiencies in T cell-mediated immunity.	mouse	Thymus tissue	High+Lowthroughput	The effect of curcumin and PI3K/Akt inhibitor on monosodium glutamate-induced rat thymocytes toxicity	否	无	nothing	thymocyte	E_02_0276	FCM,Caspase-3 activity assay,MMP,	Inhibition of PI3K/Akt signaling pathway abolished protective effect of curcumin in MSG-induced toxicity in rat thymocytes. Obtained findings suggest that curcumin may attenuate the MSG-induced apoptosis through PI3K/Akt signaling pathway which could be useful in preventing the potential deficiencies in T cell-mediated immunity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Inhibition of PI3K/Akt signaling pathway abolished protective effect of curcumin in MSG-induced toxicity in rat thymocytes. Obtained findings suggest that curcumin may attenuate the MSG-induced apoptosis through PI3K/Akt signaling pathway which could be useful in preventing the potential deficiencies in T cell-mediated immunity.		Inhibition of PI3K/Akt signaling pathway abolished protective effect of curcumin in MSG-induced toxicity in rat thymocytes. Obtained findings suggest that curcumin may attenuate the MSG-induced apoptosis through PI3K/Akt signaling pathway which could be useful in preventing the potential deficiencies in T cell-mediated immunity.	Immunohistochemical staining	Inhibition of PI3K/Akt signaling pathway abolished protective effect of curcumin in MSG-induced toxicity in rat thymocytes. Obtained findings suggest that curcumin may attenuate the MSG-induced apoptosis through PI3K/Akt signaling pathway which could be useful in preventing the potential deficiencies in T cell-mediated immunity.			FCM,Caspase-3 activity assay,MMP,				Bax
29934339	chr16	53698968	53700968	FTO	We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebpβ-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebpβ-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. 	human	adipose tissue	High+Lowthroughput	FTO mediates cell-autonomous effects on adipogenesis and adipocyte lipid content by regulating gene expression via 6mA DNA modifications	是	rs9939609,rs8050136,rs1421085,	Diabetes mellitus, obesity	fat cell	E_01_0391	transfection,RNA expression studies, RNA-Seq,m6A-RIP,6mA DNA Immunoprecipitation,Lipid Staining,Quantitative real time PCR,ChIP,Western blot,	We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebpβ-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebpβ-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebpβ-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebpβ-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. 		We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebpβ-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebpβ-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. 	Immunohistochemical staining	We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebpβ-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebpβ-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. 			transfection,RNA expression studies, RNA-Seq,m6A-RIP,6mA DNA Immunoprecipitation,Lipid Staining,Quantitative real time PCR,ChIP,Western blot,				FTO
29934339	chr20	50188384	50190384	CEBPB	We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebpβ-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebpβ-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. 	human	adipose tissue	High+Lowthroughput	FTO mediates cell-autonomous effects on adipogenesis and adipocyte lipid content by regulating gene expression via 6mA DNA modifications	是	rs9939609,rs8050136,rs1421085,	Diabetes mellitus, obesity	fat cell	E_01_0391	transfection,RNA expression studies, RNA-Seq,m6A-RIP,6mA DNA Immunoprecipitation,Lipid Staining,Quantitative real time PCR,ChIP,Western blot,	We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebpβ-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebpβ-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebpβ-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebpβ-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. 	Immunohistochemical staining	We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebpβ-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebpβ-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. 	CEBPB		transfection,RNA expression studies, RNA-Seq,m6A-RIP,6mA DNA Immunoprecipitation,Lipid Staining,Quantitative real time PCR,ChIP,Western blot,	We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebpβ-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebpβ-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. 			
29932212	chr21	34784999	34786999	RUNX1	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	human	Nervous tissue	High+Lowthroughput	CSF3R Mutations are frequently associated with abnormalities of RUNX1, CBFB, CEBPA, and NPM1 genes in acute myeloid leukemia	否	无	Acute myeloid leukemia	neutrophils	E_01_0392	DNA-Seq,RT-PCR,Mutation Analysis,	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	Immunohistochemical staining	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	RUNX1		DNA-Seq,RT-PCR,Mutation Analysis,	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.			
29932212	chr16	67026170	67028170	CBFB	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	human	Nervous tissue	High+Lowthroughput	CSF3R Mutations are frequently associated with abnormalities of RUNX1, CBFB, CEBPA, and NPM1 genes in acute myeloid leukemia	否	无	Acute myeloid leukemia	neutrophils	E_01_0392	DNA-Seq,RT-PCR,Mutation Analysis,	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	Immunohistochemical staining	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	CBFB		DNA-Seq,RT-PCR,Mutation Analysis,	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.			
29932212	chr19	33297034	33299034	CEBPA	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	human	Nervous tissue	High+Lowthroughput	CSF3R Mutations are frequently associated with abnormalities of RUNX1, CBFB, CEBPA, and NPM1 genes in acute myeloid leukemia	否	无	Acute myeloid leukemia	neutrophils	E_01_0392	DNA-Seq,RT-PCR,Mutation Analysis,	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	Immunohistochemical staining	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	CEBPA		DNA-Seq,RT-PCR,Mutation Analysis,	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.			
29932212	chr5	171384575	171386575	NPM1	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	human	Nervous tissue	High+Lowthroughput	CSF3R Mutations are frequently associated with abnormalities of RUNX1, CBFB, CEBPA, and NPM1 genes in acute myeloid leukemia	否	无	Acute myeloid leukemia	neutrophils	E_01_0392	DNA-Seq,RT-PCR,Mutation Analysis,	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.		CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	Immunohistochemical staining	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.			DNA-Seq,RT-PCR,Mutation Analysis,				NPM1
29932212	chr1	36463217	36465217	CSF3R	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	human	Nervous tissue	High+Lowthroughput	CSF3R Mutations are frequently associated with abnormalities of RUNX1, CBFB, CEBPA, and NPM1 genes in acute myeloid leukemia	否	无	Acute myeloid leukemia	neutrophils	E_01_0392	DNA-Seq,RT-PCR,Mutation Analysis,	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.		CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.	Immunohistochemical staining	CSF3R mutations are uncommon in AML; however, when they occur, they are often associated with core-binding factor gene abnormalities and CEBPAdm. An in-depth understanding of the interaction between these genetic alterations could facilitate a clearer understanding of the role of CSF3R mutations in AML development and may be used for disease classification, prognosis, and the development of targeted therapy.			DNA-Seq,RT-PCR,Mutation Analysis,				CSF3R
29930094	chr12	86405578	86407578	Esrrb	Mediator and Pol II are colocalized in the stable clusters, which associate with chromatin, have properties of phase-separated condensates, and are sensitive to transcriptional inhibitors. We suggest that large clusters of Mediator, recruited by transcription factors at large or clustered enhancer elements, interact with large Pol II clusters in transcriptional condensates in vivo.	mouse	Nervous tissue	High+Lowthroughput	Mediator and RNA polymerase II clusters associate in transcription-dependent condensates	否	无	nothing	embryonic stem cell	E_02_0277	Western blot,ChIP-seq,FISH,	Mediator and Pol II are colocalized in the stable clusters, which associate with chromatin, have properties of phase-separated condensates, and are sensitive to transcriptional inhibitors. We suggest that large clusters of Mediator, recruited by transcription factors at large or clustered enhancer elements, interact with large Pol II clusters in transcriptional condensates in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mediator and Pol II are colocalized in the stable clusters, which associate with chromatin, have properties of phase-separated condensates, and are sensitive to transcriptional inhibitors. We suggest that large clusters of Mediator, recruited by transcription factors at large or clustered enhancer elements, interact with large Pol II clusters in transcriptional condensates in vivo.		Mediator and Pol II are colocalized in the stable clusters, which associate with chromatin, have properties of phase-separated condensates, and are sensitive to transcriptional inhibitors. We suggest that large clusters of Mediator, recruited by transcription factors at large or clustered enhancer elements, interact with large Pol II clusters in transcriptional condensates in vivo.	Immunohistochemical staining	Mediator and Pol II are colocalized in the stable clusters, which associate with chromatin, have properties of phase-separated condensates, and are sensitive to transcriptional inhibitors. We suggest that large clusters of Mediator, recruited by transcription factors at large or clustered enhancer elements, interact with large Pol II clusters in transcriptional condensates in vivo.			Western blot,ChIP-seq,FISH,				Esrrb
29930094	chr19	15232852	15234852	BRD4	Mediator and Pol II are colocalized in the stable clusters, which associate with chromatin, have properties of phase-separated condensates, and are sensitive to transcriptional inhibitors. We suggest that large clusters of Mediator, recruited by transcription factors at large or clustered enhancer elements, interact with large Pol II clusters in transcriptional condensates in vivo.	mouse	Nervous tissue	High+Lowthroughput	Mediator and RNA polymerase II clusters associate in transcription-dependent condensates	否	无	nothing	embryonic stem cell	E_02_0277	Western blot,ChIP-seq,FISH,	Mediator and Pol II are colocalized in the stable clusters, which associate with chromatin, have properties of phase-separated condensates, and are sensitive to transcriptional inhibitors. We suggest that large clusters of Mediator, recruited by transcription factors at large or clustered enhancer elements, interact with large Pol II clusters in transcriptional condensates in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mediator and Pol II are colocalized in the stable clusters, which associate with chromatin, have properties of phase-separated condensates, and are sensitive to transcriptional inhibitors. We suggest that large clusters of Mediator, recruited by transcription factors at large or clustered enhancer elements, interact with large Pol II clusters in transcriptional condensates in vivo.		Mediator and Pol II are colocalized in the stable clusters, which associate with chromatin, have properties of phase-separated condensates, and are sensitive to transcriptional inhibitors. We suggest that large clusters of Mediator, recruited by transcription factors at large or clustered enhancer elements, interact with large Pol II clusters in transcriptional condensates in vivo.	Immunohistochemical staining	Mediator and Pol II are colocalized in the stable clusters, which associate with chromatin, have properties of phase-separated condensates, and are sensitive to transcriptional inhibitors. We suggest that large clusters of Mediator, recruited by transcription factors at large or clustered enhancer elements, interact with large Pol II clusters in transcriptional condensates in vivo.			Western blot,ChIP-seq,FISH,				BRD4
29930005	chr1	162042029	162044029	Dnm3os	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 	mouse	lymphoid tissue	High+Lowthroughput	Diabetes Mellitus-Induced Long Noncoding RNA Dnm3os Regulates Macrophage Functions and Inflammation via Nuclear Mechanisms	否	无	Diabetes mellitus, atherosclerosis	macrophage	E_02_0278	RNA Isolation,Western Blot,ELISA,ChIP,FISH,RNA-Seq,qRT-PCR,	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 		Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 	Immunohistochemical staining	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 			RNA Isolation,Western Blot,ELISA,ChIP,FISH,RNA-Seq,qRT-PCR,				Dnm3os
29930005	chr11	6362675	6364675	Ppia	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 	mouse	lymphoid tissue	High+Lowthroughput	Diabetes Mellitus-Induced Long Noncoding RNA Dnm3os Regulates Macrophage Functions and Inflammation via Nuclear Mechanisms	否	无	Diabetes mellitus, atherosclerosis	macrophage	E_02_0278	RNA Isolation,Western Blot,ELISA,ChIP,FISH,RNA-Seq,qRT-PCR,	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 		Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 	Immunohistochemical staining	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 			RNA Isolation,Western Blot,ELISA,ChIP,FISH,RNA-Seq,qRT-PCR,				Ppia
29930005	chrX	134457450	134459450	HPRT1	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 	mouse	lymphoid tissue	High+Lowthroughput	Diabetes Mellitus-Induced Long Noncoding RNA Dnm3os Regulates Macrophage Functions and Inflammation via Nuclear Mechanisms	否	无	Diabetes mellitus, atherosclerosis	macrophage	E_02_0278	RNA Isolation,Western Blot,ELISA,ChIP,FISH,RNA-Seq,qRT-PCR,	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 		Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 	Immunohistochemical staining	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 			RNA Isolation,Western Blot,ELISA,ChIP,FISH,RNA-Seq,qRT-PCR,				HPRT1
29930005	chr5	115694819	115696819	Rplp0	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 	mouse	lymphoid tissue	High+Lowthroughput	Diabetes Mellitus-Induced Long Noncoding RNA Dnm3os Regulates Macrophage Functions and Inflammation via Nuclear Mechanisms	否	无	Diabetes mellitus, atherosclerosis	macrophage	E_02_0278	RNA Isolation,Western Blot,ELISA,ChIP,FISH,RNA-Seq,qRT-PCR,	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 		Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 	Immunohistochemical staining	Hese results demonstrate novel mechanisms involving upregulation of long noncoding RNA Dnm3os, disruption of its interaction with nucleolin, and epigenetic modifications at target genes that promote macrophage inflammatory phenotype in diabetes mellitus. The data could lead to long noncoding RNA-based therapies for inflammatory diabetes mellitus complications. 			RNA Isolation,Western Blot,ELISA,ChIP,FISH,RNA-Seq,qRT-PCR,				Rplp0
29929436	chr1	45508017	45510017	PRDX1	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.	human	Epithelial tissues	High+Lowthroughput	Inhibition of TRAF6 ubiquitin-ligase activity by PRDX1 leads to inhibition of NFKB activation and autophagy activation	否	无	nothing	THP-1	E_01_0393	Luciferase reporter assay,Western blot,Immunoprecipitation (IP),qRT-PCR,Immunofluorescence microscopy,Salmonella Infection Assay,transwell migration assay,	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.		Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.	Immunohistochemical staining	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.			Luciferase reporter assay,Western blot,Immunoprecipitation (IP),qRT-PCR,Immunofluorescence microscopy,Salmonella Infection Assay,transwell migration assay,				PRDX1
29929436	chr11	36480938	36482938	TRAF6	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.	human	Epithelial tissues	High+Lowthroughput	Inhibition of TRAF6 ubiquitin-ligase activity by PRDX1 leads to inhibition of NFKB activation and autophagy activation	否	无	nothing	THP-1	E_01_0393	Luciferase reporter assay,Western blot,Immunoprecipitation (IP),qRT-PCR,Immunofluorescence microscopy,Salmonella Infection Assay,transwell migration assay,	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.		Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.	Immunohistochemical staining	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.			Luciferase reporter assay,Western blot,Immunoprecipitation (IP),qRT-PCR,Immunofluorescence microscopy,Salmonella Infection Assay,transwell migration assay,				TRAF6
29929436	chr9	117701240	117703240	TLR4	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.	human	Epithelial tissues	High+Lowthroughput	Inhibition of TRAF6 ubiquitin-ligase activity by PRDX1 leads to inhibition of NFKB activation and autophagy activation	否	无	nothing	THP-1	E_01_0393	Luciferase reporter assay,Western blot,Immunoprecipitation (IP),qRT-PCR,Immunofluorescence microscopy,Salmonella Infection Assay,transwell migration assay,	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.	Immunohistochemical staining	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.	TLR4		Luciferase reporter assay,Western blot,Immunoprecipitation (IP),qRT-PCR,Immunofluorescence microscopy,Salmonella Infection Assay,transwell migration assay,	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.			
29929436	chr17	42807339	42809339	BECN1	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.	human	Epithelial tissues	High+Lowthroughput	Inhibition of TRAF6 ubiquitin-ligase activity by PRDX1 leads to inhibition of NFKB activation and autophagy activation	否	无	nothing	THP-1	E_01_0393	Luciferase reporter assay,Western blot,Immunoprecipitation (IP),qRT-PCR,Immunofluorescence microscopy,Salmonella Infection Assay,transwell migration assay,	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.		Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.	Immunohistochemical staining	Additionally, migration and invasion abilities of PRDX1KD MDA-MB-231 and PRDX1KD SK-HEP-1 cancer cells were significantly enhanced compared to those of control cancer cells. Taken together, these results suggest that PRDX1 negatively regulates TLR4 signaling for NFKB activation and autophagy functions such as bactericidal activity, cancer cell migration, and cancer cell invasion by inhibiting TRAF6 ubiquitin-ligase activity.			Luciferase reporter assay,Western blot,Immunoprecipitation (IP),qRT-PCR,Immunofluorescence microscopy,Salmonella Infection Assay,transwell migration assay,				BECN1
29928592	chr8	19898949	19900949	LPL	TBBPA did not influence osteoblast differentiation, but TCDD suppressed ALP staining and activity, calcium deposition, and osteoblast-related mRNA levels. In a mixture of TBBPA and TCDD, TBBPA inhibited TCDD suppression of adipocyte and osteoblast differentiation in a dose-dependent manner. Interestingly, we observed lipid droplets in TBBPA-treated cells differentiated into osteoblasts. These results suggest that TBBPA and TCDD disrupted differentiation into adipocytes and osteoblasts and contributes to a more complete toxicological understanding of exposure to these chemical substances.	human	Nervous tissue	High+Lowthroughput	Complex toxicity as disruption of adipocyte or osteoblast differentiation in human mesenchymal stem cells under the mixed condition of TBBPA and TCDD	否	无		mesenchymal stem cell	E_01_0394	RT-qPCR,oil red O staining,ALP activity assay,cell matrix ALP staining, alizarin red S staining,	TBBPA did not influence osteoblast differentiation, but TCDD suppressed ALP staining and activity, calcium deposition, and osteoblast-related mRNA levels. In a mixture of TBBPA and TCDD, TBBPA inhibited TCDD suppression of adipocyte and osteoblast differentiation in a dose-dependent manner. Interestingly, we observed lipid droplets in TBBPA-treated cells differentiated into osteoblasts. These results suggest that TBBPA and TCDD disrupted differentiation into adipocytes and osteoblasts and contributes to a more complete toxicological understanding of exposure to these chemical substances.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TBBPA did not influence osteoblast differentiation, but TCDD suppressed ALP staining and activity, calcium deposition, and osteoblast-related mRNA levels. In a mixture of TBBPA and TCDD, TBBPA inhibited TCDD suppression of adipocyte and osteoblast differentiation in a dose-dependent manner. Interestingly, we observed lipid droplets in TBBPA-treated cells differentiated into osteoblasts. These results suggest that TBBPA and TCDD disrupted differentiation into adipocytes and osteoblasts and contributes to a more complete toxicological understanding of exposure to these chemical substances.	Immunohistochemical staining	TBBPA did not influence osteoblast differentiation, but TCDD suppressed ALP staining and activity, calcium deposition, and osteoblast-related mRNA levels. In a mixture of TBBPA and TCDD, TBBPA inhibited TCDD suppression of adipocyte and osteoblast differentiation in a dose-dependent manner. Interestingly, we observed lipid droplets in TBBPA-treated cells differentiated into osteoblasts. These results suggest that TBBPA and TCDD disrupted differentiation into adipocytes and osteoblasts and contributes to a more complete toxicological understanding of exposure to these chemical substances.	LPL		RT-qPCR,oil red O staining,ALP activity assay,cell matrix ALP staining, alizarin red S staining,	TBBPA did not influence osteoblast differentiation, but TCDD suppressed ALP staining and activity, calcium deposition, and osteoblast-related mRNA levels. In a mixture of TBBPA and TCDD, TBBPA inhibited TCDD suppression of adipocyte and osteoblast differentiation in a dose-dependent manner. Interestingly, we observed lipid droplets in TBBPA-treated cells differentiated into osteoblasts. These results suggest that TBBPA and TCDD disrupted differentiation into adipocytes and osteoblasts and contributes to a more complete toxicological understanding of exposure to these chemical substances.			
29928447	chr2	15937740	15939740	MYCN	The CTC-specific mutations were enhancer of zeste polycomb repressive complex 2 subunit, notch 1, AT-rich interaction domain 1A, serine/threonine kinase 11, fms related tyrosine kinase 3, MYCN proto-oncogene, bHLH transcription factor, APC, WNT signaling pathway regulator, and phosphatase and tensin homolog. The technique used by the present study was demonstrated to be effective at isolating CTCs at a sufficiently high purity for genomic analysis, and supported the use of comprehensive cancer panel analysis as a potential application for precision medicine.	human		High+Lowthroughput	Cancer panel analysis of circulating tumor cells in patients with breast cancer	否	无	mammary cancer	NCI-H358	E_01_0395	Immunofluorescent staining,Whole genome amplification,CCP,	The CTC-specific mutations were enhancer of zeste polycomb repressive complex 2 subunit, notch 1, AT-rich interaction domain 1A, serine/threonine kinase 11, fms related tyrosine kinase 3, MYCN proto-oncogene, bHLH transcription factor, APC, WNT signaling pathway regulator, and phosphatase and tensin homolog. The technique used by the present study was demonstrated to be effective at isolating CTCs at a sufficiently high purity for genomic analysis, and supported the use of comprehensive cancer panel analysis as a potential application for precision medicine.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The CTC-specific mutations were enhancer of zeste polycomb repressive complex 2 subunit, notch 1, AT-rich interaction domain 1A, serine/threonine kinase 11, fms related tyrosine kinase 3, MYCN proto-oncogene, bHLH transcription factor, APC, WNT signaling pathway regulator, and phosphatase and tensin homolog. The technique used by the present study was demonstrated to be effective at isolating CTCs at a sufficiently high purity for genomic analysis, and supported the use of comprehensive cancer panel analysis as a potential application for precision medicine.	Immunohistochemical staining	The CTC-specific mutations were enhancer of zeste polycomb repressive complex 2 subunit, notch 1, AT-rich interaction domain 1A, serine/threonine kinase 11, fms related tyrosine kinase 3, MYCN proto-oncogene, bHLH transcription factor, APC, WNT signaling pathway regulator, and phosphatase and tensin homolog. The technique used by the present study was demonstrated to be effective at isolating CTCs at a sufficiently high purity for genomic analysis, and supported the use of comprehensive cancer panel analysis as a potential application for precision medicine.	MYCN		Immunofluorescent staining,Whole genome amplification,CCP,	The CTC-specific mutations were enhancer of zeste polycomb repressive complex 2 subunit, notch 1, AT-rich interaction domain 1A, serine/threonine kinase 11, fms related tyrosine kinase 3, MYCN proto-oncogene, bHLH transcription factor, APC, WNT signaling pathway regulator, and phosphatase and tensin homolog. The technique used by the present study was demonstrated to be effective at isolating CTCs at a sufficiently high purity for genomic analysis, and supported the use of comprehensive cancer panel analysis as a potential application for precision medicine.			
29928447	chr5	112704931	112706931	APC	The CTC-specific mutations were enhancer of zeste polycomb repressive complex 2 subunit, notch 1, AT-rich interaction domain 1A, serine/threonine kinase 11, fms related tyrosine kinase 3, MYCN proto-oncogene, bHLH transcription factor, APC, WNT signaling pathway regulator, and phosphatase and tensin homolog. The technique used by the present study was demonstrated to be effective at isolating CTCs at a sufficiently high purity for genomic analysis, and supported the use of comprehensive cancer panel analysis as a potential application for precision medicine.	human		High+Lowthroughput	Cancer panel analysis of circulating tumor cells in patients with breast cancer	否	无	mammary cancer	NCI-H358	E_01_0395	Immunofluorescent staining,Whole genome amplification,CCP,	The CTC-specific mutations were enhancer of zeste polycomb repressive complex 2 subunit, notch 1, AT-rich interaction domain 1A, serine/threonine kinase 11, fms related tyrosine kinase 3, MYCN proto-oncogene, bHLH transcription factor, APC, WNT signaling pathway regulator, and phosphatase and tensin homolog. The technique used by the present study was demonstrated to be effective at isolating CTCs at a sufficiently high purity for genomic analysis, and supported the use of comprehensive cancer panel analysis as a potential application for precision medicine.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The CTC-specific mutations were enhancer of zeste polycomb repressive complex 2 subunit, notch 1, AT-rich interaction domain 1A, serine/threonine kinase 11, fms related tyrosine kinase 3, MYCN proto-oncogene, bHLH transcription factor, APC, WNT signaling pathway regulator, and phosphatase and tensin homolog. The technique used by the present study was demonstrated to be effective at isolating CTCs at a sufficiently high purity for genomic analysis, and supported the use of comprehensive cancer panel analysis as a potential application for precision medicine.	Immunohistochemical staining	The CTC-specific mutations were enhancer of zeste polycomb repressive complex 2 subunit, notch 1, AT-rich interaction domain 1A, serine/threonine kinase 11, fms related tyrosine kinase 3, MYCN proto-oncogene, bHLH transcription factor, APC, WNT signaling pathway regulator, and phosphatase and tensin homolog. The technique used by the present study was demonstrated to be effective at isolating CTCs at a sufficiently high purity for genomic analysis, and supported the use of comprehensive cancer panel analysis as a potential application for precision medicine.	APC		Immunofluorescent staining,Whole genome amplification,CCP,	The CTC-specific mutations were enhancer of zeste polycomb repressive complex 2 subunit, notch 1, AT-rich interaction domain 1A, serine/threonine kinase 11, fms related tyrosine kinase 3, MYCN proto-oncogene, bHLH transcription factor, APC, WNT signaling pathway regulator, and phosphatase and tensin homolog. The technique used by the present study was demonstrated to be effective at isolating CTCs at a sufficiently high purity for genomic analysis, and supported the use of comprehensive cancer panel analysis as a potential application for precision medicine.			
29928394	chr10	52311539	52313539	DKK1	In the present study, DNase I hypersensitive sites and histone modifications of DKK1 were investigated in the A549 lung cancer cell line using the UCSC Genome Browser. A set of cis-acting enhancer elements were identified by a dual-luciferase reporter gene assay system to increase activity of the DKK1 promoter with lung cancer specificity. To the best of our knowledge, these data provide the first insight into the role of the DKK1 locus in lung cancer, and confirm the contribution of intronic cis-acting elements to the regulation of DKK1 expression, providing a new insight into gene regulation in lung cancer, which could inform the development of targeted therapy.	human	Lung cancer tissues	High+Lowthroughput	Prediction and identification of transcriptional regulatory elements at the lung cancer-specific DKK1 locus	否	无	lung cancer		E_01_0396	PCR,Plasmid transfection,Firefly/Renilla luciferase quantification,	In the present study, DNase I hypersensitive sites and histone modifications of DKK1 were investigated in the A549 lung cancer cell line using the UCSC Genome Browser. A set of cis-acting enhancer elements were identified by a dual-luciferase reporter gene assay system to increase activity of the DKK1 promoter with lung cancer specificity. To the best of our knowledge, these data provide the first insight into the role of the DKK1 locus in lung cancer, and confirm the contribution of intronic cis-acting elements to the regulation of DKK1 expression, providing a new insight into gene regulation in lung cancer, which could inform the development of targeted therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, DNase I hypersensitive sites and histone modifications of DKK1 were investigated in the A549 lung cancer cell line using the UCSC Genome Browser. A set of cis-acting enhancer elements were identified by a dual-luciferase reporter gene assay system to increase activity of the DKK1 promoter with lung cancer specificity. To the best of our knowledge, these data provide the first insight into the role of the DKK1 locus in lung cancer, and confirm the contribution of intronic cis-acting elements to the regulation of DKK1 expression, providing a new insight into gene regulation in lung cancer, which could inform the development of targeted therapy.		In the present study, DNase I hypersensitive sites and histone modifications of DKK1 were investigated in the A549 lung cancer cell line using the UCSC Genome Browser. A set of cis-acting enhancer elements were identified by a dual-luciferase reporter gene assay system to increase activity of the DKK1 promoter with lung cancer specificity. To the best of our knowledge, these data provide the first insight into the role of the DKK1 locus in lung cancer, and confirm the contribution of intronic cis-acting elements to the regulation of DKK1 expression, providing a new insight into gene regulation in lung cancer, which could inform the development of targeted therapy.	Immunohistochemical staining	In the present study, DNase I hypersensitive sites and histone modifications of DKK1 were investigated in the A549 lung cancer cell line using the UCSC Genome Browser. A set of cis-acting enhancer elements were identified by a dual-luciferase reporter gene assay system to increase activity of the DKK1 promoter with lung cancer specificity. To the best of our knowledge, these data provide the first insight into the role of the DKK1 locus in lung cancer, and confirm the contribution of intronic cis-acting elements to the regulation of DKK1 expression, providing a new insight into gene regulation in lung cancer, which could inform the development of targeted therapy.			PCR,Plasmid transfection,Firefly/Renilla luciferase quantification,				DKK1
29927026	chr4	108044908	108046908	LEF1	Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis	human	Skeletal tissues	High+Lowthroughput	Novel lymphoid enhancer-binding factor 1-cytoglobin axis promotes extravasation of osteosarcoma cells into the lungs	否	无	Osteosarcoma (OS)	LM8-C3H	E_01_0397	Histology analysis,Western blot,Cell‐proliferation assay,Extravasation assay,Cell‐adhesion assay,Transmigration assay,Genomewide meta‐analysis,Reverse transcription‐PCR,qPCR,CRISPR‐Cas9 ,	Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis	Immunohistochemical staining	Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis	LEF1		Histology analysis,Western blot,Cell‐proliferation assay,Extravasation assay,Cell‐adhesion assay,Transmigration assay,Genomewide meta‐analysis,Reverse transcription‐PCR,qPCR,CRISPR‐Cas9 ,	Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis			
29927026	chr11	116533443	116535443	Cygb	Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis	human	Skeletal tissues	High+Lowthroughput	Novel lymphoid enhancer-binding factor 1-cytoglobin axis promotes extravasation of osteosarcoma cells into the lungs	否	无	Osteosarcoma (OS)	LM8-C3H	E_01_0397	Histology analysis,Western blot,Cell‐proliferation assay,Extravasation assay,Cell‐adhesion assay,Transmigration assay,Genomewide meta‐analysis,Reverse transcription‐PCR,qPCR,CRISPR‐Cas9 ,	Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis		Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis	Immunohistochemical staining	Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis			Histology analysis,Western blot,Cell‐proliferation assay,Extravasation assay,Cell‐adhesion assay,Transmigration assay,Genomewide meta‐analysis,Reverse transcription‐PCR,qPCR,CRISPR‐Cas9 ,				Cygb
29927026	chr17	76524788	76526788	CYGB	Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis	human	Skeletal tissues	High+Lowthroughput	Novel lymphoid enhancer-binding factor 1-cytoglobin axis promotes extravasation of osteosarcoma cells into the lungs	否	无	Osteosarcoma (OS)	LM8-C3H	E_01_0397	Histology analysis,Western blot,Cell‐proliferation assay,Extravasation assay,Cell‐adhesion assay,Transmigration assay,Genomewide meta‐analysis,Reverse transcription‐PCR,qPCR,CRISPR‐Cas9 ,	Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis		Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis	Immunohistochemical staining	Our results showed a novel LEF1‐CYGB axis in OS lung metastasis and may provide a new way of developing therapeutic strategies to prevent OS lung metastasis			Histology analysis,Western blot,Cell‐proliferation assay,Extravasation assay,Cell‐adhesion assay,Transmigration assay,Genomewide meta‐analysis,Reverse transcription‐PCR,qPCR,CRISPR‐Cas9 ,				CYGB
29925637	chr3	185640391	185642391	IGF2BP2	We demonstrated that linc-ADAL interacts with heterogeneous nuclear ribonucleoprotein U (hnRNPU) and insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) at distinct subcellular locations to regulate adipocyte differentiation and lipogenesis.	human	adipose tissue	High+Lowthroughput	Interrogation of nonconserved human adipose lincRNAs identifies a regulatory role of linc-ADAL in adipocyte metabolism	否	无	nothing	fat cell	E_01_0398	RNA knockdown,RNA-seq,ChIP-seq,Western blot, immunoblot, CLIP-seq,	We demonstrated that linc-ADAL interacts with heterogeneous nuclear ribonucleoprotein U (hnRNPU) and insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) at distinct subcellular locations to regulate adipocyte differentiation and lipogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We demonstrated that linc-ADAL interacts with heterogeneous nuclear ribonucleoprotein U (hnRNPU) and insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) at distinct subcellular locations to regulate adipocyte differentiation and lipogenesis.	Immunohistochemical staining	We demonstrated that linc-ADAL interacts with heterogeneous nuclear ribonucleoprotein U (hnRNPU) and insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) at distinct subcellular locations to regulate adipocyte differentiation and lipogenesis.	IGF2BP2		RNA knockdown,RNA-seq,ChIP-seq,Western blot, immunoblot, CLIP-seq,	We demonstrated that linc-ADAL interacts with heterogeneous nuclear ribonucleoprotein U (hnRNPU) and insulin-like growth factor 2 mRNA binding protein 2 (IGF2BP2) at distinct subcellular locations to regulate adipocyte differentiation and lipogenesis.			
29923177	chr10	22317950	22319950	BMI1	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	human	lymphoid tissue	High+Lowthroughput	BMI1 enhancer polymorphism underlies chromosome 10p12.31 association with childhood acute lymphoblastic leukemia	是	rs11591377,rs4748812	Childhood acute lymphoblastic leukaemia (all)		E_01_0399	CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Immunohistochemical staining	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	BMI1		CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.			
29923177	chr10	22532096	22534096	PIP4K2A	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	human	lymphoid tissue	High+Lowthroughput	BMI1 enhancer polymorphism underlies chromosome 10p12.31 association with childhood acute lymphoblastic leukemia	是	rs11591377,rs4748812	Childhood acute lymphoblastic leukaemia (all)		E_01_0399	CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.		At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Immunohistochemical staining	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.			CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,				PIP4K2A
29923177	chr20	43664291	43666291	MYBL2	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	human	lymphoid tissue	High+Lowthroughput	BMI1 enhancer polymorphism underlies chromosome 10p12.31 association with childhood acute lymphoblastic leukemia	是	rs11591377,rs4748812	Childhood acute lymphoblastic leukaemia (all)		E_01_0399	CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Immunohistochemical staining	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	MYBL2		CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.			
29923177	chr21	34784475	34786475	RUNX1	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	human	lymphoid tissue	High+Lowthroughput	BMI1 enhancer polymorphism underlies chromosome 10p12.31 association with childhood acute lymphoblastic leukemia	是	rs11591377,rs4748812	Childhood acute lymphoblastic leukaemia (all)		E_01_0399	CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Immunohistochemical staining	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	RUNX1		CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.			
29923177	chr10	61898870	61900870	ARID5B	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	human	lymphoid tissue	High+Lowthroughput	BMI1 enhancer polymorphism underlies chromosome 10p12.31 association with childhood acute lymphoblastic leukemia	是	rs11591377,rs4748812	Childhood acute lymphoblastic leukaemia (all)		E_01_0399	CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Immunohistochemical staining	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	ARID5B		CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.			
29923177	chr7	50300977	50302977	IKZF1	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	human	lymphoid tissue	High+Lowthroughput	BMI1 enhancer polymorphism underlies chromosome 10p12.31 association with childhood acute lymphoblastic leukemia	是	rs11591377,rs4748812	Childhood acute lymphoblastic leukaemia (all)		E_01_0399	CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Immunohistochemical staining	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	IKZF1		CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.			
29923177	chr14	23113950	23115950	CEBPE	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	human	lymphoid tissue	High+Lowthroughput	BMI1 enhancer polymorphism underlies chromosome 10p12.31 association with childhood acute lymphoblastic leukemia	是	rs11591377,rs4748812	Childhood acute lymphoblastic leukaemia (all)		E_01_0399	CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Immunohistochemical staining	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	CEBPE		CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.			
29923177	chr10	8042809	8044809	GATA3	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	human	lymphoid tissue	High+Lowthroughput	BMI1 enhancer polymorphism underlies chromosome 10p12.31 association with childhood acute lymphoblastic leukemia	是	rs11591377,rs4748812	Childhood acute lymphoblastic leukaemia (all)		E_01_0399	CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	Immunohistochemical staining	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.	GATA3		CHIP-seq,GWS,Enhancer assay,H3k27ac HiChIP data analysis,MethylC-Seq Analysis,Transcription factor binding analysis,	At PIP4K2A, we identified rs4748812 (Pmeta=1.3x10-15), which alters a RUNX1 binding motif and demonstrated chromosomal looping to the PIP4K2A promoter. Fine-mapping chromosome 10p12 in a multi-ethnic ALL GWAS confirmed independent associations and identified putative functional variants upstream of BMI1 and at PIP4K2A.			
29916899	chr11	65495083	65497083	MALAT1	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	human	Esophageal tissues	High+Lowthroughput	LncRNA MALAT1 promotes epithelial-to-mesenchymal transition of esophageal cancer through Ezh2-Notch1 signaling pathway	否	无	Esophageal cancer (EC)	TE-1	E_01_0400	transfection,RT-PCR,Western blot,	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	Immunohistochemical staining	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	MALAT1		transfection,RT-PCR,Western blot,	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.			
29916899	chr6	47504029	47506029	Ezh2	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	human	Esophageal tissues	High+Lowthroughput	LncRNA MALAT1 promotes epithelial-to-mesenchymal transition of esophageal cancer through Ezh2-Notch1 signaling pathway	否	无	Esophageal cancer (EC)	TE-1	E_01_0400	transfection,RT-PCR,Western blot,	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.		MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	Immunohistochemical staining	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.			transfection,RT-PCR,Western blot,				Ezh2
29916899	chr2	26345124	26347124	Notch1	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	human	Esophageal tissues	High+Lowthroughput	LncRNA MALAT1 promotes epithelial-to-mesenchymal transition of esophageal cancer through Ezh2-Notch1 signaling pathway	否	无	Esophageal cancer (EC)	TE-1	E_01_0400	transfection,RT-PCR,Western blot,	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.		MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	Immunohistochemical staining	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.			transfection,RT-PCR,Western blot,				Notch1
29916899	chr16	29880511	29882511	Hes1	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	human	Esophageal tissues	High+Lowthroughput	LncRNA MALAT1 promotes epithelial-to-mesenchymal transition of esophageal cancer through Ezh2-Notch1 signaling pathway	否	无	Esophageal cancer (EC)	TE-1	E_01_0400	transfection,RT-PCR,Western blot,	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.		MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.	Immunohistochemical staining	MALAT1 could affect EMT and metastasis of EC cells through Ezh2-Notch1 signaling pathway. This study can give deeper understandings of the role of MALAT1 in EC and may provide some new directions for treatment of patients with EC.			transfection,RT-PCR,Western blot,				Hes1
29915186	chr4	108045032	108047032	LEF1	Altogether, we provide evidence that BMP signalling is an important regulator for the neuronal fate specification of AH-NSPCs cultures and we show that it significantly cooperates with the previously described master regulator of adult hippocampal neurogenesis, the WNT signalling pathway.	human	Nervous tissue	High+Lowthroughput	BMP and WNT signalling cooperate through LEF1 in the neuronal specification of adult hippocampal neural stem and progenitor cells	否	无	Hippocampal dentate gyrus		E_01_0401	Immunostaining,Gene Expression analysis,Western blot,ChIP,	Altogether, we provide evidence that BMP signalling is an important regulator for the neuronal fate specification of AH-NSPCs cultures and we show that it significantly cooperates with the previously described master regulator of adult hippocampal neurogenesis, the WNT signalling pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Altogether, we provide evidence that BMP signalling is an important regulator for the neuronal fate specification of AH-NSPCs cultures and we show that it significantly cooperates with the previously described master regulator of adult hippocampal neurogenesis, the WNT signalling pathway.	Immunohistochemical staining	Altogether, we provide evidence that BMP signalling is an important regulator for the neuronal fate specification of AH-NSPCs cultures and we show that it significantly cooperates with the previously described master regulator of adult hippocampal neurogenesis, the WNT signalling pathway.	LEF1		Immunostaining,Gene Expression analysis,Western blot,ChIP,	Altogether, we provide evidence that BMP signalling is an important regulator for the neuronal fate specification of AH-NSPCs cultures and we show that it significantly cooperates with the previously described master regulator of adult hippocampal neurogenesis, the WNT signalling pathway.			
29914089	chr5	17983939	17985939	Cd36	Gene analysis identified a Gamma interferon activation site (GAS) element in the CD36 gene promoter that acts as a STAT3 binding site, an interaction that was confirmed by ChIP assay. STAT3 interacts with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), suggesting that nobiletin also acts through the CD36/ (STAT3)/NF-κB signaling axis. Nobiletin inhibited CD36-dependent breast cancer cell migration and invasion as well as CD36-mediated tumor sphere formation. Taken together, these results suggest that nobiletin inhibits cancer stem cells in multiple ways.	human	Epithelial tissues	High+Lowthroughput	Nobiletin Inhibits CD36-Dependent Tumor Angiogenesis, Migration, Invasion, and Sphere Formation Through the Cd36/Stat3/Nf-Κb Signaling Axis	否	无	cancer	MCF-7	E_01_0402	Reverse Transcription-PCR,Western Blot,EMSA,Wound Healing Assay,Matrigel Invasion Assay,siRNA Analysis,In vitro Angiogenesis Assay,Molecular Docking,	Gene analysis identified a Gamma interferon activation site (GAS) element in the CD36 gene promoter that acts as a STAT3 binding site, an interaction that was confirmed by ChIP assay. STAT3 interacts with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), suggesting that nobiletin also acts through the CD36/ (STAT3)/NF-κB signaling axis. Nobiletin inhibited CD36-dependent breast cancer cell migration and invasion as well as CD36-mediated tumor sphere formation. Taken together, these results suggest that nobiletin inhibits cancer stem cells in multiple ways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gene analysis identified a Gamma interferon activation site (GAS) element in the CD36 gene promoter that acts as a STAT3 binding site, an interaction that was confirmed by ChIP assay. STAT3 interacts with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), suggesting that nobiletin also acts through the CD36/ (STAT3)/NF-κB signaling axis. Nobiletin inhibited CD36-dependent breast cancer cell migration and invasion as well as CD36-mediated tumor sphere formation. Taken together, these results suggest that nobiletin inhibits cancer stem cells in multiple ways.		Gene analysis identified a Gamma interferon activation site (GAS) element in the CD36 gene promoter that acts as a STAT3 binding site, an interaction that was confirmed by ChIP assay. STAT3 interacts with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), suggesting that nobiletin also acts through the CD36/ (STAT3)/NF-κB signaling axis. Nobiletin inhibited CD36-dependent breast cancer cell migration and invasion as well as CD36-mediated tumor sphere formation. Taken together, these results suggest that nobiletin inhibits cancer stem cells in multiple ways.	Immunohistochemical staining	Gene analysis identified a Gamma interferon activation site (GAS) element in the CD36 gene promoter that acts as a STAT3 binding site, an interaction that was confirmed by ChIP assay. STAT3 interacts with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), suggesting that nobiletin also acts through the CD36/ (STAT3)/NF-κB signaling axis. Nobiletin inhibited CD36-dependent breast cancer cell migration and invasion as well as CD36-mediated tumor sphere formation. Taken together, these results suggest that nobiletin inhibits cancer stem cells in multiple ways.			Reverse Transcription-PCR,Western Blot,EMSA,Wound Healing Assay,Matrigel Invasion Assay,siRNA Analysis,In vitro Angiogenesis Assay,Molecular Docking,				Cd36
29914089	chr11	100773150	100775150	Stat3	Gene analysis identified a Gamma interferon activation site (GAS) element in the CD36 gene promoter that acts as a STAT3 binding site, an interaction that was confirmed by ChIP assay. STAT3 interacts with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), suggesting that nobiletin also acts through the CD36/ (STAT3)/NF-κB signaling axis. Nobiletin inhibited CD36-dependent breast cancer cell migration and invasion as well as CD36-mediated tumor sphere formation. Taken together, these results suggest that nobiletin inhibits cancer stem cells in multiple ways.	human	Epithelial tissues	High+Lowthroughput	Nobiletin Inhibits CD36-Dependent Tumor Angiogenesis, Migration, Invasion, and Sphere Formation Through the Cd36/Stat3/Nf-Κb Signaling Axis	否	无	cancer	MCF-7	E_01_0402	Reverse Transcription-PCR,Western Blot,EMSA,Wound Healing Assay,Matrigel Invasion Assay,siRNA Analysis,In vitro Angiogenesis Assay,Molecular Docking,	Gene analysis identified a Gamma interferon activation site (GAS) element in the CD36 gene promoter that acts as a STAT3 binding site, an interaction that was confirmed by ChIP assay. STAT3 interacts with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), suggesting that nobiletin also acts through the CD36/ (STAT3)/NF-κB signaling axis. Nobiletin inhibited CD36-dependent breast cancer cell migration and invasion as well as CD36-mediated tumor sphere formation. Taken together, these results suggest that nobiletin inhibits cancer stem cells in multiple ways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gene analysis identified a Gamma interferon activation site (GAS) element in the CD36 gene promoter that acts as a STAT3 binding site, an interaction that was confirmed by ChIP assay. STAT3 interacts with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), suggesting that nobiletin also acts through the CD36/ (STAT3)/NF-κB signaling axis. Nobiletin inhibited CD36-dependent breast cancer cell migration and invasion as well as CD36-mediated tumor sphere formation. Taken together, these results suggest that nobiletin inhibits cancer stem cells in multiple ways.		Gene analysis identified a Gamma interferon activation site (GAS) element in the CD36 gene promoter that acts as a STAT3 binding site, an interaction that was confirmed by ChIP assay. STAT3 interacts with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), suggesting that nobiletin also acts through the CD36/ (STAT3)/NF-κB signaling axis. Nobiletin inhibited CD36-dependent breast cancer cell migration and invasion as well as CD36-mediated tumor sphere formation. Taken together, these results suggest that nobiletin inhibits cancer stem cells in multiple ways.	Immunohistochemical staining	Gene analysis identified a Gamma interferon activation site (GAS) element in the CD36 gene promoter that acts as a STAT3 binding site, an interaction that was confirmed by ChIP assay. STAT3 interacts with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), suggesting that nobiletin also acts through the CD36/ (STAT3)/NF-κB signaling axis. Nobiletin inhibited CD36-dependent breast cancer cell migration and invasion as well as CD36-mediated tumor sphere formation. Taken together, these results suggest that nobiletin inhibits cancer stem cells in multiple ways.			Reverse Transcription-PCR,Western Blot,EMSA,Wound Healing Assay,Matrigel Invasion Assay,siRNA Analysis,In vitro Angiogenesis Assay,Molecular Docking,				Stat3
29913133	chr1	209782740	209784740	IRF6	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	human	Epithelial tissues	High+Lowthroughput	IRF6 and AP2A Interaction Regulates Epidermal Development	否	rs642961	Van der Woude syndrome (cleft lip / palate), popliteal pterygium syndrome (eye disease)	epidermal cell	E_01_0403	Western blot,	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	Immunohistochemical staining	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	IRF6		Western blot,	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.			
29913133	chr3	189628962	189630962	TP63	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	human	Epithelial tissues	High+Lowthroughput	IRF6 and AP2A Interaction Regulates Epidermal Development	否	rs642961	Van der Woude syndrome (cleft lip / palate), popliteal pterygium syndrome (eye disease)	epidermal cell	E_01_0403	Western blot,	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	Immunohistochemical staining	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	TP63		Western blot,	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.			
29913133	chr2	172388642	172390642	Tfap2c	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	human	Epithelial tissues	High+Lowthroughput	IRF6 and AP2A Interaction Regulates Epidermal Development	否	rs642961	Van der Woude syndrome (cleft lip / palate), popliteal pterygium syndrome (eye disease)	epidermal cell	E_01_0403	Western blot,	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.		Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	Immunohistochemical staining	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.			Western blot,				Tfap2c
29913133	chr13	40866038	40868038	Tfap2a	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	human	Epithelial tissues	High+Lowthroughput	IRF6 and AP2A Interaction Regulates Epidermal Development	否	rs642961	Van der Woude syndrome (cleft lip / palate), popliteal pterygium syndrome (eye disease)	epidermal cell	E_01_0403	Western blot,	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.		Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	Immunohistochemical staining	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.			Western blot,				Tfap2a
29913133	chr1	192832174	192834174	Irf6	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	human	Epithelial tissues	High+Lowthroughput	IRF6 and AP2A Interaction Regulates Epidermal Development	否	rs642961	Van der Woude syndrome (cleft lip / palate), popliteal pterygium syndrome (eye disease)	epidermal cell	E_01_0403	Western blot,	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.		Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	Immunohistochemical staining	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.			Western blot,				Irf6
29913133	chr1	24196668	24198668	GRHL3	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	human	Epithelial tissues	High+Lowthroughput	IRF6 and AP2A Interaction Regulates Epidermal Development	否	rs642961	Van der Woude syndrome (cleft lip / palate), popliteal pterygium syndrome (eye disease)	epidermal cell	E_01_0403	Western blot,	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	Immunohistochemical staining	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.	GRHL3		Western blot,	Therefore, we conclude that IRF6 and TFAP2A are part of a genetic regulatory network that is critical in epithelial development, with implications for both orofacial and cutaneous tissues. Our work provides in vivo, functional data to explain the relationship between AP2A protein binding and the MCS9.7 enhancer in orofacial clefting. This work is important because the MCS9.7 enhancer element contains a variant that abrogates AP2A protein binding and increases risk for orofacial clefting worldwide.			
29911120	chr13	40552875	40554875	FOXO1	Increasing of the apoptotic ratio was linked to miR-182-5p inhibition in the LNA-anti-miR group rather than other groups. Similarly, the necrotic ratio in the LNA-anti-miR group was higher.Our results supported the hypothesis that miR-182-5p inhibition can reduce the cell viability predominantly due to induces apoptosis and necrosis. The present results can apply in translational medicine for investigation of antisense therapy and drug development in leukemia.	human	Nervous tissue	High+Lowthroughput	Apoptosis induction in acute promyelocytic leukemia cells through upregulation of CEBPα by miR-182 blockage	否	无	Acute promyelocytic leukemia	HL-60	E_01_0404	Cell transfection,Reverse transcriptase microRNA real-time PCR,qRT-PCR,Cell viability assay,	Increasing of the apoptotic ratio was linked to miR-182-5p inhibition in the LNA-anti-miR group rather than other groups. Similarly, the necrotic ratio in the LNA-anti-miR group was higher.Our results supported the hypothesis that miR-182-5p inhibition can reduce the cell viability predominantly due to induces apoptosis and necrosis. The present results can apply in translational medicine for investigation of antisense therapy and drug development in leukemia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Increasing of the apoptotic ratio was linked to miR-182-5p inhibition in the LNA-anti-miR group rather than other groups. Similarly, the necrotic ratio in the LNA-anti-miR group was higher.Our results supported the hypothesis that miR-182-5p inhibition can reduce the cell viability predominantly due to induces apoptosis and necrosis. The present results can apply in translational medicine for investigation of antisense therapy and drug development in leukemia.	Immunohistochemical staining	Increasing of the apoptotic ratio was linked to miR-182-5p inhibition in the LNA-anti-miR group rather than other groups. Similarly, the necrotic ratio in the LNA-anti-miR group was higher.Our results supported the hypothesis that miR-182-5p inhibition can reduce the cell viability predominantly due to induces apoptosis and necrosis. The present results can apply in translational medicine for investigation of antisense therapy and drug development in leukemia.	FOXO1		Cell transfection,Reverse transcriptase microRNA real-time PCR,qRT-PCR,Cell viability assay,	Increasing of the apoptotic ratio was linked to miR-182-5p inhibition in the LNA-anti-miR group rather than other groups. Similarly, the necrotic ratio in the LNA-anti-miR group was higher.Our results supported the hypothesis that miR-182-5p inhibition can reduce the cell viability predominantly due to induces apoptosis and necrosis. The present results can apply in translational medicine for investigation of antisense therapy and drug development in leukemia.			
29910149	chr12	86404702	86406702	Esrrb	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	mouse	Nervous tissue	High+Lowthroughput	Esrrb Unlocks Silenced Enhancers for Reprogramming to Naive Pluripotency	否	无	nothing	embryonic stem cell	E_02_0279	RT-PCR,Immunofluorescence,Western Blot,Flow Cytometry,Bisulfite Sequencing,ChIP,NOMe-seq,GlucMS-PCR,Luciferase Reporter Assays,Microarray,ChIP-seq,RNA-seq,	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.		These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	Immunohistochemical staining	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.			RT-PCR,Immunofluorescence,Western Blot,Flow Cytometry,Bisulfite Sequencing,ChIP,NOMe-seq,GlucMS-PCR,Luciferase Reporter Assays,Microarray,ChIP-seq,RNA-seq,				Esrrb
29910149	chr3	34701839	34703839	Sox2	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	mouse	Nervous tissue	High+Lowthroughput	Esrrb Unlocks Silenced Enhancers for Reprogramming to Naive Pluripotency	否	无	nothing	embryonic stem cell	E_02_0279	RT-PCR,Immunofluorescence,Western Blot,Flow Cytometry,Bisulfite Sequencing,ChIP,NOMe-seq,GlucMS-PCR,Luciferase Reporter Assays,Microarray,ChIP-seq,RNA-seq,	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.		These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	Immunohistochemical staining	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.			RT-PCR,Immunofluorescence,Western Blot,Flow Cytometry,Bisulfite Sequencing,ChIP,NOMe-seq,GlucMS-PCR,Luciferase Reporter Assays,Microarray,ChIP-seq,RNA-seq,				Sox2
29910149	chr6	122681019	122683019	Nanog	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	mouse	Nervous tissue	High+Lowthroughput	Esrrb Unlocks Silenced Enhancers for Reprogramming to Naive Pluripotency	否	无	nothing	embryonic stem cell	E_02_0279	RT-PCR,Immunofluorescence,Western Blot,Flow Cytometry,Bisulfite Sequencing,ChIP,NOMe-seq,GlucMS-PCR,Luciferase Reporter Assays,Microarray,ChIP-seq,RNA-seq,	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.		These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	Immunohistochemical staining	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.			RT-PCR,Immunofluorescence,Western Blot,Flow Cytometry,Bisulfite Sequencing,ChIP,NOMe-seq,GlucMS-PCR,Luciferase Reporter Assays,Microarray,ChIP-seq,RNA-seq,				Nanog
29910149	chr4	55524480	55526480	Klf4	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	mouse	Nervous tissue	High+Lowthroughput	Esrrb Unlocks Silenced Enhancers for Reprogramming to Naive Pluripotency	否	无	nothing	embryonic stem cell	E_02_0279	RT-PCR,Immunofluorescence,Western Blot,Flow Cytometry,Bisulfite Sequencing,ChIP,NOMe-seq,GlucMS-PCR,Luciferase Reporter Assays,Microarray,ChIP-seq,RNA-seq,	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.		These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	Immunohistochemical staining	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.			RT-PCR,Immunofluorescence,Western Blot,Flow Cytometry,Bisulfite Sequencing,ChIP,NOMe-seq,GlucMS-PCR,Luciferase Reporter Assays,Microarray,ChIP-seq,RNA-seq,				Klf4
29910149	chr8	73069965	73071965	Klf2	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	mouse	Nervous tissue	High+Lowthroughput	Esrrb Unlocks Silenced Enhancers for Reprogramming to Naive Pluripotency	否	无	nothing	embryonic stem cell	E_02_0279	RT-PCR,Immunofluorescence,Western Blot,Flow Cytometry,Bisulfite Sequencing,ChIP,NOMe-seq,GlucMS-PCR,Luciferase Reporter Assays,Microarray,ChIP-seq,RNA-seq,	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.		These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	Immunohistochemical staining	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.			RT-PCR,Immunofluorescence,Western Blot,Flow Cytometry,Bisulfite Sequencing,ChIP,NOMe-seq,GlucMS-PCR,Luciferase Reporter Assays,Microarray,ChIP-seq,RNA-seq,				Klf2
29910149	chr5	119805939	119807939	Tbx3	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	mouse	Nervous tissue	High+Lowthroughput	Esrrb Unlocks Silenced Enhancers for Reprogramming to Naive Pluripotency	否	无	nothing	embryonic stem cell	E_02_0279	RT-PCR,Immunofluorescence,Western Blot,Flow Cytometry,Bisulfite Sequencing,ChIP,NOMe-seq,GlucMS-PCR,Luciferase Reporter Assays,Microarray,ChIP-seq,RNA-seq,	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.		These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.	Immunohistochemical staining	These results suggest that TFs can drive rapid remodeling of the local chromatin structure, highlighting the remarkable plasticity of stable epigenetic information.			RT-PCR,Immunofluorescence,Western Blot,Flow Cytometry,Bisulfite Sequencing,ChIP,NOMe-seq,GlucMS-PCR,Luciferase Reporter Assays,Microarray,ChIP-seq,RNA-seq,				Tbx3
29909987	chrX	67541571	67543571	AR	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.	human	connective tissue	High+Lowthroughput	A Somatically Acquired Enhancer of the Androgen Receptor Is a Noncoding Driver in Advanced Prostate Cancer	否	无	prostatic cancer		E_01_0405	PCR,CRISPR/Cas9,Proliferation Assays,Competition Experiments,Quantitative RT-PCR,Immunoblotting,Cloning,Chromosome Conformation Capture(3C),Crystal Violet Proliferation Assays,ChIP-seq,ChIP,ChIP-qPCR,Whole-Genome Bisulfite Sequencing analysis(WGBS),	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.	Immunohistochemical staining	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.	AR		PCR,CRISPR/Cas9,Proliferation Assays,Competition Experiments,Quantitative RT-PCR,Immunoblotting,Cloning,Chromosome Conformation Capture(3C),Crystal Violet Proliferation Assays,ChIP-seq,ChIP,ChIP-qPCR,Whole-Genome Bisulfite Sequencing analysis(WGBS),	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.			
29909987	chr17	80131587	80133587	EIF4A3	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.	human	connective tissue	High+Lowthroughput	A Somatically Acquired Enhancer of the Androgen Receptor Is a Noncoding Driver in Advanced Prostate Cancer	否	无	prostatic cancer		E_01_0405	PCR,CRISPR/Cas9,Proliferation Assays,Competition Experiments,Quantitative RT-PCR,Immunoblotting,Cloning,Chromosome Conformation Capture(3C),Crystal Violet Proliferation Assays,ChIP-seq,ChIP,ChIP-qPCR,Whole-Genome Bisulfite Sequencing analysis(WGBS),	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.		Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.	Immunohistochemical staining	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.			PCR,CRISPR/Cas9,Proliferation Assays,Competition Experiments,Quantitative RT-PCR,Immunoblotting,Cloning,Chromosome Conformation Capture(3C),Crystal Violet Proliferation Assays,ChIP-seq,ChIP,ChIP-qPCR,Whole-Genome Bisulfite Sequencing analysis(WGBS),				EIF4A3
29909987	chr16	70520712	70522712	SF3B3	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.	human	connective tissue	High+Lowthroughput	A Somatically Acquired Enhancer of the Androgen Receptor Is a Noncoding Driver in Advanced Prostate Cancer	否	无	prostatic cancer		E_01_0405	PCR,CRISPR/Cas9,Proliferation Assays,Competition Experiments,Quantitative RT-PCR,Immunoblotting,Cloning,Chromosome Conformation Capture(3C),Crystal Violet Proliferation Assays,ChIP-seq,ChIP,ChIP-qPCR,Whole-Genome Bisulfite Sequencing analysis(WGBS),	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.		Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.	Immunohistochemical staining	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.			PCR,CRISPR/Cas9,Proliferation Assays,Competition Experiments,Quantitative RT-PCR,Immunoblotting,Cloning,Chromosome Conformation Capture(3C),Crystal Violet Proliferation Assays,ChIP-seq,ChIP,ChIP-qPCR,Whole-Genome Bisulfite Sequencing analysis(WGBS),				SF3B3
29909987	chr17	38845127	38847127	RPL23	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.	human	connective tissue	High+Lowthroughput	A Somatically Acquired Enhancer of the Androgen Receptor Is a Noncoding Driver in Advanced Prostate Cancer	否	无	prostatic cancer		E_01_0405	PCR,CRISPR/Cas9,Proliferation Assays,Competition Experiments,Quantitative RT-PCR,Immunoblotting,Cloning,Chromosome Conformation Capture(3C),Crystal Violet Proliferation Assays,ChIP-seq,ChIP,ChIP-qPCR,Whole-Genome Bisulfite Sequencing analysis(WGBS),	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.		Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.	Immunohistochemical staining	Collectively, these observations underscore the importance of epigenomic profiling in primary specimens and the value of deploying genome editing to functionally characterize noncoding elements. More broadly, this work identifies a therapeutic vulnerability for targeting the AR and emphasizes the importance of regulatory elements as highly recurrent oncogenic drivers.			PCR,CRISPR/Cas9,Proliferation Assays,Competition Experiments,Quantitative RT-PCR,Immunoblotting,Cloning,Chromosome Conformation Capture(3C),Crystal Violet Proliferation Assays,ChIP-seq,ChIP,ChIP-qPCR,Whole-Genome Bisulfite Sequencing analysis(WGBS),				RPL23
29909985	chrX	67541233	67543233	AR	A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.	human	Myotome	High+Lowthroughput	Structural Alterations Driving Castration-Resistant Prostate Cancer Revealed by Linked-Read Genome Sequencing	否	无	Metastatic castration resistant prostate cancer (mcrpc)	LNCaP	E_01_0406	WGS,qPCR,Hi-C,CHIP,DNA seq,	A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.	Immunohistochemical staining	A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.	AR		WGS,qPCR,Hi-C,CHIP,DNA seq,	A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.			
29909985	chr17	39458509	39460509	CDK12	A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.	human	Myotome	High+Lowthroughput	Structural Alterations Driving Castration-Resistant Prostate Cancer Revealed by Linked-Read Genome Sequencing	否	无	Metastatic castration resistant prostate cancer (mcrpc)	LNCaP	E_01_0406	WGS,qPCR,Hi-C,CHIP,DNA seq,	A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.		A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.	Immunohistochemical staining	A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.			WGS,qPCR,Hi-C,CHIP,DNA seq,				CDK12
29909985	chr8	127732595	127734595	MYC	A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.	human	Myotome	High+Lowthroughput	Structural Alterations Driving Castration-Resistant Prostate Cancer Revealed by Linked-Read Genome Sequencing	否	无	Metastatic castration resistant prostate cancer (mcrpc)	LNCaP	E_01_0406	WGS,qPCR,Hi-C,CHIP,DNA seq,	A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.	Immunohistochemical staining	A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.	MYC		WGS,qPCR,Hi-C,CHIP,DNA seq,	A subset of cases displayed AR or MYC enhancer duplication in the context of a genome-wide tandem duplicator phenotype associated with CDK12 inactivation. Our findings highlight the complex genomic structure of mCRPC, nominate alterations that may inform prostate cancer treatment, and suggest that additional recurrent events in the non-coding mCRPC genome remain to be discovered.			
29909962	chr8	11792732	11794732	FDFT1	Whole-exome sequencing was used to identify recessive disease-causing variants in FDFT1. Functional characterization of one variant demonstrated a partial splicing defect and altered promoter and/or enhancer activity, reflecting essential mechanisms for regulating cholesterol biosynthesis/uptake in steady state.	human	connective tissue	High+Lowthroughput	Squalene Synthase Deficiency: Clinical, Biochemical, and Molecular Characterization of a Defect in Cholesterol Biosynthesis	否	无	Squalene synthase deficiency	fibroblast	E_01_0407	PCR,WES,Western blot,	Whole-exome sequencing was used to identify recessive disease-causing variants in FDFT1. Functional characterization of one variant demonstrated a partial splicing defect and altered promoter and/or enhancer activity, reflecting essential mechanisms for regulating cholesterol biosynthesis/uptake in steady state.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Whole-exome sequencing was used to identify recessive disease-causing variants in FDFT1. Functional characterization of one variant demonstrated a partial splicing defect and altered promoter and/or enhancer activity, reflecting essential mechanisms for regulating cholesterol biosynthesis/uptake in steady state.		Whole-exome sequencing was used to identify recessive disease-causing variants in FDFT1. Functional characterization of one variant demonstrated a partial splicing defect and altered promoter and/or enhancer activity, reflecting essential mechanisms for regulating cholesterol biosynthesis/uptake in steady state.	Immunohistochemical staining	Whole-exome sequencing was used to identify recessive disease-causing variants in FDFT1. Functional characterization of one variant demonstrated a partial splicing defect and altered promoter and/or enhancer activity, reflecting essential mechanisms for regulating cholesterol biosynthesis/uptake in steady state.			PCR,WES,Western blot,				FDFT1
29908199	chrX	55006337	55008337	ALAS2	These results suggest that the induction of mitochondrial ferritin expression might be essential for, but not the primary cause of, ring sideroblast formation. Our results also suggest that the insufficient supply of protoporphyrin IX due to ALAS2 deficiency in combination with increased iron import into mitochondria during erythroid differentiation results in the formation of ring sideroblasts. Furthermore, HA2low cells are a useful tool for characterizing ring sideroblasts in vitro.	human	connective tissue	High+Lowthroughput	Establishment of a cell model of X-linked sideroblastic anemia using genome editing	否	无	X-linked sideroblastic anemia		E_01_0408	Quantitative real-time polymerase chain reaction,Western blot,Electron microscopy,Flow cytometry,Staining,	These results suggest that the induction of mitochondrial ferritin expression might be essential for, but not the primary cause of, ring sideroblast formation. Our results also suggest that the insufficient supply of protoporphyrin IX due to ALAS2 deficiency in combination with increased iron import into mitochondria during erythroid differentiation results in the formation of ring sideroblasts. Furthermore, HA2low cells are a useful tool for characterizing ring sideroblasts in vitro.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that the induction of mitochondrial ferritin expression might be essential for, but not the primary cause of, ring sideroblast formation. Our results also suggest that the insufficient supply of protoporphyrin IX due to ALAS2 deficiency in combination with increased iron import into mitochondria during erythroid differentiation results in the formation of ring sideroblasts. Furthermore, HA2low cells are a useful tool for characterizing ring sideroblasts in vitro.		These results suggest that the induction of mitochondrial ferritin expression might be essential for, but not the primary cause of, ring sideroblast formation. Our results also suggest that the insufficient supply of protoporphyrin IX due to ALAS2 deficiency in combination with increased iron import into mitochondria during erythroid differentiation results in the formation of ring sideroblasts. Furthermore, HA2low cells are a useful tool for characterizing ring sideroblasts in vitro.	Immunohistochemical staining	These results suggest that the induction of mitochondrial ferritin expression might be essential for, but not the primary cause of, ring sideroblast formation. Our results also suggest that the insufficient supply of protoporphyrin IX due to ALAS2 deficiency in combination with increased iron import into mitochondria during erythroid differentiation results in the formation of ring sideroblasts. Furthermore, HA2low cells are a useful tool for characterizing ring sideroblasts in vitro.			Quantitative real-time polymerase chain reaction,Western blot,Electron microscopy,Flow cytometry,Staining,				ALAS2
29908180	chr11	98246620	98248620	Stard3	Moreover, Stard3 silencing reduced the expression of peroxisome proliferator-activated receptor-γ (PPARγ) and CCAAT/enhancer binding protein (C/EBP)α in 3T3- L1 cells. In conclusion, Stard3 enhanced the adipogenesis of preadipocytes by enhancement of cholesterol redistribution to the mitochondrial, increasing mitochondrial ROS production. These results suggest that Stard3 is an essential factor for the 3T3-L1 cells' differentiation.	mouse	adipose tissue	High+Lowthroughput	Knocking down Stard3 decreases adipogenesis with decreased mitochondrial ROS in 3T3-L1 cells	否	无	cholesterol	3T3-L1	E_02_0280	Oil red-O staining,Small interfering RNA,Quantitative real-time PCR,Protein isolation,western blot,transfection	Moreover, Stard3 silencing reduced the expression of peroxisome proliferator-activated receptor-γ (PPARγ) and CCAAT/enhancer binding protein (C/EBP)α in 3T3- L1 cells. In conclusion, Stard3 enhanced the adipogenesis of preadipocytes by enhancement of cholesterol redistribution to the mitochondrial, increasing mitochondrial ROS production. These results suggest that Stard3 is an essential factor for the 3T3-L1 cells' differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, Stard3 silencing reduced the expression of peroxisome proliferator-activated receptor-γ (PPARγ) and CCAAT/enhancer binding protein (C/EBP)α in 3T3- L1 cells. In conclusion, Stard3 enhanced the adipogenesis of preadipocytes by enhancement of cholesterol redistribution to the mitochondrial, increasing mitochondrial ROS production. These results suggest that Stard3 is an essential factor for the 3T3-L1 cells' differentiation.		Moreover, Stard3 silencing reduced the expression of peroxisome proliferator-activated receptor-γ (PPARγ) and CCAAT/enhancer binding protein (C/EBP)α in 3T3- L1 cells. In conclusion, Stard3 enhanced the adipogenesis of preadipocytes by enhancement of cholesterol redistribution to the mitochondrial, increasing mitochondrial ROS production. These results suggest that Stard3 is an essential factor for the 3T3-L1 cells' differentiation.	Immunohistochemical staining	Moreover, Stard3 silencing reduced the expression of peroxisome proliferator-activated receptor-γ (PPARγ) and CCAAT/enhancer binding protein (C/EBP)α in 3T3- L1 cells. In conclusion, Stard3 enhanced the adipogenesis of preadipocytes by enhancement of cholesterol redistribution to the mitochondrial, increasing mitochondrial ROS production. These results suggest that Stard3 is an essential factor for the 3T3-L1 cells' differentiation.			Oil red-O staining,Small interfering RNA,Quantitative real-time PCR,Protein isolation,western blot,transfection				Stard3
29907651	chr12	6567592	6569592	CHD4	The results emphasize the function of lncRNAs in guiding chromatin remodeling complexes to specific genomic loci and uncover a phosphorylation-dependent mechanism of CHD4/NuRD-mediated transcriptional regulation.	mouse	Nervous tissue	High+Lowthroughput	lncRNA PAPAS tethered to the rDNA enhancer recruits hypophosphorylated CHD4/NuRD to repress rRNA synthesis at elevated temperatures	否	无	nothing	NIH3T3	E_02_0281	PCR,siRNA,transfection,competition experiments,In vivo RNA–protein interaction assays,In vitro protein–RNA interaction assays,RNase footprinting,EMSA,Western Blot,Northwestern blot showing binding,Immunoblot,Chromatin immunoprecipitation (ChIP),CLIP,RT–PCR,RNA immunoprecipitation (fRIP) assays,	The results emphasize the function of lncRNAs in guiding chromatin remodeling complexes to specific genomic loci and uncover a phosphorylation-dependent mechanism of CHD4/NuRD-mediated transcriptional regulation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The results emphasize the function of lncRNAs in guiding chromatin remodeling complexes to specific genomic loci and uncover a phosphorylation-dependent mechanism of CHD4/NuRD-mediated transcriptional regulation.		The results emphasize the function of lncRNAs in guiding chromatin remodeling complexes to specific genomic loci and uncover a phosphorylation-dependent mechanism of CHD4/NuRD-mediated transcriptional regulation.	Immunohistochemical staining	The results emphasize the function of lncRNAs in guiding chromatin remodeling complexes to specific genomic loci and uncover a phosphorylation-dependent mechanism of CHD4/NuRD-mediated transcriptional regulation.			PCR,siRNA,transfection,competition experiments,In vivo RNA–protein interaction assays,In vitro protein–RNA interaction assays,RNase footprinting,EMSA,Western Blot,Northwestern blot showing binding,Immunoblot,Chromatin immunoprecipitation (ChIP),CLIP,RT–PCR,RNA immunoprecipitation (fRIP) assays,				CHD4
29907596	chr17	44074243	44076243	HDAC5	In vivo, endotoxemia in MEF2-reporter mice induced upregulation of PGE2 and MEF2 activation. Our findings provide an unexpected new link between inflammation and cardiac remodeling by de-repression of MEF2 through HDAC5 inactivation, which has potential implications for new strategies to treat inflammatory cardiomyopathies.	human	Nervous tissue	High+Lowthroughput	Inflammation leads through PGE/EP(3) signaling to HDAC5/MEF2-dependent transcription in cardiac myocytes	否	无	Inflammatory cardiomyopathy	nrvm	E_01_0409	Luciferase reporter assay,Immunoblotting,Immunostaining,RNA analysis,Western Blot	In vivo, endotoxemia in MEF2-reporter mice induced upregulation of PGE2 and MEF2 activation. Our findings provide an unexpected new link between inflammation and cardiac remodeling by de-repression of MEF2 through HDAC5 inactivation, which has potential implications for new strategies to treat inflammatory cardiomyopathies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In vivo, endotoxemia in MEF2-reporter mice induced upregulation of PGE2 and MEF2 activation. Our findings provide an unexpected new link between inflammation and cardiac remodeling by de-repression of MEF2 through HDAC5 inactivation, which has potential implications for new strategies to treat inflammatory cardiomyopathies.		In vivo, endotoxemia in MEF2-reporter mice induced upregulation of PGE2 and MEF2 activation. Our findings provide an unexpected new link between inflammation and cardiac remodeling by de-repression of MEF2 through HDAC5 inactivation, which has potential implications for new strategies to treat inflammatory cardiomyopathies.	Immunohistochemical staining	In vivo, endotoxemia in MEF2-reporter mice induced upregulation of PGE2 and MEF2 activation. Our findings provide an unexpected new link between inflammation and cardiac remodeling by de-repression of MEF2 through HDAC5 inactivation, which has potential implications for new strategies to treat inflammatory cardiomyopathies.			Luciferase reporter assay,Immunoblotting,Immunostaining,RNA analysis,Western Blot				HDAC5
29906314	chr6	38673142	38675142	GLO1	We show GR extract and shikonin dose-dependently inhibited glycation and enhanced oxidative defenses through nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element activation. Inflammatory targets, nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) and tumor necrosis factor alpha, were suppressed by GR extract and shikonin. Glyoxalase 1 (GLO1) and glutathione synthesis genes were significantly upregulated by GR extract and shikonin. GR extract boosted higher wavelength UV absorption in select cosmetic matrices. Rationale for the use of GR extract and shikonin are supported by our research. By inhibiting glycation, modulating oxidative stress, suppressing inflammation and UV-absorptive properties, GR extract and shikonin potentially offer multiple skin benefits.	human	connective tissue	High+Lowthroughput	Gromwell (Lithospermum erythrorhizon) root extract protects against glycation and related inflammatory and oxidative stress while offering UV absorption capability	否	无	Glycosylation	HepG2 cell	E_01_0410	qRT-PCR,qPCR	We show GR extract and shikonin dose-dependently inhibited glycation and enhanced oxidative defenses through nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element activation. Inflammatory targets, nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) and tumor necrosis factor alpha, were suppressed by GR extract and shikonin. Glyoxalase 1 (GLO1) and glutathione synthesis genes were significantly upregulated by GR extract and shikonin. GR extract boosted higher wavelength UV absorption in select cosmetic matrices. Rationale for the use of GR extract and shikonin are supported by our research. By inhibiting glycation, modulating oxidative stress, suppressing inflammation and UV-absorptive properties, GR extract and shikonin potentially offer multiple skin benefits.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We show GR extract and shikonin dose-dependently inhibited glycation and enhanced oxidative defenses through nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element activation. Inflammatory targets, nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) and tumor necrosis factor alpha, were suppressed by GR extract and shikonin. Glyoxalase 1 (GLO1) and glutathione synthesis genes were significantly upregulated by GR extract and shikonin. GR extract boosted higher wavelength UV absorption in select cosmetic matrices. Rationale for the use of GR extract and shikonin are supported by our research. By inhibiting glycation, modulating oxidative stress, suppressing inflammation and UV-absorptive properties, GR extract and shikonin potentially offer multiple skin benefits.		We show GR extract and shikonin dose-dependently inhibited glycation and enhanced oxidative defenses through nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element activation. Inflammatory targets, nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) and tumor necrosis factor alpha, were suppressed by GR extract and shikonin. Glyoxalase 1 (GLO1) and glutathione synthesis genes were significantly upregulated by GR extract and shikonin. GR extract boosted higher wavelength UV absorption in select cosmetic matrices. Rationale for the use of GR extract and shikonin are supported by our research. By inhibiting glycation, modulating oxidative stress, suppressing inflammation and UV-absorptive properties, GR extract and shikonin potentially offer multiple skin benefits.	Immunohistochemical staining	We show GR extract and shikonin dose-dependently inhibited glycation and enhanced oxidative defenses through nuclear factor erythroid 2-related factor 2 (Nrf2)/antioxidant response element activation. Inflammatory targets, nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB) and tumor necrosis factor alpha, were suppressed by GR extract and shikonin. Glyoxalase 1 (GLO1) and glutathione synthesis genes were significantly upregulated by GR extract and shikonin. GR extract boosted higher wavelength UV absorption in select cosmetic matrices. Rationale for the use of GR extract and shikonin are supported by our research. By inhibiting glycation, modulating oxidative stress, suppressing inflammation and UV-absorptive properties, GR extract and shikonin potentially offer multiple skin benefits.			qRT-PCR,qPCR				GLO1
29905573	chr7	148804380	148806380	EZH2	Collectively, our data demonstrated that modulating EZH2 expression in T cells can improve antitumor responses elicited by anti-CTLA-4 therapy, which provides a strong rationale for a combination trial of CPI-1205 plus ipilimumab.	human	lymphoid tissue	High+Lowthroughput	Modulation of EZH2 expression in T cells improves efficacy of anti-CTLA-4 therapy	否	无	tumour	T cell	E_01_0411	RNA-seq	Collectively, our data demonstrated that modulating EZH2 expression in T cells can improve antitumor responses elicited by anti-CTLA-4 therapy, which provides a strong rationale for a combination trial of CPI-1205 plus ipilimumab.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Collectively, our data demonstrated that modulating EZH2 expression in T cells can improve antitumor responses elicited by anti-CTLA-4 therapy, which provides a strong rationale for a combination trial of CPI-1205 plus ipilimumab.	Immunohistochemical staining	Collectively, our data demonstrated that modulating EZH2 expression in T cells can improve antitumor responses elicited by anti-CTLA-4 therapy, which provides a strong rationale for a combination trial of CPI-1205 plus ipilimumab.	EZH2		RNA-seq	Collectively, our data demonstrated that modulating EZH2 expression in T cells can improve antitumor responses elicited by anti-CTLA-4 therapy, which provides a strong rationale for a combination trial of CPI-1205 plus ipilimumab.			
29903884	chr11	112217210	112217767	Sox9	In vivo high-throughput chromatin accessibility techniques, transgenic assays, and genome editing revealed several novel gonadal regulatory elements in the 2-megabase gene desert upstream of Sox9 Although others are redundant, enhancer 13 (Enh13), a 557-base pair element located 565 kilobases 5' from the transcriptional start site, is essential to initiate mouse testis development; its deletion results in XY females with Sox9 transcript levels equivalent to those in XX gonads. Our data are consistent with the time-sensitive activity of SRY and indicate a strict order of enhancer usage. Enh13 is conserved and embedded within a 32.5-kilobase region whose deletion in humans is associated with XY sex reversal, suggesting that it is also critical in humans.	mouse	connective tissue	Low+High throughput	Sex reversal following deletion of a single distal enhancer of Sox9	否	--	--	Sertoli cell	E_02_0282	DNaseI-seq,ChIP-seq	In vivo high-throughput chromatin accessibility techniques, transgenic assays, and genome editing revealed several novel gonadal regulatory elements in the 2 Mb gene desert upstream of Sox9.Although others are redundant, Enh13, a 557 bp element located 565 kb 5’, is essential to initiate mouse testis development.	Enhancer	CRISPR/Cas9	ChIP-seq,RT-PCR	There was a 30 to 50% decrease in Sox9 mRNA levels in E11.5 XX Enh13-/- gonads compared to the wild type, as reflected by reduced immunofluorescence for SOX9 protein (fig. S11). These data indicate that Enh13 also plays a role in the very early expression of Sox9 in the XX gonad.	2010306G03Rik,AV220920,mKIAA4243	Enh13 is conserved and embedded within a 32.5-kilobase region whose deletion in humans is associated with XY sex reversal, suggesting that it is also critical in humans.	CRISPR/Cas9,RT-qPCR	This again supports the conclusion that Enh13 plays a more substantial role than TES during early gonadal development.	Sry	Tdf,Tdy	ChIP-qPCR	We performed ChIP-qPCR on E11.5 gonads dissected from Sry-Myc transgenic embryos by using a specific antibody against the MYC tag.SRY-MYC–positive gonads had an 11-fold enrichment versus SRY-MYC–negative gonads with primers spanning the SOX9 consensus site and a sixfold enrichment with primers spanning the SRY site, whereas primers against the strongest SRY binding site in TESCO showed fivefold enrichment.This reveals the strong binding of SRY to Enh13 at E11.5, with a preference for the SOX9 consensus site, possibly due to the adjacent SF1 binding site.	--	--	Sox9
29903884	chr11	112217210	112217767	Sry	In vivo high-throughput chromatin accessibility techniques, transgenic assays, and genome editing revealed several novel gonadal regulatory elements in the 2-megabase gene desert upstream of Sox9 Although others are redundant, enhancer 13 (Enh13), a 557-base pair element located 565 kilobases 5' from the transcriptional start site, is essential to initiate mouse testis development; its deletion results in XY females with Sox9 transcript levels equivalent to those in XX gonads. Our data are consistent with the time-sensitive activity of SRY and indicate a strict order of enhancer usage. Enh13 is conserved and embedded within a 32.5-kilobase region whose deletion in humans is associated with XY sex reversal, suggesting that it is also critical in humans.	mouse	connective tissue	Low+High throughput	Sex reversal following deletion of a single distal enhancer of Sox9	否	--	--	Sertoli cell	E_02_0282	DNaseI-seq,ChIP-seq	In vivo high-throughput chromatin accessibility techniques, transgenic assays, and genome editing revealed several novel gonadal regulatory elements in the 2 Mb gene desert upstream of Sox9.Although others are redundant, Enh13, a 557 bp element located 565 kb 5’, is essential to initiate mouse testis development.	Enhancer	CRISPR/Cas9	ChIP-seq,RT-PCR	There was a 30 to 50% decrease in Sox9 mRNA levels in E11.5 XX Enh13-/- gonads compared to the wild type, as reflected by reduced immunofluorescence for SOX9 protein (fig. S11). These data indicate that Enh13 also plays a role in the very early expression of Sox9 in the XX gonad.	2010306G03Rik,AV220920,mKIAA4243	Enh13 is conserved and embedded within a 32.5-kilobase region whose deletion in humans is associated with XY sex reversal, suggesting that it is also critical in humans.	CRISPR/Cas9,RT-qPCR	This again supports the conclusion that Enh13 plays a more substantial role than TES during early gonadal development.	Sry	Tdf,Tdy	ChIP-qPCR	We performed ChIP-qPCR on E11.5 gonads dissected from Sry-Myc transgenic embryos by using a specific antibody against the MYC tag.SRY-MYC–positive gonads had an 11-fold enrichment versus SRY-MYC–negative gonads with primers spanning the SOX9 consensus site and a sixfold enrichment with primers spanning the SRY site, whereas primers against the strongest SRY binding site in TESCO showed fivefold enrichment.This reveals the strong binding of SRY to Enh13 at E11.5, with a preference for the SOX9 consensus site, possibly due to the adjacent SF1 binding site.	--	--	Sox9
29903884	chr11	112217210	112217767	Sox8	In vivo high-throughput chromatin accessibility techniques, transgenic assays, and genome editing revealed several novel gonadal regulatory elements in the 2-megabase gene desert upstream of Sox9 Although others are redundant, enhancer 13 (Enh13), a 557-base pair element located 565 kilobases 5' from the transcriptional start site, is essential to initiate mouse testis development; its deletion results in XY females with Sox9 transcript levels equivalent to those in XX gonads. Our data are consistent with the time-sensitive activity of SRY and indicate a strict order of enhancer usage. Enh13 is conserved and embedded within a 32.5-kilobase region whose deletion in humans is associated with XY sex reversal, suggesting that it is also critical in humans.	mouse	connective tissue	Low+High throughput	Sex reversal following deletion of a single distal enhancer of Sox9	否	--	--	Sertoli cell	E_02_0282	DNaseI-seq,ChIP-seq	In vivo high-throughput chromatin accessibility techniques, transgenic assays, and genome editing revealed several novel gonadal regulatory elements in the 2 Mb gene desert upstream of Sox9.Although others are redundant, Enh13, a 557 bp element located 565 kb 5’, is essential to initiate mouse testis development.	Enhancer	CRISPR/Cas9	ChIP-seq,RT-PCR	There was a 30 to 50% decrease in Sox9 mRNA levels in E11.5 XX Enh13-/- gonads compared to the wild type, as reflected by reduced immunofluorescence for SOX9 protein (fig. S11). These data indicate that Enh13 also plays a role in the very early expression of Sox9 in the XX gonad.	2010306G03Rik,AV220920,mKIAA4243	Enh13 is conserved and embedded within a 32.5-kilobase region whose deletion in humans is associated with XY sex reversal, suggesting that it is also critical in humans.	CRISPR/Cas9,RT-qPCR	This again supports the conclusion that Enh13 plays a more substantial role than TES during early gonadal development.	Sry	Tdf,Tdy	ChIP-qPCR	We performed ChIP-qPCR on E11.5 gonads dissected from Sry-Myc transgenic embryos by using a specific antibody against the MYC tag.SRY-MYC–positive gonads had an 11-fold enrichment versus SRY-MYC–negative gonads with primers spanning the SOX9 consensus site and a sixfold enrichment with primers spanning the SRY site, whereas primers against the strongest SRY binding site in TESCO showed fivefold enrichment.This reveals the strong binding of SRY to Enh13 at E11.5, with a preference for the SOX9 consensus site, possibly due to the adjacent SF1 binding site.	--	--	Sox9
29903884	chr11	112217210	112217767	Dmrt1	In vivo high-throughput chromatin accessibility techniques, transgenic assays, and genome editing revealed several novel gonadal regulatory elements in the 2-megabase gene desert upstream of Sox9 Although others are redundant, enhancer 13 (Enh13), a 557-base pair element located 565 kilobases 5' from the transcriptional start site, is essential to initiate mouse testis development; its deletion results in XY females with Sox9 transcript levels equivalent to those in XX gonads. Our data are consistent with the time-sensitive activity of SRY and indicate a strict order of enhancer usage. Enh13 is conserved and embedded within a 32.5-kilobase region whose deletion in humans is associated with XY sex reversal, suggesting that it is also critical in humans.	mouse	connective tissue	Low+High throughput	Sex reversal following deletion of a single distal enhancer of Sox9	否	--	--	Sertoli cell	E_02_0282	DNaseI-seq,ChIP-seq	In vivo high-throughput chromatin accessibility techniques, transgenic assays, and genome editing revealed several novel gonadal regulatory elements in the 2 Mb gene desert upstream of Sox9.Although others are redundant, Enh13, a 557 bp element located 565 kb 5’, is essential to initiate mouse testis development.	Enhancer	CRISPR/Cas9	ChIP-seq,RT-PCR	There was a 30 to 50% decrease in Sox9 mRNA levels in E11.5 XX Enh13-/- gonads compared to the wild type, as reflected by reduced immunofluorescence for SOX9 protein (fig. S11). These data indicate that Enh13 also plays a role in the very early expression of Sox9 in the XX gonad.	2010306G03Rik,AV220920,mKIAA4243	Enh13 is conserved and embedded within a 32.5-kilobase region whose deletion in humans is associated with XY sex reversal, suggesting that it is also critical in humans.	CRISPR/Cas9,RT-qPCR	This again supports the conclusion that Enh13 plays a more substantial role than TES during early gonadal development.	Sry	Tdf,Tdy	ChIP-qPCR	We performed ChIP-qPCR on E11.5 gonads dissected from Sry-Myc transgenic embryos by using a specific antibody against the MYC tag.SRY-MYC–positive gonads had an 11-fold enrichment versus SRY-MYC–negative gonads with primers spanning the SOX9 consensus site and a sixfold enrichment with primers spanning the SRY site, whereas primers against the strongest SRY binding site in TESCO showed fivefold enrichment.This reveals the strong binding of SRY to Enh13 at E11.5, with a preference for the SOX9 consensus site, possibly due to the adjacent SF1 binding site.	--	--	Sox9
29903739	chr15	96725740	96737960	Tbx20	Myocardial TBX20 directly regulates a subset of genes required for fetal cardiomyocyte proliferation, including those required for the G1-S transition. TBX20 also directly downregulates progenitor-specific genes and, in addition to regulating genes that specify chamber versus nonchamber myocardium, directly activates genes required for establishment or maintenance of atrial and ventricular identity. TBX20 plays a previously unappreciated key role in atrial development through direct regulation of an evolutionarily conserved COUPT-FII enhancer.	human	Nervous tissue	Low+High throughput	Tbx20 Is Required in Mid-Gestation Cardiomyocytes and Plays a Central Role in Atrial Development	否	--	Congenital Heart Disease	cardiac muscle cell (sensu Arthopoda)	E_02_0283	ChIP-seq,Hi-C	we made use of our TBX20 ChIP-Seq analysis in E11.5 hearts and attributed TBX20 bound sites to the nearest expressed gene in E11.5 control or Tbx20 cKO cardiomyocytes. Next, we overlaid our RNA-Seq data with that of our TBX20 ChIP-Seq analysis in E11.5 hearts and identified 548 genes that were differentially expressed in Tbx20 cKO cardiomyocytes and were marked by one or more TBX20 binding events in the vicinity of the gene.	Enhancer	--	Hi-C	We next established that this Enhancer was functionally connected with COUP-TFII. We performed a promoter-based Capture Hi-C in iPSC-derived human cardiomyocytes to identify long-range physical interactions between genes and Enhancers. We observed that this Enhancer directly loops and contacts the COUP-TFII promoter,140-Kb away,confirming that this is a COUP-TFII Enhancer.	ARP-1,ARP1,CHTD4,COUPTF2,COUPTFB,COUPTFII,NF-E3,SVP40,TFCOUP2	This Enhancer interacted with the NR2F2 promoter in human cardiomyocytes and conferred atrial specific gene expression in a transgenic mouse in a TBX20 dependent manner.	Hi-C	Taken together, these results linked TBX20 binding to an evolutionary conserved Enhancer that regulates COUP-TFII expression in developing atrial cardiomyocytes, uncovering a mechanism by which COUP-TFII expression is TBX20 dependent.	TBX20	ASD4	X-Gal Staining Assay 	Section analysis of COUP-TFII enh1::lacZ transgenic embryo demonstrates X-gal staining in developing atrial myocardium (arrows) and caval vein (arrowheads). 	--	--	NR2F2
29903739	chr15	96725740	96737960	Nr2f2	Myocardial TBX20 directly regulates a subset of genes required for fetal cardiomyocyte proliferation, including those required for the G1-S transition. TBX20 also directly downregulates progenitor-specific genes and, in addition to regulating genes that specify chamber versus nonchamber myocardium, directly activates genes required for establishment or maintenance of atrial and ventricular identity. TBX20 plays a previously unappreciated key role in atrial development through direct regulation of an evolutionarily conserved COUPT-FII enhancer.	human	Nervous tissue	Low+High throughput	Tbx20 Is Required in Mid-Gestation Cardiomyocytes and Plays a Central Role in Atrial Development	否	--	Congenital Heart Disease	cardiac muscle cell (sensu Arthopoda)	E_02_0283	ChIP-seq,Hi-C	we made use of our TBX20 ChIP-Seq analysis in E11.5 hearts and attributed TBX20 bound sites to the nearest expressed gene in E11.5 control or Tbx20 cKO cardiomyocytes. Next, we overlaid our RNA-Seq data with that of our TBX20 ChIP-Seq analysis in E11.5 hearts and identified 548 genes that were differentially expressed in Tbx20 cKO cardiomyocytes and were marked by one or more TBX20 binding events in the vicinity of the gene.	Enhancer	--	Hi-C	We next established that this Enhancer was functionally connected with COUP-TFII. We performed a promoter-based Capture Hi-C in iPSC-derived human cardiomyocytes to identify long-range physical interactions between genes and Enhancers. We observed that this Enhancer directly loops and contacts the COUP-TFII promoter,140-Kb away,confirming that this is a COUP-TFII Enhancer.	ARP-1,ARP1,CHTD4,COUPTF2,COUPTFB,COUPTFII,NF-E3,SVP40,TFCOUP2	This Enhancer interacted with the NR2F2 promoter in human cardiomyocytes and conferred atrial specific gene expression in a transgenic mouse in a TBX20 dependent manner.	Hi-C	Taken together, these results linked TBX20 binding to an evolutionary conserved Enhancer that regulates COUP-TFII expression in developing atrial cardiomyocytes, uncovering a mechanism by which COUP-TFII expression is TBX20 dependent.	TBX20	ASD4	X-Gal Staining Assay 	Section analysis of COUP-TFII enh1::lacZ transgenic embryo demonstrates X-gal staining in developing atrial myocardium (arrows) and caval vein (arrowheads). 	--	--	NR2F2
29902458	chr16	29880836	29882836	Hes1	In addition, knockdown of Hes1 abrogated the miR-374b inhibition-mediated effect on NSC proliferation and differentiation. Taken together, these results demonstrate that miR-374b regulates the proliferation and differentiation of NSCs through targeting Hes1 and suggest that miR-374b is a potential target for modulating NSC-mediated neurogenesis.	mouse	Nervous tissue	High+Lowthroughput	MicroRNA-374b promotes the proliferation and differentiation of neural stem cells through targeting Hes1	否	无	nothing	neuronal stem cell	E_02_0284	RT-qPCR,Immunocytochemistry,Western blot,Cell transfection,Dual-luciferase reporter assay,Cell proliferation assay,	In addition, knockdown of Hes1 abrogated the miR-374b inhibition-mediated effect on NSC proliferation and differentiation. Taken together, these results demonstrate that miR-374b regulates the proliferation and differentiation of NSCs through targeting Hes1 and suggest that miR-374b is a potential target for modulating NSC-mediated neurogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, knockdown of Hes1 abrogated the miR-374b inhibition-mediated effect on NSC proliferation and differentiation. Taken together, these results demonstrate that miR-374b regulates the proliferation and differentiation of NSCs through targeting Hes1 and suggest that miR-374b is a potential target for modulating NSC-mediated neurogenesis.		In addition, knockdown of Hes1 abrogated the miR-374b inhibition-mediated effect on NSC proliferation and differentiation. Taken together, these results demonstrate that miR-374b regulates the proliferation and differentiation of NSCs through targeting Hes1 and suggest that miR-374b is a potential target for modulating NSC-mediated neurogenesis.	Immunohistochemical staining	In addition, knockdown of Hes1 abrogated the miR-374b inhibition-mediated effect on NSC proliferation and differentiation. Taken together, these results demonstrate that miR-374b regulates the proliferation and differentiation of NSCs through targeting Hes1 and suggest that miR-374b is a potential target for modulating NSC-mediated neurogenesis.			RT-qPCR,Immunocytochemistry,Western blot,Cell transfection,Dual-luciferase reporter assay,Cell proliferation assay,				Hes1
29899688	chr21	25877858	25879858	APP	To study the relationship between Mg2+ and TNF-α, we used human- or mouse-derived glial and neuronal cell lines or APP/PS1 transgenic (Tg) mice as in vitro and in vivo experimental models, respectively. Our data demonstrates that magnesium-L-threonate (MgT) can decrease the expression of TNF-α by restoring the levels of Mg2+ in glial cells. In addition, PI3-K/AKT and NF-κB signals play critical roles in mediating the effects of Mg2+ on suppressing the expression of TNF-α. In neurons, Mg2+ elevation showed similar suppressive effects on the expression of presenilin enhancer 2 (PEN2) and nicastrin (NCT) through a PI3-K/AKT and NF-κB-dependent mechanism. As the major components of γ-secretase, overexpression of presenilin 1 (PS1), PEN2 and NCT potentially promote the synthesis of Aβ, which in turn activates TNF-α in glial cells. Reciprocally, TNF-α stimulates the expression of PEN2 and NCT in neurons. The crosstalk between TNF-α and Aβ in glial cells and neurons could ultimately aggravate the development and progression of AD.	human	Nervous tissue	High+Lowthroughput	Magnesium Ions Inhibit the Expression of Tumor Necrosis Factor α and the Activity of γ-Secretase in a β-Amyloid Protein-Dependent Mechanism in APP/PS1 Transgenic Mice	否	无	Alzheimer's disease (AD)	A172	E_01_0412	transgenic mice,qRT-PCR,SDS-PAGE,Western blot,Immunohistochemistry,	To study the relationship between Mg2+ and TNF-α, we used human- or mouse-derived glial and neuronal cell lines or APP/PS1 transgenic (Tg) mice as in vitro and in vivo experimental models, respectively. Our data demonstrates that magnesium-L-threonate (MgT) can decrease the expression of TNF-α by restoring the levels of Mg2+ in glial cells. In addition, PI3-K/AKT and NF-κB signals play critical roles in mediating the effects of Mg2+ on suppressing the expression of TNF-α. In neurons, Mg2+ elevation showed similar suppressive effects on the expression of presenilin enhancer 2 (PEN2) and nicastrin (NCT) through a PI3-K/AKT and NF-κB-dependent mechanism. As the major components of γ-secretase, overexpression of presenilin 1 (PS1), PEN2 and NCT potentially promote the synthesis of Aβ, which in turn activates TNF-α in glial cells. Reciprocally, TNF-α stimulates the expression of PEN2 and NCT in neurons. The crosstalk between TNF-α and Aβ in glial cells and neurons could ultimately aggravate the development and progression of AD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			To study the relationship between Mg2+ and TNF-α, we used human- or mouse-derived glial and neuronal cell lines or APP/PS1 transgenic (Tg) mice as in vitro and in vivo experimental models, respectively. Our data demonstrates that magnesium-L-threonate (MgT) can decrease the expression of TNF-α by restoring the levels of Mg2+ in glial cells. In addition, PI3-K/AKT and NF-κB signals play critical roles in mediating the effects of Mg2+ on suppressing the expression of TNF-α. In neurons, Mg2+ elevation showed similar suppressive effects on the expression of presenilin enhancer 2 (PEN2) and nicastrin (NCT) through a PI3-K/AKT and NF-κB-dependent mechanism. As the major components of γ-secretase, overexpression of presenilin 1 (PS1), PEN2 and NCT potentially promote the synthesis of Aβ, which in turn activates TNF-α in glial cells. Reciprocally, TNF-α stimulates the expression of PEN2 and NCT in neurons. The crosstalk between TNF-α and Aβ in glial cells and neurons could ultimately aggravate the development and progression of AD.	Immunohistochemical staining	To study the relationship between Mg2+ and TNF-α, we used human- or mouse-derived glial and neuronal cell lines or APP/PS1 transgenic (Tg) mice as in vitro and in vivo experimental models, respectively. Our data demonstrates that magnesium-L-threonate (MgT) can decrease the expression of TNF-α by restoring the levels of Mg2+ in glial cells. In addition, PI3-K/AKT and NF-κB signals play critical roles in mediating the effects of Mg2+ on suppressing the expression of TNF-α. In neurons, Mg2+ elevation showed similar suppressive effects on the expression of presenilin enhancer 2 (PEN2) and nicastrin (NCT) through a PI3-K/AKT and NF-κB-dependent mechanism. As the major components of γ-secretase, overexpression of presenilin 1 (PS1), PEN2 and NCT potentially promote the synthesis of Aβ, which in turn activates TNF-α in glial cells. Reciprocally, TNF-α stimulates the expression of PEN2 and NCT in neurons. The crosstalk between TNF-α and Aβ in glial cells and neurons could ultimately aggravate the development and progression of AD.	APP		transgenic mice,qRT-PCR,SDS-PAGE,Western blot,Immunohistochemistry,	To study the relationship between Mg2+ and TNF-α, we used human- or mouse-derived glial and neuronal cell lines or APP/PS1 transgenic (Tg) mice as in vitro and in vivo experimental models, respectively. Our data demonstrates that magnesium-L-threonate (MgT) can decrease the expression of TNF-α by restoring the levels of Mg2+ in glial cells. In addition, PI3-K/AKT and NF-κB signals play critical roles in mediating the effects of Mg2+ on suppressing the expression of TNF-α. In neurons, Mg2+ elevation showed similar suppressive effects on the expression of presenilin enhancer 2 (PEN2) and nicastrin (NCT) through a PI3-K/AKT and NF-κB-dependent mechanism. As the major components of γ-secretase, overexpression of presenilin 1 (PS1), PEN2 and NCT potentially promote the synthesis of Aβ, which in turn activates TNF-α in glial cells. Reciprocally, TNF-α stimulates the expression of PEN2 and NCT in neurons. The crosstalk between TNF-α and Aβ in glial cells and neurons could ultimately aggravate the development and progression of AD.			
29898397	chr7	148805021	148807021	EZH2	Here, we reveal a mechanism to selectively target and reprogram the function of tumor-infiltrating Tregs (TI-Tregs) by exploiting their dependency on the histone H3K27 methyltransferase enhancer of zeste homolog 2 (EZH2) in tumors. Disruption of EZH2 activity in Tregs, either pharmacologically or genetically, drove the acquisition of pro-inflammatory functions in TI-Tregs, remodeling the tumor microenvironment and enhancing the recruitment and function of CD8 and CD4 effector T cells that eliminate tumors. Moreover, abolishing EZH2 function in Tregs was mechanistically distinct from, more potent than, and less toxic than a generalized Treg depletion approach. This study reveals a strategy to target Tregs in cancer that mitigates autoimmunity by reprogramming their function in tumors to enhance anti-cancer immunity.	human	lymphoid tissue	High+Lowthroughput	Targeting EZH2 Reprograms Intratumoral Regulatory T Cells to Enhance Cancer Immunity	否	无	cancer	lymphocyte	E_01_0413	Flow Cytometry,Histology, RNA-seq,transgenic mice	Here, we reveal a mechanism to selectively target and reprogram the function of tumor-infiltrating Tregs (TI-Tregs) by exploiting their dependency on the histone H3K27 methyltransferase enhancer of zeste homolog 2 (EZH2) in tumors. Disruption of EZH2 activity in Tregs, either pharmacologically or genetically, drove the acquisition of pro-inflammatory functions in TI-Tregs, remodeling the tumor microenvironment and enhancing the recruitment and function of CD8 and CD4 effector T cells that eliminate tumors. Moreover, abolishing EZH2 function in Tregs was mechanistically distinct from, more potent than, and less toxic than a generalized Treg depletion approach. This study reveals a strategy to target Tregs in cancer that mitigates autoimmunity by reprogramming their function in tumors to enhance anti-cancer immunity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we reveal a mechanism to selectively target and reprogram the function of tumor-infiltrating Tregs (TI-Tregs) by exploiting their dependency on the histone H3K27 methyltransferase enhancer of zeste homolog 2 (EZH2) in tumors. Disruption of EZH2 activity in Tregs, either pharmacologically or genetically, drove the acquisition of pro-inflammatory functions in TI-Tregs, remodeling the tumor microenvironment and enhancing the recruitment and function of CD8 and CD4 effector T cells that eliminate tumors. Moreover, abolishing EZH2 function in Tregs was mechanistically distinct from, more potent than, and less toxic than a generalized Treg depletion approach. This study reveals a strategy to target Tregs in cancer that mitigates autoimmunity by reprogramming their function in tumors to enhance anti-cancer immunity.	Immunohistochemical staining	Here, we reveal a mechanism to selectively target and reprogram the function of tumor-infiltrating Tregs (TI-Tregs) by exploiting their dependency on the histone H3K27 methyltransferase enhancer of zeste homolog 2 (EZH2) in tumors. Disruption of EZH2 activity in Tregs, either pharmacologically or genetically, drove the acquisition of pro-inflammatory functions in TI-Tregs, remodeling the tumor microenvironment and enhancing the recruitment and function of CD8 and CD4 effector T cells that eliminate tumors. Moreover, abolishing EZH2 function in Tregs was mechanistically distinct from, more potent than, and less toxic than a generalized Treg depletion approach. This study reveals a strategy to target Tregs in cancer that mitigates autoimmunity by reprogramming their function in tumors to enhance anti-cancer immunity.	EZH2		Flow Cytometry,Histology, RNA-seq,transgenic mice	Here, we reveal a mechanism to selectively target and reprogram the function of tumor-infiltrating Tregs (TI-Tregs) by exploiting their dependency on the histone H3K27 methyltransferase enhancer of zeste homolog 2 (EZH2) in tumors. Disruption of EZH2 activity in Tregs, either pharmacologically or genetically, drove the acquisition of pro-inflammatory functions in TI-Tregs, remodeling the tumor microenvironment and enhancing the recruitment and function of CD8 and CD4 effector T cells that eliminate tumors. Moreover, abolishing EZH2 function in Tregs was mechanistically distinct from, more potent than, and less toxic than a generalized Treg depletion approach. This study reveals a strategy to target Tregs in cancer that mitigates autoimmunity by reprogramming their function in tumors to enhance anti-cancer immunity.			
29898397	chrX	49247860	49249860	FOXP3	Here, we reveal a mechanism to selectively target and reprogram the function of tumor-infiltrating Tregs (TI-Tregs) by exploiting their dependency on the histone H3K27 methyltransferase enhancer of zeste homolog 2 (EZH2) in tumors. Disruption of EZH2 activity in Tregs, either pharmacologically or genetically, drove the acquisition of pro-inflammatory functions in TI-Tregs, remodeling the tumor microenvironment and enhancing the recruitment and function of CD8 and CD4 effector T cells that eliminate tumors. Moreover, abolishing EZH2 function in Tregs was mechanistically distinct from, more potent than, and less toxic than a generalized Treg depletion approach. This study reveals a strategy to target Tregs in cancer that mitigates autoimmunity by reprogramming their function in tumors to enhance anti-cancer immunity.	human	lymphoid tissue	High+Lowthroughput	Targeting EZH2 Reprograms Intratumoral Regulatory T Cells to Enhance Cancer Immunity	否	无	cancer	lymphocyte	E_01_0413	Flow Cytometry,Histology, RNA-seq,transgenic mice	Here, we reveal a mechanism to selectively target and reprogram the function of tumor-infiltrating Tregs (TI-Tregs) by exploiting their dependency on the histone H3K27 methyltransferase enhancer of zeste homolog 2 (EZH2) in tumors. Disruption of EZH2 activity in Tregs, either pharmacologically or genetically, drove the acquisition of pro-inflammatory functions in TI-Tregs, remodeling the tumor microenvironment and enhancing the recruitment and function of CD8 and CD4 effector T cells that eliminate tumors. Moreover, abolishing EZH2 function in Tregs was mechanistically distinct from, more potent than, and less toxic than a generalized Treg depletion approach. This study reveals a strategy to target Tregs in cancer that mitigates autoimmunity by reprogramming their function in tumors to enhance anti-cancer immunity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we reveal a mechanism to selectively target and reprogram the function of tumor-infiltrating Tregs (TI-Tregs) by exploiting their dependency on the histone H3K27 methyltransferase enhancer of zeste homolog 2 (EZH2) in tumors. Disruption of EZH2 activity in Tregs, either pharmacologically or genetically, drove the acquisition of pro-inflammatory functions in TI-Tregs, remodeling the tumor microenvironment and enhancing the recruitment and function of CD8 and CD4 effector T cells that eliminate tumors. Moreover, abolishing EZH2 function in Tregs was mechanistically distinct from, more potent than, and less toxic than a generalized Treg depletion approach. This study reveals a strategy to target Tregs in cancer that mitigates autoimmunity by reprogramming their function in tumors to enhance anti-cancer immunity.	Immunohistochemical staining	Here, we reveal a mechanism to selectively target and reprogram the function of tumor-infiltrating Tregs (TI-Tregs) by exploiting their dependency on the histone H3K27 methyltransferase enhancer of zeste homolog 2 (EZH2) in tumors. Disruption of EZH2 activity in Tregs, either pharmacologically or genetically, drove the acquisition of pro-inflammatory functions in TI-Tregs, remodeling the tumor microenvironment and enhancing the recruitment and function of CD8 and CD4 effector T cells that eliminate tumors. Moreover, abolishing EZH2 function in Tregs was mechanistically distinct from, more potent than, and less toxic than a generalized Treg depletion approach. This study reveals a strategy to target Tregs in cancer that mitigates autoimmunity by reprogramming their function in tumors to enhance anti-cancer immunity.	FOXP3		Flow Cytometry,Histology, RNA-seq,transgenic mice	Here, we reveal a mechanism to selectively target and reprogram the function of tumor-infiltrating Tregs (TI-Tregs) by exploiting their dependency on the histone H3K27 methyltransferase enhancer of zeste homolog 2 (EZH2) in tumors. Disruption of EZH2 activity in Tregs, either pharmacologically or genetically, drove the acquisition of pro-inflammatory functions in TI-Tregs, remodeling the tumor microenvironment and enhancing the recruitment and function of CD8 and CD4 effector T cells that eliminate tumors. Moreover, abolishing EZH2 function in Tregs was mechanistically distinct from, more potent than, and less toxic than a generalized Treg depletion approach. This study reveals a strategy to target Tregs in cancer that mitigates autoimmunity by reprogramming their function in tumors to enhance anti-cancer immunity.			
29897487	chr4	55524704	55526704	Klf4	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).	mouse	Epithelial tissues	High+Lowthroughput	Dietary Red Raspberry Reduces Colorectal Inflammation and Carcinogenic Risk in Mice with Dextran Sulfate Sodium-Induced Colitis	否	无	Colorectal inflammation	goblet cell	E_02_0285	qRT-PCR,Immunohistochemical analysis,Immunoblotting analysis	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).		Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).	Immunohistochemical staining	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).			qRT-PCR,Immunohistochemical analysis,Immunoblotting analysis				Klf4
29897487	chr16	29880535	29882535	Hes1	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).	mouse	Epithelial tissues	High+Lowthroughput	Dietary Red Raspberry Reduces Colorectal Inflammation and Carcinogenic Risk in Mice with Dextran Sulfate Sodium-Induced Colitis	否	无	Colorectal inflammation	goblet cell	E_02_0285	qRT-PCR,Immunohistochemical analysis,Immunoblotting analysis	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).		Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).	Immunohistochemical staining	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).			qRT-PCR,Immunohistochemical analysis,Immunoblotting analysis				Hes1
29897487	chr7	141273629	141275629	Muc2	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).	mouse	Epithelial tissues	High+Lowthroughput	Dietary Red Raspberry Reduces Colorectal Inflammation and Carcinogenic Risk in Mice with Dextran Sulfate Sodium-Induced Colitis	否	无	Colorectal inflammation	goblet cell	E_02_0285	qRT-PCR,Immunohistochemical analysis,Immunoblotting analysis	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).		Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).	Immunohistochemical staining	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).			qRT-PCR,Immunohistochemical analysis,Immunoblotting analysis				Muc2
29897487	chr17	42310769	42312769	STAT3	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).	mouse	Epithelial tissues	High+Lowthroughput	Dietary Red Raspberry Reduces Colorectal Inflammation and Carcinogenic Risk in Mice with Dextran Sulfate Sodium-Induced Colitis	否	无	Colorectal inflammation	goblet cell	E_02_0285	qRT-PCR,Immunohistochemical analysis,Immunoblotting analysis	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).		Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).	Immunohistochemical staining	Furthermore, RB supplementation facilitated epithelium repair, as evidenced by enhanced goblet cell density, expression of transcription factors including Kruppel-like factor 4 (Klf4) and Hairy and enhancer of split 1 (Hes1), terminal differentiation markers, mucin 2 (Muc2), and intestinal alkaline phosphatase (by 20-200%; P ≤ 0.01). Conversely, proliferating cell nuclear antigen (by 70%; P ≤ 0.01), β-catenin, and signal transducer and activator of transcription 3 (STAT3) signaling (by 19-33%; P ≤ 0.05) were reduced by RB supplementation. In addition, RB supplementation enhanced p53 stability (by 53%) and reduced oncogenic gene expression (by 50-60%).			qRT-PCR,Immunohistochemical analysis,Immunoblotting analysis				STAT3
29896299	chr2	216669551	216671551	IGFBP5	Taken together, our findings reveal that atheroprotective flow reduces H3K27me3 as a chromatin-based mechanism to augment the expression of genes that confer an anti-inflammatory response in the endothelium. Our study exemplifies flow-dependent epigenetic regulation of endothelial gene expression, and also suggests that targeting the EZH2/H3K27me3/IGFBP5 pathway may offer novel therapeutics for inflammatory disorders such as atherosclerosis.	human	Epithelial tissues	High+Lowthroughput	Flow-dependent epigenetic regulation of IGFBP5 expression by H3K27me3 contributes to endothelial anti-inflammatory effects	否	无	atherosclerosis	HUVECs	E_01_0414	ChIP,RNA-seq,ChIP-qPCR,Western blot ,siRNA,miRNA transfection,Luciferase reporter assay,immunofluorescent staining,	Taken together, our findings reveal that atheroprotective flow reduces H3K27me3 as a chromatin-based mechanism to augment the expression of genes that confer an anti-inflammatory response in the endothelium. Our study exemplifies flow-dependent epigenetic regulation of endothelial gene expression, and also suggests that targeting the EZH2/H3K27me3/IGFBP5 pathway may offer novel therapeutics for inflammatory disorders such as atherosclerosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, our findings reveal that atheroprotective flow reduces H3K27me3 as a chromatin-based mechanism to augment the expression of genes that confer an anti-inflammatory response in the endothelium. Our study exemplifies flow-dependent epigenetic regulation of endothelial gene expression, and also suggests that targeting the EZH2/H3K27me3/IGFBP5 pathway may offer novel therapeutics for inflammatory disorders such as atherosclerosis.		Taken together, our findings reveal that atheroprotective flow reduces H3K27me3 as a chromatin-based mechanism to augment the expression of genes that confer an anti-inflammatory response in the endothelium. Our study exemplifies flow-dependent epigenetic regulation of endothelial gene expression, and also suggests that targeting the EZH2/H3K27me3/IGFBP5 pathway may offer novel therapeutics for inflammatory disorders such as atherosclerosis.	Immunohistochemical staining	Taken together, our findings reveal that atheroprotective flow reduces H3K27me3 as a chromatin-based mechanism to augment the expression of genes that confer an anti-inflammatory response in the endothelium. Our study exemplifies flow-dependent epigenetic regulation of endothelial gene expression, and also suggests that targeting the EZH2/H3K27me3/IGFBP5 pathway may offer novel therapeutics for inflammatory disorders such as atherosclerosis.			ChIP,RNA-seq,ChIP-qPCR,Western blot ,siRNA,miRNA transfection,Luciferase reporter assay,immunofluorescent staining,				IGFBP5
29896299	chr7	148804460	148806460	EZH2	Taken together, our findings reveal that atheroprotective flow reduces H3K27me3 as a chromatin-based mechanism to augment the expression of genes that confer an anti-inflammatory response in the endothelium. Our study exemplifies flow-dependent epigenetic regulation of endothelial gene expression, and also suggests that targeting the EZH2/H3K27me3/IGFBP5 pathway may offer novel therapeutics for inflammatory disorders such as atherosclerosis.	human	Epithelial tissues	High+Lowthroughput	Flow-dependent epigenetic regulation of IGFBP5 expression by H3K27me3 contributes to endothelial anti-inflammatory effects	否	无	atherosclerosis	HUVECs	E_01_0414	ChIP,RNA-seq,ChIP-qPCR,Western blot ,siRNA,miRNA transfection,Luciferase reporter assay,immunofluorescent staining,	Taken together, our findings reveal that atheroprotective flow reduces H3K27me3 as a chromatin-based mechanism to augment the expression of genes that confer an anti-inflammatory response in the endothelium. Our study exemplifies flow-dependent epigenetic regulation of endothelial gene expression, and also suggests that targeting the EZH2/H3K27me3/IGFBP5 pathway may offer novel therapeutics for inflammatory disorders such as atherosclerosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Taken together, our findings reveal that atheroprotective flow reduces H3K27me3 as a chromatin-based mechanism to augment the expression of genes that confer an anti-inflammatory response in the endothelium. Our study exemplifies flow-dependent epigenetic regulation of endothelial gene expression, and also suggests that targeting the EZH2/H3K27me3/IGFBP5 pathway may offer novel therapeutics for inflammatory disorders such as atherosclerosis.	Immunohistochemical staining	Taken together, our findings reveal that atheroprotective flow reduces H3K27me3 as a chromatin-based mechanism to augment the expression of genes that confer an anti-inflammatory response in the endothelium. Our study exemplifies flow-dependent epigenetic regulation of endothelial gene expression, and also suggests that targeting the EZH2/H3K27me3/IGFBP5 pathway may offer novel therapeutics for inflammatory disorders such as atherosclerosis.	EZH2		ChIP,RNA-seq,ChIP-qPCR,Western blot ,siRNA,miRNA transfection,Luciferase reporter assay,immunofluorescent staining,	Taken together, our findings reveal that atheroprotective flow reduces H3K27me3 as a chromatin-based mechanism to augment the expression of genes that confer an anti-inflammatory response in the endothelium. Our study exemplifies flow-dependent epigenetic regulation of endothelial gene expression, and also suggests that targeting the EZH2/H3K27me3/IGFBP5 pathway may offer novel therapeutics for inflammatory disorders such as atherosclerosis.			
29894816	chr2	136111792	136113792	CXCR4	The current results indicate that 4DV3 might serve as a prototype for a new type of dual function ligand, one that acts as a HIV-1 entry inhibitor and a CXCR4 drug delivery targeting ligand.	human	lymphoid tissue	High+Lowthroughput	Design and evaluation of a CXCR4 targeting peptide 4DV3 as an HIV entry inhibitor and a ligand for targeted drug delivery	否	无	AIDS		E_01_0415	competitive binding assay,MTT assay,luciferase activity	The current results indicate that 4DV3 might serve as a prototype for a new type of dual function ligand, one that acts as a HIV-1 entry inhibitor and a CXCR4 drug delivery targeting ligand.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The current results indicate that 4DV3 might serve as a prototype for a new type of dual function ligand, one that acts as a HIV-1 entry inhibitor and a CXCR4 drug delivery targeting ligand.	Immunohistochemical staining	The current results indicate that 4DV3 might serve as a prototype for a new type of dual function ligand, one that acts as a HIV-1 entry inhibitor and a CXCR4 drug delivery targeting ligand.	CXCR4		competitive binding assay,MTT assay,luciferase activity	The current results indicate that 4DV3 might serve as a prototype for a new type of dual function ligand, one that acts as a HIV-1 entry inhibitor and a CXCR4 drug delivery targeting ligand.			
29893919	chr8	38139821	38141821	STAR	Herein, we provide investigators with rationale for each step in the MMARGE pipeline and key differences for analysis of datasets with different experimental designs. We demonstrate the utility of MMARGE using mouse peritoneal macrophages, liver cells, and human lymphoblastoid cells. MMARGE provides a powerful tool to identify combinations of cell type-specific transcription factors while simultaneously interpreting functional effects of non-coding genetic variation.	mouse	lymphoid tissue	High+Lowthroughput	MMARGE: Motif Mutation Analysis for Regulatory Genomic Elements	否	无	nothing	peritoneal macrophages	E_02_0286	ATAC-seq,DNase I,CHIP-seq,GWAS,	Herein, we provide investigators with rationale for each step in the MMARGE pipeline and key differences for analysis of datasets with different experimental designs. We demonstrate the utility of MMARGE using mouse peritoneal macrophages, liver cells, and human lymphoblastoid cells. MMARGE provides a powerful tool to identify combinations of cell type-specific transcription factors while simultaneously interpreting functional effects of non-coding genetic variation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Herein, we provide investigators with rationale for each step in the MMARGE pipeline and key differences for analysis of datasets with different experimental designs. We demonstrate the utility of MMARGE using mouse peritoneal macrophages, liver cells, and human lymphoblastoid cells. MMARGE provides a powerful tool to identify combinations of cell type-specific transcription factors while simultaneously interpreting functional effects of non-coding genetic variation.		Herein, we provide investigators with rationale for each step in the MMARGE pipeline and key differences for analysis of datasets with different experimental designs. We demonstrate the utility of MMARGE using mouse peritoneal macrophages, liver cells, and human lymphoblastoid cells. MMARGE provides a powerful tool to identify combinations of cell type-specific transcription factors while simultaneously interpreting functional effects of non-coding genetic variation.	Immunohistochemical staining	Herein, we provide investigators with rationale for each step in the MMARGE pipeline and key differences for analysis of datasets with different experimental designs. We demonstrate the utility of MMARGE using mouse peritoneal macrophages, liver cells, and human lymphoblastoid cells. MMARGE provides a powerful tool to identify combinations of cell type-specific transcription factors while simultaneously interpreting functional effects of non-coding genetic variation.			ATAC-seq,DNase I,CHIP-seq,GWAS,				STAR
29889836	chr1	169719974	169721974	SELE	In conclusion, everolimus attenuates EC activation via reduced NF-κB p65 translocation causing decreased E-selectin and VCAM-1 expression at transcriptional and post-transcriptional level after DES.	human	Epithelial tissues	High+Lowthroughput	Endothelial cell activation is attenuated by everolimus via transcriptional and post-transcriptional regulatory mechanisms after drug-eluting coronary stenting	否	无	nothing	HCAEC	E_01_0416	RT-qPCR,ELISA,ChIP-seq,Transfection,	In conclusion, everolimus attenuates EC activation via reduced NF-κB p65 translocation causing decreased E-selectin and VCAM-1 expression at transcriptional and post-transcriptional level after DES.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, everolimus attenuates EC activation via reduced NF-κB p65 translocation causing decreased E-selectin and VCAM-1 expression at transcriptional and post-transcriptional level after DES.		In conclusion, everolimus attenuates EC activation via reduced NF-κB p65 translocation causing decreased E-selectin and VCAM-1 expression at transcriptional and post-transcriptional level after DES.	Immunohistochemical staining	In conclusion, everolimus attenuates EC activation via reduced NF-κB p65 translocation causing decreased E-selectin and VCAM-1 expression at transcriptional and post-transcriptional level after DES.			RT-qPCR,ELISA,ChIP-seq,Transfection,				SELE
29889836	chr1	100717343	100719343	VCAM1	In conclusion, everolimus attenuates EC activation via reduced NF-κB p65 translocation causing decreased E-selectin and VCAM-1 expression at transcriptional and post-transcriptional level after DES.	human	Epithelial tissues	High+Lowthroughput	Endothelial cell activation is attenuated by everolimus via transcriptional and post-transcriptional regulatory mechanisms after drug-eluting coronary stenting	否	无	nothing	HCAEC	E_01_0416	RT-qPCR,ELISA,ChIP-seq,Transfection,	In conclusion, everolimus attenuates EC activation via reduced NF-κB p65 translocation causing decreased E-selectin and VCAM-1 expression at transcriptional and post-transcriptional level after DES.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, everolimus attenuates EC activation via reduced NF-κB p65 translocation causing decreased E-selectin and VCAM-1 expression at transcriptional and post-transcriptional level after DES.		In conclusion, everolimus attenuates EC activation via reduced NF-κB p65 translocation causing decreased E-selectin and VCAM-1 expression at transcriptional and post-transcriptional level after DES.	Immunohistochemical staining	In conclusion, everolimus attenuates EC activation via reduced NF-κB p65 translocation causing decreased E-selectin and VCAM-1 expression at transcriptional and post-transcriptional level after DES.			RT-qPCR,ELISA,ChIP-seq,Transfection,				VCAM1
29888110	chr4	7751285	7753285	AFAP1-AS1	Here, we identify a lncRNA AFAP1-AS1 that facilitates colorectal cancer, where it is upregulated. AFAP1-AS1 expression was associated with colorectal cancer patient survival. AFAP1-AS1 knockdown inhibited cell proliferation, cell cycle, and tumorigenesis in an subcutaneous mouse xenograft model system. Further data demonstrated that AFAP1-AS1 was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of EZH2 target genes. Our findings indicate that AFAP1-AS1 is an oncogenic lncRNA that promotes tumor progression and may be a novel prognostic factor in colorectal cancer. Targeting AFAP1-AS1 might be a potential therapeutic strategy for colorectal cancer treatment.	human	Colon tissue	High+Lowthroughput	Long noncoding RNA AFAP1-AS1 facilitates tumor growth through enhancer of zeste homolog 2 in colorectal cancer	否	无	colorectal cancer 	LOVO cell	E_01_0417	ChIP-qPCR,RNA pull-down assay,RNA immunoprecipitation,RNA extraction,quantitative RT-PCR,Western blot,	Here, we identify a lncRNA AFAP1-AS1 that facilitates colorectal cancer, where it is upregulated. AFAP1-AS1 expression was associated with colorectal cancer patient survival. AFAP1-AS1 knockdown inhibited cell proliferation, cell cycle, and tumorigenesis in an subcutaneous mouse xenograft model system. Further data demonstrated that AFAP1-AS1 was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of EZH2 target genes. Our findings indicate that AFAP1-AS1 is an oncogenic lncRNA that promotes tumor progression and may be a novel prognostic factor in colorectal cancer. Targeting AFAP1-AS1 might be a potential therapeutic strategy for colorectal cancer treatment.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we identify a lncRNA AFAP1-AS1 that facilitates colorectal cancer, where it is upregulated. AFAP1-AS1 expression was associated with colorectal cancer patient survival. AFAP1-AS1 knockdown inhibited cell proliferation, cell cycle, and tumorigenesis in an subcutaneous mouse xenograft model system. Further data demonstrated that AFAP1-AS1 was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of EZH2 target genes. Our findings indicate that AFAP1-AS1 is an oncogenic lncRNA that promotes tumor progression and may be a novel prognostic factor in colorectal cancer. Targeting AFAP1-AS1 might be a potential therapeutic strategy for colorectal cancer treatment.		Here, we identify a lncRNA AFAP1-AS1 that facilitates colorectal cancer, where it is upregulated. AFAP1-AS1 expression was associated with colorectal cancer patient survival. AFAP1-AS1 knockdown inhibited cell proliferation, cell cycle, and tumorigenesis in an subcutaneous mouse xenograft model system. Further data demonstrated that AFAP1-AS1 was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of EZH2 target genes. Our findings indicate that AFAP1-AS1 is an oncogenic lncRNA that promotes tumor progression and may be a novel prognostic factor in colorectal cancer. Targeting AFAP1-AS1 might be a potential therapeutic strategy for colorectal cancer treatment.	Immunohistochemical staining	Here, we identify a lncRNA AFAP1-AS1 that facilitates colorectal cancer, where it is upregulated. AFAP1-AS1 expression was associated with colorectal cancer patient survival. AFAP1-AS1 knockdown inhibited cell proliferation, cell cycle, and tumorigenesis in an subcutaneous mouse xenograft model system. Further data demonstrated that AFAP1-AS1 was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of EZH2 target genes. Our findings indicate that AFAP1-AS1 is an oncogenic lncRNA that promotes tumor progression and may be a novel prognostic factor in colorectal cancer. Targeting AFAP1-AS1 might be a potential therapeutic strategy for colorectal cancer treatment.			ChIP-qPCR,RNA pull-down assay,RNA immunoprecipitation,RNA extraction,quantitative RT-PCR,Western blot,				AFAP1-AS1
29888110	chr7	148804522	148806522	EZH2	Here, we identify a lncRNA AFAP1-AS1 that facilitates colorectal cancer, where it is upregulated. AFAP1-AS1 expression was associated with colorectal cancer patient survival. AFAP1-AS1 knockdown inhibited cell proliferation, cell cycle, and tumorigenesis in an subcutaneous mouse xenograft model system. Further data demonstrated that AFAP1-AS1 was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of EZH2 target genes. Our findings indicate that AFAP1-AS1 is an oncogenic lncRNA that promotes tumor progression and may be a novel prognostic factor in colorectal cancer. Targeting AFAP1-AS1 might be a potential therapeutic strategy for colorectal cancer treatment.	human	Colon tissue	High+Lowthroughput	Long noncoding RNA AFAP1-AS1 facilitates tumor growth through enhancer of zeste homolog 2 in colorectal cancer	否	无	colorectal cancer 	LOVO cell	E_01_0417	ChIP-qPCR,RNA pull-down assay,RNA immunoprecipitation,RNA extraction,quantitative RT-PCR,Western blot,	Here, we identify a lncRNA AFAP1-AS1 that facilitates colorectal cancer, where it is upregulated. AFAP1-AS1 expression was associated with colorectal cancer patient survival. AFAP1-AS1 knockdown inhibited cell proliferation, cell cycle, and tumorigenesis in an subcutaneous mouse xenograft model system. Further data demonstrated that AFAP1-AS1 was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of EZH2 target genes. Our findings indicate that AFAP1-AS1 is an oncogenic lncRNA that promotes tumor progression and may be a novel prognostic factor in colorectal cancer. Targeting AFAP1-AS1 might be a potential therapeutic strategy for colorectal cancer treatment.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we identify a lncRNA AFAP1-AS1 that facilitates colorectal cancer, where it is upregulated. AFAP1-AS1 expression was associated with colorectal cancer patient survival. AFAP1-AS1 knockdown inhibited cell proliferation, cell cycle, and tumorigenesis in an subcutaneous mouse xenograft model system. Further data demonstrated that AFAP1-AS1 was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of EZH2 target genes. Our findings indicate that AFAP1-AS1 is an oncogenic lncRNA that promotes tumor progression and may be a novel prognostic factor in colorectal cancer. Targeting AFAP1-AS1 might be a potential therapeutic strategy for colorectal cancer treatment.	Immunohistochemical staining	Here, we identify a lncRNA AFAP1-AS1 that facilitates colorectal cancer, where it is upregulated. AFAP1-AS1 expression was associated with colorectal cancer patient survival. AFAP1-AS1 knockdown inhibited cell proliferation, cell cycle, and tumorigenesis in an subcutaneous mouse xenograft model system. Further data demonstrated that AFAP1-AS1 was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of EZH2 target genes. Our findings indicate that AFAP1-AS1 is an oncogenic lncRNA that promotes tumor progression and may be a novel prognostic factor in colorectal cancer. Targeting AFAP1-AS1 might be a potential therapeutic strategy for colorectal cancer treatment.	EZH2		ChIP-qPCR,RNA pull-down assay,RNA immunoprecipitation,RNA extraction,quantitative RT-PCR,Western blot,	Here, we identify a lncRNA AFAP1-AS1 that facilitates colorectal cancer, where it is upregulated. AFAP1-AS1 expression was associated with colorectal cancer patient survival. AFAP1-AS1 knockdown inhibited cell proliferation, cell cycle, and tumorigenesis in an subcutaneous mouse xenograft model system. Further data demonstrated that AFAP1-AS1 was associated with enhancer of zeste homolog 2 (EZH2) and that this association was required for the repression of EZH2 target genes. Our findings indicate that AFAP1-AS1 is an oncogenic lncRNA that promotes tumor progression and may be a novel prognostic factor in colorectal cancer. Targeting AFAP1-AS1 might be a potential therapeutic strategy for colorectal cancer treatment.			
29887316	chr22	39516355	39518355	ATF4	ATF4 knockdown by siRNA significantly attenuated the suppressive effect of palmitate on EPO production. Studies utilizing inherited super-anemic mice (ISAM) mated with EPO-Cre mice (ISAM-REC mice) for lineage-labeling of REP cells showed that ATF4 activation by palmitate suppressed EPO production in REP cells. Laser capture microdissection confirmed ATF4 activation in the interstitial area of ISAM-REC mice treated with palmitate-conjugated BSA. Thus, endoplasmic reticulum stress induced by palmitate suppressed EPO expression by REP cells in a manner independent of HIF activation. The link between endoplasmic reticulum stress, dyslipidemia, and hypoxia may contribute to development and progression of anemia in CKD.	human	Liver tissue	High+Lowthroughput	Palmitate deranges erythropoietin production via transcription factor ATF4 activation of unfolded protein response	否	无	Chronic kidney injury	HepG2	E_01_0418	Oil red O staining,Western blot,Luciferase assays,quantitative real-time PCR,Histological analysis,Immunofluorescence analysis,Electron microscopy,Laser microdissection,	ATF4 knockdown by siRNA significantly attenuated the suppressive effect of palmitate on EPO production. Studies utilizing inherited super-anemic mice (ISAM) mated with EPO-Cre mice (ISAM-REC mice) for lineage-labeling of REP cells showed that ATF4 activation by palmitate suppressed EPO production in REP cells. Laser capture microdissection confirmed ATF4 activation in the interstitial area of ISAM-REC mice treated with palmitate-conjugated BSA. Thus, endoplasmic reticulum stress induced by palmitate suppressed EPO expression by REP cells in a manner independent of HIF activation. The link between endoplasmic reticulum stress, dyslipidemia, and hypoxia may contribute to development and progression of anemia in CKD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			ATF4 knockdown by siRNA significantly attenuated the suppressive effect of palmitate on EPO production. Studies utilizing inherited super-anemic mice (ISAM) mated with EPO-Cre mice (ISAM-REC mice) for lineage-labeling of REP cells showed that ATF4 activation by palmitate suppressed EPO production in REP cells. Laser capture microdissection confirmed ATF4 activation in the interstitial area of ISAM-REC mice treated with palmitate-conjugated BSA. Thus, endoplasmic reticulum stress induced by palmitate suppressed EPO expression by REP cells in a manner independent of HIF activation. The link between endoplasmic reticulum stress, dyslipidemia, and hypoxia may contribute to development and progression of anemia in CKD.	Immunohistochemical staining	ATF4 knockdown by siRNA significantly attenuated the suppressive effect of palmitate on EPO production. Studies utilizing inherited super-anemic mice (ISAM) mated with EPO-Cre mice (ISAM-REC mice) for lineage-labeling of REP cells showed that ATF4 activation by palmitate suppressed EPO production in REP cells. Laser capture microdissection confirmed ATF4 activation in the interstitial area of ISAM-REC mice treated with palmitate-conjugated BSA. Thus, endoplasmic reticulum stress induced by palmitate suppressed EPO expression by REP cells in a manner independent of HIF activation. The link between endoplasmic reticulum stress, dyslipidemia, and hypoxia may contribute to development and progression of anemia in CKD.	ATF4		Oil red O staining,Western blot,Luciferase assays,quantitative real-time PCR,Histological analysis,Immunofluorescence analysis,Electron microscopy,Laser microdissection,	ATF4 knockdown by siRNA significantly attenuated the suppressive effect of palmitate on EPO production. Studies utilizing inherited super-anemic mice (ISAM) mated with EPO-Cre mice (ISAM-REC mice) for lineage-labeling of REP cells showed that ATF4 activation by palmitate suppressed EPO production in REP cells. Laser capture microdissection confirmed ATF4 activation in the interstitial area of ISAM-REC mice treated with palmitate-conjugated BSA. Thus, endoplasmic reticulum stress induced by palmitate suppressed EPO expression by REP cells in a manner independent of HIF activation. The link between endoplasmic reticulum stress, dyslipidemia, and hypoxia may contribute to development and progression of anemia in CKD.			
29887316	chr7	100717869	100719869	EPO	ATF4 knockdown by siRNA significantly attenuated the suppressive effect of palmitate on EPO production. Studies utilizing inherited super-anemic mice (ISAM) mated with EPO-Cre mice (ISAM-REC mice) for lineage-labeling of REP cells showed that ATF4 activation by palmitate suppressed EPO production in REP cells. Laser capture microdissection confirmed ATF4 activation in the interstitial area of ISAM-REC mice treated with palmitate-conjugated BSA. Thus, endoplasmic reticulum stress induced by palmitate suppressed EPO expression by REP cells in a manner independent of HIF activation. The link between endoplasmic reticulum stress, dyslipidemia, and hypoxia may contribute to development and progression of anemia in CKD.	human	Liver tissue	High+Lowthroughput	Palmitate deranges erythropoietin production via transcription factor ATF4 activation of unfolded protein response	否	无	Chronic kidney injury	HepG2	E_01_0418	Oil red O staining,Western blot,Luciferase assays,quantitative real-time PCR,Histological analysis,Immunofluorescence analysis,Electron microscopy,Laser microdissection,	ATF4 knockdown by siRNA significantly attenuated the suppressive effect of palmitate on EPO production. Studies utilizing inherited super-anemic mice (ISAM) mated with EPO-Cre mice (ISAM-REC mice) for lineage-labeling of REP cells showed that ATF4 activation by palmitate suppressed EPO production in REP cells. Laser capture microdissection confirmed ATF4 activation in the interstitial area of ISAM-REC mice treated with palmitate-conjugated BSA. Thus, endoplasmic reticulum stress induced by palmitate suppressed EPO expression by REP cells in a manner independent of HIF activation. The link between endoplasmic reticulum stress, dyslipidemia, and hypoxia may contribute to development and progression of anemia in CKD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			ATF4 knockdown by siRNA significantly attenuated the suppressive effect of palmitate on EPO production. Studies utilizing inherited super-anemic mice (ISAM) mated with EPO-Cre mice (ISAM-REC mice) for lineage-labeling of REP cells showed that ATF4 activation by palmitate suppressed EPO production in REP cells. Laser capture microdissection confirmed ATF4 activation in the interstitial area of ISAM-REC mice treated with palmitate-conjugated BSA. Thus, endoplasmic reticulum stress induced by palmitate suppressed EPO expression by REP cells in a manner independent of HIF activation. The link between endoplasmic reticulum stress, dyslipidemia, and hypoxia may contribute to development and progression of anemia in CKD.	Immunohistochemical staining	ATF4 knockdown by siRNA significantly attenuated the suppressive effect of palmitate on EPO production. Studies utilizing inherited super-anemic mice (ISAM) mated with EPO-Cre mice (ISAM-REC mice) for lineage-labeling of REP cells showed that ATF4 activation by palmitate suppressed EPO production in REP cells. Laser capture microdissection confirmed ATF4 activation in the interstitial area of ISAM-REC mice treated with palmitate-conjugated BSA. Thus, endoplasmic reticulum stress induced by palmitate suppressed EPO expression by REP cells in a manner independent of HIF activation. The link between endoplasmic reticulum stress, dyslipidemia, and hypoxia may contribute to development and progression of anemia in CKD.	EPO		Oil red O staining,Western blot,Luciferase assays,quantitative real-time PCR,Histological analysis,Immunofluorescence analysis,Electron microscopy,Laser microdissection,	ATF4 knockdown by siRNA significantly attenuated the suppressive effect of palmitate on EPO production. Studies utilizing inherited super-anemic mice (ISAM) mated with EPO-Cre mice (ISAM-REC mice) for lineage-labeling of REP cells showed that ATF4 activation by palmitate suppressed EPO production in REP cells. Laser capture microdissection confirmed ATF4 activation in the interstitial area of ISAM-REC mice treated with palmitate-conjugated BSA. Thus, endoplasmic reticulum stress induced by palmitate suppressed EPO expression by REP cells in a manner independent of HIF activation. The link between endoplasmic reticulum stress, dyslipidemia, and hypoxia may contribute to development and progression of anemia in CKD.			
29885843	chr11	46853631	46855631	LRP4	Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.	human	Parathyroid tissue	High+Lowthroughput	LRP4 promotes proliferation, migration, and invasion in papillary thyroid cancer	否	无	Thyroid cancer	TPC1	E_01_0419	qRT-PCR,Cell transfection,Cell proliferation assay,Colony formation assay,Cell migration and invasion assays,Western blot,LRP4 siRNA	Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.		Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.	Immunohistochemical staining	Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.			qRT-PCR,Cell transfection,Cell proliferation assay,Colony formation assay,Cell migration and invasion assays,Western blot,LRP4 siRNA				LRP4
29885843	chr7	148804573	148806573	EZH2	Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.	human	Parathyroid tissue	High+Lowthroughput	LRP4 promotes proliferation, migration, and invasion in papillary thyroid cancer	否	无	Thyroid cancer	TPC1	E_01_0419	qRT-PCR,Cell transfection,Cell proliferation assay,Colony formation assay,Cell migration and invasion assays,Western blot,LRP4 siRNA	Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.	Immunohistochemical staining	Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.	EZH2		qRT-PCR,Cell transfection,Cell proliferation assay,Colony formation assay,Cell migration and invasion assays,Western blot,LRP4 siRNA	Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.			
29885843	chr10	31315705	31317705	ZEB1	Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.	human	Parathyroid tissue	High+Lowthroughput	LRP4 promotes proliferation, migration, and invasion in papillary thyroid cancer	否	无	Thyroid cancer	TPC1	E_01_0419	qRT-PCR,Cell transfection,Cell proliferation assay,Colony formation assay,Cell migration and invasion assays,Western blot,LRP4 siRNA	Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.	Immunohistochemical staining	Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.	ZEB1		qRT-PCR,Cell transfection,Cell proliferation assay,Colony formation assay,Cell migration and invasion assays,Western blot,LRP4 siRNA	Thus, the biological role of LRP4 in the thyroid cancer in the present study was investigated using the PTC cell lines TPC1, BCPAP and KTC-1. In these cell lines, the mRNA level of LRP4 was higher than normal thyroid cancer cell named HTORI3. In vitro experiments demonstrated that LRP4 downregulation significantly inhibited the colony formation, proliferation, migration, and invasion of the three PTC cell lines. Knockdown of LRP4 by small interfering RNA (siRNA) in those cell lines decreased the protein expression of N-cadherin, Enhancer of zeste homolog 2 (EZH2), and Zinc finger E-box-binding home-box 1 (ZEB1). Furthermore, LRP4 knockdown significantly reduced the levels of phosphorylated PI3K in the PTC cell lines. In conclusion, the present study indicated that LRP4 is a gene associated with PTC and might become a potential therapeutic target.			
29885461	chr6	131945329	131947329	CCN2	Loss of CCN2 in CAFs resulted in reduced CAF activation, as detected by staining with anti-α-smooth muscle actin antibodies, and reduced tumor-induced neovascularization, as detected by micro-computed tomography (micro-CT) and staining with anti-CD31 antibodies. CCN2-deficient B16(F10) cells were defective in a tubule formation/vasculogenic mimicry assay in vitro. Mice deleted for CCN2 in CAFs also showed impaired vasculogenic mimicry of subcutaneously-injected B16-F10 cells in vivo. Our results provide new insights into the cross-talk among different cell types in the tumor microenvironment and suggest CAFs play a heretofore unappreciated role by being essential for tumor neovascularization via the production of CCN2. Our data are consistent with the hypothesis that activated CAFs are essential for melanoma metastasis and that, due to its role in this process, CCN2 is a therapeutic target for melanoma.	human	Nervous tissue	High+Lowthroughput	Activation of cancer-associated fibroblasts is required for tumor neovascularization in a murine model of melanoma	否	无	Metastatic melanoma	B16-F10	E_01_0420	ELISA,Histological analysis,transfection,RNA-seq,immunohistochemistry experiments,	Loss of CCN2 in CAFs resulted in reduced CAF activation, as detected by staining with anti-α-smooth muscle actin antibodies, and reduced tumor-induced neovascularization, as detected by micro-computed tomography (micro-CT) and staining with anti-CD31 antibodies. CCN2-deficient B16(F10) cells were defective in a tubule formation/vasculogenic mimicry assay in vitro. Mice deleted for CCN2 in CAFs also showed impaired vasculogenic mimicry of subcutaneously-injected B16-F10 cells in vivo. Our results provide new insights into the cross-talk among different cell types in the tumor microenvironment and suggest CAFs play a heretofore unappreciated role by being essential for tumor neovascularization via the production of CCN2. Our data are consistent with the hypothesis that activated CAFs are essential for melanoma metastasis and that, due to its role in this process, CCN2 is a therapeutic target for melanoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Loss of CCN2 in CAFs resulted in reduced CAF activation, as detected by staining with anti-α-smooth muscle actin antibodies, and reduced tumor-induced neovascularization, as detected by micro-computed tomography (micro-CT) and staining with anti-CD31 antibodies. CCN2-deficient B16(F10) cells were defective in a tubule formation/vasculogenic mimicry assay in vitro. Mice deleted for CCN2 in CAFs also showed impaired vasculogenic mimicry of subcutaneously-injected B16-F10 cells in vivo. Our results provide new insights into the cross-talk among different cell types in the tumor microenvironment and suggest CAFs play a heretofore unappreciated role by being essential for tumor neovascularization via the production of CCN2. Our data are consistent with the hypothesis that activated CAFs are essential for melanoma metastasis and that, due to its role in this process, CCN2 is a therapeutic target for melanoma.	Immunohistochemical staining	Loss of CCN2 in CAFs resulted in reduced CAF activation, as detected by staining with anti-α-smooth muscle actin antibodies, and reduced tumor-induced neovascularization, as detected by micro-computed tomography (micro-CT) and staining with anti-CD31 antibodies. CCN2-deficient B16(F10) cells were defective in a tubule formation/vasculogenic mimicry assay in vitro. Mice deleted for CCN2 in CAFs also showed impaired vasculogenic mimicry of subcutaneously-injected B16-F10 cells in vivo. Our results provide new insights into the cross-talk among different cell types in the tumor microenvironment and suggest CAFs play a heretofore unappreciated role by being essential for tumor neovascularization via the production of CCN2. Our data are consistent with the hypothesis that activated CAFs are essential for melanoma metastasis and that, due to its role in this process, CCN2 is a therapeutic target for melanoma.	CCN2		ELISA,Histological analysis,transfection,RNA-seq,immunohistochemistry experiments,	Loss of CCN2 in CAFs resulted in reduced CAF activation, as detected by staining with anti-α-smooth muscle actin antibodies, and reduced tumor-induced neovascularization, as detected by micro-computed tomography (micro-CT) and staining with anti-CD31 antibodies. CCN2-deficient B16(F10) cells were defective in a tubule formation/vasculogenic mimicry assay in vitro. Mice deleted for CCN2 in CAFs also showed impaired vasculogenic mimicry of subcutaneously-injected B16-F10 cells in vivo. Our results provide new insights into the cross-talk among different cell types in the tumor microenvironment and suggest CAFs play a heretofore unappreciated role by being essential for tumor neovascularization via the production of CCN2. Our data are consistent with the hypothesis that activated CAFs are essential for melanoma metastasis and that, due to its role in this process, CCN2 is a therapeutic target for melanoma.			
29885461	chr7	94392263	94394263	COL1A2	Loss of CCN2 in CAFs resulted in reduced CAF activation, as detected by staining with anti-α-smooth muscle actin antibodies, and reduced tumor-induced neovascularization, as detected by micro-computed tomography (micro-CT) and staining with anti-CD31 antibodies. CCN2-deficient B16(F10) cells were defective in a tubule formation/vasculogenic mimicry assay in vitro. Mice deleted for CCN2 in CAFs also showed impaired vasculogenic mimicry of subcutaneously-injected B16-F10 cells in vivo. Our results provide new insights into the cross-talk among different cell types in the tumor microenvironment and suggest CAFs play a heretofore unappreciated role by being essential for tumor neovascularization via the production of CCN2. Our data are consistent with the hypothesis that activated CAFs are essential for melanoma metastasis and that, due to its role in this process, CCN2 is a therapeutic target for melanoma.	human	Nervous tissue	High+Lowthroughput	Activation of cancer-associated fibroblasts is required for tumor neovascularization in a murine model of melanoma	否	无	Metastatic melanoma	B16-F10	E_01_0420	ELISA,Histological analysis,transfection,RNA-seq,immunohistochemistry experiments,	Loss of CCN2 in CAFs resulted in reduced CAF activation, as detected by staining with anti-α-smooth muscle actin antibodies, and reduced tumor-induced neovascularization, as detected by micro-computed tomography (micro-CT) and staining with anti-CD31 antibodies. CCN2-deficient B16(F10) cells were defective in a tubule formation/vasculogenic mimicry assay in vitro. Mice deleted for CCN2 in CAFs also showed impaired vasculogenic mimicry of subcutaneously-injected B16-F10 cells in vivo. Our results provide new insights into the cross-talk among different cell types in the tumor microenvironment and suggest CAFs play a heretofore unappreciated role by being essential for tumor neovascularization via the production of CCN2. Our data are consistent with the hypothesis that activated CAFs are essential for melanoma metastasis and that, due to its role in this process, CCN2 is a therapeutic target for melanoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Loss of CCN2 in CAFs resulted in reduced CAF activation, as detected by staining with anti-α-smooth muscle actin antibodies, and reduced tumor-induced neovascularization, as detected by micro-computed tomography (micro-CT) and staining with anti-CD31 antibodies. CCN2-deficient B16(F10) cells were defective in a tubule formation/vasculogenic mimicry assay in vitro. Mice deleted for CCN2 in CAFs also showed impaired vasculogenic mimicry of subcutaneously-injected B16-F10 cells in vivo. Our results provide new insights into the cross-talk among different cell types in the tumor microenvironment and suggest CAFs play a heretofore unappreciated role by being essential for tumor neovascularization via the production of CCN2. Our data are consistent with the hypothesis that activated CAFs are essential for melanoma metastasis and that, due to its role in this process, CCN2 is a therapeutic target for melanoma.	Immunohistochemical staining	Loss of CCN2 in CAFs resulted in reduced CAF activation, as detected by staining with anti-α-smooth muscle actin antibodies, and reduced tumor-induced neovascularization, as detected by micro-computed tomography (micro-CT) and staining with anti-CD31 antibodies. CCN2-deficient B16(F10) cells were defective in a tubule formation/vasculogenic mimicry assay in vitro. Mice deleted for CCN2 in CAFs also showed impaired vasculogenic mimicry of subcutaneously-injected B16-F10 cells in vivo. Our results provide new insights into the cross-talk among different cell types in the tumor microenvironment and suggest CAFs play a heretofore unappreciated role by being essential for tumor neovascularization via the production of CCN2. Our data are consistent with the hypothesis that activated CAFs are essential for melanoma metastasis and that, due to its role in this process, CCN2 is a therapeutic target for melanoma.	COL1A2		ELISA,Histological analysis,transfection,RNA-seq,immunohistochemistry experiments,	Loss of CCN2 in CAFs resulted in reduced CAF activation, as detected by staining with anti-α-smooth muscle actin antibodies, and reduced tumor-induced neovascularization, as detected by micro-computed tomography (micro-CT) and staining with anti-CD31 antibodies. CCN2-deficient B16(F10) cells were defective in a tubule formation/vasculogenic mimicry assay in vitro. Mice deleted for CCN2 in CAFs also showed impaired vasculogenic mimicry of subcutaneously-injected B16-F10 cells in vivo. Our results provide new insights into the cross-talk among different cell types in the tumor microenvironment and suggest CAFs play a heretofore unappreciated role by being essential for tumor neovascularization via the production of CCN2. Our data are consistent with the hypothesis that activated CAFs are essential for melanoma metastasis and that, due to its role in this process, CCN2 is a therapeutic target for melanoma.			
29885262	chr1	55036580	55038580	PCSK9	We, therefore, studied the effect of PCSK9 on interferon (IFN) β expression. We show that PCSK9 decreases IFNβ promoter/enhancer activity, mRNA and protein levels, and its downstream 2',5'-oligoadenylate synthetase-1 mRNA level. ProPCSK9, but not the cleaved PCSK9, down-regulates IFNβ promoter/enhancer activity. Moreover, PCSK9 decreases IFNβ promoter/enhancer activity through the positive regulatory domain IV region where the activating transcription factor-2 (ATF-2)/c-Jun heterodimer binds. Mechanistically, we demonstrate an interaction between PCSK9 and ATF-2, which reduces ATF-2/c-Jun dimerization and ATF-2/c-Jun binding to the IFNβ enhancer. This novel function of PCSK9 should have important implications in optimizing the clinical use of PCSK9 inhibitors.	human	Liver tissue	High+Lowthroughput	Proprotein convertase subtilisin/kexin type 9 inhibits interferon β expression through interacting with ATF-2	否	无	cancer	Huh-7 cell	E_01_0421	transcription,luciferase assay,Western blot,RT-qPCR,ELISA,ChIP,	We, therefore, studied the effect of PCSK9 on interferon (IFN) β expression. We show that PCSK9 decreases IFNβ promoter/enhancer activity, mRNA and protein levels, and its downstream 2',5'-oligoadenylate synthetase-1 mRNA level. ProPCSK9, but not the cleaved PCSK9, down-regulates IFNβ promoter/enhancer activity. Moreover, PCSK9 decreases IFNβ promoter/enhancer activity through the positive regulatory domain IV region where the activating transcription factor-2 (ATF-2)/c-Jun heterodimer binds. Mechanistically, we demonstrate an interaction between PCSK9 and ATF-2, which reduces ATF-2/c-Jun dimerization and ATF-2/c-Jun binding to the IFNβ enhancer. This novel function of PCSK9 should have important implications in optimizing the clinical use of PCSK9 inhibitors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We, therefore, studied the effect of PCSK9 on interferon (IFN) β expression. We show that PCSK9 decreases IFNβ promoter/enhancer activity, mRNA and protein levels, and its downstream 2',5'-oligoadenylate synthetase-1 mRNA level. ProPCSK9, but not the cleaved PCSK9, down-regulates IFNβ promoter/enhancer activity. Moreover, PCSK9 decreases IFNβ promoter/enhancer activity through the positive regulatory domain IV region where the activating transcription factor-2 (ATF-2)/c-Jun heterodimer binds. Mechanistically, we demonstrate an interaction between PCSK9 and ATF-2, which reduces ATF-2/c-Jun dimerization and ATF-2/c-Jun binding to the IFNβ enhancer. This novel function of PCSK9 should have important implications in optimizing the clinical use of PCSK9 inhibitors.		We, therefore, studied the effect of PCSK9 on interferon (IFN) β expression. We show that PCSK9 decreases IFNβ promoter/enhancer activity, mRNA and protein levels, and its downstream 2',5'-oligoadenylate synthetase-1 mRNA level. ProPCSK9, but not the cleaved PCSK9, down-regulates IFNβ promoter/enhancer activity. Moreover, PCSK9 decreases IFNβ promoter/enhancer activity through the positive regulatory domain IV region where the activating transcription factor-2 (ATF-2)/c-Jun heterodimer binds. Mechanistically, we demonstrate an interaction between PCSK9 and ATF-2, which reduces ATF-2/c-Jun dimerization and ATF-2/c-Jun binding to the IFNβ enhancer. This novel function of PCSK9 should have important implications in optimizing the clinical use of PCSK9 inhibitors.	Immunohistochemical staining	We, therefore, studied the effect of PCSK9 on interferon (IFN) β expression. We show that PCSK9 decreases IFNβ promoter/enhancer activity, mRNA and protein levels, and its downstream 2',5'-oligoadenylate synthetase-1 mRNA level. ProPCSK9, but not the cleaved PCSK9, down-regulates IFNβ promoter/enhancer activity. Moreover, PCSK9 decreases IFNβ promoter/enhancer activity through the positive regulatory domain IV region where the activating transcription factor-2 (ATF-2)/c-Jun heterodimer binds. Mechanistically, we demonstrate an interaction between PCSK9 and ATF-2, which reduces ATF-2/c-Jun dimerization and ATF-2/c-Jun binding to the IFNβ enhancer. This novel function of PCSK9 should have important implications in optimizing the clinical use of PCSK9 inhibitors.			transcription,luciferase assay,Western blot,RT-qPCR,ELISA,ChIP,				PCSK9
29884649	chr13	110709998	110711998	ING1	Correspondingly, GADD45α occupies C/EBPβ/δ-dependent superenhancers and, cooperatively with ING1, promotes local DNA demethylation via long-range chromatin loops to permit C/EBPβ recruitment. The results indicate that enhancer methylation can affect aging and imply that C/EBP proteins play an unexpected role in this process. Our study suggests a causal nexus between DNA demethylation, metabolism, and organismal aging.	human	Nervous tissue	High+Lowthroughput	Impaired DNA demethylation of C/EBP sites causes premature aging	否	无	Premature ageing	MEF	E_01_0422	WGBS-seq,Oil Red O staining,RNA isolation,cDNA synthesis,qPCR,RNA-seq,RNA expression microarrays,ChIP,ChIP-seq,NG Capture-C,Methylation-sensitive PCR,Hematoxylin and eosin (H&E) staining,SA-β-Gal staining,Luciferase reporter assays,Co-IP,immunoblotting,Immunostaining	Correspondingly, GADD45α occupies C/EBPβ/δ-dependent superenhancers and, cooperatively with ING1, promotes local DNA demethylation via long-range chromatin loops to permit C/EBPβ recruitment. The results indicate that enhancer methylation can affect aging and imply that C/EBP proteins play an unexpected role in this process. Our study suggests a causal nexus between DNA demethylation, metabolism, and organismal aging.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Correspondingly, GADD45α occupies C/EBPβ/δ-dependent superenhancers and, cooperatively with ING1, promotes local DNA demethylation via long-range chromatin loops to permit C/EBPβ recruitment. The results indicate that enhancer methylation can affect aging and imply that C/EBP proteins play an unexpected role in this process. Our study suggests a causal nexus between DNA demethylation, metabolism, and organismal aging.		Correspondingly, GADD45α occupies C/EBPβ/δ-dependent superenhancers and, cooperatively with ING1, promotes local DNA demethylation via long-range chromatin loops to permit C/EBPβ recruitment. The results indicate that enhancer methylation can affect aging and imply that C/EBP proteins play an unexpected role in this process. Our study suggests a causal nexus between DNA demethylation, metabolism, and organismal aging.	Immunohistochemical staining	Correspondingly, GADD45α occupies C/EBPβ/δ-dependent superenhancers and, cooperatively with ING1, promotes local DNA demethylation via long-range chromatin loops to permit C/EBPβ recruitment. The results indicate that enhancer methylation can affect aging and imply that C/EBP proteins play an unexpected role in this process. Our study suggests a causal nexus between DNA demethylation, metabolism, and organismal aging.			WGBS-seq,Oil Red O staining,RNA isolation,cDNA synthesis,qPCR,RNA-seq,RNA expression microarrays,ChIP,ChIP-seq,NG Capture-C,Methylation-sensitive PCR,Hematoxylin and eosin (H&E) staining,SA-β-Gal staining,Luciferase reporter assays,Co-IP,immunoblotting,Immunostaining				ING1
29883697	chr11	47266314	47268314	MADD	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.	human	Nervous tissue	High+Lowthroughput	Integrative analysis of genome-wide association study and brain region related enhancer maps identifies biological pathways for insomnia	否	无	insomnia	neuronal stem cell	E_01_0423	GWAS	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.		The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.	Immunohistochemical staining	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.			GWAS				MADD
29883697	chr14	35082401	35084401	PPP2R3C	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.	human	Nervous tissue	High+Lowthroughput	Integrative analysis of genome-wide association study and brain region related enhancer maps identifies biological pathways for insomnia	否	无	insomnia	neuronal stem cell	E_01_0423	GWAS	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.		The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.	Immunohistochemical staining	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.			GWAS				PPP2R3C
29883697	chr1	15488363	15490363	CASP9	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.	human	Nervous tissue	High+Lowthroughput	Integrative analysis of genome-wide association study and brain region related enhancer maps identifies biological pathways for insomnia	否	无	insomnia	neuronal stem cell	E_01_0423	GWAS	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.		The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.	Immunohistochemical staining	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.			GWAS				CASP9
29883697	chr1	15681611	15683611	PLEKHM2	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.	human	Nervous tissue	High+Lowthroughput	Integrative analysis of genome-wide association study and brain region related enhancer maps identifies biological pathways for insomnia	否	无	insomnia	neuronal stem cell	E_01_0423	GWAS	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.		The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.	Immunohistochemical staining	The chromosomal enhancer maps of 6 brain regions were then aligned with the GWAS summary data to obtain the association testing results of enhancer regions for insomnia. Gene prioritization, tissue/cell and pathway enrichment analysis were implemented by Data-driven Expression Prioritized Integration for Complex Traits (DEPICT) tool. We identified multiple cross-brain regions or brain-region specific prioritized genes for insomnia, such as MADD (P = .0013 in angular gyrus), PPP2R3C (P = .0319 in cingulate gyrus), CASP9 (P = .0066 in angular gyrus and P = .0278 in hippocampus middle), PLEKHM2 (P = .0032 in angular gyrus, P = .0052 in anterior caudate, P = .0385 in cingulate gyrus and P = .0011 in inferior temporal lobe). This study also detected a group of insomnia associated biological pathways within multiple or specific brain regions, such as REACTOME_SIGNALING_BY_NOTCH and KEGG_GLYCEROPHOSPHOLIPID_METABOLISM. Our results showed that insomnia associated genes were significantly enriched in neural stem cells. Our results highlight a set of potential points, particularly neural stem cells, for subsequent biological studies for insomnia.			GWAS				PLEKHM2
29882899	chr8	127732924	127734924	MYC	Moreover, we show that in colon carcinoma cells, Wnt-responsive enhancers preferentially upregulate transcription from the P1 promoter using reporter assays and in the context of the endogenous Wnt induction. In addition, multiple enhancer deletions using CRISPR/Cas9 corroborate the regulatory specificity of P1. Finally, we show that preferential activation between Wnt-responsive enhancers and the P1 promoter is influenced by the distinct core promoter elements that are present in the MYC promoters. Taken together, our results provide new insight into how enhancers can specifically target alternative promoters and suggest that formation of these selective interactions could allow more precise combinatorial regulation of transcription initiation.	human	Colon tissue	High+Lowthroughput	Selective Activation of Alternative MYC Core Promoters by Wnt-Responsive Enhancers	否	无	nothing	HCT-116	E_01_0424	PCR,Luciferase Reporter Assay,Real Time qPCR,Genome Editing,ChIP-Seq,	Moreover, we show that in colon carcinoma cells, Wnt-responsive enhancers preferentially upregulate transcription from the P1 promoter using reporter assays and in the context of the endogenous Wnt induction. In addition, multiple enhancer deletions using CRISPR/Cas9 corroborate the regulatory specificity of P1. Finally, we show that preferential activation between Wnt-responsive enhancers and the P1 promoter is influenced by the distinct core promoter elements that are present in the MYC promoters. Taken together, our results provide new insight into how enhancers can specifically target alternative promoters and suggest that formation of these selective interactions could allow more precise combinatorial regulation of transcription initiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Moreover, we show that in colon carcinoma cells, Wnt-responsive enhancers preferentially upregulate transcription from the P1 promoter using reporter assays and in the context of the endogenous Wnt induction. In addition, multiple enhancer deletions using CRISPR/Cas9 corroborate the regulatory specificity of P1. Finally, we show that preferential activation between Wnt-responsive enhancers and the P1 promoter is influenced by the distinct core promoter elements that are present in the MYC promoters. Taken together, our results provide new insight into how enhancers can specifically target alternative promoters and suggest that formation of these selective interactions could allow more precise combinatorial regulation of transcription initiation.	Immunohistochemical staining	Moreover, we show that in colon carcinoma cells, Wnt-responsive enhancers preferentially upregulate transcription from the P1 promoter using reporter assays and in the context of the endogenous Wnt induction. In addition, multiple enhancer deletions using CRISPR/Cas9 corroborate the regulatory specificity of P1. Finally, we show that preferential activation between Wnt-responsive enhancers and the P1 promoter is influenced by the distinct core promoter elements that are present in the MYC promoters. Taken together, our results provide new insight into how enhancers can specifically target alternative promoters and suggest that formation of these selective interactions could allow more precise combinatorial regulation of transcription initiation.	MYC		PCR,Luciferase Reporter Assay,Real Time qPCR,Genome Editing,ChIP-Seq,	Moreover, we show that in colon carcinoma cells, Wnt-responsive enhancers preferentially upregulate transcription from the P1 promoter using reporter assays and in the context of the endogenous Wnt induction. In addition, multiple enhancer deletions using CRISPR/Cas9 corroborate the regulatory specificity of P1. Finally, we show that preferential activation between Wnt-responsive enhancers and the P1 promoter is influenced by the distinct core promoter elements that are present in the MYC promoters. Taken together, our results provide new insight into how enhancers can specifically target alternative promoters and suggest that formation of these selective interactions could allow more precise combinatorial regulation of transcription initiation.			
29881822	chr15	59517953	59519953	Trib1	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.	mouse	Nervous tissue	High+Lowthroughput	Neutrophils alleviate fibrosis in the CCl(4)-induced mouse chronic liver injury model	否	无	Chronic liver injury	neutrophils	E_02_0287	qPCR,Western Blot,RT-PCR,real-time PCR,flow cytometry	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.		Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.	Immunohistochemical staining	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.			qPCR,Western Blot,RT-PCR,real-time PCR,flow cytometry				Trib1
29881822	chr9	7555828	7557828	Mmp8	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.	mouse	Nervous tissue	High+Lowthroughput	Neutrophils alleviate fibrosis in the CCl(4)-induced mouse chronic liver injury model	否	无	Chronic liver injury	neutrophils	E_02_0287	qPCR,Western Blot,RT-PCR,real-time PCR,flow cytometry	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.		Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.	Immunohistochemical staining	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.			qPCR,Western Blot,RT-PCR,real-time PCR,flow cytometry				Mmp8
29881822	chr2	164779751	164781751	Mmp9	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.	mouse	Nervous tissue	High+Lowthroughput	Neutrophils alleviate fibrosis in the CCl(4)-induced mouse chronic liver injury model	否	无	Chronic liver injury	neutrophils	E_02_0287	qPCR,Western Blot,RT-PCR,real-time PCR,flow cytometry	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.		Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.	Immunohistochemical staining	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.			qPCR,Western Blot,RT-PCR,real-time PCR,flow cytometry				Mmp9
29881822	chr5	91036112	91038112	Cxcl1	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.	mouse	Nervous tissue	High+Lowthroughput	Neutrophils alleviate fibrosis in the CCl(4)-induced mouse chronic liver injury model	否	无	Chronic liver injury	neutrophils	E_02_0287	qPCR,Western Blot,RT-PCR,real-time PCR,flow cytometry	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.		Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.	Immunohistochemical staining	Consistently, transplantation of Trib1-deficient bone marrow cells into wild-type mice alleviated CCl4-induced fibrosis. Furthermore, expression of chemokine (C-X-C motif) ligand 1 (Cxcl1) by adeno-associated viral vector in the normal liver recruited neutrophils and suppressed CCl4-induced fibrosis; infusion of wild-type neutrophils in CCl4-treated mice also ameliorated fibrosis. Using recombinant adeno-associated virus-mediated expression of Mmp8 and Mmp9 alleviated liver fibrosis. Finally, neutrophil depletion by infusion of Ly6G antibody significantly enhanced CCl4-induced fibrosis. Conclusion: While neutrophils are well known to exacerbate acute liver injury, our results demonstrate a beneficial role of neutrophils in chronic liver injury by promoting fibrolysis.			qPCR,Western Blot,RT-PCR,real-time PCR,flow cytometry				Cxcl1
29881302	chr7	27736725	27738725	TAX1BP1	We describe a potential mechanism related to failure of A20 to suppress inflammation in CD, characterized by high A20 expression and low A20 protein levels. The dysregulation of A20 is potentially due to alterations in ABIN-1, and infection with E. coli strain LF82 could affect the function and stability of A20. Our study signifies an important finding in A20 regulation in IBD, which prevents it from suppressing inflammation.	human	Colon tissue	High+Lowthroughput	Tumor necrosis factor α-induced protein 3 (A20) is dysregulated in pediatric Crohn disease	否	无	Pediatric inflammatory bowel disease (IBD)	T-84	E_01_0425	Total RNA extraction,reverse transcription PCR,Cytokine analysis,Immunofluorescence microscopy,ELISA,	We describe a potential mechanism related to failure of A20 to suppress inflammation in CD, characterized by high A20 expression and low A20 protein levels. The dysregulation of A20 is potentially due to alterations in ABIN-1, and infection with E. coli strain LF82 could affect the function and stability of A20. Our study signifies an important finding in A20 regulation in IBD, which prevents it from suppressing inflammation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We describe a potential mechanism related to failure of A20 to suppress inflammation in CD, characterized by high A20 expression and low A20 protein levels. The dysregulation of A20 is potentially due to alterations in ABIN-1, and infection with E. coli strain LF82 could affect the function and stability of A20. Our study signifies an important finding in A20 regulation in IBD, which prevents it from suppressing inflammation.		We describe a potential mechanism related to failure of A20 to suppress inflammation in CD, characterized by high A20 expression and low A20 protein levels. The dysregulation of A20 is potentially due to alterations in ABIN-1, and infection with E. coli strain LF82 could affect the function and stability of A20. Our study signifies an important finding in A20 regulation in IBD, which prevents it from suppressing inflammation.	Immunohistochemical staining	We describe a potential mechanism related to failure of A20 to suppress inflammation in CD, characterized by high A20 expression and low A20 protein levels. The dysregulation of A20 is potentially due to alterations in ABIN-1, and infection with E. coli strain LF82 could affect the function and stability of A20. Our study signifies an important finding in A20 regulation in IBD, which prevents it from suppressing inflammation.			Total RNA extraction,reverse transcription PCR,Cytokine analysis,Immunofluorescence microscopy,ELISA,				TAX1BP1
29880601	chr12	7916539	7918539	SLC2A3	Finally, we investigated expression of the SLC2A3 and SLC2A14 genes, adjacently positioned to the eRNA07573 locus,in eRNA07573 KO cells.  Here, we show that 145 unstable nuclear RNAs, including enhancer RNAs (eRNAs) and long noncoding RNAs (lncRNAs) such as NEAT1v2, are stabilized upon Salmonella infection in HeLa cells. In uninfected cells, the RNA exosome, aided by the Nuclear EXosome Targeting (NEXT) complex, degrades these labile transcripts. Upon infection, the levels of the exosome/NEXT components, RRP6 and MTR4, dramatically decrease, resulting in transcript stabilization. Depletion of lncRNAs, NEAT1v2, or eRNA07573 in HeLa cells triggers increased susceptibility to Salmonella infection concomitant with the deregulated expression of a distinct class of immunity-related genes, indicating that the accumulation of unstable nuclear RNAs contributes to antibacterial defense. Our results highlight a fundamental role for regulated degradation of nuclear RNA in the response to pathogenic infection.	human	connective tissue	High+Lowthroughput	Diminished nuclear RNA decay upon Salmonella infection upregulates antibacterial noncoding RNAs	否	无	Salmonella infection	HeLa	E_01_0426	transfection,RT–qPCR,siRNA,Immunoblotting,FISH,immunocytochemistry,Northern blot	Finally, we investigated expression of the SLC2A3 and SLC2A14 genes, adjacently positioned to the eRNA07573 locus,in eRNA07573 KO cells.  Here, we show that 145 unstable nuclear RNAs, including enhancer RNAs (eRNAs) and long noncoding RNAs (lncRNAs) such as NEAT1v2, are stabilized upon Salmonella infection in HeLa cells. In uninfected cells, the RNA exosome, aided by the Nuclear EXosome Targeting (NEXT) complex, degrades these labile transcripts. Upon infection, the levels of the exosome/NEXT components, RRP6 and MTR4, dramatically decrease, resulting in transcript stabilization. Depletion of lncRNAs, NEAT1v2, or eRNA07573 in HeLa cells triggers increased susceptibility to Salmonella infection concomitant with the deregulated expression of a distinct class of immunity-related genes, indicating that the accumulation of unstable nuclear RNAs contributes to antibacterial defense. Our results highlight a fundamental role for regulated degradation of nuclear RNA in the response to pathogenic infection.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Finally, we investigated expression of the SLC2A3 and SLC2A14 genes, adjacently positioned to the eRNA07573 locus,in eRNA07573 KO cells.  Here, we show that 145 unstable nuclear RNAs, including enhancer RNAs (eRNAs) and long noncoding RNAs (lncRNAs) such as NEAT1v2, are stabilized upon Salmonella infection in HeLa cells. In uninfected cells, the RNA exosome, aided by the Nuclear EXosome Targeting (NEXT) complex, degrades these labile transcripts. Upon infection, the levels of the exosome/NEXT components, RRP6 and MTR4, dramatically decrease, resulting in transcript stabilization. Depletion of lncRNAs, NEAT1v2, or eRNA07573 in HeLa cells triggers increased susceptibility to Salmonella infection concomitant with the deregulated expression of a distinct class of immunity-related genes, indicating that the accumulation of unstable nuclear RNAs contributes to antibacterial defense. Our results highlight a fundamental role for regulated degradation of nuclear RNA in the response to pathogenic infection.		Finally, we investigated expression of the SLC2A3 and SLC2A14 genes, adjacently positioned to the eRNA07573 locus,in eRNA07573 KO cells.  Here, we show that 145 unstable nuclear RNAs, including enhancer RNAs (eRNAs) and long noncoding RNAs (lncRNAs) such as NEAT1v2, are stabilized upon Salmonella infection in HeLa cells. In uninfected cells, the RNA exosome, aided by the Nuclear EXosome Targeting (NEXT) complex, degrades these labile transcripts. Upon infection, the levels of the exosome/NEXT components, RRP6 and MTR4, dramatically decrease, resulting in transcript stabilization. Depletion of lncRNAs, NEAT1v2, or eRNA07573 in HeLa cells triggers increased susceptibility to Salmonella infection concomitant with the deregulated expression of a distinct class of immunity-related genes, indicating that the accumulation of unstable nuclear RNAs contributes to antibacterial defense. Our results highlight a fundamental role for regulated degradation of nuclear RNA in the response to pathogenic infection.	Immunohistochemical staining	Finally, we investigated expression of the SLC2A3 and SLC2A14 genes, adjacently positioned to the eRNA07573 locus,in eRNA07573 KO cells.  Here, we show that 145 unstable nuclear RNAs, including enhancer RNAs (eRNAs) and long noncoding RNAs (lncRNAs) such as NEAT1v2, are stabilized upon Salmonella infection in HeLa cells. In uninfected cells, the RNA exosome, aided by the Nuclear EXosome Targeting (NEXT) complex, degrades these labile transcripts. Upon infection, the levels of the exosome/NEXT components, RRP6 and MTR4, dramatically decrease, resulting in transcript stabilization. Depletion of lncRNAs, NEAT1v2, or eRNA07573 in HeLa cells triggers increased susceptibility to Salmonella infection concomitant with the deregulated expression of a distinct class of immunity-related genes, indicating that the accumulation of unstable nuclear RNAs contributes to antibacterial defense. Our results highlight a fundamental role for regulated degradation of nuclear RNA in the response to pathogenic infection.			transfection,RT–qPCR,siRNA,Immunoblotting,FISH,immunocytochemistry,Northern blot				SLC2A3
29880601	chr17	78353905	78355905	SOCS3	Finally, we investigated expression of the SLC2A3 and SLC2A14 genes, adjacently positioned to the eRNA07573 locus,in eRNA07573 KO cells.  Here, we show that 145 unstable nuclear RNAs, including enhancer RNAs (eRNAs) and long noncoding RNAs (lncRNAs) such as NEAT1v2, are stabilized upon Salmonella infection in HeLa cells. In uninfected cells, the RNA exosome, aided by the Nuclear EXosome Targeting (NEXT) complex, degrades these labile transcripts. Upon infection, the levels of the exosome/NEXT components, RRP6 and MTR4, dramatically decrease, resulting in transcript stabilization. Depletion of lncRNAs, NEAT1v2, or eRNA07573 in HeLa cells triggers increased susceptibility to Salmonella infection concomitant with the deregulated expression of a distinct class of immunity-related genes, indicating that the accumulation of unstable nuclear RNAs contributes to antibacterial defense. Our results highlight a fundamental role for regulated degradation of nuclear RNA in the response to pathogenic infection.	human	connective tissue	High+Lowthroughput	Diminished nuclear RNA decay upon Salmonella infection upregulates antibacterial noncoding RNAs	否	无	Salmonella infection	HeLa	E_01_0426	transfection,RT–qPCR,siRNA,Immunoblotting,FISH,immunocytochemistry,Northern blot	Finally, we investigated expression of the SLC2A3 and SLC2A14 genes, adjacently positioned to the eRNA07573 locus,in eRNA07573 KO cells.  Here, we show that 145 unstable nuclear RNAs, including enhancer RNAs (eRNAs) and long noncoding RNAs (lncRNAs) such as NEAT1v2, are stabilized upon Salmonella infection in HeLa cells. In uninfected cells, the RNA exosome, aided by the Nuclear EXosome Targeting (NEXT) complex, degrades these labile transcripts. Upon infection, the levels of the exosome/NEXT components, RRP6 and MTR4, dramatically decrease, resulting in transcript stabilization. Depletion of lncRNAs, NEAT1v2, or eRNA07573 in HeLa cells triggers increased susceptibility to Salmonella infection concomitant with the deregulated expression of a distinct class of immunity-related genes, indicating that the accumulation of unstable nuclear RNAs contributes to antibacterial defense. Our results highlight a fundamental role for regulated degradation of nuclear RNA in the response to pathogenic infection.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Finally, we investigated expression of the SLC2A3 and SLC2A14 genes, adjacently positioned to the eRNA07573 locus,in eRNA07573 KO cells.  Here, we show that 145 unstable nuclear RNAs, including enhancer RNAs (eRNAs) and long noncoding RNAs (lncRNAs) such as NEAT1v2, are stabilized upon Salmonella infection in HeLa cells. In uninfected cells, the RNA exosome, aided by the Nuclear EXosome Targeting (NEXT) complex, degrades these labile transcripts. Upon infection, the levels of the exosome/NEXT components, RRP6 and MTR4, dramatically decrease, resulting in transcript stabilization. Depletion of lncRNAs, NEAT1v2, or eRNA07573 in HeLa cells triggers increased susceptibility to Salmonella infection concomitant with the deregulated expression of a distinct class of immunity-related genes, indicating that the accumulation of unstable nuclear RNAs contributes to antibacterial defense. Our results highlight a fundamental role for regulated degradation of nuclear RNA in the response to pathogenic infection.	Immunohistochemical staining	Finally, we investigated expression of the SLC2A3 and SLC2A14 genes, adjacently positioned to the eRNA07573 locus,in eRNA07573 KO cells.  Here, we show that 145 unstable nuclear RNAs, including enhancer RNAs (eRNAs) and long noncoding RNAs (lncRNAs) such as NEAT1v2, are stabilized upon Salmonella infection in HeLa cells. In uninfected cells, the RNA exosome, aided by the Nuclear EXosome Targeting (NEXT) complex, degrades these labile transcripts. Upon infection, the levels of the exosome/NEXT components, RRP6 and MTR4, dramatically decrease, resulting in transcript stabilization. Depletion of lncRNAs, NEAT1v2, or eRNA07573 in HeLa cells triggers increased susceptibility to Salmonella infection concomitant with the deregulated expression of a distinct class of immunity-related genes, indicating that the accumulation of unstable nuclear RNAs contributes to antibacterial defense. Our results highlight a fundamental role for regulated degradation of nuclear RNA in the response to pathogenic infection.	SOCS3		transfection,RT–qPCR,siRNA,Immunoblotting,FISH,immunocytochemistry,Northern blot	Finally, we investigated expression of the SLC2A3 and SLC2A14 genes, adjacently positioned to the eRNA07573 locus,in eRNA07573 KO cells.  Here, we show that 145 unstable nuclear RNAs, including enhancer RNAs (eRNAs) and long noncoding RNAs (lncRNAs) such as NEAT1v2, are stabilized upon Salmonella infection in HeLa cells. In uninfected cells, the RNA exosome, aided by the Nuclear EXosome Targeting (NEXT) complex, degrades these labile transcripts. Upon infection, the levels of the exosome/NEXT components, RRP6 and MTR4, dramatically decrease, resulting in transcript stabilization. Depletion of lncRNAs, NEAT1v2, or eRNA07573 in HeLa cells triggers increased susceptibility to Salmonella infection concomitant with the deregulated expression of a distinct class of immunity-related genes, indicating that the accumulation of unstable nuclear RNAs contributes to antibacterial defense. Our results highlight a fundamental role for regulated degradation of nuclear RNA in the response to pathogenic infection.			
29879032	chr14	51429786	51431786	Ang2	Initially, we found that BAY11-7082 inhibited NF-κB expression in a concentration-dependent manner. According to the findings of MTT assay and flow cytometry, we understood that RA-HFLS treated by BAY11-7082 (an inhibitor of NF-κB), the inhibition of NF-κB pathway, suppressed RA-HFLS proliferation and induced RA-HFLS apoptosis in a concentration and time-dependent manner. Furthermore, RA-HFLS treated by BAY11-7082 presented decreased VEGF, Ang1 and Ang2 expressions in a concentration-dependent manner.The study concluded that inhibition of NF-κB pathway induced cell apoptosis and suppressed proliferation and angiogenesis of RA-HFLS, which could serve as a novel target in the treatment of RA.	human		High+Lowthroughput	Inhibition of NF-κB signaling pathway induces apoptosis and suppresses proliferation and angiogenesis of human fibroblast-like synovial cells in rheumatoid arthritis	否	无	Rheumatoid arthritis (RA)	HFLS cell	E_01_0427	MTT,Flow cytometry,Western blot	Initially, we found that BAY11-7082 inhibited NF-κB expression in a concentration-dependent manner. According to the findings of MTT assay and flow cytometry, we understood that RA-HFLS treated by BAY11-7082 (an inhibitor of NF-κB), the inhibition of NF-κB pathway, suppressed RA-HFLS proliferation and induced RA-HFLS apoptosis in a concentration and time-dependent manner. Furthermore, RA-HFLS treated by BAY11-7082 presented decreased VEGF, Ang1 and Ang2 expressions in a concentration-dependent manner.The study concluded that inhibition of NF-κB pathway induced cell apoptosis and suppressed proliferation and angiogenesis of RA-HFLS, which could serve as a novel target in the treatment of RA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Initially, we found that BAY11-7082 inhibited NF-κB expression in a concentration-dependent manner. According to the findings of MTT assay and flow cytometry, we understood that RA-HFLS treated by BAY11-7082 (an inhibitor of NF-κB), the inhibition of NF-κB pathway, suppressed RA-HFLS proliferation and induced RA-HFLS apoptosis in a concentration and time-dependent manner. Furthermore, RA-HFLS treated by BAY11-7082 presented decreased VEGF, Ang1 and Ang2 expressions in a concentration-dependent manner.The study concluded that inhibition of NF-κB pathway induced cell apoptosis and suppressed proliferation and angiogenesis of RA-HFLS, which could serve as a novel target in the treatment of RA.		Initially, we found that BAY11-7082 inhibited NF-κB expression in a concentration-dependent manner. According to the findings of MTT assay and flow cytometry, we understood that RA-HFLS treated by BAY11-7082 (an inhibitor of NF-κB), the inhibition of NF-κB pathway, suppressed RA-HFLS proliferation and induced RA-HFLS apoptosis in a concentration and time-dependent manner. Furthermore, RA-HFLS treated by BAY11-7082 presented decreased VEGF, Ang1 and Ang2 expressions in a concentration-dependent manner.The study concluded that inhibition of NF-κB pathway induced cell apoptosis and suppressed proliferation and angiogenesis of RA-HFLS, which could serve as a novel target in the treatment of RA.	Immunohistochemical staining	Initially, we found that BAY11-7082 inhibited NF-κB expression in a concentration-dependent manner. According to the findings of MTT assay and flow cytometry, we understood that RA-HFLS treated by BAY11-7082 (an inhibitor of NF-κB), the inhibition of NF-κB pathway, suppressed RA-HFLS proliferation and induced RA-HFLS apoptosis in a concentration and time-dependent manner. Furthermore, RA-HFLS treated by BAY11-7082 presented decreased VEGF, Ang1 and Ang2 expressions in a concentration-dependent manner.The study concluded that inhibition of NF-κB pathway induced cell apoptosis and suppressed proliferation and angiogenesis of RA-HFLS, which could serve as a novel target in the treatment of RA.			MTT,Flow cytometry,Western blot				Ang2
29877106	chr10	24788525	24790525	Arg1	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	human	lymphoid tissue	High+Lowthroughput	Polysaccharides from Citrus grandis associate with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophages	否	无	chronic pharyngitis	macrophage	E_01_0428	Western blot,Enzyme-linked immunosorbent assay(ELISA),RT-PCR	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.		PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	Immunohistochemical staining	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.			Western blot,Enzyme-linked immunosorbent assay(ELISA),RT-PCR				Arg1
29877106	chr2	14231594	14233594	Mrc1	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	human	lymphoid tissue	High+Lowthroughput	Polysaccharides from Citrus grandis associate with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophages	否	无	chronic pharyngitis	macrophage	E_01_0428	Western blot,Enzyme-linked immunosorbent assay(ELISA),RT-PCR	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.		PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	Immunohistochemical staining	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.			Western blot,Enzyme-linked immunosorbent assay(ELISA),RT-PCR				Mrc1
29877106	chr5	132438005	132440005	IRF1	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	human	lymphoid tissue	High+Lowthroughput	Polysaccharides from Citrus grandis associate with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophages	否	无	chronic pharyngitis	macrophage	E_01_0428	Western blot,Enzyme-linked immunosorbent assay(ELISA),RT-PCR	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	Immunohistochemical staining	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	IRF1		Western blot,Enzyme-linked immunosorbent assay(ELISA),RT-PCR	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.			
29877106	chr7	128935031	128937031	IRF5	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	human	lymphoid tissue	High+Lowthroughput	Polysaccharides from Citrus grandis associate with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophages	否	无	chronic pharyngitis	macrophage	E_01_0428	Western blot,Enzyme-linked immunosorbent assay(ELISA),RT-PCR	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	Immunohistochemical staining	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.	IRF5		Western blot,Enzyme-linked immunosorbent assay(ELISA),RT-PCR	PCG and luteolin suppress the productions of pro-inflammatory cytokines interlukin-6 (IL-6), interlukin-12 (IL-12) and tumor necrosis factor alpha (TNF-α) in macrophages. Luteolin promotes macrophage M2 polarization by enhancing expressions of arginase (Arg1) and mannose receptor C type 1 (Mrc1). PCG and luteolin suppress nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation and interferon regulatory factor 1 (IRF1), interferon regulatory factor 5 (IRF5) expression. PCG together with luteolin relieves chronic pharyngitis by anti-inflammatory via suppressing NF-κB pathway and the polarization of M1 macrophage.			
29876014	chr18	63121048	63123048	BCL2	Here, we analyzed the epigenome of two high-risk APL (hrAPL) patients and compared it to non-high-risk APL cases. Despite the lack of common genetic signatures, we found that human hrAPL blasts from patients with extremely poor prognosis display specific patterns of histone H3 acetylation, specifically hyperacetylation at a common set of enhancer regions. In addition, unique profiles of the repressive marks H3K27me3 and DNA methylation were exposed in high-risk APLs. Epigenetic comparison with low/intermediate-risk APLs and AMLs revealed hrAPL-specific patterns of histone acetylation and DNA methylation, suggesting these could be further developed into markers for clinical identification. The epigenetic drug MC2884, a newly generated general HAT/EZH2 inhibitor, induces apoptosis of high-risk APL blasts and reshapes their epigenomes by targeting both active and repressive marks. Together, our analysis uncovers distinctive epigenome signatures of hrAPL patients, and provides proof of concept for use of epigenome profiling coupled to epigenetic drugs to 'personalize' precision medicine.	human	Nervous tissue	High+Lowthroughput	Multi-omics profiling reveals a distinctive epigenome signature for high-risk acute promyelocytic leukemia	是	无	Acute promyelocytic leukemia (APL)	promyelocyte	E_01_0429	NGS,ChIP,RNA extraction,RT-PCR,Whole-genome bisulfite sequencing(WGBS),RNA-seq	Here, we analyzed the epigenome of two high-risk APL (hrAPL) patients and compared it to non-high-risk APL cases. Despite the lack of common genetic signatures, we found that human hrAPL blasts from patients with extremely poor prognosis display specific patterns of histone H3 acetylation, specifically hyperacetylation at a common set of enhancer regions. In addition, unique profiles of the repressive marks H3K27me3 and DNA methylation were exposed in high-risk APLs. Epigenetic comparison with low/intermediate-risk APLs and AMLs revealed hrAPL-specific patterns of histone acetylation and DNA methylation, suggesting these could be further developed into markers for clinical identification. The epigenetic drug MC2884, a newly generated general HAT/EZH2 inhibitor, induces apoptosis of high-risk APL blasts and reshapes their epigenomes by targeting both active and repressive marks. Together, our analysis uncovers distinctive epigenome signatures of hrAPL patients, and provides proof of concept for use of epigenome profiling coupled to epigenetic drugs to 'personalize' precision medicine.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we analyzed the epigenome of two high-risk APL (hrAPL) patients and compared it to non-high-risk APL cases. Despite the lack of common genetic signatures, we found that human hrAPL blasts from patients with extremely poor prognosis display specific patterns of histone H3 acetylation, specifically hyperacetylation at a common set of enhancer regions. In addition, unique profiles of the repressive marks H3K27me3 and DNA methylation were exposed in high-risk APLs. Epigenetic comparison with low/intermediate-risk APLs and AMLs revealed hrAPL-specific patterns of histone acetylation and DNA methylation, suggesting these could be further developed into markers for clinical identification. The epigenetic drug MC2884, a newly generated general HAT/EZH2 inhibitor, induces apoptosis of high-risk APL blasts and reshapes their epigenomes by targeting both active and repressive marks. Together, our analysis uncovers distinctive epigenome signatures of hrAPL patients, and provides proof of concept for use of epigenome profiling coupled to epigenetic drugs to 'personalize' precision medicine.	Immunohistochemical staining	Here, we analyzed the epigenome of two high-risk APL (hrAPL) patients and compared it to non-high-risk APL cases. Despite the lack of common genetic signatures, we found that human hrAPL blasts from patients with extremely poor prognosis display specific patterns of histone H3 acetylation, specifically hyperacetylation at a common set of enhancer regions. In addition, unique profiles of the repressive marks H3K27me3 and DNA methylation were exposed in high-risk APLs. Epigenetic comparison with low/intermediate-risk APLs and AMLs revealed hrAPL-specific patterns of histone acetylation and DNA methylation, suggesting these could be further developed into markers for clinical identification. The epigenetic drug MC2884, a newly generated general HAT/EZH2 inhibitor, induces apoptosis of high-risk APL blasts and reshapes their epigenomes by targeting both active and repressive marks. Together, our analysis uncovers distinctive epigenome signatures of hrAPL patients, and provides proof of concept for use of epigenome profiling coupled to epigenetic drugs to 'personalize' precision medicine.	BCL2		NGS,ChIP,RNA extraction,RT-PCR,Whole-genome bisulfite sequencing(WGBS),RNA-seq	Here, we analyzed the epigenome of two high-risk APL (hrAPL) patients and compared it to non-high-risk APL cases. Despite the lack of common genetic signatures, we found that human hrAPL blasts from patients with extremely poor prognosis display specific patterns of histone H3 acetylation, specifically hyperacetylation at a common set of enhancer regions. In addition, unique profiles of the repressive marks H3K27me3 and DNA methylation were exposed in high-risk APLs. Epigenetic comparison with low/intermediate-risk APLs and AMLs revealed hrAPL-specific patterns of histone acetylation and DNA methylation, suggesting these could be further developed into markers for clinical identification. The epigenetic drug MC2884, a newly generated general HAT/EZH2 inhibitor, induces apoptosis of high-risk APL blasts and reshapes their epigenomes by targeting both active and repressive marks. Together, our analysis uncovers distinctive epigenome signatures of hrAPL patients, and provides proof of concept for use of epigenome profiling coupled to epigenetic drugs to 'personalize' precision medicine.			
29876014	chr1	33005121	33007121	AK2	Here, we analyzed the epigenome of two high-risk APL (hrAPL) patients and compared it to non-high-risk APL cases. Despite the lack of common genetic signatures, we found that human hrAPL blasts from patients with extremely poor prognosis display specific patterns of histone H3 acetylation, specifically hyperacetylation at a common set of enhancer regions. In addition, unique profiles of the repressive marks H3K27me3 and DNA methylation were exposed in high-risk APLs. Epigenetic comparison with low/intermediate-risk APLs and AMLs revealed hrAPL-specific patterns of histone acetylation and DNA methylation, suggesting these could be further developed into markers for clinical identification. The epigenetic drug MC2884, a newly generated general HAT/EZH2 inhibitor, induces apoptosis of high-risk APL blasts and reshapes their epigenomes by targeting both active and repressive marks. Together, our analysis uncovers distinctive epigenome signatures of hrAPL patients, and provides proof of concept for use of epigenome profiling coupled to epigenetic drugs to 'personalize' precision medicine.	human	Nervous tissue	High+Lowthroughput	Multi-omics profiling reveals a distinctive epigenome signature for high-risk acute promyelocytic leukemia	是	无	Acute promyelocytic leukemia (APL)	promyelocyte	E_01_0429	NGS,ChIP,RNA extraction,RT-PCR,Whole-genome bisulfite sequencing(WGBS),RNA-seq	Here, we analyzed the epigenome of two high-risk APL (hrAPL) patients and compared it to non-high-risk APL cases. Despite the lack of common genetic signatures, we found that human hrAPL blasts from patients with extremely poor prognosis display specific patterns of histone H3 acetylation, specifically hyperacetylation at a common set of enhancer regions. In addition, unique profiles of the repressive marks H3K27me3 and DNA methylation were exposed in high-risk APLs. Epigenetic comparison with low/intermediate-risk APLs and AMLs revealed hrAPL-specific patterns of histone acetylation and DNA methylation, suggesting these could be further developed into markers for clinical identification. The epigenetic drug MC2884, a newly generated general HAT/EZH2 inhibitor, induces apoptosis of high-risk APL blasts and reshapes their epigenomes by targeting both active and repressive marks. Together, our analysis uncovers distinctive epigenome signatures of hrAPL patients, and provides proof of concept for use of epigenome profiling coupled to epigenetic drugs to 'personalize' precision medicine.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we analyzed the epigenome of two high-risk APL (hrAPL) patients and compared it to non-high-risk APL cases. Despite the lack of common genetic signatures, we found that human hrAPL blasts from patients with extremely poor prognosis display specific patterns of histone H3 acetylation, specifically hyperacetylation at a common set of enhancer regions. In addition, unique profiles of the repressive marks H3K27me3 and DNA methylation were exposed in high-risk APLs. Epigenetic comparison with low/intermediate-risk APLs and AMLs revealed hrAPL-specific patterns of histone acetylation and DNA methylation, suggesting these could be further developed into markers for clinical identification. The epigenetic drug MC2884, a newly generated general HAT/EZH2 inhibitor, induces apoptosis of high-risk APL blasts and reshapes their epigenomes by targeting both active and repressive marks. Together, our analysis uncovers distinctive epigenome signatures of hrAPL patients, and provides proof of concept for use of epigenome profiling coupled to epigenetic drugs to 'personalize' precision medicine.		Here, we analyzed the epigenome of two high-risk APL (hrAPL) patients and compared it to non-high-risk APL cases. Despite the lack of common genetic signatures, we found that human hrAPL blasts from patients with extremely poor prognosis display specific patterns of histone H3 acetylation, specifically hyperacetylation at a common set of enhancer regions. In addition, unique profiles of the repressive marks H3K27me3 and DNA methylation were exposed in high-risk APLs. Epigenetic comparison with low/intermediate-risk APLs and AMLs revealed hrAPL-specific patterns of histone acetylation and DNA methylation, suggesting these could be further developed into markers for clinical identification. The epigenetic drug MC2884, a newly generated general HAT/EZH2 inhibitor, induces apoptosis of high-risk APL blasts and reshapes their epigenomes by targeting both active and repressive marks. Together, our analysis uncovers distinctive epigenome signatures of hrAPL patients, and provides proof of concept for use of epigenome profiling coupled to epigenetic drugs to 'personalize' precision medicine.	Immunohistochemical staining	Here, we analyzed the epigenome of two high-risk APL (hrAPL) patients and compared it to non-high-risk APL cases. Despite the lack of common genetic signatures, we found that human hrAPL blasts from patients with extremely poor prognosis display specific patterns of histone H3 acetylation, specifically hyperacetylation at a common set of enhancer regions. In addition, unique profiles of the repressive marks H3K27me3 and DNA methylation were exposed in high-risk APLs. Epigenetic comparison with low/intermediate-risk APLs and AMLs revealed hrAPL-specific patterns of histone acetylation and DNA methylation, suggesting these could be further developed into markers for clinical identification. The epigenetic drug MC2884, a newly generated general HAT/EZH2 inhibitor, induces apoptosis of high-risk APL blasts and reshapes their epigenomes by targeting both active and repressive marks. Together, our analysis uncovers distinctive epigenome signatures of hrAPL patients, and provides proof of concept for use of epigenome profiling coupled to epigenetic drugs to 'personalize' precision medicine.			NGS,ChIP,RNA extraction,RT-PCR,Whole-genome bisulfite sequencing(WGBS),RNA-seq				AK2
29875794	chrX	67541120	67543120	AR	To find relevant epigenetic signatures enriched at the ARA-lincRNAs' transcription start sites (TSSs) we used a machine learning approach and identified that the ARA-lincRNA genomic loci in LNCaP cells are significantly enriched with epigenetic marks that are characteristic of in cis enhancer RNA regulators, and that the H3K27ac mark of active enhancers is conspicuously enriched at the TSS of ARA-lincRNAs adjacent to androgen-activated protein-coding genes. In addition, LNCaP topologically associating domains (TADs) that comprise chromatin regions with ARA-lincRNAs exhibit transcription factor contents, epigenetic marks and gene transcriptional activities that are significantly different from TADs not containing ARA-lincRNAs. This work highlights the possible involvement of hundreds of lincRNAs working in synergy with the AR on the genome-wide androgen-induced gene regulatory program in prostate cells.	human	Myotome	High+Lowthroughput	Chromatin Landscape Distinguishes the Genomic Loci of Hundreds of Androgen-Receptor-Associated LincRNAs From the Loci of Non-associated LincRNAs	否	无		LNCaP	E_01_0430	RNA-seq,RIP-Seq,RT-qPCR,Reverse Transcription PCR,GSEA,DNAseI Datasets	To find relevant epigenetic signatures enriched at the ARA-lincRNAs' transcription start sites (TSSs) we used a machine learning approach and identified that the ARA-lincRNA genomic loci in LNCaP cells are significantly enriched with epigenetic marks that are characteristic of in cis enhancer RNA regulators, and that the H3K27ac mark of active enhancers is conspicuously enriched at the TSS of ARA-lincRNAs adjacent to androgen-activated protein-coding genes. In addition, LNCaP topologically associating domains (TADs) that comprise chromatin regions with ARA-lincRNAs exhibit transcription factor contents, epigenetic marks and gene transcriptional activities that are significantly different from TADs not containing ARA-lincRNAs. This work highlights the possible involvement of hundreds of lincRNAs working in synergy with the AR on the genome-wide androgen-induced gene regulatory program in prostate cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			To find relevant epigenetic signatures enriched at the ARA-lincRNAs' transcription start sites (TSSs) we used a machine learning approach and identified that the ARA-lincRNA genomic loci in LNCaP cells are significantly enriched with epigenetic marks that are characteristic of in cis enhancer RNA regulators, and that the H3K27ac mark of active enhancers is conspicuously enriched at the TSS of ARA-lincRNAs adjacent to androgen-activated protein-coding genes. In addition, LNCaP topologically associating domains (TADs) that comprise chromatin regions with ARA-lincRNAs exhibit transcription factor contents, epigenetic marks and gene transcriptional activities that are significantly different from TADs not containing ARA-lincRNAs. This work highlights the possible involvement of hundreds of lincRNAs working in synergy with the AR on the genome-wide androgen-induced gene regulatory program in prostate cells.	Immunohistochemical staining	To find relevant epigenetic signatures enriched at the ARA-lincRNAs' transcription start sites (TSSs) we used a machine learning approach and identified that the ARA-lincRNA genomic loci in LNCaP cells are significantly enriched with epigenetic marks that are characteristic of in cis enhancer RNA regulators, and that the H3K27ac mark of active enhancers is conspicuously enriched at the TSS of ARA-lincRNAs adjacent to androgen-activated protein-coding genes. In addition, LNCaP topologically associating domains (TADs) that comprise chromatin regions with ARA-lincRNAs exhibit transcription factor contents, epigenetic marks and gene transcriptional activities that are significantly different from TADs not containing ARA-lincRNAs. This work highlights the possible involvement of hundreds of lincRNAs working in synergy with the AR on the genome-wide androgen-induced gene regulatory program in prostate cells.	AR		RNA-seq,RIP-Seq,RT-qPCR,Reverse Transcription PCR,GSEA,DNAseI Datasets	To find relevant epigenetic signatures enriched at the ARA-lincRNAs' transcription start sites (TSSs) we used a machine learning approach and identified that the ARA-lincRNA genomic loci in LNCaP cells are significantly enriched with epigenetic marks that are characteristic of in cis enhancer RNA regulators, and that the H3K27ac mark of active enhancers is conspicuously enriched at the TSS of ARA-lincRNAs adjacent to androgen-activated protein-coding genes. In addition, LNCaP topologically associating domains (TADs) that comprise chromatin regions with ARA-lincRNAs exhibit transcription factor contents, epigenetic marks and gene transcriptional activities that are significantly different from TADs not containing ARA-lincRNAs. This work highlights the possible involvement of hundreds of lincRNAs working in synergy with the AR on the genome-wide androgen-induced gene regulatory program in prostate cells.			
29875794	chr12	49185847	49187847	TUBA1C	To find relevant epigenetic signatures enriched at the ARA-lincRNAs' transcription start sites (TSSs) we used a machine learning approach and identified that the ARA-lincRNA genomic loci in LNCaP cells are significantly enriched with epigenetic marks that are characteristic of in cis enhancer RNA regulators, and that the H3K27ac mark of active enhancers is conspicuously enriched at the TSS of ARA-lincRNAs adjacent to androgen-activated protein-coding genes. In addition, LNCaP topologically associating domains (TADs) that comprise chromatin regions with ARA-lincRNAs exhibit transcription factor contents, epigenetic marks and gene transcriptional activities that are significantly different from TADs not containing ARA-lincRNAs. This work highlights the possible involvement of hundreds of lincRNAs working in synergy with the AR on the genome-wide androgen-induced gene regulatory program in prostate cells.	human	Myotome	High+Lowthroughput	Chromatin Landscape Distinguishes the Genomic Loci of Hundreds of Androgen-Receptor-Associated LincRNAs From the Loci of Non-associated LincRNAs	否	无		LNCaP	E_01_0430	RNA-seq,RIP-Seq,RT-qPCR,Reverse Transcription PCR,GSEA,DNAseI Datasets	To find relevant epigenetic signatures enriched at the ARA-lincRNAs' transcription start sites (TSSs) we used a machine learning approach and identified that the ARA-lincRNA genomic loci in LNCaP cells are significantly enriched with epigenetic marks that are characteristic of in cis enhancer RNA regulators, and that the H3K27ac mark of active enhancers is conspicuously enriched at the TSS of ARA-lincRNAs adjacent to androgen-activated protein-coding genes. In addition, LNCaP topologically associating domains (TADs) that comprise chromatin regions with ARA-lincRNAs exhibit transcription factor contents, epigenetic marks and gene transcriptional activities that are significantly different from TADs not containing ARA-lincRNAs. This work highlights the possible involvement of hundreds of lincRNAs working in synergy with the AR on the genome-wide androgen-induced gene regulatory program in prostate cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To find relevant epigenetic signatures enriched at the ARA-lincRNAs' transcription start sites (TSSs) we used a machine learning approach and identified that the ARA-lincRNA genomic loci in LNCaP cells are significantly enriched with epigenetic marks that are characteristic of in cis enhancer RNA regulators, and that the H3K27ac mark of active enhancers is conspicuously enriched at the TSS of ARA-lincRNAs adjacent to androgen-activated protein-coding genes. In addition, LNCaP topologically associating domains (TADs) that comprise chromatin regions with ARA-lincRNAs exhibit transcription factor contents, epigenetic marks and gene transcriptional activities that are significantly different from TADs not containing ARA-lincRNAs. This work highlights the possible involvement of hundreds of lincRNAs working in synergy with the AR on the genome-wide androgen-induced gene regulatory program in prostate cells.		To find relevant epigenetic signatures enriched at the ARA-lincRNAs' transcription start sites (TSSs) we used a machine learning approach and identified that the ARA-lincRNA genomic loci in LNCaP cells are significantly enriched with epigenetic marks that are characteristic of in cis enhancer RNA regulators, and that the H3K27ac mark of active enhancers is conspicuously enriched at the TSS of ARA-lincRNAs adjacent to androgen-activated protein-coding genes. In addition, LNCaP topologically associating domains (TADs) that comprise chromatin regions with ARA-lincRNAs exhibit transcription factor contents, epigenetic marks and gene transcriptional activities that are significantly different from TADs not containing ARA-lincRNAs. This work highlights the possible involvement of hundreds of lincRNAs working in synergy with the AR on the genome-wide androgen-induced gene regulatory program in prostate cells.	Immunohistochemical staining	To find relevant epigenetic signatures enriched at the ARA-lincRNAs' transcription start sites (TSSs) we used a machine learning approach and identified that the ARA-lincRNA genomic loci in LNCaP cells are significantly enriched with epigenetic marks that are characteristic of in cis enhancer RNA regulators, and that the H3K27ac mark of active enhancers is conspicuously enriched at the TSS of ARA-lincRNAs adjacent to androgen-activated protein-coding genes. In addition, LNCaP topologically associating domains (TADs) that comprise chromatin regions with ARA-lincRNAs exhibit transcription factor contents, epigenetic marks and gene transcriptional activities that are significantly different from TADs not containing ARA-lincRNAs. This work highlights the possible involvement of hundreds of lincRNAs working in synergy with the AR on the genome-wide androgen-induced gene regulatory program in prostate cells.			RNA-seq,RIP-Seq,RT-qPCR,Reverse Transcription PCR,GSEA,DNAseI Datasets				TUBA1C
29875318	chr19	30520129	30522129	Dkk1	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.	human	connective tissue	High+Lowthroughput	Sclerostin neutralization unleashes the osteoanabolic effects of Dkk1 inhibition	否	无	Osteoporosis	osteocyte	E_01_0431	DXA,μCT,pQCT,Histology,transgenic mice,ELISA,	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.		In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.	Immunohistochemical staining	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.			DXA,μCT,pQCT,Histology,transgenic mice,ELISA,				Dkk1
29875318	chr5	104347639	104349639	Dmp1	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.	human	connective tissue	High+Lowthroughput	Sclerostin neutralization unleashes the osteoanabolic effects of Dkk1 inhibition	否	无	Osteoporosis	osteocyte	E_01_0431	DXA,μCT,pQCT,Histology,transgenic mice,ELISA,	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.		In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.	Immunohistochemical staining	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.			DXA,μCT,pQCT,Histology,transgenic mice,ELISA,				Dmp1
29875318	chr17	43751649	43753649	SOST	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.	human	connective tissue	High+Lowthroughput	Sclerostin neutralization unleashes the osteoanabolic effects of Dkk1 inhibition	否	无	Osteoporosis	osteocyte	E_01_0431	DXA,μCT,pQCT,Histology,transgenic mice,ELISA,	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.		In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.	Immunohistochemical staining	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.			DXA,μCT,pQCT,Histology,transgenic mice,ELISA,				SOST
29875318	chr11	68309810	68311810	LRP5	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.	human	connective tissue	High+Lowthroughput	Sclerostin neutralization unleashes the osteoanabolic effects of Dkk1 inhibition	否	无	Osteoporosis	osteocyte	E_01_0431	DXA,μCT,pQCT,Histology,transgenic mice,ELISA,	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.		In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.	Immunohistochemical staining	In conclusion, the osteoanabolic effects of Dkk1 inhibition can be realized if sclerostin upregulation is prevented. Anabolic therapies for patients with low bone mass might benefit from a strategy that accounts for the compensatory milieu of WNT inhibitors in bone tissue.			DXA,μCT,pQCT,Histology,transgenic mice,ELISA,				LRP5
29874879	chr14	74473514	74475514	NPC2	Our study demonstrated that NPC2-mediated free cholesterol homeostasis controls HSC proliferation and mitochondrial function.	human	connective tissue	High+Lowthroughput	Niemann-Pick Type C2 Protein Regulates Free Cholesterol Accumulation and Influences Hepatic Stellate Cell Proliferation and Mitochondrial Respiration Function	否	无	hepatic fibrosis 	HSC-T6 cell	E_01_0432	Western Blot,Real-Time PCR,Seahorse Assay	Our study demonstrated that NPC2-mediated free cholesterol homeostasis controls HSC proliferation and mitochondrial function.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our study demonstrated that NPC2-mediated free cholesterol homeostasis controls HSC proliferation and mitochondrial function.		Our study demonstrated that NPC2-mediated free cholesterol homeostasis controls HSC proliferation and mitochondrial function.	Immunohistochemical staining	Our study demonstrated that NPC2-mediated free cholesterol homeostasis controls HSC proliferation and mitochondrial function.			Western Blot,Real-Time PCR,Seahorse Assay				NPC2
29874879	chr9	117701781	117703781	TLR4	Our study demonstrated that NPC2-mediated free cholesterol homeostasis controls HSC proliferation and mitochondrial function.	human	connective tissue	High+Lowthroughput	Niemann-Pick Type C2 Protein Regulates Free Cholesterol Accumulation and Influences Hepatic Stellate Cell Proliferation and Mitochondrial Respiration Function	否	无	hepatic fibrosis 	HSC-T6 cell	E_01_0432	Western Blot,Real-Time PCR,Seahorse Assay	Our study demonstrated that NPC2-mediated free cholesterol homeostasis controls HSC proliferation and mitochondrial function.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our study demonstrated that NPC2-mediated free cholesterol homeostasis controls HSC proliferation and mitochondrial function.	Immunohistochemical staining	Our study demonstrated that NPC2-mediated free cholesterol homeostasis controls HSC proliferation and mitochondrial function.	TLR4		Western Blot,Real-Time PCR,Seahorse Assay	Our study demonstrated that NPC2-mediated free cholesterol homeostasis controls HSC proliferation and mitochondrial function.			
29874843	chr9	4981763	4983763	JAK2	Our data showed that COSCs can regulate body weight gain, lipids, serum alanine aminotransferase, and aspartate aminotransferase, as well as upregulate the hepatic leptin receptor-b (LepRb) and the phosphorylation of JAK2 and STAT3. Meanwhile, marked increased expressions of liver sterol regulatory element-binding protein-1c, fatty acid synthase, acetyl-CoA carboxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, adiponectin, adipose peroxisome proliferator-activated receptor γ, CCAAT-enhancer binding protein α, adipose differentiation-related protein, and SREBP-1c were observed. The results suggested that COSCs activate the JAK2-STAT3 signaling pathway to alleviate leptin resistance and suppress adipogenesis to reduce lipid accumulation. Thus, they can potentially be used for obesity treatment.	mouse	hepatic tissue	High+Lowthroughput	Anti-Obesity Effect of Chitosan Oligosaccharide Capsules (COSCs) in Obese Rats by Ameliorating Leptin Resistance and Adipogenesis	否	无	Obesity	hepatocyte	E_02_0288	RT-PCR,Western Blot,AST,ALT,	Our data showed that COSCs can regulate body weight gain, lipids, serum alanine aminotransferase, and aspartate aminotransferase, as well as upregulate the hepatic leptin receptor-b (LepRb) and the phosphorylation of JAK2 and STAT3. Meanwhile, marked increased expressions of liver sterol regulatory element-binding protein-1c, fatty acid synthase, acetyl-CoA carboxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, adiponectin, adipose peroxisome proliferator-activated receptor γ, CCAAT-enhancer binding protein α, adipose differentiation-related protein, and SREBP-1c were observed. The results suggested that COSCs activate the JAK2-STAT3 signaling pathway to alleviate leptin resistance and suppress adipogenesis to reduce lipid accumulation. Thus, they can potentially be used for obesity treatment.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data showed that COSCs can regulate body weight gain, lipids, serum alanine aminotransferase, and aspartate aminotransferase, as well as upregulate the hepatic leptin receptor-b (LepRb) and the phosphorylation of JAK2 and STAT3. Meanwhile, marked increased expressions of liver sterol regulatory element-binding protein-1c, fatty acid synthase, acetyl-CoA carboxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, adiponectin, adipose peroxisome proliferator-activated receptor γ, CCAAT-enhancer binding protein α, adipose differentiation-related protein, and SREBP-1c were observed. The results suggested that COSCs activate the JAK2-STAT3 signaling pathway to alleviate leptin resistance and suppress adipogenesis to reduce lipid accumulation. Thus, they can potentially be used for obesity treatment.		Our data showed that COSCs can regulate body weight gain, lipids, serum alanine aminotransferase, and aspartate aminotransferase, as well as upregulate the hepatic leptin receptor-b (LepRb) and the phosphorylation of JAK2 and STAT3. Meanwhile, marked increased expressions of liver sterol regulatory element-binding protein-1c, fatty acid synthase, acetyl-CoA carboxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, adiponectin, adipose peroxisome proliferator-activated receptor γ, CCAAT-enhancer binding protein α, adipose differentiation-related protein, and SREBP-1c were observed. The results suggested that COSCs activate the JAK2-STAT3 signaling pathway to alleviate leptin resistance and suppress adipogenesis to reduce lipid accumulation. Thus, they can potentially be used for obesity treatment.	Immunohistochemical staining	Our data showed that COSCs can regulate body weight gain, lipids, serum alanine aminotransferase, and aspartate aminotransferase, as well as upregulate the hepatic leptin receptor-b (LepRb) and the phosphorylation of JAK2 and STAT3. Meanwhile, marked increased expressions of liver sterol regulatory element-binding protein-1c, fatty acid synthase, acetyl-CoA carboxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, adiponectin, adipose peroxisome proliferator-activated receptor γ, CCAAT-enhancer binding protein α, adipose differentiation-related protein, and SREBP-1c were observed. The results suggested that COSCs activate the JAK2-STAT3 signaling pathway to alleviate leptin resistance and suppress adipogenesis to reduce lipid accumulation. Thus, they can potentially be used for obesity treatment.			RT-PCR,Western Blot,AST,ALT,				JAK2
29874843	chr17	42310467	42312467	STAT3	Our data showed that COSCs can regulate body weight gain, lipids, serum alanine aminotransferase, and aspartate aminotransferase, as well as upregulate the hepatic leptin receptor-b (LepRb) and the phosphorylation of JAK2 and STAT3. Meanwhile, marked increased expressions of liver sterol regulatory element-binding protein-1c, fatty acid synthase, acetyl-CoA carboxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, adiponectin, adipose peroxisome proliferator-activated receptor γ, CCAAT-enhancer binding protein α, adipose differentiation-related protein, and SREBP-1c were observed. The results suggested that COSCs activate the JAK2-STAT3 signaling pathway to alleviate leptin resistance and suppress adipogenesis to reduce lipid accumulation. Thus, they can potentially be used for obesity treatment.	mouse	hepatic tissue	High+Lowthroughput	Anti-Obesity Effect of Chitosan Oligosaccharide Capsules (COSCs) in Obese Rats by Ameliorating Leptin Resistance and Adipogenesis	否	无	Obesity	hepatocyte	E_02_0288	RT-PCR,Western Blot,AST,ALT,	Our data showed that COSCs can regulate body weight gain, lipids, serum alanine aminotransferase, and aspartate aminotransferase, as well as upregulate the hepatic leptin receptor-b (LepRb) and the phosphorylation of JAK2 and STAT3. Meanwhile, marked increased expressions of liver sterol regulatory element-binding protein-1c, fatty acid synthase, acetyl-CoA carboxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, adiponectin, adipose peroxisome proliferator-activated receptor γ, CCAAT-enhancer binding protein α, adipose differentiation-related protein, and SREBP-1c were observed. The results suggested that COSCs activate the JAK2-STAT3 signaling pathway to alleviate leptin resistance and suppress adipogenesis to reduce lipid accumulation. Thus, they can potentially be used for obesity treatment.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data showed that COSCs can regulate body weight gain, lipids, serum alanine aminotransferase, and aspartate aminotransferase, as well as upregulate the hepatic leptin receptor-b (LepRb) and the phosphorylation of JAK2 and STAT3. Meanwhile, marked increased expressions of liver sterol regulatory element-binding protein-1c, fatty acid synthase, acetyl-CoA carboxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, adiponectin, adipose peroxisome proliferator-activated receptor γ, CCAAT-enhancer binding protein α, adipose differentiation-related protein, and SREBP-1c were observed. The results suggested that COSCs activate the JAK2-STAT3 signaling pathway to alleviate leptin resistance and suppress adipogenesis to reduce lipid accumulation. Thus, they can potentially be used for obesity treatment.		Our data showed that COSCs can regulate body weight gain, lipids, serum alanine aminotransferase, and aspartate aminotransferase, as well as upregulate the hepatic leptin receptor-b (LepRb) and the phosphorylation of JAK2 and STAT3. Meanwhile, marked increased expressions of liver sterol regulatory element-binding protein-1c, fatty acid synthase, acetyl-CoA carboxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, adiponectin, adipose peroxisome proliferator-activated receptor γ, CCAAT-enhancer binding protein α, adipose differentiation-related protein, and SREBP-1c were observed. The results suggested that COSCs activate the JAK2-STAT3 signaling pathway to alleviate leptin resistance and suppress adipogenesis to reduce lipid accumulation. Thus, they can potentially be used for obesity treatment.	Immunohistochemical staining	Our data showed that COSCs can regulate body weight gain, lipids, serum alanine aminotransferase, and aspartate aminotransferase, as well as upregulate the hepatic leptin receptor-b (LepRb) and the phosphorylation of JAK2 and STAT3. Meanwhile, marked increased expressions of liver sterol regulatory element-binding protein-1c, fatty acid synthase, acetyl-CoA carboxylase, 3-hydroxy-3-methylglutaryl-CoA reductase, adiponectin, adipose peroxisome proliferator-activated receptor γ, CCAAT-enhancer binding protein α, adipose differentiation-related protein, and SREBP-1c were observed. The results suggested that COSCs activate the JAK2-STAT3 signaling pathway to alleviate leptin resistance and suppress adipogenesis to reduce lipid accumulation. Thus, they can potentially be used for obesity treatment.			RT-PCR,Western Blot,AST,ALT,				STAT3
29871881	chr4	102498539	102500539	NFKB1	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	human		High+Lowthroughput	Human Enhancers Harboring Specific Sequence Composition, Activity, and Genome Organization Are Linked to the Immune Response	是	无	nothing		E_01_0433	Hi-C,RELA ChIP-seq, DNA seq	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	Immunohistochemical staining	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	NFKB1		Hi-C,RELA ChIP-seq, DNA seq	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.			
29871881	chr2	60878901	60880901	REL	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	human		High+Lowthroughput	Human Enhancers Harboring Specific Sequence Composition, Activity, and Genome Organization Are Linked to the Immune Response	是	无	nothing		E_01_0433	Hi-C,RELA ChIP-seq, DNA seq	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	Immunohistochemical staining	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	REL		Hi-C,RELA ChIP-seq, DNA seq	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.			
29871881	chr11	65650710	65652710	RELA	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	human		High+Lowthroughput	Human Enhancers Harboring Specific Sequence Composition, Activity, and Genome Organization Are Linked to the Immune Response	是	无	nothing		E_01_0433	Hi-C,RELA ChIP-seq, DNA seq	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	Immunohistochemical staining	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	RELA		Hi-C,RELA ChIP-seq, DNA seq	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.			
29871881	chr6	89924213	89926213	BACH2	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	human		High+Lowthroughput	Human Enhancers Harboring Specific Sequence Composition, Activity, and Genome Organization Are Linked to the Immune Response	是	无	nothing		E_01_0433	Hi-C,RELA ChIP-seq, DNA seq	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.		Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	Immunohistochemical staining	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.			Hi-C,RELA ChIP-seq, DNA seq				BACH2
29871881	chr17	67823197	67825197	BPTF	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	human		High+Lowthroughput	Human Enhancers Harboring Specific Sequence Composition, Activity, and Genome Organization Are Linked to the Immune Response	是	无	nothing		E_01_0433	Hi-C,RELA ChIP-seq, DNA seq	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	Immunohistochemical staining	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.	BPTF		Hi-C,RELA ChIP-seq, DNA seq	Looking at chromatin capture data, we found that the two classes of enhancers were lying in distinct topologically associating domains and chromatin loops. Our results suggest that specific nucleotide compositions encode for classes of enhancers that are functionally distinct and specifically organized in the human genome.			
29869821	chr2	15587927	15589927	DDX1	These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.	human	Colon tissue	High+Lowthroughput	DEAD box protein DDX1 promotes colorectal tumorigenesis through transcriptional activation of the LGR5 gene	否	无	Colorectal neoplasms	LoVo cell	E_01_0434	CRISPR / Cas9,knockdown,Quantitative RT‐PCR,Western blot,Luciferase reporter assay,Immunohistochemistry, Immunofluorescence analysis,ChIP	These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.		These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.	Immunohistochemical staining	These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.			CRISPR / Cas9,knockdown,Quantitative RT‐PCR,Western blot,Luciferase reporter assay,Immunohistochemistry, Immunofluorescence analysis,ChIP				DDX1
29869821	chr12	71436962	71438962	LGR5	These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.	human	Colon tissue	High+Lowthroughput	DEAD box protein DDX1 promotes colorectal tumorigenesis through transcriptional activation of the LGR5 gene	否	无	Colorectal neoplasms	LoVo cell	E_01_0434	CRISPR / Cas9,knockdown,Quantitative RT‐PCR,Western blot,Luciferase reporter assay,Immunohistochemistry, Immunofluorescence analysis,ChIP	These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.	Immunohistochemical staining	These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.	LGR5		CRISPR / Cas9,knockdown,Quantitative RT‐PCR,Western blot,Luciferase reporter assay,Immunohistochemistry, Immunofluorescence analysis,ChIP	These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.			
29869821	chr3	181709198	181711198	SOX2	These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.	human	Colon tissue	High+Lowthroughput	DEAD box protein DDX1 promotes colorectal tumorigenesis through transcriptional activation of the LGR5 gene	否	无	Colorectal neoplasms	LoVo cell	E_01_0434	CRISPR / Cas9,knockdown,Quantitative RT‐PCR,Western blot,Luciferase reporter assay,Immunohistochemistry, Immunofluorescence analysis,ChIP	These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.	Immunohistochemical staining	These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.	SOX2		CRISPR / Cas9,knockdown,Quantitative RT‐PCR,Western blot,Luciferase reporter assay,Immunohistochemistry, Immunofluorescence analysis,ChIP	These results suggest that LGR5 is a critical effector of DDX1 in colorectal cancer cells. The DDX1-LGR5 axis could be a new drug target for this type of malignant cancer.			
29867706	chr13	30454393	30456393	HMGB1	We provide novel evidence that UA reduces inflammatory cytokine production to protect the brain from cerebral ischemia and reperfusion injury possibly through the HMGB1/TLR4/NFκB signaling pathway.	mouse	Nervous tissue	High+Lowthroughput	Ursolic Acid Ameliorates Inflammation in Cerebral Ischemia and Reperfusion Injury Possibly via High Mobility Group Box 1/Toll-Like Receptor 4/NFκB Pathway	否	无	Inflammation in cerebral ischemia, reperfusion injury	microglial cell	E_02_0289	Nissl staining, ELISA,immunofluorescence staining,Western Blot,immunohistochemical staining	We provide novel evidence that UA reduces inflammatory cytokine production to protect the brain from cerebral ischemia and reperfusion injury possibly through the HMGB1/TLR4/NFκB signaling pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We provide novel evidence that UA reduces inflammatory cytokine production to protect the brain from cerebral ischemia and reperfusion injury possibly through the HMGB1/TLR4/NFκB signaling pathway.		We provide novel evidence that UA reduces inflammatory cytokine production to protect the brain from cerebral ischemia and reperfusion injury possibly through the HMGB1/TLR4/NFκB signaling pathway.	Immunohistochemical staining	We provide novel evidence that UA reduces inflammatory cytokine production to protect the brain from cerebral ischemia and reperfusion injury possibly through the HMGB1/TLR4/NFκB signaling pathway.			Nissl staining, ELISA,immunofluorescence staining,Western Blot,immunohistochemical staining				HMGB1
29867706	chr9	117701209	117703209	TLR4	We provide novel evidence that UA reduces inflammatory cytokine production to protect the brain from cerebral ischemia and reperfusion injury possibly through the HMGB1/TLR4/NFκB signaling pathway.	mouse	Nervous tissue	High+Lowthroughput	Ursolic Acid Ameliorates Inflammation in Cerebral Ischemia and Reperfusion Injury Possibly via High Mobility Group Box 1/Toll-Like Receptor 4/NFκB Pathway	否	无	Inflammation in cerebral ischemia, reperfusion injury	microglial cell	E_02_0289	Nissl staining, ELISA,immunofluorescence staining,Western Blot,immunohistochemical staining	We provide novel evidence that UA reduces inflammatory cytokine production to protect the brain from cerebral ischemia and reperfusion injury possibly through the HMGB1/TLR4/NFκB signaling pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We provide novel evidence that UA reduces inflammatory cytokine production to protect the brain from cerebral ischemia and reperfusion injury possibly through the HMGB1/TLR4/NFκB signaling pathway.		We provide novel evidence that UA reduces inflammatory cytokine production to protect the brain from cerebral ischemia and reperfusion injury possibly through the HMGB1/TLR4/NFκB signaling pathway.	Immunohistochemical staining	We provide novel evidence that UA reduces inflammatory cytokine production to protect the brain from cerebral ischemia and reperfusion injury possibly through the HMGB1/TLR4/NFκB signaling pathway.			Nissl staining, ELISA,immunofluorescence staining,Western Blot,immunohistochemical staining				TLR4
29866822	chr4	54654583	54656583	KIT	Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.	human	Kidney tissue	High+Lowthroughput	Gastrointestinal stromal tumor enhancers support a transcription factor network predictive of clinical outcome	否	无	Gastrointestinal stromal tumor (GIST)	293FT	E_01_0435	Transfection,RNA-Seq,ATAC-seq,ChIP-Seq,Quantitative RT-PCR,Cloning,CRISPR Assays,Immunoblotting	Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.	Immunohistochemical staining	Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.	KIT		Transfection,RNA-Seq,ATAC-seq,ChIP-Seq,Quantitative RT-PCR,Cloning,CRISPR Assays,Immunoblotting	Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.			
29866822	chr4	54226460	54228460	PDGFRA	Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.	human	Kidney tissue	High+Lowthroughput	Gastrointestinal stromal tumor enhancers support a transcription factor network predictive of clinical outcome	否	无	Gastrointestinal stromal tumor (GIST)	293FT	E_01_0435	Transfection,RNA-Seq,ATAC-seq,ChIP-Seq,Quantitative RT-PCR,Cloning,CRISPR Assays,Immunoblotting	Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.	Immunohistochemical staining	Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.	PDGFRA		Transfection,RNA-Seq,ATAC-seq,ChIP-Seq,Quantitative RT-PCR,Cloning,CRISPR Assays,Immunoblotting	Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.			
29866822	chr5	154472237	154474237	HAND1	Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.	human	Kidney tissue	High+Lowthroughput	Gastrointestinal stromal tumor enhancers support a transcription factor network predictive of clinical outcome	否	无	Gastrointestinal stromal tumor (GIST)	293FT	E_01_0435	Transfection,RNA-Seq,ATAC-seq,ChIP-Seq,Quantitative RT-PCR,Cloning,CRISPR Assays,Immunoblotting	Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.	Immunohistochemical staining	Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.	HAND1		Transfection,RNA-Seq,ATAC-seq,ChIP-Seq,Quantitative RT-PCR,Cloning,CRISPR Assays,Immunoblotting	Utilizing chromatin immunoprecipitation with sequencing of tumor samples and cell lines, we describe the enhancer landscape of GIST, highlighting genes that reinforce and extend our understanding of these neoplasms. A group of core transcription factors can be distinguished from others unique to localized and metastatic disease. The transcription factor HAND1 emerges in metastatic disease, binds to established GIST-associated enhancers, and facilitates GIST cell proliferation and KIT gene expression. The pattern of transcription factor expression in primary tumors is predictive of metastasis-free survival in GIST patients. These results provide insight into the enhancer landscape and transcription factor network underlying GIST, and define a unique strategy for predicting clinical behavior of this disease.			
29864144	chrX	71530253	71532253	OGT	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	human	Mammary tissue	High+Lowthroughput	Impact of OGT deregulation on EZH2 target genes FOXA1 and FOXC1 expression in breast cancer cells	否	无	mammary cancer	MCF10A	E_01_0436	RT-PCR,RNA isolation,Western blot,Chromatin immunoprecipitation assay(CHIP),Migration/invasion assay,	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	Immunohistochemical staining	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	OGT		RT-PCR,RNA isolation,Western blot,Chromatin immunoprecipitation assay(CHIP),Migration/invasion assay,	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.			
29864144	chr7	148804114	148806114	EZH2	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	human	Mammary tissue	High+Lowthroughput	Impact of OGT deregulation on EZH2 target genes FOXA1 and FOXC1 expression in breast cancer cells	否	无	mammary cancer	MCF10A	E_01_0436	RT-PCR,RNA isolation,Western blot,Chromatin immunoprecipitation assay(CHIP),Migration/invasion assay,	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	Immunohistochemical staining	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	EZH2		RT-PCR,RNA isolation,Western blot,Chromatin immunoprecipitation assay(CHIP),Migration/invasion assay,	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.			
29864144	chr14	37587703	37589703	FOXA1	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	human	Mammary tissue	High+Lowthroughput	Impact of OGT deregulation on EZH2 target genes FOXA1 and FOXC1 expression in breast cancer cells	否	无	mammary cancer	MCF10A	E_01_0436	RT-PCR,RNA isolation,Western blot,Chromatin immunoprecipitation assay(CHIP),Migration/invasion assay,	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	Immunohistochemical staining	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	FOXA1		RT-PCR,RNA isolation,Western blot,Chromatin immunoprecipitation assay(CHIP),Migration/invasion assay,	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.			
29864144	chr6	1606662	1608662	FOXC1	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	human	Mammary tissue	High+Lowthroughput	Impact of OGT deregulation on EZH2 target genes FOXA1 and FOXC1 expression in breast cancer cells	否	无	mammary cancer	MCF10A	E_01_0436	RT-PCR,RNA isolation,Western blot,Chromatin immunoprecipitation assay(CHIP),Migration/invasion assay,	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	Immunohistochemical staining	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	FOXC1		RT-PCR,RNA isolation,Western blot,Chromatin immunoprecipitation assay(CHIP),Migration/invasion assay,	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.			
29864144	chr17	31934265	31936265	SUZ12	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	human	Mammary tissue	High+Lowthroughput	Impact of OGT deregulation on EZH2 target genes FOXA1 and FOXC1 expression in breast cancer cells	否	无	mammary cancer	MCF10A	E_01_0436	RT-PCR,RNA isolation,Western blot,Chromatin immunoprecipitation assay(CHIP),Migration/invasion assay,	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	Immunohistochemical staining	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.	SUZ12		RT-PCR,RNA isolation,Western blot,Chromatin immunoprecipitation assay(CHIP),Migration/invasion assay,	The results showed that OGT silencing affects EZH2 binding to FOXC1 promoter but the effect is cell-context dependent. Despite the slight decrease in EZH2 protein level in cells with OGT depletion, EZH2 binding to FOXC1 was increased. Moreover, OGT binding to promoter regions of FOXA1 and FOXC1 was increased in cells with knockdown of EZH2. Increased expression of FOXA1 and FOXC1 in cells with OGT deregulation was associated with increased acetylation level of histone H3. The results suggest that OGT is involved in regulation of FOXA1 and FOXC1 expression but its role is not associated with regulation of EZH2 protein stability.			
29858072	chr5	138462604	138464604	EGR1	Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.	human	Nervous tissue	High+Lowthroughput	Inflammatory-Related P62 Triggers Malignant Transformation of Mesenchymal Stem Cells through the Cascade of CUDR-CTCF-IGFII-RAS Signaling	否	无	Inflammation, tumour	HBMMSCs cell	E_01_0437	Transfection,RT-PCR,Western Blot,GST Pull-Down,Super-EMSA,ChIP,Co-IP,ChIP-3C/ChIP-Loop Assays,Cells Proliferation CCK8 Assay,Soft-Agar Colony Formation Assay,Xenograft Transplantation In Vivo,Histological Analysis	Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.	Immunohistochemical staining	Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.	EGR1		Transfection,RT-PCR,Western Blot,GST Pull-Down,Super-EMSA,ChIP,Co-IP,ChIP-3C/ChIP-Loop Assays,Cells Proliferation CCK8 Assay,Soft-Agar Colony Formation Assay,Xenograft Transplantation In Vivo,Histological Analysis	Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.			
29858072	chr9	117701610	117703610	TLR4	Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.	human	Nervous tissue	High+Lowthroughput	Inflammatory-Related P62 Triggers Malignant Transformation of Mesenchymal Stem Cells through the Cascade of CUDR-CTCF-IGFII-RAS Signaling	否	无	Inflammation, tumour	HBMMSCs cell	E_01_0437	Transfection,RT-PCR,Western Blot,GST Pull-Down,Super-EMSA,ChIP,Co-IP,ChIP-3C/ChIP-Loop Assays,Cells Proliferation CCK8 Assay,Soft-Agar Colony Formation Assay,Xenograft Transplantation In Vivo,Histological Analysis	Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.	Immunohistochemical staining	Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.	TLR4		Transfection,RT-PCR,Western Blot,GST Pull-Down,Super-EMSA,ChIP,Co-IP,ChIP-3C/ChIP-Loop Assays,Cells Proliferation CCK8 Assay,Soft-Agar Colony Formation Assay,Xenograft Transplantation In Vivo,Histological Analysis	Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.			
29858072	chr16	67559941	67561941	CTCF	Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.	human	Nervous tissue	High+Lowthroughput	Inflammatory-Related P62 Triggers Malignant Transformation of Mesenchymal Stem Cells through the Cascade of CUDR-CTCF-IGFII-RAS Signaling	否	无	Inflammation, tumour	HBMMSCs cell	E_01_0437	Transfection,RT-PCR,Western Blot,GST Pull-Down,Super-EMSA,ChIP,Co-IP,ChIP-3C/ChIP-Loop Assays,Cells Proliferation CCK8 Assay,Soft-Agar Colony Formation Assay,Xenograft Transplantation In Vivo,Histological Analysis	Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.	Immunohistochemical staining	Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.	CTCF		Transfection,RT-PCR,Western Blot,GST Pull-Down,Super-EMSA,ChIP,Co-IP,ChIP-3C/ChIP-Loop Assays,Cells Proliferation CCK8 Assay,Soft-Agar Colony Formation Assay,Xenograft Transplantation In Vivo,Histological Analysis	Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.			
29854630	chr10	71059112	71061112	Tfam	These results suggest CAPs with regular exercise may enhance lipid metabolism by regulation of gene products involved in lipid and antioxidant metabolism including SREBP-1c, PPAR-γ, and Nrf2 pathways in rats. 	mouse	Epithelial tissues	High+Lowthroughput	Capsaicinoids improve consequences of physical activity	否	无	inflammation	endothelial cell	E_02_0290	Western blot	These results suggest CAPs with regular exercise may enhance lipid metabolism by regulation of gene products involved in lipid and antioxidant metabolism including SREBP-1c, PPAR-γ, and Nrf2 pathways in rats. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest CAPs with regular exercise may enhance lipid metabolism by regulation of gene products involved in lipid and antioxidant metabolism including SREBP-1c, PPAR-γ, and Nrf2 pathways in rats. 		These results suggest CAPs with regular exercise may enhance lipid metabolism by regulation of gene products involved in lipid and antioxidant metabolism including SREBP-1c, PPAR-γ, and Nrf2 pathways in rats. 	Immunohistochemical staining	These results suggest CAPs with regular exercise may enhance lipid metabolism by regulation of gene products involved in lipid and antioxidant metabolism including SREBP-1c, PPAR-γ, and Nrf2 pathways in rats. 			Western blot				Tfam
29853604	chr4	186066731	186068731	TLR3	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	human	connective tissue	High+Lowthroughput	Helicase-Driven Activation of NFκB-COX2 Pathway Mediates the Immunosuppressive Component of dsRNA-Driven Inflammation in the Human Tumor Microenvironment	否	无	Inflammation, cancer	C0135C	E_01_0438	Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 		This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Immunohistochemical staining	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 			Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,				TLR3
29853604	chr14	102774482	102776482	TRAF3	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	human	connective tissue	High+Lowthroughput	Helicase-Driven Activation of NFκB-COX2 Pathway Mediates the Immunosuppressive Component of dsRNA-Driven Inflammation in the Human Tumor Microenvironment	否	无	Inflammation, cancer	C0135C	E_01_0438	Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Immunohistochemical staining	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	TRAF3		Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 			
29853604	chr19	49656925	49658925	IRF3	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	human	connective tissue	High+Lowthroughput	Helicase-Driven Activation of NFκB-COX2 Pathway Mediates the Immunosuppressive Component of dsRNA-Driven Inflammation in the Human Tumor Microenvironment	否	无	Inflammation, cancer	C0135C	E_01_0438	Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Immunohistochemical staining	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	IRF3		Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 			
29853604	chr4	76018223	76020223	CXCL10	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	human	connective tissue	High+Lowthroughput	Helicase-Driven Activation of NFκB-COX2 Pathway Mediates the Immunosuppressive Component of dsRNA-Driven Inflammation in the Human Tumor Microenvironment	否	无	Inflammation, cancer	C0135C	E_01_0438	Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Immunohistochemical staining	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	CXCL10		Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 			
29853604	chr1	206764397	206766397	IL10	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	human	connective tissue	High+Lowthroughput	Helicase-Driven Activation of NFκB-COX2 Pathway Mediates the Immunosuppressive Component of dsRNA-Driven Inflammation in the Human Tumor Microenvironment	否	无	Inflammation, cancer	C0135C	E_01_0438	Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Immunohistochemical staining	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	IL10		Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 			
29853604	chr16	57355768	57357768	CCL22	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	human	connective tissue	High+Lowthroughput	Helicase-Driven Activation of NFκB-COX2 Pathway Mediates the Immunosuppressive Component of dsRNA-Driven Inflammation in the Human Tumor Microenvironment	否	无	Inflammation, cancer	C0135C	E_01_0438	Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 		This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Immunohistochemical staining	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 			Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,				CCL22
29853604	chr10	44367998	44369998	CXCL12	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	human	connective tissue	High+Lowthroughput	Helicase-Driven Activation of NFκB-COX2 Pathway Mediates the Immunosuppressive Component of dsRNA-Driven Inflammation in the Human Tumor Microenvironment	否	无	Inflammation, cancer	C0135C	E_01_0438	Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 		This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 	Immunohistochemical staining	This study characterizes two different poly-I:C-induced signaling pathways in their induction of immunostimulatory and suppressive factors and suggests improved ways to reprogram the TME to enhance the antitumor efficacy of immunotherapies. 			Western blot,Image flow analysis,Immunofluorescence,Phospho-CREB activation,RT-PCR,ELISA,chemotaxis assays,				CXCL12
29853569	chr3	97917797	97919797	Notch2	We identified unique protein signatures that represent temporal changes in the vessel wall during neointimal lesion formation in the presence and absence of Notch2. Overall lesion formation was not affected with loss of smooth muscle Notch2, suggesting compensatory pathways. We also validated the regulation of known injury- or Notch-related targets identified in other vascular contexts, providing additional insight into conserved pathways involved in vascular remodeling.	human	Myotome	High+Lowthroughput	Notch2 and Proteomic Signatures in Mouse Neointimal Lesion Formation	否	无	Neointimal lesions	VSMC	E_01_0439	PCR, immunohistochemical staining,Vessel morphometric analysis,immunostaining,Transgenic mice,	We identified unique protein signatures that represent temporal changes in the vessel wall during neointimal lesion formation in the presence and absence of Notch2. Overall lesion formation was not affected with loss of smooth muscle Notch2, suggesting compensatory pathways. We also validated the regulation of known injury- or Notch-related targets identified in other vascular contexts, providing additional insight into conserved pathways involved in vascular remodeling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identified unique protein signatures that represent temporal changes in the vessel wall during neointimal lesion formation in the presence and absence of Notch2. Overall lesion formation was not affected with loss of smooth muscle Notch2, suggesting compensatory pathways. We also validated the regulation of known injury- or Notch-related targets identified in other vascular contexts, providing additional insight into conserved pathways involved in vascular remodeling.		We identified unique protein signatures that represent temporal changes in the vessel wall during neointimal lesion formation in the presence and absence of Notch2. Overall lesion formation was not affected with loss of smooth muscle Notch2, suggesting compensatory pathways. We also validated the regulation of known injury- or Notch-related targets identified in other vascular contexts, providing additional insight into conserved pathways involved in vascular remodeling.	Immunohistochemical staining	We identified unique protein signatures that represent temporal changes in the vessel wall during neointimal lesion formation in the presence and absence of Notch2. Overall lesion formation was not affected with loss of smooth muscle Notch2, suggesting compensatory pathways. We also validated the regulation of known injury- or Notch-related targets identified in other vascular contexts, providing additional insight into conserved pathways involved in vascular remodeling.			PCR, immunohistochemical staining,Vessel morphometric analysis,immunostaining,Transgenic mice,				Notch2
29853569	chr2	26345191	26347191	Notch1	We identified unique protein signatures that represent temporal changes in the vessel wall during neointimal lesion formation in the presence and absence of Notch2. Overall lesion formation was not affected with loss of smooth muscle Notch2, suggesting compensatory pathways. We also validated the regulation of known injury- or Notch-related targets identified in other vascular contexts, providing additional insight into conserved pathways involved in vascular remodeling.	human	Myotome	High+Lowthroughput	Notch2 and Proteomic Signatures in Mouse Neointimal Lesion Formation	否	无	Neointimal lesions	VSMC	E_01_0439	PCR, immunohistochemical staining,Vessel morphometric analysis,immunostaining,Transgenic mice,	We identified unique protein signatures that represent temporal changes in the vessel wall during neointimal lesion formation in the presence and absence of Notch2. Overall lesion formation was not affected with loss of smooth muscle Notch2, suggesting compensatory pathways. We also validated the regulation of known injury- or Notch-related targets identified in other vascular contexts, providing additional insight into conserved pathways involved in vascular remodeling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identified unique protein signatures that represent temporal changes in the vessel wall during neointimal lesion formation in the presence and absence of Notch2. Overall lesion formation was not affected with loss of smooth muscle Notch2, suggesting compensatory pathways. We also validated the regulation of known injury- or Notch-related targets identified in other vascular contexts, providing additional insight into conserved pathways involved in vascular remodeling.		We identified unique protein signatures that represent temporal changes in the vessel wall during neointimal lesion formation in the presence and absence of Notch2. Overall lesion formation was not affected with loss of smooth muscle Notch2, suggesting compensatory pathways. We also validated the regulation of known injury- or Notch-related targets identified in other vascular contexts, providing additional insight into conserved pathways involved in vascular remodeling.	Immunohistochemical staining	We identified unique protein signatures that represent temporal changes in the vessel wall during neointimal lesion formation in the presence and absence of Notch2. Overall lesion formation was not affected with loss of smooth muscle Notch2, suggesting compensatory pathways. We also validated the regulation of known injury- or Notch-related targets identified in other vascular contexts, providing additional insight into conserved pathways involved in vascular remodeling.			PCR, immunohistochemical staining,Vessel morphometric analysis,immunostaining,Transgenic mice,				Notch1
29852820	chr11	102833101	102835101	MMP3	miR-155 is a sustainable factor for intervertebral disk and suppresses the expression of catabolic genes induced by TNF-α and IL-1β by targeting C/EBPβ in rat NP cells.	mouse	lymphoid tissue	High+Lowthroughput	MicroRNA-155 suppresses the catabolic effect induced by TNF-α and IL-1β by targeting C/EBPβ in rat nucleus pulposus cells	否	无	Disc degeneration	natural killer cell	E_02_0291	Dual Luciferase Reporter Assay, real-time PCR,Western Blot,MRI,HE staining,collagen II immunochemistry,transgenic mice,Histology,immunohistochemistry,C/EBPβ knockdown,transfection,PCR	miR-155 is a sustainable factor for intervertebral disk and suppresses the expression of catabolic genes induced by TNF-α and IL-1β by targeting C/EBPβ in rat NP cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	miR-155 is a sustainable factor for intervertebral disk and suppresses the expression of catabolic genes induced by TNF-α and IL-1β by targeting C/EBPβ in rat NP cells.		miR-155 is a sustainable factor for intervertebral disk and suppresses the expression of catabolic genes induced by TNF-α and IL-1β by targeting C/EBPβ in rat NP cells.	Immunohistochemical staining	miR-155 is a sustainable factor for intervertebral disk and suppresses the expression of catabolic genes induced by TNF-α and IL-1β by targeting C/EBPβ in rat NP cells.			Dual Luciferase Reporter Assay, real-time PCR,Western Blot,MRI,HE staining,collagen II immunochemistry,transgenic mice,Histology,immunohistochemistry,C/EBPβ knockdown,transfection,PCR				MMP3
29852820	chr12	6531940	6533940	GAPDH	miR-155 is a sustainable factor for intervertebral disk and suppresses the expression of catabolic genes induced by TNF-α and IL-1β by targeting C/EBPβ in rat NP cells.	mouse	lymphoid tissue	High+Lowthroughput	MicroRNA-155 suppresses the catabolic effect induced by TNF-α and IL-1β by targeting C/EBPβ in rat nucleus pulposus cells	否	无	Disc degeneration	natural killer cell	E_02_0291	Dual Luciferase Reporter Assay, real-time PCR,Western Blot,MRI,HE staining,collagen II immunochemistry,transgenic mice,Histology,immunohistochemistry,C/EBPβ knockdown,transfection,PCR	miR-155 is a sustainable factor for intervertebral disk and suppresses the expression of catabolic genes induced by TNF-α and IL-1β by targeting C/EBPβ in rat NP cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	miR-155 is a sustainable factor for intervertebral disk and suppresses the expression of catabolic genes induced by TNF-α and IL-1β by targeting C/EBPβ in rat NP cells.		miR-155 is a sustainable factor for intervertebral disk and suppresses the expression of catabolic genes induced by TNF-α and IL-1β by targeting C/EBPβ in rat NP cells.	Immunohistochemical staining	miR-155 is a sustainable factor for intervertebral disk and suppresses the expression of catabolic genes induced by TNF-α and IL-1β by targeting C/EBPβ in rat NP cells.			Dual Luciferase Reporter Assay, real-time PCR,Western Blot,MRI,HE staining,collagen II immunochemistry,transgenic mice,Histology,immunohistochemistry,C/EBPβ knockdown,transfection,PCR				GAPDH
29851521	chr6	151654399	151656399	ESR1	This study successfully used TP to develop a DA patch with good anti-inflammatory and analgesic effects, proving that TP promotes the release of DA by reducing the interaction between DA and PSA and increasing the mobility of PSA.	mouse	Epithelial tissues	High+Lowthroughput	Development of a daphnetin transdermal patch using chemical enhancer strategy: insights of the enhancement effect of Transcutol P and the assessment of pharmacodynamics	否	无	nothing	stratified squamous epithelium cell	E_02_0292	HPLC,DSC,FTIR	This study successfully used TP to develop a DA patch with good anti-inflammatory and analgesic effects, proving that TP promotes the release of DA by reducing the interaction between DA and PSA and increasing the mobility of PSA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This study successfully used TP to develop a DA patch with good anti-inflammatory and analgesic effects, proving that TP promotes the release of DA by reducing the interaction between DA and PSA and increasing the mobility of PSA.		This study successfully used TP to develop a DA patch with good anti-inflammatory and analgesic effects, proving that TP promotes the release of DA by reducing the interaction between DA and PSA and increasing the mobility of PSA.	Immunohistochemical staining	This study successfully used TP to develop a DA patch with good anti-inflammatory and analgesic effects, proving that TP promotes the release of DA by reducing the interaction between DA and PSA and increasing the mobility of PSA.			HPLC,DSC,FTIR				ESR1
29851165	chr11	32385307	32387307	WT1	Our data suggest that the methylation pattern of the WT1 promoter and enhancers in human podocytes are distinctive from those in HK2. Furthermore, TGF-β1 alters the methylation levels of the WT1 promoter and enhancers in human podocytes. This modification may be relevant to the attenuation of WT1 by TGF-β1, which could contribute to podocyte injury.	human		High+Lowthroughput	TGF-β1 alters DNA methylation levels in promoter and enhancer regions of the WT1 gene in human podocytes	否	无	Wilms tumor 1 (WT1)	AB8/13 	E_01_0440	ChIP-seq,Quantitative methylation-specific PCR,Quantitative methylation-specific PCR,Western blot,	Our data suggest that the methylation pattern of the WT1 promoter and enhancers in human podocytes are distinctive from those in HK2. Furthermore, TGF-β1 alters the methylation levels of the WT1 promoter and enhancers in human podocytes. This modification may be relevant to the attenuation of WT1 by TGF-β1, which could contribute to podocyte injury.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data suggest that the methylation pattern of the WT1 promoter and enhancers in human podocytes are distinctive from those in HK2. Furthermore, TGF-β1 alters the methylation levels of the WT1 promoter and enhancers in human podocytes. This modification may be relevant to the attenuation of WT1 by TGF-β1, which could contribute to podocyte injury.		Our data suggest that the methylation pattern of the WT1 promoter and enhancers in human podocytes are distinctive from those in HK2. Furthermore, TGF-β1 alters the methylation levels of the WT1 promoter and enhancers in human podocytes. This modification may be relevant to the attenuation of WT1 by TGF-β1, which could contribute to podocyte injury.	Immunohistochemical staining	Our data suggest that the methylation pattern of the WT1 promoter and enhancers in human podocytes are distinctive from those in HK2. Furthermore, TGF-β1 alters the methylation levels of the WT1 promoter and enhancers in human podocytes. This modification may be relevant to the attenuation of WT1 by TGF-β1, which could contribute to podocyte injury.			ChIP-seq,Quantitative methylation-specific PCR,Quantitative methylation-specific PCR,Western blot,				WT1
29849691	chr10	88950862	88952862	FAS	We determined the expression levels of the adipogenesis-related proteins by RT-PCR and western blotting in HFD-induced obese mice. The GLE dose-dependently inhibited 3T3-L1 adipocyte differentiation and intracellular lipid accumulation in differentiated adipocytes. Further, body weight gain and fat accumulation were significantly lower in the GLE-treated HFD mice than in the untreated HFD mice. GLE treatment suppressed the expression of adipogenic genes such as peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/enhancer-binding protein (C/EBP) α, fatty acid synthase (aP2), and fatty acid synthase (FAS). These results suggest that the GLE inhibits adipocyte differentiation and intracellular lipid accumulation by downregulating the adipogenic gene expression both in vitro and in vivo.	mouse	adipose tissue	High+Lowthroughput	Glehnia littoralis Root Extract Inhibits Fat Accumulation in 3T3-L1 Cells and High-Fat Diet-Induced Obese Mice by Downregulating Adipogenic Gene Expression	否	无	Obesity	3T3-L1	E_02_0293	RT-PCR,western blot,oil red O staining,High-Performance Liquid Chromatography (HPLC)	We determined the expression levels of the adipogenesis-related proteins by RT-PCR and western blotting in HFD-induced obese mice. The GLE dose-dependently inhibited 3T3-L1 adipocyte differentiation and intracellular lipid accumulation in differentiated adipocytes. Further, body weight gain and fat accumulation were significantly lower in the GLE-treated HFD mice than in the untreated HFD mice. GLE treatment suppressed the expression of adipogenic genes such as peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/enhancer-binding protein (C/EBP) α, fatty acid synthase (aP2), and fatty acid synthase (FAS). These results suggest that the GLE inhibits adipocyte differentiation and intracellular lipid accumulation by downregulating the adipogenic gene expression both in vitro and in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We determined the expression levels of the adipogenesis-related proteins by RT-PCR and western blotting in HFD-induced obese mice. The GLE dose-dependently inhibited 3T3-L1 adipocyte differentiation and intracellular lipid accumulation in differentiated adipocytes. Further, body weight gain and fat accumulation were significantly lower in the GLE-treated HFD mice than in the untreated HFD mice. GLE treatment suppressed the expression of adipogenic genes such as peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/enhancer-binding protein (C/EBP) α, fatty acid synthase (aP2), and fatty acid synthase (FAS). These results suggest that the GLE inhibits adipocyte differentiation and intracellular lipid accumulation by downregulating the adipogenic gene expression both in vitro and in vivo.		We determined the expression levels of the adipogenesis-related proteins by RT-PCR and western blotting in HFD-induced obese mice. The GLE dose-dependently inhibited 3T3-L1 adipocyte differentiation and intracellular lipid accumulation in differentiated adipocytes. Further, body weight gain and fat accumulation were significantly lower in the GLE-treated HFD mice than in the untreated HFD mice. GLE treatment suppressed the expression of adipogenic genes such as peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/enhancer-binding protein (C/EBP) α, fatty acid synthase (aP2), and fatty acid synthase (FAS). These results suggest that the GLE inhibits adipocyte differentiation and intracellular lipid accumulation by downregulating the adipogenic gene expression both in vitro and in vivo.	Immunohistochemical staining	We determined the expression levels of the adipogenesis-related proteins by RT-PCR and western blotting in HFD-induced obese mice. The GLE dose-dependently inhibited 3T3-L1 adipocyte differentiation and intracellular lipid accumulation in differentiated adipocytes. Further, body weight gain and fat accumulation were significantly lower in the GLE-treated HFD mice than in the untreated HFD mice. GLE treatment suppressed the expression of adipogenic genes such as peroxisome proliferator-activated receptor (PPAR) γ, CCAAT/enhancer-binding protein (C/EBP) α, fatty acid synthase (aP2), and fatty acid synthase (FAS). These results suggest that the GLE inhibits adipocyte differentiation and intracellular lipid accumulation by downregulating the adipogenic gene expression both in vitro and in vivo.			RT-PCR,western blot,oil red O staining,High-Performance Liquid Chromatography (HPLC)				FAS
29848731	chr7	148804383	148806383	EZH2	EZH2 was frequently observed in patients with resected SCLC, but no significant associations were found between its expression and the clinicopathological characteristics and postoperative survivals.	human	Lung tissue	High+Lowthroughput	Prevalence of Enhancer of Zeste Homolog 2 in Patients with Resected Small Cell Lung Cancer	否	无	Small cell lung cancer (SCLC)	NSCC cell	E_01_0441	Immunohistochemical analyses,	EZH2 was frequently observed in patients with resected SCLC, but no significant associations were found between its expression and the clinicopathological characteristics and postoperative survivals.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2 was frequently observed in patients with resected SCLC, but no significant associations were found between its expression and the clinicopathological characteristics and postoperative survivals.	Immunohistochemical staining	EZH2 was frequently observed in patients with resected SCLC, but no significant associations were found between its expression and the clinicopathological characteristics and postoperative survivals.	EZH2		Immunohistochemical analyses,	EZH2 was frequently observed in patients with resected SCLC, but no significant associations were found between its expression and the clinicopathological characteristics and postoperative survivals.			
29848344	chr14	73418621	73420621	Rb1	Our study identified dysregulated lncRNAs in the M-MDSCs of E. granulosus infection mouse models; they might be involved in M-MDSC-derived immunosuppression in related diseases.	mouse	connective tissue	High+Lowthroughput	Microarray analysis of long non-coding RNA expression profiles in monocytic myeloid-derived suppressor cells in Echinococcus granulosus-infected mice	否	无	Cystic echinococcosis, a chronic zoonotic disease		E_02_0294	Microarray profiling,Quantitative reverse transcription-PCR (qRT-PCR),Cis- and trans-regulation analysis	Our study identified dysregulated lncRNAs in the M-MDSCs of E. granulosus infection mouse models; they might be involved in M-MDSC-derived immunosuppression in related diseases.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our study identified dysregulated lncRNAs in the M-MDSCs of E. granulosus infection mouse models; they might be involved in M-MDSC-derived immunosuppression in related diseases.		Our study identified dysregulated lncRNAs in the M-MDSCs of E. granulosus infection mouse models; they might be involved in M-MDSC-derived immunosuppression in related diseases.	Immunohistochemical staining	Our study identified dysregulated lncRNAs in the M-MDSCs of E. granulosus infection mouse models; they might be involved in M-MDSC-derived immunosuppression in related diseases.			Microarray profiling,Quantitative reverse transcription-PCR (qRT-PCR),Cis- and trans-regulation analysis				Rb1
29847803	chr7	34815681	34817681	Cebpa	Taken together, our data provide insights into how PU.1 and CEBPA functionally interact to drive GM-lineage differentiation.	mouse	connective tissue	High+Lowthroughput	Enhancer and Transcription Factor Dynamics during Myeloid Differentiation Reveal an Early Differentiation Block in Cebpa null Progenitors	否	无	nothing		E_02_0295	ChIP-seq,ATAC-seq,scRNA-seq,RNA-Seq,ATAC-qPCR	Taken together, our data provide insights into how PU.1 and CEBPA functionally interact to drive GM-lineage differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, our data provide insights into how PU.1 and CEBPA functionally interact to drive GM-lineage differentiation.		Taken together, our data provide insights into how PU.1 and CEBPA functionally interact to drive GM-lineage differentiation.	Immunohistochemical staining	Taken together, our data provide insights into how PU.1 and CEBPA functionally interact to drive GM-lineage differentiation.			ChIP-seq,ATAC-seq,scRNA-seq,RNA-Seq,ATAC-qPCR				Cebpa
29847803	chr19	33296790	33298790	CEBPA	Taken together, our data provide insights into how PU.1 and CEBPA functionally interact to drive GM-lineage differentiation.	mouse	connective tissue	High+Lowthroughput	Enhancer and Transcription Factor Dynamics during Myeloid Differentiation Reveal an Early Differentiation Block in Cebpa null Progenitors	否	无	nothing		E_02_0295	ChIP-seq,ATAC-seq,scRNA-seq,RNA-Seq,ATAC-qPCR	Taken together, our data provide insights into how PU.1 and CEBPA functionally interact to drive GM-lineage differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, our data provide insights into how PU.1 and CEBPA functionally interact to drive GM-lineage differentiation.		Taken together, our data provide insights into how PU.1 and CEBPA functionally interact to drive GM-lineage differentiation.	Immunohistochemical staining	Taken together, our data provide insights into how PU.1 and CEBPA functionally interact to drive GM-lineage differentiation.			ChIP-seq,ATAC-seq,scRNA-seq,RNA-Seq,ATAC-qPCR				CEBPA
29846108	chrX	154019316	154021316	MECP2	In conclusion, we identified miR-132 as a first miRNA regulating the osmotic balance by regulating the hypothalamic AVP gene mRNA expression.	mouse	Nervous tissue	High+Lowthroughput	MicroRNA-132 controls water homeostasis through regulating MECP2-mediated vasopressin synthesis	否	无	nothing		E_02_0296	AVP-enhancer reporter assay,Western blot,RT-qPCR,Immunohistochemistry	In conclusion, we identified miR-132 as a first miRNA regulating the osmotic balance by regulating the hypothalamic AVP gene mRNA expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, we identified miR-132 as a first miRNA regulating the osmotic balance by regulating the hypothalamic AVP gene mRNA expression.		In conclusion, we identified miR-132 as a first miRNA regulating the osmotic balance by regulating the hypothalamic AVP gene mRNA expression.	Immunohistochemical staining	In conclusion, we identified miR-132 as a first miRNA regulating the osmotic balance by regulating the hypothalamic AVP gene mRNA expression.			AVP-enhancer reporter assay,Western blot,RT-qPCR,Immunohistochemistry				MECP2
29846108	chr20	3079791	3081791	AVP	In conclusion, we identified miR-132 as a first miRNA regulating the osmotic balance by regulating the hypothalamic AVP gene mRNA expression.	mouse	Nervous tissue	High+Lowthroughput	MicroRNA-132 controls water homeostasis through regulating MECP2-mediated vasopressin synthesis	否	无	nothing		E_02_0296	AVP-enhancer reporter assay,Western blot,RT-qPCR,Immunohistochemistry	In conclusion, we identified miR-132 as a first miRNA regulating the osmotic balance by regulating the hypothalamic AVP gene mRNA expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, we identified miR-132 as a first miRNA regulating the osmotic balance by regulating the hypothalamic AVP gene mRNA expression.		In conclusion, we identified miR-132 as a first miRNA regulating the osmotic balance by regulating the hypothalamic AVP gene mRNA expression.	Immunohistochemical staining	In conclusion, we identified miR-132 as a first miRNA regulating the osmotic balance by regulating the hypothalamic AVP gene mRNA expression.			AVP-enhancer reporter assay,Western blot,RT-qPCR,Immunohistochemistry				AVP
29845218	chr16	4254258	4256258	TFAP4	In addition, there was a positive correlation between the TFAP4 and TRERNA1 expression level in clinical GC cases, which also indicated that TFAP4 can directly modulate the expression of TRERNA1. In the present study, we provide a novel potential therapeutic target and strategy for GC.	human	Gastric tissues	High+Lowthroughput	Elevated TFAP4 regulates lncRNA TRERNA1 to promote cell migration and invasion in gastric cancer	否	无	gastric cancer	AGS, SGC‑7901 and BGC‑823	E_01_0442	Reverse transcription‑quantitative PCR (RT‑qPCR),transfection,Cell migration and invasion assays,Luciferase reporter assay,Chromatin immunoprecipitation (ChIP) assay	In addition, there was a positive correlation between the TFAP4 and TRERNA1 expression level in clinical GC cases, which also indicated that TFAP4 can directly modulate the expression of TRERNA1. In the present study, we provide a novel potential therapeutic target and strategy for GC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, there was a positive correlation between the TFAP4 and TRERNA1 expression level in clinical GC cases, which also indicated that TFAP4 can directly modulate the expression of TRERNA1. In the present study, we provide a novel potential therapeutic target and strategy for GC.	Immunohistochemical staining	In addition, there was a positive correlation between the TFAP4 and TRERNA1 expression level in clinical GC cases, which also indicated that TFAP4 can directly modulate the expression of TRERNA1. In the present study, we provide a novel potential therapeutic target and strategy for GC.	TFAP4		Reverse transcription‑quantitative PCR (RT‑qPCR),transfection,Cell migration and invasion assays,Luciferase reporter assay,Chromatin immunoprecipitation (ChIP) assay	In addition, there was a positive correlation between the TFAP4 and TRERNA1 expression level in clinical GC cases, which also indicated that TFAP4 can directly modulate the expression of TRERNA1. In the present study, we provide a novel potential therapeutic target and strategy for GC.			
29845218	chr20	50037523	50039523	TRERNA1	In addition, there was a positive correlation between the TFAP4 and TRERNA1 expression level in clinical GC cases, which also indicated that TFAP4 can directly modulate the expression of TRERNA1. In the present study, we provide a novel potential therapeutic target and strategy for GC.	human	Gastric tissues	High+Lowthroughput	Elevated TFAP4 regulates lncRNA TRERNA1 to promote cell migration and invasion in gastric cancer	否	无	gastric cancer	AGS, SGC‑7901 and BGC‑823	E_01_0442	Reverse transcription‑quantitative PCR (RT‑qPCR),transfection,Cell migration and invasion assays,Luciferase reporter assay,Chromatin immunoprecipitation (ChIP) assay	In addition, there was a positive correlation between the TFAP4 and TRERNA1 expression level in clinical GC cases, which also indicated that TFAP4 can directly modulate the expression of TRERNA1. In the present study, we provide a novel potential therapeutic target and strategy for GC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, there was a positive correlation between the TFAP4 and TRERNA1 expression level in clinical GC cases, which also indicated that TFAP4 can directly modulate the expression of TRERNA1. In the present study, we provide a novel potential therapeutic target and strategy for GC.		In addition, there was a positive correlation between the TFAP4 and TRERNA1 expression level in clinical GC cases, which also indicated that TFAP4 can directly modulate the expression of TRERNA1. In the present study, we provide a novel potential therapeutic target and strategy for GC.	Immunohistochemical staining	In addition, there was a positive correlation between the TFAP4 and TRERNA1 expression level in clinical GC cases, which also indicated that TFAP4 can directly modulate the expression of TRERNA1. In the present study, we provide a novel potential therapeutic target and strategy for GC.			Reverse transcription‑quantitative PCR (RT‑qPCR),transfection,Cell migration and invasion assays,Luciferase reporter assay,Chromatin immunoprecipitation (ChIP) assay				TRERNA1
29844424	chr17	63474572	63476572	ACE	In conclusion, PDE induced the low peak bone mass and its intergenerational effect, which was mediated by sustained activation of RAS via increasing H3K27ac level of ACE.	mouse	Nervous tissue	High+Lowthroughput	Increased H3K27ac level of ACE mediates the intergenerational effect of low peak bone mass induced by prenatal dexamethasone exposure in male offspring rats	否	无	Low peak bone mass	BMSCs	E_02_0297	ELISA,Total RNA extraction,RT-qPCR,Alizarin Red S staining,siRNA knockdown,Western blot,Histological,immunohistochemistry analysis,Chromatin immunoprecipitation (ChIP) assay	In conclusion, PDE induced the low peak bone mass and its intergenerational effect, which was mediated by sustained activation of RAS via increasing H3K27ac level of ACE.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, PDE induced the low peak bone mass and its intergenerational effect, which was mediated by sustained activation of RAS via increasing H3K27ac level of ACE.		In conclusion, PDE induced the low peak bone mass and its intergenerational effect, which was mediated by sustained activation of RAS via increasing H3K27ac level of ACE.	Immunohistochemical staining	In conclusion, PDE induced the low peak bone mass and its intergenerational effect, which was mediated by sustained activation of RAS via increasing H3K27ac level of ACE.			ELISA,Total RNA extraction,RT-qPCR,Alizarin Red S staining,siRNA knockdown,Western blot,Histological,immunohistochemistry analysis,Chromatin immunoprecipitation (ChIP) assay				ACE
29842805	chr15	99562745	99564745	MEF2A	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	human	Epithelial tissues	High+Lowthroughput	The MEF2A and MEF2D function as scaffold proteins that interact with HDAC1 or p300 in SOD3 expression in THP-1 cells	否	无	Neoplasm, vascular disease	THP-1	E_01_0443	Western blot,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,transfection,Immunoprecipitation (IP),small interfering RNA transfection	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	Immunohistochemical staining	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	MEF2A		Western blot,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,transfection,Immunoprecipitation (IP),small interfering RNA transfection	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.			
29842805	chr1	156460878	156462878	MEF2D	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	human	Epithelial tissues	High+Lowthroughput	The MEF2A and MEF2D function as scaffold proteins that interact with HDAC1 or p300 in SOD3 expression in THP-1 cells	否	无	Neoplasm, vascular disease	THP-1	E_01_0443	Western blot,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,transfection,Immunoprecipitation (IP),small interfering RNA transfection	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.		The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	Immunohistochemical staining	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.			Western blot,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,transfection,Immunoprecipitation (IP),small interfering RNA transfection				MEF2D
29842805	chr4	24786853	24788853	SOD3	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	human	Epithelial tissues	High+Lowthroughput	The MEF2A and MEF2D function as scaffold proteins that interact with HDAC1 or p300 in SOD3 expression in THP-1 cells	否	无	Neoplasm, vascular disease	THP-1	E_01_0443	Western blot,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,transfection,Immunoprecipitation (IP),small interfering RNA transfection	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.		The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	Immunohistochemical staining	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.			Western blot,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,transfection,Immunoprecipitation (IP),small interfering RNA transfection				SOD3
29842805	chr1	32289204	32291204	HDAC1	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	human	Epithelial tissues	High+Lowthroughput	The MEF2A and MEF2D function as scaffold proteins that interact with HDAC1 or p300 in SOD3 expression in THP-1 cells	否	无	Neoplasm, vascular disease	THP-1	E_01_0443	Western blot,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,transfection,Immunoprecipitation (IP),small interfering RNA transfection	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	Immunohistochemical staining	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.	HDAC1		Western blot,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,transfection,Immunoprecipitation (IP),small interfering RNA transfection	The results of the present study demonstrated that the binding of histone deacetylase 1 (HDAC1) to the SOD3 promoter region contributed to SOD3 silencing in basal THP-1 cells. On the other hand, the dissociation of HDAC1 from the SOD3 promoter region and the enrichment of p300, a histone acetyltransferase (HAT), within that region were observed in TPA-induced THP-1 cells. Myocyte enhancer factor 2 (MEF2) functions as a scaffold protein that interacts with histone deacetylases (HDAC) or HAT and regulates gene expression. The present results showed that the MEF2A and MEF2D function as mediators for TPA-elicited SOD3 expression by interacting with HDAC or p300. Additionally, the knockdown of MEF2A or MEF2D in human skin fibroblasts suppressed SOD3 expression at the mRNA and protein levels. Our results provide an insight into epigenetic regulation of redox gene expression, and may ultimately contribute to suppressing the progression of tumours and vascular diseases.			
29813070	chr10	80968670	80970670	Zbtb7a	Moreover, the presence of prebound Zbtb7a can specify promoters that are amenable to TF-induced changes in accessibility. Therefore, Zbtb7a represents a widely used promoter factor that transduces signals from other TFs to enable control of accessibility and regulation of gene expression.	human	Nervous tissue	High+Lowthroughput	Zbtb7a is a transducer for the control of promoter accessibility by NF-kappa B and multiple other transcription factors	否	无	nothing	3T3	E_01_0444	Zbtb7a knockdown,quantitative real-time PCR,ChIP,ChIP-seq,DHS sequencing,Reporter assays,BiFC,GST pull-down,MS,Analysis of genomic datasets	Moreover, the presence of prebound Zbtb7a can specify promoters that are amenable to TF-induced changes in accessibility. Therefore, Zbtb7a represents a widely used promoter factor that transduces signals from other TFs to enable control of accessibility and regulation of gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, the presence of prebound Zbtb7a can specify promoters that are amenable to TF-induced changes in accessibility. Therefore, Zbtb7a represents a widely used promoter factor that transduces signals from other TFs to enable control of accessibility and regulation of gene expression.		Moreover, the presence of prebound Zbtb7a can specify promoters that are amenable to TF-induced changes in accessibility. Therefore, Zbtb7a represents a widely used promoter factor that transduces signals from other TFs to enable control of accessibility and regulation of gene expression.	Immunohistochemical staining	Moreover, the presence of prebound Zbtb7a can specify promoters that are amenable to TF-induced changes in accessibility. Therefore, Zbtb7a represents a widely used promoter factor that transduces signals from other TFs to enable control of accessibility and regulation of gene expression.			Zbtb7a knockdown,quantitative real-time PCR,ChIP,ChIP-seq,DHS sequencing,Reporter assays,BiFC,GST pull-down,MS,Analysis of genomic datasets				Zbtb7a
29808619	chr17	34252611	34254611	CCL2	AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.	human	Prostate tissue	High+Lowthroughput	Loss of androgen receptor signaling in prostate cancer-associated fibroblasts (CAFs) promotes CCL2- and CXCL8-mediated cancer cell migration	否	无	Prostate cancer (PCA)	LNCaPs、cwr1	E_01_0445	ChiP-seq,ChIP-seq,western blot,immunohistochemistry (IHC)	AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.	Immunohistochemical staining	AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.	CCL2		ChiP-seq,ChIP-seq,western blot,immunohistochemistry (IHC)	AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.			
29808619	chr4	73737863	73739863	CXCL8	AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.	human	Prostate tissue	High+Lowthroughput	Loss of androgen receptor signaling in prostate cancer-associated fibroblasts (CAFs) promotes CCL2- and CXCL8-mediated cancer cell migration	否	无	Prostate cancer (PCA)	LNCaPs、cwr1	E_01_0445	ChiP-seq,ChIP-seq,western blot,immunohistochemistry (IHC)	AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.	Immunohistochemical staining	AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.	CXCL8		ChiP-seq,ChIP-seq,western blot,immunohistochemistry (IHC)	AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.			
29808619	chrX	67541054	67543054	AR	AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.	human	Prostate tissue	High+Lowthroughput	Loss of androgen receptor signaling in prostate cancer-associated fibroblasts (CAFs) promotes CCL2- and CXCL8-mediated cancer cell migration	否	无	Prostate cancer (PCA)	LNCaPs、cwr1	E_01_0445	ChiP-seq,ChIP-seq,western blot,immunohistochemistry (IHC)	AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.	Immunohistochemical staining	AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.	AR		ChiP-seq,ChIP-seq,western blot,immunohistochemistry (IHC)	AR signaling in CAF-like cells decreased expression of multiple cytokines; most notably CCL2 and CXCL8 and both cytokines increased migration of PCa cells. These results suggest direct paracrine regulation of PCa cell migration by CAFs through AR signaling.			
29807547	chr21	38377160	38379160	ERG	"Our results demonstrate that megakaryopoietic profiles are established early in hematopoiesis and are present in the majority of the hematopoietic progenitor population. However, megakaryopoiesis does not constitute a ""default"" differentiation pathway, as extensive de novo DNA methylation accompanies megakaryopoietic commitment. In contrast, erythropoietic profiles are not established until a later stage of hematopoiesis, and require more dramatic changes to the transcriptional and epigenetic programs. These data provide important insights into lineage commitment and can contribute to ongoing studies related to diseases associated with differentiation defects."	mouse	connective tissue	High+Lowthroughput	Establishment of regulatory elements during erythro-megakaryopoiesis identifies hematopoietic lineage-commitment points	否	无	nothing	LSK cell	E_02_0298	ATAC-Seq,ChIP-Seq,MBD‑Seq,RNA‑Seq,flow cytometry,indexing-first immunoprecipitation(iChIP)	"Our results demonstrate that megakaryopoietic profiles are established early in hematopoiesis and are present in the majority of the hematopoietic progenitor population. However, megakaryopoiesis does not constitute a ""default"" differentiation pathway, as extensive de novo DNA methylation accompanies megakaryopoietic commitment. In contrast, erythropoietic profiles are not established until a later stage of hematopoiesis, and require more dramatic changes to the transcriptional and epigenetic programs. These data provide important insights into lineage commitment and can contribute to ongoing studies related to diseases associated with differentiation defects."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Our results demonstrate that megakaryopoietic profiles are established early in hematopoiesis and are present in the majority of the hematopoietic progenitor population. However, megakaryopoiesis does not constitute a ""default"" differentiation pathway, as extensive de novo DNA methylation accompanies megakaryopoietic commitment. In contrast, erythropoietic profiles are not established until a later stage of hematopoiesis, and require more dramatic changes to the transcriptional and epigenetic programs. These data provide important insights into lineage commitment and can contribute to ongoing studies related to diseases associated with differentiation defects."		"Our results demonstrate that megakaryopoietic profiles are established early in hematopoiesis and are present in the majority of the hematopoietic progenitor population. However, megakaryopoiesis does not constitute a ""default"" differentiation pathway, as extensive de novo DNA methylation accompanies megakaryopoietic commitment. In contrast, erythropoietic profiles are not established until a later stage of hematopoiesis, and require more dramatic changes to the transcriptional and epigenetic programs. These data provide important insights into lineage commitment and can contribute to ongoing studies related to diseases associated with differentiation defects."	Immunohistochemical staining	"Our results demonstrate that megakaryopoietic profiles are established early in hematopoiesis and are present in the majority of the hematopoietic progenitor population. However, megakaryopoiesis does not constitute a ""default"" differentiation pathway, as extensive de novo DNA methylation accompanies megakaryopoietic commitment. In contrast, erythropoietic profiles are not established until a later stage of hematopoiesis, and require more dramatic changes to the transcriptional and epigenetic programs. These data provide important insights into lineage commitment and can contribute to ongoing studies related to diseases associated with differentiation defects."			ATAC-Seq,ChIP-Seq,MBD‑Seq,RNA‑Seq,flow cytometry,indexing-first immunoprecipitation(iChIP)				ERG
29807547	chr11	128456195	128458195	ETS1	"Our results demonstrate that megakaryopoietic profiles are established early in hematopoiesis and are present in the majority of the hematopoietic progenitor population. However, megakaryopoiesis does not constitute a ""default"" differentiation pathway, as extensive de novo DNA methylation accompanies megakaryopoietic commitment. In contrast, erythropoietic profiles are not established until a later stage of hematopoiesis, and require more dramatic changes to the transcriptional and epigenetic programs. These data provide important insights into lineage commitment and can contribute to ongoing studies related to diseases associated with differentiation defects."	mouse	connective tissue	High+Lowthroughput	Establishment of regulatory elements during erythro-megakaryopoiesis identifies hematopoietic lineage-commitment points	否	无	nothing	LSK cell	E_02_0298	ATAC-Seq,ChIP-Seq,MBD‑Seq,RNA‑Seq,flow cytometry,indexing-first immunoprecipitation(iChIP)	"Our results demonstrate that megakaryopoietic profiles are established early in hematopoiesis and are present in the majority of the hematopoietic progenitor population. However, megakaryopoiesis does not constitute a ""default"" differentiation pathway, as extensive de novo DNA methylation accompanies megakaryopoietic commitment. In contrast, erythropoietic profiles are not established until a later stage of hematopoiesis, and require more dramatic changes to the transcriptional and epigenetic programs. These data provide important insights into lineage commitment and can contribute to ongoing studies related to diseases associated with differentiation defects."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Our results demonstrate that megakaryopoietic profiles are established early in hematopoiesis and are present in the majority of the hematopoietic progenitor population. However, megakaryopoiesis does not constitute a ""default"" differentiation pathway, as extensive de novo DNA methylation accompanies megakaryopoietic commitment. In contrast, erythropoietic profiles are not established until a later stage of hematopoiesis, and require more dramatic changes to the transcriptional and epigenetic programs. These data provide important insights into lineage commitment and can contribute to ongoing studies related to diseases associated with differentiation defects."		"Our results demonstrate that megakaryopoietic profiles are established early in hematopoiesis and are present in the majority of the hematopoietic progenitor population. However, megakaryopoiesis does not constitute a ""default"" differentiation pathway, as extensive de novo DNA methylation accompanies megakaryopoietic commitment. In contrast, erythropoietic profiles are not established until a later stage of hematopoiesis, and require more dramatic changes to the transcriptional and epigenetic programs. These data provide important insights into lineage commitment and can contribute to ongoing studies related to diseases associated with differentiation defects."	Immunohistochemical staining	"Our results demonstrate that megakaryopoietic profiles are established early in hematopoiesis and are present in the majority of the hematopoietic progenitor population. However, megakaryopoiesis does not constitute a ""default"" differentiation pathway, as extensive de novo DNA methylation accompanies megakaryopoietic commitment. In contrast, erythropoietic profiles are not established until a later stage of hematopoiesis, and require more dramatic changes to the transcriptional and epigenetic programs. These data provide important insights into lineage commitment and can contribute to ongoing studies related to diseases associated with differentiation defects."			ATAC-Seq,ChIP-Seq,MBD‑Seq,RNA‑Seq,flow cytometry,indexing-first immunoprecipitation(iChIP)				ETS1
29806631	chr4	106918996	106920996	DKK2	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	human	Facet joint tissue	High+Lowthroughput	Altered Wnt and NF-κB Signaling in Facet Joint Osteoarthritis: Insights from RNA Deep Sequencing	否	无	Facet joint osteoarthritis, lumbar spine osteoarthritis	mutant lymphoma cell	E_01_0446	RNA-seq,Bioinformatic analysis,qRT-PCR,	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.		In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Immunohistochemical staining	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.			RNA-seq,Bioinformatic analysis,qRT-PCR,				DKK2
29806631	chr8	54455086	54457086	SOX17	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	human	Facet joint tissue	High+Lowthroughput	Altered Wnt and NF-κB Signaling in Facet Joint Osteoarthritis: Insights from RNA Deep Sequencing	否	无	Facet joint osteoarthritis, lumbar spine osteoarthritis	mutant lymphoma cell	E_01_0446	RNA-seq,Bioinformatic analysis,qRT-PCR,	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Immunohistochemical staining	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	SOX17		RNA-seq,Bioinformatic analysis,qRT-PCR,	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.			
29806631	chr8	127732858	127734858	MYC	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	human	Facet joint tissue	High+Lowthroughput	Altered Wnt and NF-κB Signaling in Facet Joint Osteoarthritis: Insights from RNA Deep Sequencing	否	无	Facet joint osteoarthritis, lumbar spine osteoarthritis	mutant lymphoma cell	E_01_0446	RNA-seq,Bioinformatic analysis,qRT-PCR,	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Immunohistochemical staining	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	MYC		RNA-seq,Bioinformatic analysis,qRT-PCR,	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.			
29806631	chr5	150216613	150218613	CAMK2A	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	human	Facet joint tissue	High+Lowthroughput	Altered Wnt and NF-κB Signaling in Facet Joint Osteoarthritis: Insights from RNA Deep Sequencing	否	无	Facet joint osteoarthritis, lumbar spine osteoarthritis	mutant lymphoma cell	E_01_0446	RNA-seq,Bioinformatic analysis,qRT-PCR,	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Immunohistochemical staining	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	CAMK2A		RNA-seq,Bioinformatic analysis,qRT-PCR,	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.			
29806631	chr5	134111712	134113712	TCF7	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	human	Facet joint tissue	High+Lowthroughput	Altered Wnt and NF-κB Signaling in Facet Joint Osteoarthritis: Insights from RNA Deep Sequencing	否	无	Facet joint osteoarthritis, lumbar spine osteoarthritis	mutant lymphoma cell	E_01_0446	RNA-seq,Bioinformatic analysis,qRT-PCR,	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.		In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Immunohistochemical staining	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.			RNA-seq,Bioinformatic analysis,qRT-PCR,				TCF7
29806631	chr4	108045007	108047007	LEF1	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	human	Facet joint tissue	High+Lowthroughput	Altered Wnt and NF-κB Signaling in Facet Joint Osteoarthritis: Insights from RNA Deep Sequencing	否	无	Facet joint osteoarthritis, lumbar spine osteoarthritis	mutant lymphoma cell	E_01_0446	RNA-seq,Bioinformatic analysis,qRT-PCR,	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Immunohistochemical staining	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	LEF1		RNA-seq,Bioinformatic analysis,qRT-PCR,	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.			
29806631	chr17	36100950	36102950	CCL4	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	human	Facet joint tissue	High+Lowthroughput	Altered Wnt and NF-κB Signaling in Facet Joint Osteoarthritis: Insights from RNA Deep Sequencing	否	无	Facet joint osteoarthritis, lumbar spine osteoarthritis	mutant lymphoma cell	E_01_0446	RNA-seq,Bioinformatic analysis,qRT-PCR,	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.		In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Immunohistochemical staining	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.			RNA-seq,Bioinformatic analysis,qRT-PCR,				CCL4
29806631	chr17	36208360	36210360	CCL4L2	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	human	Facet joint tissue	High+Lowthroughput	Altered Wnt and NF-κB Signaling in Facet Joint Osteoarthritis: Insights from RNA Deep Sequencing	否	无	Facet joint osteoarthritis, lumbar spine osteoarthritis	mutant lymphoma cell	E_01_0446	RNA-seq,Bioinformatic analysis,qRT-PCR,	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.		In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.	Immunohistochemical staining	In NF-κB signaling pathway, the mRNA levels of C-C Motif Chemokine Ligand 4 (CCL4) and C-C Motif Chemokine Ligand 4 Like 2 (CCL4L2) were increased, while the mRNA levels of BCL2 Related Protein A1 were decreased. These results suggest that Wnt and NF-κB signaling may be altered in the process of facet joint cartilage degeneration. The present study will expand our understanding of the molecular bases underlying facet joint osteoarthritis.			RNA-seq,Bioinformatic analysis,qRT-PCR,				CCL4L2
29805666	chr7	148804346	148806346	EZH2	Collectively, these data demonstrate that EZH2 is frequently overexpressed in EC cells and its overexpression is associated with promoting the proliferation and invasion and decreasing the apoptosis of EC cells, suggesting that EZH2 may provide potential therapeutic targets for treatment of endometrial carcinoma.	human	Endometrial cancer tissues	High+Lowthroughput	Enhancer of zeste homolog 2 blockade by RNA interference is implicated with inhibited proliferation, invasion and promoted apoptosis in endometrial carcinoma	否	无	Endometrial cancer (EC)	monoblast	E_01_0447	Western blot,EZH2 small interfering (si)RNA transfection,Quantitative reverse transcription‑polymerase chain reaction (RT‑qPCR) analysis,In vitro cell proliferation assay,Annexin V/propidium iodide (PI) staining,Matrigel invasion assay,immunohistochemical analysis 	Collectively, these data demonstrate that EZH2 is frequently overexpressed in EC cells and its overexpression is associated with promoting the proliferation and invasion and decreasing the apoptosis of EC cells, suggesting that EZH2 may provide potential therapeutic targets for treatment of endometrial carcinoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Collectively, these data demonstrate that EZH2 is frequently overexpressed in EC cells and its overexpression is associated with promoting the proliferation and invasion and decreasing the apoptosis of EC cells, suggesting that EZH2 may provide potential therapeutic targets for treatment of endometrial carcinoma.	Immunohistochemical staining	Collectively, these data demonstrate that EZH2 is frequently overexpressed in EC cells and its overexpression is associated with promoting the proliferation and invasion and decreasing the apoptosis of EC cells, suggesting that EZH2 may provide potential therapeutic targets for treatment of endometrial carcinoma.	EZH2		Western blot,EZH2 small interfering (si)RNA transfection,Quantitative reverse transcription‑polymerase chain reaction (RT‑qPCR) analysis,In vitro cell proliferation assay,Annexin V/propidium iodide (PI) staining,Matrigel invasion assay,immunohistochemical analysis 	Collectively, these data demonstrate that EZH2 is frequently overexpressed in EC cells and its overexpression is associated with promoting the proliferation and invasion and decreasing the apoptosis of EC cells, suggesting that EZH2 may provide potential therapeutic targets for treatment of endometrial carcinoma.			
29805666	chr18	63120106	63122106	BCL2	Collectively, these data demonstrate that EZH2 is frequently overexpressed in EC cells and its overexpression is associated with promoting the proliferation and invasion and decreasing the apoptosis of EC cells, suggesting that EZH2 may provide potential therapeutic targets for treatment of endometrial carcinoma.	human	Endometrial cancer tissues	High+Lowthroughput	Enhancer of zeste homolog 2 blockade by RNA interference is implicated with inhibited proliferation, invasion and promoted apoptosis in endometrial carcinoma	否	无	Endometrial cancer (EC)	monoblast	E_01_0447	Western blot,EZH2 small interfering (si)RNA transfection,Quantitative reverse transcription‑polymerase chain reaction (RT‑qPCR) analysis,In vitro cell proliferation assay,Annexin V/propidium iodide (PI) staining,Matrigel invasion assay,immunohistochemical analysis 	Collectively, these data demonstrate that EZH2 is frequently overexpressed in EC cells and its overexpression is associated with promoting the proliferation and invasion and decreasing the apoptosis of EC cells, suggesting that EZH2 may provide potential therapeutic targets for treatment of endometrial carcinoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Collectively, these data demonstrate that EZH2 is frequently overexpressed in EC cells and its overexpression is associated with promoting the proliferation and invasion and decreasing the apoptosis of EC cells, suggesting that EZH2 may provide potential therapeutic targets for treatment of endometrial carcinoma.	Immunohistochemical staining	Collectively, these data demonstrate that EZH2 is frequently overexpressed in EC cells and its overexpression is associated with promoting the proliferation and invasion and decreasing the apoptosis of EC cells, suggesting that EZH2 may provide potential therapeutic targets for treatment of endometrial carcinoma.	BCL2		Western blot,EZH2 small interfering (si)RNA transfection,Quantitative reverse transcription‑polymerase chain reaction (RT‑qPCR) analysis,In vitro cell proliferation assay,Annexin V/propidium iodide (PI) staining,Matrigel invasion assay,immunohistochemical analysis 	Collectively, these data demonstrate that EZH2 is frequently overexpressed in EC cells and its overexpression is associated with promoting the proliferation and invasion and decreasing the apoptosis of EC cells, suggesting that EZH2 may provide potential therapeutic targets for treatment of endometrial carcinoma.			
29805099	chr20	50188232	50190232	CEBPB	Collectively, tumor glycolysis orchestrates a molecular network of the AMPK-ULK1, autophagy, and CEBPB pathways to affect MDSCs and maintain tumor immunosuppression.	human	Mammary tissue	High+Lowthroughput	Aerobic Glycolysis Controls Myeloid-Derived Suppressor Cells and Tumor Immunity via a Specific CEBPB Isoform in Triple-Negative Breast Cancer	否	无	Triple negative breast cancer (TNBC)	4T1	E_01_0448	Short Pairpin RNAs (shRNA),Small Interfering RNA (siRNA),Genetic Knockout,Western Blot,RNA Extraction,Reverse Transcription,Real-Time Polymerase Chain Reaction,Flow Cytometry Analysis (FACS),Immunofluorescence Staining,Metabolic Assay,Bioinformatics Analysis	Collectively, tumor glycolysis orchestrates a molecular network of the AMPK-ULK1, autophagy, and CEBPB pathways to affect MDSCs and maintain tumor immunosuppression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Collectively, tumor glycolysis orchestrates a molecular network of the AMPK-ULK1, autophagy, and CEBPB pathways to affect MDSCs and maintain tumor immunosuppression.	Immunohistochemical staining	Collectively, tumor glycolysis orchestrates a molecular network of the AMPK-ULK1, autophagy, and CEBPB pathways to affect MDSCs and maintain tumor immunosuppression.	CEBPB		Short Pairpin RNAs (shRNA),Small Interfering RNA (siRNA),Genetic Knockout,Western Blot,RNA Extraction,Reverse Transcription,Real-Time Polymerase Chain Reaction,Flow Cytometry Analysis (FACS),Immunofluorescence Staining,Metabolic Assay,Bioinformatics Analysis	Collectively, tumor glycolysis orchestrates a molecular network of the AMPK-ULK1, autophagy, and CEBPB pathways to affect MDSCs and maintain tumor immunosuppression.			
29802990	chr15	102311121	102313121	Sp1	We identified two alternative nine-SNPs haplotypes strictly linked to the allele *1 and *2 of hs1.2, that could be used as markers to further investigate the region and associations to pathology. Finally, we identified two haplotypes, namely E2A1 and E2A2, that strongly support the hypothesis of a relevant effect of the rs35216181 in the onset of Psoriasis when the *2 allele is present.	human	lymphoid tissue	High+Lowthroughput	Association between Psoriasis and haplotypes of the IgH 3' Regulatory Region 1	是	rs35216181,rs373084296	Autoimmune disease, psoriasis	T cell	E_01_0449	nested-PCR	We identified two alternative nine-SNPs haplotypes strictly linked to the allele *1 and *2 of hs1.2, that could be used as markers to further investigate the region and associations to pathology. Finally, we identified two haplotypes, namely E2A1 and E2A2, that strongly support the hypothesis of a relevant effect of the rs35216181 in the onset of Psoriasis when the *2 allele is present.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identified two alternative nine-SNPs haplotypes strictly linked to the allele *1 and *2 of hs1.2, that could be used as markers to further investigate the region and associations to pathology. Finally, we identified two haplotypes, namely E2A1 and E2A2, that strongly support the hypothesis of a relevant effect of the rs35216181 in the onset of Psoriasis when the *2 allele is present.		We identified two alternative nine-SNPs haplotypes strictly linked to the allele *1 and *2 of hs1.2, that could be used as markers to further investigate the region and associations to pathology. Finally, we identified two haplotypes, namely E2A1 and E2A2, that strongly support the hypothesis of a relevant effect of the rs35216181 in the onset of Psoriasis when the *2 allele is present.	Immunohistochemical staining	We identified two alternative nine-SNPs haplotypes strictly linked to the allele *1 and *2 of hs1.2, that could be used as markers to further investigate the region and associations to pathology. Finally, we identified two haplotypes, namely E2A1 and E2A2, that strongly support the hypothesis of a relevant effect of the rs35216181 in the onset of Psoriasis when the *2 allele is present.			nested-PCR				Sp1
29799396	chr12	6784343	6786343	CD4	Employing a combined phenotypic and transcriptomic approach we disclosed a Th1/Th17 phenotype as well as innate and adaptive functions of CD4+CD8+ double-positive T-cells in GPA.	human	connective tissue	High+Lowthroughput	Circulating CD4+CD8+ double-positive T-cells display features of innate and adaptive immune function in granulomatosis with polyangiitis	否	无	Granulomatosis with polyangiitis (GPA)	whole blood cell	E_01_0450	Flow cytometric analysis,Transcriptome,biological database analysis	Employing a combined phenotypic and transcriptomic approach we disclosed a Th1/Th17 phenotype as well as innate and adaptive functions of CD4+CD8+ double-positive T-cells in GPA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Employing a combined phenotypic and transcriptomic approach we disclosed a Th1/Th17 phenotype as well as innate and adaptive functions of CD4+CD8+ double-positive T-cells in GPA.		Employing a combined phenotypic and transcriptomic approach we disclosed a Th1/Th17 phenotype as well as innate and adaptive functions of CD4+CD8+ double-positive T-cells in GPA.	Immunohistochemical staining	Employing a combined phenotypic and transcriptomic approach we disclosed a Th1/Th17 phenotype as well as innate and adaptive functions of CD4+CD8+ double-positive T-cells in GPA.			Flow cytometric analysis,Transcriptome,biological database analysis				CD4
29798841	chr1	51786244	51788244	NRDC	Nrdc inhibits pancreatitis and suppresses PDA initiation in mice.	mouse	Nervous tissue	High+Lowthroughput	Nardilysin inhibits pancreatitis and suppresses pancreatic ductal adenocarcinoma initiation in mice	否	无	Pancreatitis, murine pancreatic ductal adenocarcinoma (PDA), pancreatic intraepithelial lesion (PanIN)	ES	E_02_0299	Southern blot,PCR,qRT-PCR,immunohistochemistry,immunofluorescence staining,immunostaining,microarray analysis	Nrdc inhibits pancreatitis and suppresses PDA initiation in mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Nrdc inhibits pancreatitis and suppresses PDA initiation in mice.		Nrdc inhibits pancreatitis and suppresses PDA initiation in mice.	Immunohistochemical staining	Nrdc inhibits pancreatitis and suppresses PDA initiation in mice.			Southern blot,PCR,qRT-PCR,immunohistochemistry,immunofluorescence staining,immunostaining,microarray analysis				NRDC
29798841	chr12	25202626	25204626	KRAS	Nrdc inhibits pancreatitis and suppresses PDA initiation in mice.	mouse	Nervous tissue	High+Lowthroughput	Nardilysin inhibits pancreatitis and suppresses pancreatic ductal adenocarcinoma initiation in mice	否	无	Pancreatitis, murine pancreatic ductal adenocarcinoma (PDA), pancreatic intraepithelial lesion (PanIN)	ES	E_02_0299	Southern blot,PCR,qRT-PCR,immunohistochemistry,immunofluorescence staining,immunostaining,microarray analysis	Nrdc inhibits pancreatitis and suppresses PDA initiation in mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Nrdc inhibits pancreatitis and suppresses PDA initiation in mice.		Nrdc inhibits pancreatitis and suppresses PDA initiation in mice.	Immunohistochemical staining	Nrdc inhibits pancreatitis and suppresses PDA initiation in mice.			Southern blot,PCR,qRT-PCR,immunohistochemistry,immunofluorescence staining,immunostaining,microarray analysis				KRAS
29797095	chr3	133743341	133745341	TF	We present a workflow, integrating epigenomics and topologically associating domain data, aimed at discovering trait-associated SNP pairs from GWAS where neither SNP achieved independent genome-wide significance. Each analyzed SNP pair consists of one SNP in a putative active enhancer and another SNP in a putative physically interacting gene promoter in a trait-relevant tissue. As a proof-of-principle case study, we used this approach to identify focused collections of SNP pairs that we analyzed in three independent Type 2 diabetes (T2D) GWAS. This approach led us to discover 35 significant SNP pairs, encompassing both novel signals and signals for which we have found orthogonal support from other sources. Nine of these pairs are consistent with eQTL results, two are consistent with our own capture C experiments, and seven involve signals supported by recent T2D literature.	human	Liver tissue	High+Lowthroughput	Leveraging epigenomics and contactomics data to investigate SNP pairs in GWAS	是	rs76024800,rs7577213	Type 2 diabetes (T2D)	HEPG2	E_01_0451	GWAS,DNase-Seq,ATAC-Seq,	We present a workflow, integrating epigenomics and topologically associating domain data, aimed at discovering trait-associated SNP pairs from GWAS where neither SNP achieved independent genome-wide significance. Each analyzed SNP pair consists of one SNP in a putative active enhancer and another SNP in a putative physically interacting gene promoter in a trait-relevant tissue. As a proof-of-principle case study, we used this approach to identify focused collections of SNP pairs that we analyzed in three independent Type 2 diabetes (T2D) GWAS. This approach led us to discover 35 significant SNP pairs, encompassing both novel signals and signals for which we have found orthogonal support from other sources. Nine of these pairs are consistent with eQTL results, two are consistent with our own capture C experiments, and seven involve signals supported by recent T2D literature.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We present a workflow, integrating epigenomics and topologically associating domain data, aimed at discovering trait-associated SNP pairs from GWAS where neither SNP achieved independent genome-wide significance. Each analyzed SNP pair consists of one SNP in a putative active enhancer and another SNP in a putative physically interacting gene promoter in a trait-relevant tissue. As a proof-of-principle case study, we used this approach to identify focused collections of SNP pairs that we analyzed in three independent Type 2 diabetes (T2D) GWAS. This approach led us to discover 35 significant SNP pairs, encompassing both novel signals and signals for which we have found orthogonal support from other sources. Nine of these pairs are consistent with eQTL results, two are consistent with our own capture C experiments, and seven involve signals supported by recent T2D literature.		We present a workflow, integrating epigenomics and topologically associating domain data, aimed at discovering trait-associated SNP pairs from GWAS where neither SNP achieved independent genome-wide significance. Each analyzed SNP pair consists of one SNP in a putative active enhancer and another SNP in a putative physically interacting gene promoter in a trait-relevant tissue. As a proof-of-principle case study, we used this approach to identify focused collections of SNP pairs that we analyzed in three independent Type 2 diabetes (T2D) GWAS. This approach led us to discover 35 significant SNP pairs, encompassing both novel signals and signals for which we have found orthogonal support from other sources. Nine of these pairs are consistent with eQTL results, two are consistent with our own capture C experiments, and seven involve signals supported by recent T2D literature.	Immunohistochemical staining	We present a workflow, integrating epigenomics and topologically associating domain data, aimed at discovering trait-associated SNP pairs from GWAS where neither SNP achieved independent genome-wide significance. Each analyzed SNP pair consists of one SNP in a putative active enhancer and another SNP in a putative physically interacting gene promoter in a trait-relevant tissue. As a proof-of-principle case study, we used this approach to identify focused collections of SNP pairs that we analyzed in three independent Type 2 diabetes (T2D) GWAS. This approach led us to discover 35 significant SNP pairs, encompassing both novel signals and signals for which we have found orthogonal support from other sources. Nine of these pairs are consistent with eQTL results, two are consistent with our own capture C experiments, and seven involve signals supported by recent T2D literature.			GWAS,DNase-Seq,ATAC-Seq,				TF
29794985	chr17	17678780	17680780	RAI1	These results suggest a likely contribution of RAI1, either alone or in combination of other factors, to social behavior and reinforce the RAI1 gene as a candidate gene in patients with autistic manifestations or social behavioral abnormalities.	human	Nervous tissue	High+Lowthroughput	A Rare De Novo RAI1 Gene Mutation Affecting BDNF-Enhancer-Driven Transcription Activity Associated with Autism and Atypical Smith-Magenis Syndrome Presentation	是	无	Autism, atypical Smith Magenis syndrome	Neuro-2a	E_01_0452	AMPure,PCR,Western Blot,Immunofluorescence Analysis,Reporter Gene Assays,RNA-Seq,transfection of Neuro-2a cells	These results suggest a likely contribution of RAI1, either alone or in combination of other factors, to social behavior and reinforce the RAI1 gene as a candidate gene in patients with autistic manifestations or social behavioral abnormalities.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest a likely contribution of RAI1, either alone or in combination of other factors, to social behavior and reinforce the RAI1 gene as a candidate gene in patients with autistic manifestations or social behavioral abnormalities.		These results suggest a likely contribution of RAI1, either alone or in combination of other factors, to social behavior and reinforce the RAI1 gene as a candidate gene in patients with autistic manifestations or social behavioral abnormalities.	Immunohistochemical staining	These results suggest a likely contribution of RAI1, either alone or in combination of other factors, to social behavior and reinforce the RAI1 gene as a candidate gene in patients with autistic manifestations or social behavioral abnormalities.			AMPure,PCR,Western Blot,Immunofluorescence Analysis,Reporter Gene Assays,RNA-Seq,transfection of Neuro-2a cells				RAI1
29794985	chr11	27652058	27654058	BDNF	These results suggest a likely contribution of RAI1, either alone or in combination of other factors, to social behavior and reinforce the RAI1 gene as a candidate gene in patients with autistic manifestations or social behavioral abnormalities.	human	Nervous tissue	High+Lowthroughput	A Rare De Novo RAI1 Gene Mutation Affecting BDNF-Enhancer-Driven Transcription Activity Associated with Autism and Atypical Smith-Magenis Syndrome Presentation	是	无	Autism, atypical Smith Magenis syndrome	Neuro-2a	E_01_0452	AMPure,PCR,Western Blot,Immunofluorescence Analysis,Reporter Gene Assays,RNA-Seq,transfection of Neuro-2a cells	These results suggest a likely contribution of RAI1, either alone or in combination of other factors, to social behavior and reinforce the RAI1 gene as a candidate gene in patients with autistic manifestations or social behavioral abnormalities.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These results suggest a likely contribution of RAI1, either alone or in combination of other factors, to social behavior and reinforce the RAI1 gene as a candidate gene in patients with autistic manifestations or social behavioral abnormalities.	Immunohistochemical staining	These results suggest a likely contribution of RAI1, either alone or in combination of other factors, to social behavior and reinforce the RAI1 gene as a candidate gene in patients with autistic manifestations or social behavioral abnormalities.	BDNF		AMPure,PCR,Western Blot,Immunofluorescence Analysis,Reporter Gene Assays,RNA-Seq,transfection of Neuro-2a cells	These results suggest a likely contribution of RAI1, either alone or in combination of other factors, to social behavior and reinforce the RAI1 gene as a candidate gene in patients with autistic manifestations or social behavioral abnormalities.			
29794473	chr8	19899275	19901275	LPL	During the adipogenic differentiation of hASCs, miR-27b expression decreased, and LPL expression increased. The abnormal expression of miR-27b and LPL effectively regulated the adipogenic differentiation of hASCs.	human	adipose tissue	High+Lowthroughput	MiR-27b Impairs Adipocyte Differentiation of Human Adipose Tissue-Derived Mesenchymal Stem Cells by Targeting LPL	否	无	nothing	hASCs	E_01_0453	Double Dual Luciferase Reporter Assay,qRT-PCR,western blot,cellular immunofluorescence,oil red O staining assay,Cell transfection	During the adipogenic differentiation of hASCs, miR-27b expression decreased, and LPL expression increased. The abnormal expression of miR-27b and LPL effectively regulated the adipogenic differentiation of hASCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			During the adipogenic differentiation of hASCs, miR-27b expression decreased, and LPL expression increased. The abnormal expression of miR-27b and LPL effectively regulated the adipogenic differentiation of hASCs.	Immunohistochemical staining	During the adipogenic differentiation of hASCs, miR-27b expression decreased, and LPL expression increased. The abnormal expression of miR-27b and LPL effectively regulated the adipogenic differentiation of hASCs.	LPL		Double Dual Luciferase Reporter Assay,qRT-PCR,western blot,cellular immunofluorescence,oil red O staining assay,Cell transfection	During the adipogenic differentiation of hASCs, miR-27b expression decreased, and LPL expression increased. The abnormal expression of miR-27b and LPL effectively regulated the adipogenic differentiation of hASCs.			
29792826	chr4	56905265	56907265	REST	Using CRISPR/Cas9, we further functionally validated an enhancer on chr8p23.1 as activator counteracting REST, a master regulator known to be a transcriptional suppressor of Alzheimer disease. Our results suggest an evolutionary origin of aging-related diseases: the side effects of human-specific, neural-tissue expressed enhancers. Thus, adaptive molecular changes in human macroevolution may introduce vulnerabilities to disease development in modern populations.	human		High+Lowthroughput	Fast-Evolving Human-Specific Neural Enhancers Are Associated with Aging-Related Diseases	是	无	Alzheimer's disease, aging	HEK293T	E_01_0454	CRISPR/Cas9,chromatin immunoprecipitation sequencing,qRT-PCR,PCR, RNA-seq,transfection	Using CRISPR/Cas9, we further functionally validated an enhancer on chr8p23.1 as activator counteracting REST, a master regulator known to be a transcriptional suppressor of Alzheimer disease. Our results suggest an evolutionary origin of aging-related diseases: the side effects of human-specific, neural-tissue expressed enhancers. Thus, adaptive molecular changes in human macroevolution may introduce vulnerabilities to disease development in modern populations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Using CRISPR/Cas9, we further functionally validated an enhancer on chr8p23.1 as activator counteracting REST, a master regulator known to be a transcriptional suppressor of Alzheimer disease. Our results suggest an evolutionary origin of aging-related diseases: the side effects of human-specific, neural-tissue expressed enhancers. Thus, adaptive molecular changes in human macroevolution may introduce vulnerabilities to disease development in modern populations.	Immunohistochemical staining	Using CRISPR/Cas9, we further functionally validated an enhancer on chr8p23.1 as activator counteracting REST, a master regulator known to be a transcriptional suppressor of Alzheimer disease. Our results suggest an evolutionary origin of aging-related diseases: the side effects of human-specific, neural-tissue expressed enhancers. Thus, adaptive molecular changes in human macroevolution may introduce vulnerabilities to disease development in modern populations.	REST		CRISPR/Cas9,chromatin immunoprecipitation sequencing,qRT-PCR,PCR, RNA-seq,transfection	Using CRISPR/Cas9, we further functionally validated an enhancer on chr8p23.1 as activator counteracting REST, a master regulator known to be a transcriptional suppressor of Alzheimer disease. Our results suggest an evolutionary origin of aging-related diseases: the side effects of human-specific, neural-tissue expressed enhancers. Thus, adaptive molecular changes in human macroevolution may introduce vulnerabilities to disease development in modern populations.			
29790264	chr11	32384629	32386629	WT1	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	human	lymphoid tissue	High+Lowthroughput	Immune responses against tumour-associated antigen-derived cytotoxic T lymphocyte epitopes in cholangiocarcinoma patients	否	无	Cholangiocarcinoma	TILs	E_01_0455	ELISPOT,PCR,real-time PCR,Immunotherapy	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.		These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	Immunohistochemical staining	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.			ELISPOT,PCR,real-time PCR,Immunotherapy				WT1
29790264	chr7	148804162	148806162	EZH2	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	human	lymphoid tissue	High+Lowthroughput	Immune responses against tumour-associated antigen-derived cytotoxic T lymphocyte epitopes in cholangiocarcinoma patients	否	无	Cholangiocarcinoma	TILs	E_01_0455	ELISPOT,PCR,real-time PCR,Immunotherapy	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	Immunohistochemical staining	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	EZH2		ELISPOT,PCR,real-time PCR,Immunotherapy	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.			
29790264	chr11	1155862	1157862	MUC5AC	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	human	lymphoid tissue	High+Lowthroughput	Immune responses against tumour-associated antigen-derived cytotoxic T lymphocyte epitopes in cholangiocarcinoma patients	否	无	Cholangiocarcinoma	TILs	E_01_0455	ELISPOT,PCR,real-time PCR,Immunotherapy	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.		These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	Immunohistochemical staining	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.			ELISPOT,PCR,real-time PCR,Immunotherapy				MUC5AC
29790264	chrX	133532916	133534916	GPC3	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	human	lymphoid tissue	High+Lowthroughput	Immune responses against tumour-associated antigen-derived cytotoxic T lymphocyte epitopes in cholangiocarcinoma patients	否	无	Cholangiocarcinoma	TILs	E_01_0455	ELISPOT,PCR,real-time PCR,Immunotherapy	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.		These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	Immunohistochemical staining	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.			ELISPOT,PCR,real-time PCR,Immunotherapy				GPC3
29790264	chr5	138175964	138177964	KIF20A	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	human	lymphoid tissue	High+Lowthroughput	Immune responses against tumour-associated antigen-derived cytotoxic T lymphocyte epitopes in cholangiocarcinoma patients	否	无	Cholangiocarcinoma	TILs	E_01_0455	ELISPOT,PCR,real-time PCR,Immunotherapy	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.		These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.	Immunohistochemical staining	These results demonstrated several TAAs may be promising for immunotherapy for cholangiocarcinoma, and patients with high lymphocyte counts may benefit more from immunotherapy.			ELISPOT,PCR,real-time PCR,Immunotherapy				KIF20A
29789713	chr1	47429569	47431569	FOXD2-AS1	Mechanically, FOXD2-AS1 promoted GC tumorigenesis partly through EZH2 and LSD1 mediated EphB3 downregulation. The present results revealed that FOXD2-AS1 acted as a tumor inducer in GC partly through EphB3 inhibition by direct interaction with EZH2 and LSD1, and may prove to be a potential biomarker of carcinogenesis.	human		High+Lowthroughput	Upregulation of the long noncoding RNA FOXD2-AS1 promotes carcinogenesis by epigenetically silencing EphB3 through EZH2 and LSD1, and predicts poor prognosis in gastric cancer	否	无	Gastric cancer (GC)	BGC823	E_01_0456	GSEA,quantitative real-time PCR,transfection,Flow cytometry,Western blot,Immunohistochemistry(IHC),ChIRP,RIP,RNA pull-down assay,Cell proliferation assays,chromatin immunoprecipitation (ChIP)	Mechanically, FOXD2-AS1 promoted GC tumorigenesis partly through EZH2 and LSD1 mediated EphB3 downregulation. The present results revealed that FOXD2-AS1 acted as a tumor inducer in GC partly through EphB3 inhibition by direct interaction with EZH2 and LSD1, and may prove to be a potential biomarker of carcinogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mechanically, FOXD2-AS1 promoted GC tumorigenesis partly through EZH2 and LSD1 mediated EphB3 downregulation. The present results revealed that FOXD2-AS1 acted as a tumor inducer in GC partly through EphB3 inhibition by direct interaction with EZH2 and LSD1, and may prove to be a potential biomarker of carcinogenesis.		Mechanically, FOXD2-AS1 promoted GC tumorigenesis partly through EZH2 and LSD1 mediated EphB3 downregulation. The present results revealed that FOXD2-AS1 acted as a tumor inducer in GC partly through EphB3 inhibition by direct interaction with EZH2 and LSD1, and may prove to be a potential biomarker of carcinogenesis.	Immunohistochemical staining	Mechanically, FOXD2-AS1 promoted GC tumorigenesis partly through EZH2 and LSD1 mediated EphB3 downregulation. The present results revealed that FOXD2-AS1 acted as a tumor inducer in GC partly through EphB3 inhibition by direct interaction with EZH2 and LSD1, and may prove to be a potential biomarker of carcinogenesis.			GSEA,quantitative real-time PCR,transfection,Flow cytometry,Western blot,Immunohistochemistry(IHC),ChIRP,RIP,RNA pull-down assay,Cell proliferation assays,chromatin immunoprecipitation (ChIP)				FOXD2-AS1
29789713	chr7	148804370	148806370	EZH2	Mechanically, FOXD2-AS1 promoted GC tumorigenesis partly through EZH2 and LSD1 mediated EphB3 downregulation. The present results revealed that FOXD2-AS1 acted as a tumor inducer in GC partly through EphB3 inhibition by direct interaction with EZH2 and LSD1, and may prove to be a potential biomarker of carcinogenesis.	human		High+Lowthroughput	Upregulation of the long noncoding RNA FOXD2-AS1 promotes carcinogenesis by epigenetically silencing EphB3 through EZH2 and LSD1, and predicts poor prognosis in gastric cancer	否	无	Gastric cancer (GC)	BGC823	E_01_0456	GSEA,quantitative real-time PCR,transfection,Flow cytometry,Western blot,Immunohistochemistry(IHC),ChIRP,RIP,RNA pull-down assay,Cell proliferation assays,chromatin immunoprecipitation (ChIP)	Mechanically, FOXD2-AS1 promoted GC tumorigenesis partly through EZH2 and LSD1 mediated EphB3 downregulation. The present results revealed that FOXD2-AS1 acted as a tumor inducer in GC partly through EphB3 inhibition by direct interaction with EZH2 and LSD1, and may prove to be a potential biomarker of carcinogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mechanically, FOXD2-AS1 promoted GC tumorigenesis partly through EZH2 and LSD1 mediated EphB3 downregulation. The present results revealed that FOXD2-AS1 acted as a tumor inducer in GC partly through EphB3 inhibition by direct interaction with EZH2 and LSD1, and may prove to be a potential biomarker of carcinogenesis.	Immunohistochemical staining	Mechanically, FOXD2-AS1 promoted GC tumorigenesis partly through EZH2 and LSD1 mediated EphB3 downregulation. The present results revealed that FOXD2-AS1 acted as a tumor inducer in GC partly through EphB3 inhibition by direct interaction with EZH2 and LSD1, and may prove to be a potential biomarker of carcinogenesis.	EZH2		GSEA,quantitative real-time PCR,transfection,Flow cytometry,Western blot,Immunohistochemistry(IHC),ChIRP,RIP,RNA pull-down assay,Cell proliferation assays,chromatin immunoprecipitation (ChIP)	Mechanically, FOXD2-AS1 promoted GC tumorigenesis partly through EZH2 and LSD1 mediated EphB3 downregulation. The present results revealed that FOXD2-AS1 acted as a tumor inducer in GC partly through EphB3 inhibition by direct interaction with EZH2 and LSD1, and may prove to be a potential biomarker of carcinogenesis.			
29789597	chr6	31572755	31574755	TNF	In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.	human	lymphoid tissue	High+Lowthroughput	Enhancer of zeste homolog 2-catalysed H3K27 trimethylation plays a key role in acute-on-chronic liver failure via TNF-mediated pathway	否	无	Acute phase chronic liver failure	PBMC	E_01_0457	Western blot,reverse transcription-PCR,cytokine analysis,Immunostaining,Histological analysis,Chromatin immunoprecipitation (ChIP) assays	In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.	Immunohistochemical staining	In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.	TNF		Western blot,reverse transcription-PCR,cytokine analysis,Immunostaining,Histological analysis,Chromatin immunoprecipitation (ChIP) assays	In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.			
29789597	chr7	148804415	148806415	EZH2	In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.	human	lymphoid tissue	High+Lowthroughput	Enhancer of zeste homolog 2-catalysed H3K27 trimethylation plays a key role in acute-on-chronic liver failure via TNF-mediated pathway	否	无	Acute phase chronic liver failure	PBMC	E_01_0457	Western blot,reverse transcription-PCR,cytokine analysis,Immunostaining,Histological analysis,Chromatin immunoprecipitation (ChIP) assays	In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.	Immunohistochemical staining	In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.	EZH2		Western blot,reverse transcription-PCR,cytokine analysis,Immunostaining,Histological analysis,Chromatin immunoprecipitation (ChIP) assays	In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.			
29789597	chr17	7576424	7578424	CD68	In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.	human	lymphoid tissue	High+Lowthroughput	Enhancer of zeste homolog 2-catalysed H3K27 trimethylation plays a key role in acute-on-chronic liver failure via TNF-mediated pathway	否	无	Acute phase chronic liver failure	PBMC	E_01_0457	Western blot,reverse transcription-PCR,cytokine analysis,Immunostaining,Histological analysis,Chromatin immunoprecipitation (ChIP) assays	In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.		In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.	Immunohistochemical staining	In conclusion, EZH2 and H3K27me3 contributed to the pathogenesis of liver failure via triggering TNF and other indispensable proinflammatory cytokines. EZH2 was to modify H3K27me3 enrichment, as well as, activation of the downstream NF-κB and Akt signalling pathways.			Western blot,reverse transcription-PCR,cytokine analysis,Immunostaining,Histological analysis,Chromatin immunoprecipitation (ChIP) assays				CD68
29789579	chr14	75276080	75278080	FOS	Taken together, we resolve the long-standing controversy and uncertainty in the field, and reveal a fundamental role of OCT4A protein in regulating FOS/AP-1 signaling-centered genes that mediate the adhesion, migration, and propagation of somatic cancer cells.	human	Nervous tissue	High+Lowthroughput	Endogenous authentic OCT4A proteins directly regulate FOS/AP-1 transcription in somatic cancer cells	否	无	nothing	293T	E_01_0458	CRISPR\Cas9,PCR,western blot,qRT-PCR,immunoprecipitation(IP),Immunostaining,immunoblotting,ChIP assays,ChIP-PCR,MS analysis,RNA-Seq,western blotting (WB) analysis	Taken together, we resolve the long-standing controversy and uncertainty in the field, and reveal a fundamental role of OCT4A protein in regulating FOS/AP-1 signaling-centered genes that mediate the adhesion, migration, and propagation of somatic cancer cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Taken together, we resolve the long-standing controversy and uncertainty in the field, and reveal a fundamental role of OCT4A protein in regulating FOS/AP-1 signaling-centered genes that mediate the adhesion, migration, and propagation of somatic cancer cells.	Immunohistochemical staining	Taken together, we resolve the long-standing controversy and uncertainty in the field, and reveal a fundamental role of OCT4A protein in regulating FOS/AP-1 signaling-centered genes that mediate the adhesion, migration, and propagation of somatic cancer cells.	FOS		CRISPR\Cas9,PCR,western blot,qRT-PCR,immunoprecipitation(IP),Immunostaining,immunoblotting,ChIP assays,ChIP-PCR,MS analysis,RNA-Seq,western blotting (WB) analysis	Taken together, we resolve the long-standing controversy and uncertainty in the field, and reveal a fundamental role of OCT4A protein in regulating FOS/AP-1 signaling-centered genes that mediate the adhesion, migration, and propagation of somatic cancer cells.			
29789579	chr6	31161696	31163696	POU5F1	Taken together, we resolve the long-standing controversy and uncertainty in the field, and reveal a fundamental role of OCT4A protein in regulating FOS/AP-1 signaling-centered genes that mediate the adhesion, migration, and propagation of somatic cancer cells.	human	Nervous tissue	High+Lowthroughput	Endogenous authentic OCT4A proteins directly regulate FOS/AP-1 transcription in somatic cancer cells	否	无	nothing	293T	E_01_0458	CRISPR\Cas9,PCR,western blot,qRT-PCR,immunoprecipitation(IP),Immunostaining,immunoblotting,ChIP assays,ChIP-PCR,MS analysis,RNA-Seq,western blotting (WB) analysis	Taken together, we resolve the long-standing controversy and uncertainty in the field, and reveal a fundamental role of OCT4A protein in regulating FOS/AP-1 signaling-centered genes that mediate the adhesion, migration, and propagation of somatic cancer cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Taken together, we resolve the long-standing controversy and uncertainty in the field, and reveal a fundamental role of OCT4A protein in regulating FOS/AP-1 signaling-centered genes that mediate the adhesion, migration, and propagation of somatic cancer cells.	Immunohistochemical staining	Taken together, we resolve the long-standing controversy and uncertainty in the field, and reveal a fundamental role of OCT4A protein in regulating FOS/AP-1 signaling-centered genes that mediate the adhesion, migration, and propagation of somatic cancer cells.	POU5F1		CRISPR\Cas9,PCR,western blot,qRT-PCR,immunoprecipitation(IP),Immunostaining,immunoblotting,ChIP assays,ChIP-PCR,MS analysis,RNA-Seq,western blotting (WB) analysis	Taken together, we resolve the long-standing controversy and uncertainty in the field, and reveal a fundamental role of OCT4A protein in regulating FOS/AP-1 signaling-centered genes that mediate the adhesion, migration, and propagation of somatic cancer cells.			
29789508	chr17	82075550	82077550	FASN	Taken together, these findings demonstrate that the effect of metformin on adipocyte differentiation is biphasic and dose-dependent. Lower concentrations of metformin induce adipogenesis, which could be mediated in an AMPK-independent manner, while higher concentrations of metformin inhibit adipogenesis via AMPK activation.	human	adipose tissue	High+Lowthroughput	Dual Effects of Metformin on Adipogenic Differentiation of 3T3-L1 Preadipocyte in AMPK-Dependent and Independent Manners	否	无	Type 2 diabetes (T2D)	3T3-L1	E_01_0459	Oil Red O Staining,MTT assay,Quantitative Real-Time PCR,Western Blot	Taken together, these findings demonstrate that the effect of metformin on adipocyte differentiation is biphasic and dose-dependent. Lower concentrations of metformin induce adipogenesis, which could be mediated in an AMPK-independent manner, while higher concentrations of metformin inhibit adipogenesis via AMPK activation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, these findings demonstrate that the effect of metformin on adipocyte differentiation is biphasic and dose-dependent. Lower concentrations of metformin induce adipogenesis, which could be mediated in an AMPK-independent manner, while higher concentrations of metformin inhibit adipogenesis via AMPK activation.		Taken together, these findings demonstrate that the effect of metformin on adipocyte differentiation is biphasic and dose-dependent. Lower concentrations of metformin induce adipogenesis, which could be mediated in an AMPK-independent manner, while higher concentrations of metformin inhibit adipogenesis via AMPK activation.	Immunohistochemical staining	Taken together, these findings demonstrate that the effect of metformin on adipocyte differentiation is biphasic and dose-dependent. Lower concentrations of metformin induce adipogenesis, which could be mediated in an AMPK-independent manner, while higher concentrations of metformin inhibit adipogenesis via AMPK activation.			Oil Red O Staining,MTT assay,Quantitative Real-Time PCR,Western Blot				FASN
29785964	chr6	170551706	170553706	TBP	In contrast, TBP-TFIIB and TBP-BRF2 complexes were not recruited unless a TATA box was present, which allowed selective and efficient recruitment of the TBP-BRF2 complex. Thus, TBP both prevented BRF2 recruitment to Pol II promoters and enhanced BRF2 recruitment to Pol III promoters. On Pol II promoters, TBP recruitment was separate from TFIIB recruitment and enhanced by TFIIA. Our results provide a model for specific Pol recruitment at SNAPc-dependent promoters.	human		High+Lowthroughput	Mechanism of selective recruitment of RNA polymerases II and III to snRNA gene promoters	否	无	nothing	293 cell	E_01_0460	transfection,immunoblots,DNase I footprinting,EMSAs,In vitro transcription assay,ChIPs,Pull-down assay,ChIP-seq,ChIP-qPCRs	In contrast, TBP-TFIIB and TBP-BRF2 complexes were not recruited unless a TATA box was present, which allowed selective and efficient recruitment of the TBP-BRF2 complex. Thus, TBP both prevented BRF2 recruitment to Pol II promoters and enhanced BRF2 recruitment to Pol III promoters. On Pol II promoters, TBP recruitment was separate from TFIIB recruitment and enhanced by TFIIA. Our results provide a model for specific Pol recruitment at SNAPc-dependent promoters.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In contrast, TBP-TFIIB and TBP-BRF2 complexes were not recruited unless a TATA box was present, which allowed selective and efficient recruitment of the TBP-BRF2 complex. Thus, TBP both prevented BRF2 recruitment to Pol II promoters and enhanced BRF2 recruitment to Pol III promoters. On Pol II promoters, TBP recruitment was separate from TFIIB recruitment and enhanced by TFIIA. Our results provide a model for specific Pol recruitment at SNAPc-dependent promoters.	Immunohistochemical staining	In contrast, TBP-TFIIB and TBP-BRF2 complexes were not recruited unless a TATA box was present, which allowed selective and efficient recruitment of the TBP-BRF2 complex. Thus, TBP both prevented BRF2 recruitment to Pol II promoters and enhanced BRF2 recruitment to Pol III promoters. On Pol II promoters, TBP recruitment was separate from TFIIB recruitment and enhanced by TFIIA. Our results provide a model for specific Pol recruitment at SNAPc-dependent promoters.	TBP		transfection,immunoblots,DNase I footprinting,EMSAs,In vitro transcription assay,ChIPs,Pull-down assay,ChIP-seq,ChIP-qPCRs	In contrast, TBP-TFIIB and TBP-BRF2 complexes were not recruited unless a TATA box was present, which allowed selective and efficient recruitment of the TBP-BRF2 complex. Thus, TBP both prevented BRF2 recruitment to Pol II promoters and enhanced BRF2 recruitment to Pol III promoters. On Pol II promoters, TBP recruitment was separate from TFIIB recruitment and enhanced by TFIIA. Our results provide a model for specific Pol recruitment at SNAPc-dependent promoters.			
29785964	chr8	37840578	37842578	BRF2	In contrast, TBP-TFIIB and TBP-BRF2 complexes were not recruited unless a TATA box was present, which allowed selective and efficient recruitment of the TBP-BRF2 complex. Thus, TBP both prevented BRF2 recruitment to Pol II promoters and enhanced BRF2 recruitment to Pol III promoters. On Pol II promoters, TBP recruitment was separate from TFIIB recruitment and enhanced by TFIIA. Our results provide a model for specific Pol recruitment at SNAPc-dependent promoters.	human		High+Lowthroughput	Mechanism of selective recruitment of RNA polymerases II and III to snRNA gene promoters	否	无	nothing	293 cell	E_01_0460	transfection,immunoblots,DNase I footprinting,EMSAs,In vitro transcription assay,ChIPs,Pull-down assay,ChIP-seq,ChIP-qPCRs	In contrast, TBP-TFIIB and TBP-BRF2 complexes were not recruited unless a TATA box was present, which allowed selective and efficient recruitment of the TBP-BRF2 complex. Thus, TBP both prevented BRF2 recruitment to Pol II promoters and enhanced BRF2 recruitment to Pol III promoters. On Pol II promoters, TBP recruitment was separate from TFIIB recruitment and enhanced by TFIIA. Our results provide a model for specific Pol recruitment at SNAPc-dependent promoters.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In contrast, TBP-TFIIB and TBP-BRF2 complexes were not recruited unless a TATA box was present, which allowed selective and efficient recruitment of the TBP-BRF2 complex. Thus, TBP both prevented BRF2 recruitment to Pol II promoters and enhanced BRF2 recruitment to Pol III promoters. On Pol II promoters, TBP recruitment was separate from TFIIB recruitment and enhanced by TFIIA. Our results provide a model for specific Pol recruitment at SNAPc-dependent promoters.		In contrast, TBP-TFIIB and TBP-BRF2 complexes were not recruited unless a TATA box was present, which allowed selective and efficient recruitment of the TBP-BRF2 complex. Thus, TBP both prevented BRF2 recruitment to Pol II promoters and enhanced BRF2 recruitment to Pol III promoters. On Pol II promoters, TBP recruitment was separate from TFIIB recruitment and enhanced by TFIIA. Our results provide a model for specific Pol recruitment at SNAPc-dependent promoters.	Immunohistochemical staining	In contrast, TBP-TFIIB and TBP-BRF2 complexes were not recruited unless a TATA box was present, which allowed selective and efficient recruitment of the TBP-BRF2 complex. Thus, TBP both prevented BRF2 recruitment to Pol II promoters and enhanced BRF2 recruitment to Pol III promoters. On Pol II promoters, TBP recruitment was separate from TFIIB recruitment and enhanced by TFIIA. Our results provide a model for specific Pol recruitment at SNAPc-dependent promoters.			transfection,immunoblots,DNase I footprinting,EMSAs,In vitro transcription assay,ChIPs,Pull-down assay,ChIP-seq,ChIP-qPCRs				BRF2
29783071	chr15	99562489	99564489	MEF2A	Finally, the results of ChIP indicated that MEF2A occupied the promoter region of the Capn3 gene in rat denervated gastrocnemius muscle tissue. Based on these results, we proposed that MEF2A is a transcriptional regulator for Capn3 gene expression.	human	Gastrocnemius muscle tissue	High+Lowthroughput	MEF2A regulates Calpain 3 expression in L6 myoblasts	否	无	Muscle wasting after reversible sciatic nerve injury	L6 cell	E_01_0461	Luciferase reporter assay,EMSA,PCR,Western Blot,qRT-PCR,immunocytochemistry,ChIP,siRNA treatment,Bioinformatics analysis,plasmid construction	Finally, the results of ChIP indicated that MEF2A occupied the promoter region of the Capn3 gene in rat denervated gastrocnemius muscle tissue. Based on these results, we proposed that MEF2A is a transcriptional regulator for Capn3 gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Finally, the results of ChIP indicated that MEF2A occupied the promoter region of the Capn3 gene in rat denervated gastrocnemius muscle tissue. Based on these results, we proposed that MEF2A is a transcriptional regulator for Capn3 gene expression.	Immunohistochemical staining	Finally, the results of ChIP indicated that MEF2A occupied the promoter region of the Capn3 gene in rat denervated gastrocnemius muscle tissue. Based on these results, we proposed that MEF2A is a transcriptional regulator for Capn3 gene expression.	MEF2A		Luciferase reporter assay,EMSA,PCR,Western Blot,qRT-PCR,immunocytochemistry,ChIP,siRNA treatment,Bioinformatics analysis,plasmid construction	Finally, the results of ChIP indicated that MEF2A occupied the promoter region of the Capn3 gene in rat denervated gastrocnemius muscle tissue. Based on these results, we proposed that MEF2A is a transcriptional regulator for Capn3 gene expression.			
29783071	chr2	120291428	120293428	Capn3	Finally, the results of ChIP indicated that MEF2A occupied the promoter region of the Capn3 gene in rat denervated gastrocnemius muscle tissue. Based on these results, we proposed that MEF2A is a transcriptional regulator for Capn3 gene expression.	human	Gastrocnemius muscle tissue	High+Lowthroughput	MEF2A regulates Calpain 3 expression in L6 myoblasts	否	无	Muscle wasting after reversible sciatic nerve injury	L6 cell	E_01_0461	Luciferase reporter assay,EMSA,PCR,Western Blot,qRT-PCR,immunocytochemistry,ChIP,siRNA treatment,Bioinformatics analysis,plasmid construction	Finally, the results of ChIP indicated that MEF2A occupied the promoter region of the Capn3 gene in rat denervated gastrocnemius muscle tissue. Based on these results, we proposed that MEF2A is a transcriptional regulator for Capn3 gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Finally, the results of ChIP indicated that MEF2A occupied the promoter region of the Capn3 gene in rat denervated gastrocnemius muscle tissue. Based on these results, we proposed that MEF2A is a transcriptional regulator for Capn3 gene expression.		Finally, the results of ChIP indicated that MEF2A occupied the promoter region of the Capn3 gene in rat denervated gastrocnemius muscle tissue. Based on these results, we proposed that MEF2A is a transcriptional regulator for Capn3 gene expression.	Immunohistochemical staining	Finally, the results of ChIP indicated that MEF2A occupied the promoter region of the Capn3 gene in rat denervated gastrocnemius muscle tissue. Based on these results, we proposed that MEF2A is a transcriptional regulator for Capn3 gene expression.			Luciferase reporter assay,EMSA,PCR,Western Blot,qRT-PCR,immunocytochemistry,ChIP,siRNA treatment,Bioinformatics analysis,plasmid construction				Capn3
29779944	chr3	133743368	133745368	TF	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.	mouse		High+Lowthroughput	Analysis of Genetically Diverse Macrophages Reveals Local and Domain-wide Mechanisms that Control Transcription Factor Binding and Function	否	无	nothing	L929	E_02_0300	RNA-seq,ChIP-seq,5' GRO-seq,GRO-seq,ATAC-seq,PLAC-seq,Bisulfite Sequencing,Hi-C,WGCNA analysis	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.		Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.	Immunohistochemical staining	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.			RNA-seq,ChIP-seq,5' GRO-seq,GRO-seq,ATAC-seq,PLAC-seq,Bisulfite Sequencing,Hi-C,WGCNA analysis				TF
29779944	chr10	87691539	87693539	Igf1	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.	mouse		High+Lowthroughput	Analysis of Genetically Diverse Macrophages Reveals Local and Domain-wide Mechanisms that Control Transcription Factor Binding and Function	否	无	nothing	L929	E_02_0300	RNA-seq,ChIP-seq,5' GRO-seq,GRO-seq,ATAC-seq,PLAC-seq,Bisulfite Sequencing,Hi-C,WGCNA analysis	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.		Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.	Immunohistochemical staining	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.			RNA-seq,ChIP-seq,5' GRO-seq,GRO-seq,ATAC-seq,PLAC-seq,Bisulfite Sequencing,Hi-C,WGCNA analysis				Igf1
29779944	chr21	25731873	25733873	GABPA	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.	mouse		High+Lowthroughput	Analysis of Genetically Diverse Macrophages Reveals Local and Domain-wide Mechanisms that Control Transcription Factor Binding and Function	否	无	nothing	L929	E_02_0300	RNA-seq,ChIP-seq,5' GRO-seq,GRO-seq,ATAC-seq,PLAC-seq,Bisulfite Sequencing,Hi-C,WGCNA analysis	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.		Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.	Immunohistochemical staining	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.			RNA-seq,ChIP-seq,5' GRO-seq,GRO-seq,ATAC-seq,PLAC-seq,Bisulfite Sequencing,Hi-C,WGCNA analysis				GABPA
29779944	chr19	48627002	48629002	DBP	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.	mouse		High+Lowthroughput	Analysis of Genetically Diverse Macrophages Reveals Local and Domain-wide Mechanisms that Control Transcription Factor Binding and Function	否	无	nothing	L929	E_02_0300	RNA-seq,ChIP-seq,5' GRO-seq,GRO-seq,ATAC-seq,PLAC-seq,Bisulfite Sequencing,Hi-C,WGCNA analysis	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.		Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.	Immunohistochemical staining	Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages.			RNA-seq,ChIP-seq,5' GRO-seq,GRO-seq,ATAC-seq,PLAC-seq,Bisulfite Sequencing,Hi-C,WGCNA analysis				DBP
29779941	chr1	3066245	3068245	PRDM16	These findings provide insights into how epigenetic control of transcriptional enhancers in radial glial determines the organization of the mammalian cerebral cortex.	human	Nervous tissue	High+Lowthroughput	The Epigenetic State of PRDM16-Regulated Enhancers in Radial Glia Controls Cortical Neuron Position	否	无	nothing	HEK293	E_01_0462	RNA,Chromatin Immunoprecipitation,Native Chromatin Immunoprecipitation,Prdm16 and Pdzrn3 Knockdown,RNaseq Analysis,ChIP-Seq,Binding and Expression Target Analysis (BETA),	These findings provide insights into how epigenetic control of transcriptional enhancers in radial glial determines the organization of the mammalian cerebral cortex.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings provide insights into how epigenetic control of transcriptional enhancers in radial glial determines the organization of the mammalian cerebral cortex.		These findings provide insights into how epigenetic control of transcriptional enhancers in radial glial determines the organization of the mammalian cerebral cortex.	Immunohistochemical staining	These findings provide insights into how epigenetic control of transcriptional enhancers in radial glial determines the organization of the mammalian cerebral cortex.			RNA,Chromatin Immunoprecipitation,Native Chromatin Immunoprecipitation,Prdm16 and Pdzrn3 Knockdown,RNaseq Analysis,ChIP-Seq,Binding and Expression Target Analysis (BETA),				PRDM16
29779941	chr3	73379673	73381673	PDZRN3	These findings provide insights into how epigenetic control of transcriptional enhancers in radial glial determines the organization of the mammalian cerebral cortex.	human	Nervous tissue	High+Lowthroughput	The Epigenetic State of PRDM16-Regulated Enhancers in Radial Glia Controls Cortical Neuron Position	否	无	nothing	HEK293	E_01_0462	RNA,Chromatin Immunoprecipitation,Native Chromatin Immunoprecipitation,Prdm16 and Pdzrn3 Knockdown,RNaseq Analysis,ChIP-Seq,Binding and Expression Target Analysis (BETA),	These findings provide insights into how epigenetic control of transcriptional enhancers in radial glial determines the organization of the mammalian cerebral cortex.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings provide insights into how epigenetic control of transcriptional enhancers in radial glial determines the organization of the mammalian cerebral cortex.		These findings provide insights into how epigenetic control of transcriptional enhancers in radial glial determines the organization of the mammalian cerebral cortex.	Immunohistochemical staining	These findings provide insights into how epigenetic control of transcriptional enhancers in radial glial determines the organization of the mammalian cerebral cortex.			RNA,Chromatin Immunoprecipitation,Native Chromatin Immunoprecipitation,Prdm16 and Pdzrn3 Knockdown,RNaseq Analysis,ChIP-Seq,Binding and Expression Target Analysis (BETA),				PDZRN3
29779861	chr19	42504265	42506265	CEACAM1		human	Epithelial tissues	High+Lowthroughput	HopQ impacts the integrin α5β1-independent NF-κB activation by Helicobacter pylori in CEACAM expressing cells	否	无	Peptic ulcer disease, gastric cancer	HeLa cell	E_01_0463	siRNA transfection,Immunofluorescence (IF),immunoblotting,immunoprecipitation,PCR		Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq				Immunohistochemical staining				siRNA transfection,Immunofluorescence (IF),immunoblotting,immunoprecipitation,PCR				CEACAM1
29777912	chr19	15233026	15235026	BRD4	Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.	human	connective tissue	High+Lowthroughput	A super-enhancer maintains homeostatic expression of Regnase-1	否	无	Autoimmune diseases, cancer	HEK293T	E_01_0464	transfection,Quantitative RT-PCR,Western blot,CRISPR/Cas9	Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.	Immunohistochemical staining	Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.	BRD4		transfection,Quantitative RT-PCR,Western blot,CRISPR/Cas9	Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.			
29777912	chr17	39401448	39403448	MED1	Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.	human	connective tissue	High+Lowthroughput	A super-enhancer maintains homeostatic expression of Regnase-1	否	无	Autoimmune diseases, cancer	HEK293T	E_01_0464	transfection,Quantitative RT-PCR,Western blot,CRISPR/Cas9	Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.	Immunohistochemical staining	Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.	MED1		transfection,Quantitative RT-PCR,Western blot,CRISPR/Cas9	Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.			
29777912	chr1	37471471	37473471	ZC3H12A	Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.	human	connective tissue	High+Lowthroughput	A super-enhancer maintains homeostatic expression of Regnase-1	否	无	Autoimmune diseases, cancer	HEK293T	E_01_0464	transfection,Quantitative RT-PCR,Western blot,CRISPR/Cas9	Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.		Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.	Immunohistochemical staining	Our result reveals a novel molecular mechanism by which a super-enhancer around the second intron regulates the expression of Regnase-1, and in turn maintains a desired level of Regnase-1.			transfection,Quantitative RT-PCR,Western blot,CRISPR/Cas9				ZC3H12A
29777232	chr12	4002608	4004608	Pomc	With maternal HF diet, offspring at weaning had rapid early weight gain, increased adiposity, and hyperleptinemia. The programmed adult offspring, subsequently fed LF diet, retained the increased body weight. Maternal HF diet combined with offspring HF diet caused more pronounced hyperphagia, fat mass, and insulin resistance. The ARC Pomc gene from programmed offspring at weaning showed hypermethylation in the enhancer (nPE1 and nPE2) regions and in the promoter sequence mediating leptin effects. Interestingly, hypermethylation at the Pomc promoter but not at the enhancer region persisted long term into adulthood in the programmed offspring. However, there were no additive effects on methylation levels in the regulatory regions of Pomc in programmed offspring fed a HF diet.	mouse	/	High+Lowthroughput	Maternal overnutrition programs epigenetic changes in the regulatory regions of hypothalamic Pomc in the offspring of rats	否	无	Obesity, diabetes		E_02_0301	Quantitative reverse-transcription PCR,DNA methylation analysis,Enzyme-linked immunosorbent assay	With maternal HF diet, offspring at weaning had rapid early weight gain, increased adiposity, and hyperleptinemia. The programmed adult offspring, subsequently fed LF diet, retained the increased body weight. Maternal HF diet combined with offspring HF diet caused more pronounced hyperphagia, fat mass, and insulin resistance. The ARC Pomc gene from programmed offspring at weaning showed hypermethylation in the enhancer (nPE1 and nPE2) regions and in the promoter sequence mediating leptin effects. Interestingly, hypermethylation at the Pomc promoter but not at the enhancer region persisted long term into adulthood in the programmed offspring. However, there were no additive effects on methylation levels in the regulatory regions of Pomc in programmed offspring fed a HF diet.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	With maternal HF diet, offspring at weaning had rapid early weight gain, increased adiposity, and hyperleptinemia. The programmed adult offspring, subsequently fed LF diet, retained the increased body weight. Maternal HF diet combined with offspring HF diet caused more pronounced hyperphagia, fat mass, and insulin resistance. The ARC Pomc gene from programmed offspring at weaning showed hypermethylation in the enhancer (nPE1 and nPE2) regions and in the promoter sequence mediating leptin effects. Interestingly, hypermethylation at the Pomc promoter but not at the enhancer region persisted long term into adulthood in the programmed offspring. However, there were no additive effects on methylation levels in the regulatory regions of Pomc in programmed offspring fed a HF diet.		With maternal HF diet, offspring at weaning had rapid early weight gain, increased adiposity, and hyperleptinemia. The programmed adult offspring, subsequently fed LF diet, retained the increased body weight. Maternal HF diet combined with offspring HF diet caused more pronounced hyperphagia, fat mass, and insulin resistance. The ARC Pomc gene from programmed offspring at weaning showed hypermethylation in the enhancer (nPE1 and nPE2) regions and in the promoter sequence mediating leptin effects. Interestingly, hypermethylation at the Pomc promoter but not at the enhancer region persisted long term into adulthood in the programmed offspring. However, there were no additive effects on methylation levels in the regulatory regions of Pomc in programmed offspring fed a HF diet.	Immunohistochemical staining	With maternal HF diet, offspring at weaning had rapid early weight gain, increased adiposity, and hyperleptinemia. The programmed adult offspring, subsequently fed LF diet, retained the increased body weight. Maternal HF diet combined with offspring HF diet caused more pronounced hyperphagia, fat mass, and insulin resistance. The ARC Pomc gene from programmed offspring at weaning showed hypermethylation in the enhancer (nPE1 and nPE2) regions and in the promoter sequence mediating leptin effects. Interestingly, hypermethylation at the Pomc promoter but not at the enhancer region persisted long term into adulthood in the programmed offspring. However, there were no additive effects on methylation levels in the regulatory regions of Pomc in programmed offspring fed a HF diet.			Quantitative reverse-transcription PCR,DNA methylation analysis,Enzyme-linked immunosorbent assay				Pomc
29775615	chr4	87647723	87649723	DMP1	This study provides a new understanding of DMP1's function in regulation of osteogenesis: not only an enhancer of bone formation, but also a negative regulator of MSCs differentiation in bone.	human	connective tissue	High+Lowthroughput	Extracellular matrix protein DMP1 suppresses osteogenic differentiation of Mesenchymal Stem Cells	否	无	nothing	mouse bone marrow cell	E_01_0465	Immunofluorescence staining,Real-time PCR,Western blot,Analysis of histology	This study provides a new understanding of DMP1's function in regulation of osteogenesis: not only an enhancer of bone formation, but also a negative regulator of MSCs differentiation in bone.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This study provides a new understanding of DMP1's function in regulation of osteogenesis: not only an enhancer of bone formation, but also a negative regulator of MSCs differentiation in bone.		This study provides a new understanding of DMP1's function in regulation of osteogenesis: not only an enhancer of bone formation, but also a negative regulator of MSCs differentiation in bone.	Immunohistochemical staining	This study provides a new understanding of DMP1's function in regulation of osteogenesis: not only an enhancer of bone formation, but also a negative regulator of MSCs differentiation in bone.			Immunofluorescence staining,Real-time PCR,Western blot,Analysis of histology				DMP1
29775582	chr2	11479885	11481885	GREB1	"Collectively, these data suggest that the enhancer and promoter remain ""poised"" for transcription via their contacts with GBS1 and GBS2. Upon E2 induction, GBS1 and GBS2 disengage from the enhancer, allowing direct EPC for active transcription."	human	Epithelial tissues	High+Lowthroughput	SRC-3 Coactivator Governs Dynamic Estrogen-Induced Chromatin Looping Interactions during Transcription	否	无	nothing	HeLa S3	E_01_0466	3C,Immunoblotting,Chromatin Reconstitution,Immunodepletion,3C-qPCR,qPCR	"Collectively, these data suggest that the enhancer and promoter remain ""poised"" for transcription via their contacts with GBS1 and GBS2. Upon E2 induction, GBS1 and GBS2 disengage from the enhancer, allowing direct EPC for active transcription."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Collectively, these data suggest that the enhancer and promoter remain ""poised"" for transcription via their contacts with GBS1 and GBS2. Upon E2 induction, GBS1 and GBS2 disengage from the enhancer, allowing direct EPC for active transcription."		"Collectively, these data suggest that the enhancer and promoter remain ""poised"" for transcription via their contacts with GBS1 and GBS2. Upon E2 induction, GBS1 and GBS2 disengage from the enhancer, allowing direct EPC for active transcription."	Immunohistochemical staining	"Collectively, these data suggest that the enhancer and promoter remain ""poised"" for transcription via their contacts with GBS1 and GBS2. Upon E2 induction, GBS1 and GBS2 disengage from the enhancer, allowing direct EPC for active transcription."			3C,Immunoblotting,Chromatin Reconstitution,Immunodepletion,3C-qPCR,qPCR				GREB1
29775417	chr7	148804568	148806568	EZH2	These data indicate that EZH2 activation contributes to renal EMT and fibrosis through activation of multiple signaling pathways and suggest that EZH2 has potential as a therapeutic target for treatment of renal fibrosis.-Zhou, X., Xiong, C., Tolbert, E., Zhao, T. C., Bayliss, G., Zhuang, S. Targeting histone methyltransferase enhancer of zeste homolog-2 inhibits renal epithelial-mesenchymal transition and attenuates renal fibrosis.	mouse	Kidney tissue	High+Lowthroughput	Targeting histone methyltransferase enhancer of zeste homolog-2 inhibits renal epithelial-mesenchymal transition and attenuates renal fibrosis	否	无	Renal fibrosis	kidney tubule cell	E_02_0302	Transfection of siRNA,Immunoblot analysis,Histochemical,immunofluorescent staining,Densitometry analysis	These data indicate that EZH2 activation contributes to renal EMT and fibrosis through activation of multiple signaling pathways and suggest that EZH2 has potential as a therapeutic target for treatment of renal fibrosis.-Zhou, X., Xiong, C., Tolbert, E., Zhao, T. C., Bayliss, G., Zhuang, S. Targeting histone methyltransferase enhancer of zeste homolog-2 inhibits renal epithelial-mesenchymal transition and attenuates renal fibrosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These data indicate that EZH2 activation contributes to renal EMT and fibrosis through activation of multiple signaling pathways and suggest that EZH2 has potential as a therapeutic target for treatment of renal fibrosis.-Zhou, X., Xiong, C., Tolbert, E., Zhao, T. C., Bayliss, G., Zhuang, S. Targeting histone methyltransferase enhancer of zeste homolog-2 inhibits renal epithelial-mesenchymal transition and attenuates renal fibrosis.		These data indicate that EZH2 activation contributes to renal EMT and fibrosis through activation of multiple signaling pathways and suggest that EZH2 has potential as a therapeutic target for treatment of renal fibrosis.-Zhou, X., Xiong, C., Tolbert, E., Zhao, T. C., Bayliss, G., Zhuang, S. Targeting histone methyltransferase enhancer of zeste homolog-2 inhibits renal epithelial-mesenchymal transition and attenuates renal fibrosis.	Immunohistochemical staining	These data indicate that EZH2 activation contributes to renal EMT and fibrosis through activation of multiple signaling pathways and suggest that EZH2 has potential as a therapeutic target for treatment of renal fibrosis.-Zhou, X., Xiong, C., Tolbert, E., Zhao, T. C., Bayliss, G., Zhuang, S. Targeting histone methyltransferase enhancer of zeste homolog-2 inhibits renal epithelial-mesenchymal transition and attenuates renal fibrosis.			Transfection of siRNA,Immunoblot analysis,Histochemical,immunofluorescent staining,Densitometry analysis				EZH2
29774079	chr19	15825440	15827440	UCA1	These findings uncover for the first time that AC026904.1 and UCA1 could cooperatively upregulate Slug expression at both transcriptional and post-transcriptional levels, exerting critical roles in TGF-β-induced EMT. The present work provides new evidence that lncRNAs function as key regulators of EMT and hold great promise to be used as novel biomarkers and therapeutic targets for metastatic breast cancer.	human	Mammary tissue	High+Lowthroughput	"Long non-coding RNAs AC026904.1 and UCA1: a ""one-two punch"" for TGF-β-induced SNAI2 activation and epithelial-mesenchymal transition in breast cancer"	否	无	mammary cancer	MDA-MB-231-luc-D3H2LN	E_01_0467	ChIRP,microarray analysis,qPCR,Kaplan-Meier survival analysis,confocal laser microscopy,Western blot,chromosome conformation capture (3C),RNA purification (ChIRP), ChIP,luciferase reporter assay,transwell migration assay	These findings uncover for the first time that AC026904.1 and UCA1 could cooperatively upregulate Slug expression at both transcriptional and post-transcriptional levels, exerting critical roles in TGF-β-induced EMT. The present work provides new evidence that lncRNAs function as key regulators of EMT and hold great promise to be used as novel biomarkers and therapeutic targets for metastatic breast cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings uncover for the first time that AC026904.1 and UCA1 could cooperatively upregulate Slug expression at both transcriptional and post-transcriptional levels, exerting critical roles in TGF-β-induced EMT. The present work provides new evidence that lncRNAs function as key regulators of EMT and hold great promise to be used as novel biomarkers and therapeutic targets for metastatic breast cancer.		These findings uncover for the first time that AC026904.1 and UCA1 could cooperatively upregulate Slug expression at both transcriptional and post-transcriptional levels, exerting critical roles in TGF-β-induced EMT. The present work provides new evidence that lncRNAs function as key regulators of EMT and hold great promise to be used as novel biomarkers and therapeutic targets for metastatic breast cancer.	Immunohistochemical staining	These findings uncover for the first time that AC026904.1 and UCA1 could cooperatively upregulate Slug expression at both transcriptional and post-transcriptional levels, exerting critical roles in TGF-β-induced EMT. The present work provides new evidence that lncRNAs function as key regulators of EMT and hold great promise to be used as novel biomarkers and therapeutic targets for metastatic breast cancer.			ChIRP,microarray analysis,qPCR,Kaplan-Meier survival analysis,confocal laser microscopy,Western blot,chromosome conformation capture (3C),RNA purification (ChIRP), ChIP,luciferase reporter assay,transwell migration assay				UCA1
29774079	chr8	48915262	48917262	SNAI2	These findings uncover for the first time that AC026904.1 and UCA1 could cooperatively upregulate Slug expression at both transcriptional and post-transcriptional levels, exerting critical roles in TGF-β-induced EMT. The present work provides new evidence that lncRNAs function as key regulators of EMT and hold great promise to be used as novel biomarkers and therapeutic targets for metastatic breast cancer.	human	Mammary tissue	High+Lowthroughput	"Long non-coding RNAs AC026904.1 and UCA1: a ""one-two punch"" for TGF-β-induced SNAI2 activation and epithelial-mesenchymal transition in breast cancer"	否	无	mammary cancer	MDA-MB-231-luc-D3H2LN	E_01_0467	ChIRP,microarray analysis,qPCR,Kaplan-Meier survival analysis,confocal laser microscopy,Western blot,chromosome conformation capture (3C),RNA purification (ChIRP), ChIP,luciferase reporter assay,transwell migration assay	These findings uncover for the first time that AC026904.1 and UCA1 could cooperatively upregulate Slug expression at both transcriptional and post-transcriptional levels, exerting critical roles in TGF-β-induced EMT. The present work provides new evidence that lncRNAs function as key regulators of EMT and hold great promise to be used as novel biomarkers and therapeutic targets for metastatic breast cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These findings uncover for the first time that AC026904.1 and UCA1 could cooperatively upregulate Slug expression at both transcriptional and post-transcriptional levels, exerting critical roles in TGF-β-induced EMT. The present work provides new evidence that lncRNAs function as key regulators of EMT and hold great promise to be used as novel biomarkers and therapeutic targets for metastatic breast cancer.	Immunohistochemical staining	These findings uncover for the first time that AC026904.1 and UCA1 could cooperatively upregulate Slug expression at both transcriptional and post-transcriptional levels, exerting critical roles in TGF-β-induced EMT. The present work provides new evidence that lncRNAs function as key regulators of EMT and hold great promise to be used as novel biomarkers and therapeutic targets for metastatic breast cancer.	SNAI2		ChIRP,microarray analysis,qPCR,Kaplan-Meier survival analysis,confocal laser microscopy,Western blot,chromosome conformation capture (3C),RNA purification (ChIRP), ChIP,luciferase reporter assay,transwell migration assay	These findings uncover for the first time that AC026904.1 and UCA1 could cooperatively upregulate Slug expression at both transcriptional and post-transcriptional levels, exerting critical roles in TGF-β-induced EMT. The present work provides new evidence that lncRNAs function as key regulators of EMT and hold great promise to be used as novel biomarkers and therapeutic targets for metastatic breast cancer.			
29773854	chr12	102393392	102395392	IGF1	Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.	human	Epithelial tissues	High+Lowthroughput	Genome-wide haplotype association analysis of primary biliary cholangitis risk in Japanese	是	无	Primary biliary cholangitis (PBC)	epithelial cell	E_01_0468	ChIP-seq	Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.	Immunohistochemical staining	Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.	IGF1		ChIP-seq	Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.			
29773854	chr7	7638258	7640258	UMAD1	Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.	human	Epithelial tissues	High+Lowthroughput	Genome-wide haplotype association analysis of primary biliary cholangitis risk in Japanese	是	无	Primary biliary cholangitis (PBC)	epithelial cell	E_01_0468	ChIP-seq	Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.		Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.	Immunohistochemical staining	Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.			ChIP-seq				UMAD1
29773854	chr9	114781980	114783980	TNFSF15	Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.	human	Epithelial tissues	High+Lowthroughput	Genome-wide haplotype association analysis of primary biliary cholangitis risk in Japanese	是	无	Primary biliary cholangitis (PBC)	epithelial cell	E_01_0468	ChIP-seq	Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.		Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.	Immunohistochemical staining	Our analysis demonstrates the utility of haplotype association analyses in discovering and characterizing PBC susceptibility loci.			ChIP-seq				TNFSF15
29773832	chr3	133743689	133745689	TF	Thus, our study provides new insight into the epigenetic landscapes associated with the heterogeneity of PDAC, thereby increasing our mechanistic understanding of this disease, as well as offering potential new markers and therapeutic targets.	human	Epithelial tissues	High+Lowthroughput	Distinct epigenetic landscapes underlie the pathobiology of pancreatic cancer subtypes	否	无	Pancreatic ductal adenocarcinoma (PDAC) subtype	epithelial cell	E_01_0469	RNA extraction,RNA-seq,ChIP-seq,SNP arrays analysis,siRNA transfection,qPCR	Thus, our study provides new insight into the epigenetic landscapes associated with the heterogeneity of PDAC, thereby increasing our mechanistic understanding of this disease, as well as offering potential new markers and therapeutic targets.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, our study provides new insight into the epigenetic landscapes associated with the heterogeneity of PDAC, thereby increasing our mechanistic understanding of this disease, as well as offering potential new markers and therapeutic targets.		Thus, our study provides new insight into the epigenetic landscapes associated with the heterogeneity of PDAC, thereby increasing our mechanistic understanding of this disease, as well as offering potential new markers and therapeutic targets.	Immunohistochemical staining	Thus, our study provides new insight into the epigenetic landscapes associated with the heterogeneity of PDAC, thereby increasing our mechanistic understanding of this disease, as well as offering potential new markers and therapeutic targets.			RNA extraction,RNA-seq,ChIP-seq,SNP arrays analysis,siRNA transfection,qPCR				TF
29773832	chr7	81696419	81698419	HGF	Thus, our study provides new insight into the epigenetic landscapes associated with the heterogeneity of PDAC, thereby increasing our mechanistic understanding of this disease, as well as offering potential new markers and therapeutic targets.	human	Epithelial tissues	High+Lowthroughput	Distinct epigenetic landscapes underlie the pathobiology of pancreatic cancer subtypes	否	无	Pancreatic ductal adenocarcinoma (PDAC) subtype	epithelial cell	E_01_0469	RNA extraction,RNA-seq,ChIP-seq,SNP arrays analysis,siRNA transfection,qPCR	Thus, our study provides new insight into the epigenetic landscapes associated with the heterogeneity of PDAC, thereby increasing our mechanistic understanding of this disease, as well as offering potential new markers and therapeutic targets.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, our study provides new insight into the epigenetic landscapes associated with the heterogeneity of PDAC, thereby increasing our mechanistic understanding of this disease, as well as offering potential new markers and therapeutic targets.	Immunohistochemical staining	Thus, our study provides new insight into the epigenetic landscapes associated with the heterogeneity of PDAC, thereby increasing our mechanistic understanding of this disease, as well as offering potential new markers and therapeutic targets.	IL6		RNA extraction,RNA-seq,ChIP-seq,SNP arrays analysis,siRNA transfection,qPCR	Thus, our study provides new insight into the epigenetic landscapes associated with the heterogeneity of PDAC, thereby increasing our mechanistic understanding of this disease, as well as offering potential new markers and therapeutic targets.			
29772805	chr19	48952280	48954280	BAX	This study suggested that EFDK had antioxidant activity and a neuroprotective effect, and ameliorated cognitive abnormalities in TMT-induced mice by regulating the JNK/Akt and apoptotic pathway.	mouse	Nervous tissue	High+Lowthroughput	Ethyl Acetate Fraction from Persimmon (Diospyros kaki) Ameliorates Cerebral Neuronal Loss and Cognitive Deficit via the JNK/Akt Pathway in TMT-Induced Mice	否	无	Cerebral neuronal loss and cognitive deficits	HT22 cell	E_02_0303	Western Blot,transgenic mice	This study suggested that EFDK had antioxidant activity and a neuroprotective effect, and ameliorated cognitive abnormalities in TMT-induced mice by regulating the JNK/Akt and apoptotic pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This study suggested that EFDK had antioxidant activity and a neuroprotective effect, and ameliorated cognitive abnormalities in TMT-induced mice by regulating the JNK/Akt and apoptotic pathway.		This study suggested that EFDK had antioxidant activity and a neuroprotective effect, and ameliorated cognitive abnormalities in TMT-induced mice by regulating the JNK/Akt and apoptotic pathway.	Immunohistochemical staining	This study suggested that EFDK had antioxidant activity and a neuroprotective effect, and ameliorated cognitive abnormalities in TMT-induced mice by regulating the JNK/Akt and apoptotic pathway.			Western Blot,transgenic mice				BAX
29772677	chrX	123856883	123858883	XIAP	Overall, these findings suggest that lambertianic acid enhances TRAIL-induced apoptosis via inhibition of XIAP/NF-κB in TRAIL resistant NSCLCs.	human	Lung tissue	High+Lowthroughput	Lambertianic Acid Sensitizes Non-Small Cell Lung Cancers to TRAIL-Induced Apoptosis via Inhibition of XIAP/NF-κB and Activation of Caspases and Death Receptor 4	否	无		A549	E_01_0470	Western Blot,Co-Immunoprecipitation,Cell Cycle Analysis,Crystal Violet Assay,Cytotoxicity Assay,flow cytometry	Overall, these findings suggest that lambertianic acid enhances TRAIL-induced apoptosis via inhibition of XIAP/NF-κB in TRAIL resistant NSCLCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Overall, these findings suggest that lambertianic acid enhances TRAIL-induced apoptosis via inhibition of XIAP/NF-κB in TRAIL resistant NSCLCs.	Immunohistochemical staining	Overall, these findings suggest that lambertianic acid enhances TRAIL-induced apoptosis via inhibition of XIAP/NF-κB in TRAIL resistant NSCLCs.	XIAP		Western Blot,Co-Immunoprecipitation,Cell Cycle Analysis,Crystal Violet Assay,Cytotoxicity Assay,flow cytometry	Overall, these findings suggest that lambertianic acid enhances TRAIL-induced apoptosis via inhibition of XIAP/NF-κB in TRAIL resistant NSCLCs.			
29771444	chr6	45325483	45327483	RUNX2	In summary, LLLI can promote osteogenesis and inhibit adipocytes formation, thus attenuating bone resorption of osteoclasts. The mechanism of LLLI is that it promotes the entry of β-catenin into the nucleus and regulates the Wnt pathway and the differentiation direction of mesenchymal stem cells through the APN signal pathway, thus promoting bone formation.	mouse	connective tissue	High+Lowthroughput	Low-level laser irradiation promotes the differentiation of bone marrow stromal cells into osteoblasts through the APN/Wnt/β-catenin pathway	否	无	Non small cell lung cancer	mesenchymal stem cell	E_02_0304	Immunofluorescence,Alkaline Phosphatase (AP) Stain,Western Blot,Alizarin Red Stain,Oil Red O Stain,RT-PCR,cell transfection	In summary, LLLI can promote osteogenesis and inhibit adipocytes formation, thus attenuating bone resorption of osteoclasts. The mechanism of LLLI is that it promotes the entry of β-catenin into the nucleus and regulates the Wnt pathway and the differentiation direction of mesenchymal stem cells through the APN signal pathway, thus promoting bone formation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In summary, LLLI can promote osteogenesis and inhibit adipocytes formation, thus attenuating bone resorption of osteoclasts. The mechanism of LLLI is that it promotes the entry of β-catenin into the nucleus and regulates the Wnt pathway and the differentiation direction of mesenchymal stem cells through the APN signal pathway, thus promoting bone formation.		In summary, LLLI can promote osteogenesis and inhibit adipocytes formation, thus attenuating bone resorption of osteoclasts. The mechanism of LLLI is that it promotes the entry of β-catenin into the nucleus and regulates the Wnt pathway and the differentiation direction of mesenchymal stem cells through the APN signal pathway, thus promoting bone formation.	Immunohistochemical staining	In summary, LLLI can promote osteogenesis and inhibit adipocytes formation, thus attenuating bone resorption of osteoclasts. The mechanism of LLLI is that it promotes the entry of β-catenin into the nucleus and regulates the Wnt pathway and the differentiation direction of mesenchymal stem cells through the APN signal pathway, thus promoting bone formation.			Immunofluorescence,Alkaline Phosphatase (AP) Stain,Western Blot,Alizarin Red Stain,Oil Red O Stain,RT-PCR,cell transfection				RUNX2
29771329	chr17	15227161	15229161	PMP22	In this study, we have utilized genome editing to create a deletion of this super-enhancer to determine its role in Pmp22 regulation. Our data show a significant decrease in Pmp22 transcript expression using allele-specific internal controls. Moreover, the P2 promoter of the Pmp22 gene, which is used in other cell types, is affected, but we find that the Schwann cell-specific P1 promoter is disproportionately more sensitive to loss of the super-enhancer. These data show for the first time the requirement of these upstream enhancers for full Pmp22 expression.	human	connective tissue	High+Lowthroughput	Regulation of the neuropathy-associated Pmp22 gene by a distal super-enhancer	否	无	Inherited peripheral neuropathies		E_01_0471	CRISPR/Cas9,siRNA treatment,RT-qPCR,Spectral karyotyping	In this study, we have utilized genome editing to create a deletion of this super-enhancer to determine its role in Pmp22 regulation. Our data show a significant decrease in Pmp22 transcript expression using allele-specific internal controls. Moreover, the P2 promoter of the Pmp22 gene, which is used in other cell types, is affected, but we find that the Schwann cell-specific P1 promoter is disproportionately more sensitive to loss of the super-enhancer. These data show for the first time the requirement of these upstream enhancers for full Pmp22 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we have utilized genome editing to create a deletion of this super-enhancer to determine its role in Pmp22 regulation. Our data show a significant decrease in Pmp22 transcript expression using allele-specific internal controls. Moreover, the P2 promoter of the Pmp22 gene, which is used in other cell types, is affected, but we find that the Schwann cell-specific P1 promoter is disproportionately more sensitive to loss of the super-enhancer. These data show for the first time the requirement of these upstream enhancers for full Pmp22 expression.		In this study, we have utilized genome editing to create a deletion of this super-enhancer to determine its role in Pmp22 regulation. Our data show a significant decrease in Pmp22 transcript expression using allele-specific internal controls. Moreover, the P2 promoter of the Pmp22 gene, which is used in other cell types, is affected, but we find that the Schwann cell-specific P1 promoter is disproportionately more sensitive to loss of the super-enhancer. These data show for the first time the requirement of these upstream enhancers for full Pmp22 expression.	Immunohistochemical staining	In this study, we have utilized genome editing to create a deletion of this super-enhancer to determine its role in Pmp22 regulation. Our data show a significant decrease in Pmp22 transcript expression using allele-specific internal controls. Moreover, the P2 promoter of the Pmp22 gene, which is used in other cell types, is affected, but we find that the Schwann cell-specific P1 promoter is disproportionately more sensitive to loss of the super-enhancer. These data show for the first time the requirement of these upstream enhancers for full Pmp22 expression.			CRISPR/Cas9,siRNA treatment,RT-qPCR,Spectral karyotyping				PMP22
29771329	chr11	63017002	63019002	Pmp22	In this study, we have utilized genome editing to create a deletion of this super-enhancer to determine its role in Pmp22 regulation. Our data show a significant decrease in Pmp22 transcript expression using allele-specific internal controls. Moreover, the P2 promoter of the Pmp22 gene, which is used in other cell types, is affected, but we find that the Schwann cell-specific P1 promoter is disproportionately more sensitive to loss of the super-enhancer. These data show for the first time the requirement of these upstream enhancers for full Pmp22 expression.	human	connective tissue	High+Lowthroughput	Regulation of the neuropathy-associated Pmp22 gene by a distal super-enhancer	否	无	Inherited peripheral neuropathies		E_01_0471	CRISPR/Cas9,siRNA treatment,RT-qPCR,Spectral karyotyping	In this study, we have utilized genome editing to create a deletion of this super-enhancer to determine its role in Pmp22 regulation. Our data show a significant decrease in Pmp22 transcript expression using allele-specific internal controls. Moreover, the P2 promoter of the Pmp22 gene, which is used in other cell types, is affected, but we find that the Schwann cell-specific P1 promoter is disproportionately more sensitive to loss of the super-enhancer. These data show for the first time the requirement of these upstream enhancers for full Pmp22 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we have utilized genome editing to create a deletion of this super-enhancer to determine its role in Pmp22 regulation. Our data show a significant decrease in Pmp22 transcript expression using allele-specific internal controls. Moreover, the P2 promoter of the Pmp22 gene, which is used in other cell types, is affected, but we find that the Schwann cell-specific P1 promoter is disproportionately more sensitive to loss of the super-enhancer. These data show for the first time the requirement of these upstream enhancers for full Pmp22 expression.		In this study, we have utilized genome editing to create a deletion of this super-enhancer to determine its role in Pmp22 regulation. Our data show a significant decrease in Pmp22 transcript expression using allele-specific internal controls. Moreover, the P2 promoter of the Pmp22 gene, which is used in other cell types, is affected, but we find that the Schwann cell-specific P1 promoter is disproportionately more sensitive to loss of the super-enhancer. These data show for the first time the requirement of these upstream enhancers for full Pmp22 expression.	Immunohistochemical staining	In this study, we have utilized genome editing to create a deletion of this super-enhancer to determine its role in Pmp22 regulation. Our data show a significant decrease in Pmp22 transcript expression using allele-specific internal controls. Moreover, the P2 promoter of the Pmp22 gene, which is used in other cell types, is affected, but we find that the Schwann cell-specific P1 promoter is disproportionately more sensitive to loss of the super-enhancer. These data show for the first time the requirement of these upstream enhancers for full Pmp22 expression.			CRISPR/Cas9,siRNA treatment,RT-qPCR,Spectral karyotyping				Pmp22
29769415	chr3	41191924	41193924	CTNNB1	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.	human	Osteosarcoma tissues	High+Lowthroughput	Up-regulation of microRNA-340 promotes osteosarcoma cell apoptosis while suppressing proliferation, migration, and invasion by inactivating the CTNNB1-mediated Notch signaling pathway	否	无	Osteosarcoma (OS)		E_01_0472	Luciferase reporter assay,Western Blot,RT-QPCR,immunohistochemistry,in situ hybridization(ISH),transfection,MTT,flow cytometry,scratch test,transwell assay	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.	Immunohistochemical staining	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.	CTNNB1		Luciferase reporter assay,Western Blot,RT-QPCR,immunohistochemistry,in situ hybridization(ISH),transfection,MTT,flow cytometry,scratch test,transwell assay	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.			
29769415	chr16	29880495	29882495	Hes1	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.	human	Osteosarcoma tissues	High+Lowthroughput	Up-regulation of microRNA-340 promotes osteosarcoma cell apoptosis while suppressing proliferation, migration, and invasion by inactivating the CTNNB1-mediated Notch signaling pathway	否	无	Osteosarcoma (OS)		E_01_0472	Luciferase reporter assay,Western Blot,RT-QPCR,immunohistochemistry,in situ hybridization(ISH),transfection,MTT,flow cytometry,scratch test,transwell assay	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.		Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.	Immunohistochemical staining	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.			Luciferase reporter assay,Western Blot,RT-QPCR,immunohistochemistry,in situ hybridization(ISH),transfection,MTT,flow cytometry,scratch test,transwell assay				Hes1
29769415	chr17	44804428	44806428	Runx2	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.	human	Osteosarcoma tissues	High+Lowthroughput	Up-regulation of microRNA-340 promotes osteosarcoma cell apoptosis while suppressing proliferation, migration, and invasion by inactivating the CTNNB1-mediated Notch signaling pathway	否	无	Osteosarcoma (OS)		E_01_0472	Luciferase reporter assay,Western Blot,RT-QPCR,immunohistochemistry,in situ hybridization(ISH),transfection,MTT,flow cytometry,scratch test,transwell assay	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.		Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.	Immunohistochemical staining	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.			Luciferase reporter assay,Western Blot,RT-QPCR,immunohistochemistry,in situ hybridization(ISH),transfection,MTT,flow cytometry,scratch test,transwell assay				Runx2
29769415	chr7	45108548	45110548	Bax	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.	human	Osteosarcoma tissues	High+Lowthroughput	Up-regulation of microRNA-340 promotes osteosarcoma cell apoptosis while suppressing proliferation, migration, and invasion by inactivating the CTNNB1-mediated Notch signaling pathway	否	无	Osteosarcoma (OS)		E_01_0472	Luciferase reporter assay,Western Blot,RT-QPCR,immunohistochemistry,in situ hybridization(ISH),transfection,MTT,flow cytometry,scratch test,transwell assay	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.		Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.	Immunohistochemical staining	Our results show that miR-340 was expressed a higher level in normal tissue than OS tissue. Expression of Notch, CTNNB1, hairy and enhancer of split 1 (Hes1), Bcl-2, Runt-related transcription factor 2 (Runx2), and osteocalcin increased and that of miR-340, Bcl-2 interacting mediator of cell death (BIM), and Bcl-2 associated protein X (Bax) decreased in OS tissues. U-2OS cell line had the highest miR-340 expression. We also found that the up-regulation of miR-340 had increased expression of miR-340, BIM, and Bax but decreased expression of Notch, CTNNB1, Hes1, Bcl-2, Runx2, and osteocalcin. Up-regulation of miR-340p lead to increased cell apoptosis, suppressed cell proliferation, migration, and invasion. Our study demonstrates that overexpression of miR-340 could suppress OS cell proliferation, migration, and invasion as well as promoting OS cell apoptosis by inactivating the Notch signaling pathway via down-regulating CTNNB1. Functional miR-340 overexpression might be a future therapeutic strategy for OS.			Luciferase reporter assay,Western Blot,RT-QPCR,immunohistochemistry,in situ hybridization(ISH),transfection,MTT,flow cytometry,scratch test,transwell assay				Bax
29769310	chr17	57998205	58000205	SRSF1	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.	human	Epithelial tissues	High+Lowthroughput	Tumor-associated intronic editing of HNRPLL generates a novel splicing variant linked to cell proliferation	否	无	tumour	HeLa cell	E_01_0473	gene knockdown,RT-PCR,qPCR,RNA-immunoprecipitation (RNA-IP) experiment,RNC-mRNA,Splicing luciferase reporter assay,RNA-seq,Gene expression analysis,Chromatin immunoprecipitation assay (ChIP)	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.		Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.	Immunohistochemical staining	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.			gene knockdown,RT-PCR,qPCR,RNA-immunoprecipitation (RNA-IP) experiment,RNC-mRNA,Splicing luciferase reporter assay,RNA-seq,Gene expression analysis,Chromatin immunoprecipitation assay (ChIP)				SRSF1
29769310	chr1	154578216	154580216	ADAR	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.	human	Epithelial tissues	High+Lowthroughput	Tumor-associated intronic editing of HNRPLL generates a novel splicing variant linked to cell proliferation	否	无	tumour	HeLa cell	E_01_0473	gene knockdown,RT-PCR,qPCR,RNA-immunoprecipitation (RNA-IP) experiment,RNC-mRNA,Splicing luciferase reporter assay,RNA-seq,Gene expression analysis,Chromatin immunoprecipitation assay (ChIP)	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.		Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.	Immunohistochemical staining	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.			gene knockdown,RT-PCR,qPCR,RNA-immunoprecipitation (RNA-IP) experiment,RNC-mRNA,Splicing luciferase reporter assay,RNA-seq,Gene expression analysis,Chromatin immunoprecipitation assay (ChIP)				ADAR
29769310	chr11	69638330	69640330	CCND1	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.	human	Epithelial tissues	High+Lowthroughput	Tumor-associated intronic editing of HNRPLL generates a novel splicing variant linked to cell proliferation	否	无	tumour	HeLa cell	E_01_0473	gene knockdown,RT-PCR,qPCR,RNA-immunoprecipitation (RNA-IP) experiment,RNC-mRNA,Splicing luciferase reporter assay,RNA-seq,Gene expression analysis,Chromatin immunoprecipitation assay (ChIP)	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.	Immunohistochemical staining	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.	CCND1		gene knockdown,RT-PCR,qPCR,RNA-immunoprecipitation (RNA-IP) experiment,RNC-mRNA,Splicing luciferase reporter assay,RNA-seq,Gene expression analysis,Chromatin immunoprecipitation assay (ChIP)	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.			
29769310	chr9	99100881	99102881	TGFBR1	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.	human	Epithelial tissues	High+Lowthroughput	Tumor-associated intronic editing of HNRPLL generates a novel splicing variant linked to cell proliferation	否	无	tumour	HeLa cell	E_01_0473	gene knockdown,RT-PCR,qPCR,RNA-immunoprecipitation (RNA-IP) experiment,RNC-mRNA,Splicing luciferase reporter assay,RNA-seq,Gene expression analysis,Chromatin immunoprecipitation assay (ChIP)	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.		Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.	Immunohistochemical staining	Gene expression profiling by RNA-seq revealed that E12A acts distinctly from HNRPLL and regulates a set of growth-related genes, such as cyclin CCND1 and growth factor receptor TGFBR1 Accordingly, silencing E12A expression leads to impaired clonogenic ability and enhanced sensitivity to doxorubicin, thus highlighting the significance of this alternative isoform in tumor cell survival. In summary, we present the interplay of RNA editing and splicing as a regulatory mechanism of gene expression and also its physiological relevance. These findings extend our understanding of transcriptional dynamics and provide a mechanistic explanation to the link of RNA editors to tumorigenesis.			gene knockdown,RT-PCR,qPCR,RNA-immunoprecipitation (RNA-IP) experiment,RNC-mRNA,Splicing luciferase reporter assay,RNA-seq,Gene expression analysis,Chromatin immunoprecipitation assay (ChIP)				TGFBR1
29768655	chr7	148804347	148806347	EZH2	More importantly, we revealed that siEZH2 down-regulated NF-κB p65 within the nucleus. These findings indicate that the let-7e/EZH2/H3K27me3/NF-κB p65 pathway is a novel regulatory axis of TNFα expression. In addition, we determined the protein differences between siEZH2 and siEZH2-NC by iTRAQ and found a number of proteins that might be associated with TNFα.	human	connective tissue	High+Lowthroughput	Let-7e inhibits TNF-α expression by targeting the methyl transferase EZH2 in DENV2-infected THP-1 cells	否	无	nothing	THP-1 cells	E_01_0474	Western blot,Immunofluorescence assay,qRT-PCR,ELISA,Luciferase reporter assay,iTRAQ,miRNA or siRNA transfection,EZH2 knockdown,Smad3 knockdown	More importantly, we revealed that siEZH2 down-regulated NF-κB p65 within the nucleus. These findings indicate that the let-7e/EZH2/H3K27me3/NF-κB p65 pathway is a novel regulatory axis of TNFα expression. In addition, we determined the protein differences between siEZH2 and siEZH2-NC by iTRAQ and found a number of proteins that might be associated with TNFα.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			More importantly, we revealed that siEZH2 down-regulated NF-κB p65 within the nucleus. These findings indicate that the let-7e/EZH2/H3K27me3/NF-κB p65 pathway is a novel regulatory axis of TNFα expression. In addition, we determined the protein differences between siEZH2 and siEZH2-NC by iTRAQ and found a number of proteins that might be associated with TNFα.	Immunohistochemical staining	More importantly, we revealed that siEZH2 down-regulated NF-κB p65 within the nucleus. These findings indicate that the let-7e/EZH2/H3K27me3/NF-κB p65 pathway is a novel regulatory axis of TNFα expression. In addition, we determined the protein differences between siEZH2 and siEZH2-NC by iTRAQ and found a number of proteins that might be associated with TNFα.	EZH2		Western blot,Immunofluorescence assay,qRT-PCR,ELISA,Luciferase reporter assay,iTRAQ,miRNA or siRNA transfection,EZH2 knockdown,Smad3 knockdown	More importantly, we revealed that siEZH2 down-regulated NF-κB p65 within the nucleus. These findings indicate that the let-7e/EZH2/H3K27me3/NF-κB p65 pathway is a novel regulatory axis of TNFα expression. In addition, we determined the protein differences between siEZH2 and siEZH2-NC by iTRAQ and found a number of proteins that might be associated with TNFα.			
29768655	chr9	63551241	63553241	Smad3	More importantly, we revealed that siEZH2 down-regulated NF-κB p65 within the nucleus. These findings indicate that the let-7e/EZH2/H3K27me3/NF-κB p65 pathway is a novel regulatory axis of TNFα expression. In addition, we determined the protein differences between siEZH2 and siEZH2-NC by iTRAQ and found a number of proteins that might be associated with TNFα.	human	connective tissue	High+Lowthroughput	Let-7e inhibits TNF-α expression by targeting the methyl transferase EZH2 in DENV2-infected THP-1 cells	否	无	nothing	THP-1 cells	E_01_0474	Western blot,Immunofluorescence assay,qRT-PCR,ELISA,Luciferase reporter assay,iTRAQ,miRNA or siRNA transfection,EZH2 knockdown,Smad3 knockdown	More importantly, we revealed that siEZH2 down-regulated NF-κB p65 within the nucleus. These findings indicate that the let-7e/EZH2/H3K27me3/NF-κB p65 pathway is a novel regulatory axis of TNFα expression. In addition, we determined the protein differences between siEZH2 and siEZH2-NC by iTRAQ and found a number of proteins that might be associated with TNFα.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	More importantly, we revealed that siEZH2 down-regulated NF-κB p65 within the nucleus. These findings indicate that the let-7e/EZH2/H3K27me3/NF-κB p65 pathway is a novel regulatory axis of TNFα expression. In addition, we determined the protein differences between siEZH2 and siEZH2-NC by iTRAQ and found a number of proteins that might be associated with TNFα.		More importantly, we revealed that siEZH2 down-regulated NF-κB p65 within the nucleus. These findings indicate that the let-7e/EZH2/H3K27me3/NF-κB p65 pathway is a novel regulatory axis of TNFα expression. In addition, we determined the protein differences between siEZH2 and siEZH2-NC by iTRAQ and found a number of proteins that might be associated with TNFα.	Immunohistochemical staining	More importantly, we revealed that siEZH2 down-regulated NF-κB p65 within the nucleus. These findings indicate that the let-7e/EZH2/H3K27me3/NF-κB p65 pathway is a novel regulatory axis of TNFα expression. In addition, we determined the protein differences between siEZH2 and siEZH2-NC by iTRAQ and found a number of proteins that might be associated with TNFα.			Western blot,Immunofluorescence assay,qRT-PCR,ELISA,Luciferase reporter assay,iTRAQ,miRNA or siRNA transfection,EZH2 knockdown,Smad3 knockdown				Smad3
29768212	chr1	186669486	186671486	PTGS2	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	human	Synovial tissue	High+Lowthroughput	mTOR Senses Environmental Cues to Shape the Fibroblast-like Synoviocyte Response to Inflammation	否	无	Inflammation, rheumatoid arthritis (RA)		E_01_0475	Immunohistochemistry,Western Blot,qPCR,ELISA,EMSA,siRNA-Mediated Knockdown,Immunofluorescence Staining,Automated Imaging	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	Immunohistochemical staining	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	PTGS2		Immunohistochemistry,Western Blot,qPCR,ELISA,EMSA,siRNA-Mediated Knockdown,Immunofluorescence Staining,Automated Imaging	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).			
29768212	chr2	190905705	190907705	STAT1	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	human	Synovial tissue	High+Lowthroughput	mTOR Senses Environmental Cues to Shape the Fibroblast-like Synoviocyte Response to Inflammation	否	无	Inflammation, rheumatoid arthritis (RA)		E_01_0475	Immunohistochemistry,Western Blot,qPCR,ELISA,EMSA,siRNA-Mediated Knockdown,Immunofluorescence Staining,Automated Imaging	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	Immunohistochemical staining	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	STAT1		Immunohistochemistry,Western Blot,qPCR,ELISA,EMSA,siRNA-Mediated Knockdown,Immunofluorescence Staining,Automated Imaging	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).			
29768212	chr4	76030740	76032740	CXCL11	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	human	Synovial tissue	High+Lowthroughput	mTOR Senses Environmental Cues to Shape the Fibroblast-like Synoviocyte Response to Inflammation	否	无	Inflammation, rheumatoid arthritis (RA)		E_01_0475	Immunohistochemistry,Western Blot,qPCR,ELISA,EMSA,siRNA-Mediated Knockdown,Immunofluorescence Staining,Automated Imaging	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).		mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	Immunohistochemical staining	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).			Immunohistochemistry,Western Blot,qPCR,ELISA,EMSA,siRNA-Mediated Knockdown,Immunofluorescence Staining,Automated Imaging				CXCL11
29768212	chr13	108248345	108250345	TNFSF13B	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	human	Synovial tissue	High+Lowthroughput	mTOR Senses Environmental Cues to Shape the Fibroblast-like Synoviocyte Response to Inflammation	否	无	Inflammation, rheumatoid arthritis (RA)		E_01_0475	Immunohistochemistry,Western Blot,qPCR,ELISA,EMSA,siRNA-Mediated Knockdown,Immunofluorescence Staining,Automated Imaging	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).		mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).	Immunohistochemical staining	mTOR pathway activation is associated with decreased NF-κB-mediated gene expression (e.g., PTGS2, IL-6, and IL-8) but increased STAT1-dependent gene expression (e.g., CXCL11 and TNFSF13B). We further demonstrate how metabolic inputs, such as amino acids, impinge on TNF-mTORC1 signaling to differentially regulate pro-inflammatory signaling circuits. Our results define a critical role for mTOR in the regulation of the pro-inflammatory response in FLSs and unfold its pathogenic involvement in TNF-driven diseases, such as rheumatoid arthritis (RA).			Immunohistochemistry,Western Blot,qPCR,ELISA,EMSA,siRNA-Mediated Knockdown,Immunofluorescence Staining,Automated Imaging				TNFSF13B
29768199	chr14	21382478	21384478	CHD8		human	adipose tissue	High+Lowthroughput	The Autism-Related Protein CHD8 Cooperates with C/EBPβ to Regulate Adipogenesis	否	无	Autism spectrum disorder (ASD)	preadipocyte	E_01_0476	transgenic mice,RNA Interference,Luciferase Assay,RT-PCR,Real-Time PCR Analysis,Transfection,Immunoblot Analysis,Immunoprecipitation,ChIP,FAIRE,ChIP-Seq,RNA-Seq,Histopathology		Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq				Immunohistochemical staining				transgenic mice,RNA Interference,Luciferase Assay,RT-PCR,Real-Time PCR Analysis,Transfection,Immunoblot Analysis,Immunoprecipitation,ChIP,FAIRE,ChIP-Seq,RNA-Seq,Histopathology				CHD8
29766758	chr11	112140806	112142806	IL18	Furthermore, NBD stimulates bone formation in BMP-2-mediated spinal fusion, possibly through crosstalk of the NF-κB pathway with other pathways. The results of this study might provide the basis to develop new therapeutic bone grafting approaches with combinatory administration of BMP-2 and NBD for spinal fusion.	mouse	Nervous tissue	High+Lowthroughput	Anti-Inflammatory Peptide Attenuates Edema and Promotes BMP-2-Induced Bone Formation in Spine Fusion	否	无	inflammation	fibroblast	E_02_0305	DNA binding activity,RT-PCR,hematoxylin/eosin (H&E) staining,	Furthermore, NBD stimulates bone formation in BMP-2-mediated spinal fusion, possibly through crosstalk of the NF-κB pathway with other pathways. The results of this study might provide the basis to develop new therapeutic bone grafting approaches with combinatory administration of BMP-2 and NBD for spinal fusion.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, NBD stimulates bone formation in BMP-2-mediated spinal fusion, possibly through crosstalk of the NF-κB pathway with other pathways. The results of this study might provide the basis to develop new therapeutic bone grafting approaches with combinatory administration of BMP-2 and NBD for spinal fusion.		Furthermore, NBD stimulates bone formation in BMP-2-mediated spinal fusion, possibly through crosstalk of the NF-κB pathway with other pathways. The results of this study might provide the basis to develop new therapeutic bone grafting approaches with combinatory administration of BMP-2 and NBD for spinal fusion.	Immunohistochemical staining	Furthermore, NBD stimulates bone formation in BMP-2-mediated spinal fusion, possibly through crosstalk of the NF-κB pathway with other pathways. The results of this study might provide the basis to develop new therapeutic bone grafting approaches with combinatory administration of BMP-2 and NBD for spinal fusion.			DNA binding activity,RT-PCR,hematoxylin/eosin (H&E) staining,				IL18
29765957	chr16	67559780	67561780	CTCF	The prevalence of four SNPs (rs1324192, rs7019262, rs518054, and rs571221) risk alleles haplotype in this region was significantly higher (compared with other haplotypes) in frail older adults compared with non-frail older adults (29.7 vs. 20.8%, p = 0.0005, respectively). Functional analyses using in silico approaches placed rs518054 in the CTCF binding site as well as DNase hypersensitive region. Furthermore, rs518054 was found to be in an enhancer site of NFIB gene located downstream. NFIB is a transcription factor that promotes cell differentiation during development, has antiapoptotic effect, maintains stem cell populations in adult tissues, and also acts as epigenetic regulators. Our study found novel association of SNPs in the regulatory region in the 9p21-23 region with the frailty phenotype; signifying the importance of this locus in aging.	human	Epithelial tissues	High+Lowthroughput	Genetic Insights Into Frailty: Association of 9p21-23 Locus With Frailty	是	rs1324192,rs7019262,rs518054,rs571221	Frailty, aging		E_01_0477	WGS	The prevalence of four SNPs (rs1324192, rs7019262, rs518054, and rs571221) risk alleles haplotype in this region was significantly higher (compared with other haplotypes) in frail older adults compared with non-frail older adults (29.7 vs. 20.8%, p = 0.0005, respectively). Functional analyses using in silico approaches placed rs518054 in the CTCF binding site as well as DNase hypersensitive region. Furthermore, rs518054 was found to be in an enhancer site of NFIB gene located downstream. NFIB is a transcription factor that promotes cell differentiation during development, has antiapoptotic effect, maintains stem cell populations in adult tissues, and also acts as epigenetic regulators. Our study found novel association of SNPs in the regulatory region in the 9p21-23 region with the frailty phenotype; signifying the importance of this locus in aging.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The prevalence of four SNPs (rs1324192, rs7019262, rs518054, and rs571221) risk alleles haplotype in this region was significantly higher (compared with other haplotypes) in frail older adults compared with non-frail older adults (29.7 vs. 20.8%, p = 0.0005, respectively). Functional analyses using in silico approaches placed rs518054 in the CTCF binding site as well as DNase hypersensitive region. Furthermore, rs518054 was found to be in an enhancer site of NFIB gene located downstream. NFIB is a transcription factor that promotes cell differentiation during development, has antiapoptotic effect, maintains stem cell populations in adult tissues, and also acts as epigenetic regulators. Our study found novel association of SNPs in the regulatory region in the 9p21-23 region with the frailty phenotype; signifying the importance of this locus in aging.	Immunohistochemical staining	The prevalence of four SNPs (rs1324192, rs7019262, rs518054, and rs571221) risk alleles haplotype in this region was significantly higher (compared with other haplotypes) in frail older adults compared with non-frail older adults (29.7 vs. 20.8%, p = 0.0005, respectively). Functional analyses using in silico approaches placed rs518054 in the CTCF binding site as well as DNase hypersensitive region. Furthermore, rs518054 was found to be in an enhancer site of NFIB gene located downstream. NFIB is a transcription factor that promotes cell differentiation during development, has antiapoptotic effect, maintains stem cell populations in adult tissues, and also acts as epigenetic regulators. Our study found novel association of SNPs in the regulatory region in the 9p21-23 region with the frailty phenotype; signifying the importance of this locus in aging.	CTCF		WGS	The prevalence of four SNPs (rs1324192, rs7019262, rs518054, and rs571221) risk alleles haplotype in this region was significantly higher (compared with other haplotypes) in frail older adults compared with non-frail older adults (29.7 vs. 20.8%, p = 0.0005, respectively). Functional analyses using in silico approaches placed rs518054 in the CTCF binding site as well as DNase hypersensitive region. Furthermore, rs518054 was found to be in an enhancer site of NFIB gene located downstream. NFIB is a transcription factor that promotes cell differentiation during development, has antiapoptotic effect, maintains stem cell populations in adult tissues, and also acts as epigenetic regulators. Our study found novel association of SNPs in the regulatory region in the 9p21-23 region with the frailty phenotype; signifying the importance of this locus in aging.			
29765957	chr9	14078899	14080899	NFIB	The prevalence of four SNPs (rs1324192, rs7019262, rs518054, and rs571221) risk alleles haplotype in this region was significantly higher (compared with other haplotypes) in frail older adults compared with non-frail older adults (29.7 vs. 20.8%, p = 0.0005, respectively). Functional analyses using in silico approaches placed rs518054 in the CTCF binding site as well as DNase hypersensitive region. Furthermore, rs518054 was found to be in an enhancer site of NFIB gene located downstream. NFIB is a transcription factor that promotes cell differentiation during development, has antiapoptotic effect, maintains stem cell populations in adult tissues, and also acts as epigenetic regulators. Our study found novel association of SNPs in the regulatory region in the 9p21-23 region with the frailty phenotype; signifying the importance of this locus in aging.	human	Epithelial tissues	High+Lowthroughput	Genetic Insights Into Frailty: Association of 9p21-23 Locus With Frailty	是	rs1324192,rs7019262,rs518054,rs571221	Frailty, aging		E_01_0477	WGS	The prevalence of four SNPs (rs1324192, rs7019262, rs518054, and rs571221) risk alleles haplotype in this region was significantly higher (compared with other haplotypes) in frail older adults compared with non-frail older adults (29.7 vs. 20.8%, p = 0.0005, respectively). Functional analyses using in silico approaches placed rs518054 in the CTCF binding site as well as DNase hypersensitive region. Furthermore, rs518054 was found to be in an enhancer site of NFIB gene located downstream. NFIB is a transcription factor that promotes cell differentiation during development, has antiapoptotic effect, maintains stem cell populations in adult tissues, and also acts as epigenetic regulators. Our study found novel association of SNPs in the regulatory region in the 9p21-23 region with the frailty phenotype; signifying the importance of this locus in aging.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The prevalence of four SNPs (rs1324192, rs7019262, rs518054, and rs571221) risk alleles haplotype in this region was significantly higher (compared with other haplotypes) in frail older adults compared with non-frail older adults (29.7 vs. 20.8%, p = 0.0005, respectively). Functional analyses using in silico approaches placed rs518054 in the CTCF binding site as well as DNase hypersensitive region. Furthermore, rs518054 was found to be in an enhancer site of NFIB gene located downstream. NFIB is a transcription factor that promotes cell differentiation during development, has antiapoptotic effect, maintains stem cell populations in adult tissues, and also acts as epigenetic regulators. Our study found novel association of SNPs in the regulatory region in the 9p21-23 region with the frailty phenotype; signifying the importance of this locus in aging.		The prevalence of four SNPs (rs1324192, rs7019262, rs518054, and rs571221) risk alleles haplotype in this region was significantly higher (compared with other haplotypes) in frail older adults compared with non-frail older adults (29.7 vs. 20.8%, p = 0.0005, respectively). Functional analyses using in silico approaches placed rs518054 in the CTCF binding site as well as DNase hypersensitive region. Furthermore, rs518054 was found to be in an enhancer site of NFIB gene located downstream. NFIB is a transcription factor that promotes cell differentiation during development, has antiapoptotic effect, maintains stem cell populations in adult tissues, and also acts as epigenetic regulators. Our study found novel association of SNPs in the regulatory region in the 9p21-23 region with the frailty phenotype; signifying the importance of this locus in aging.	Immunohistochemical staining	The prevalence of four SNPs (rs1324192, rs7019262, rs518054, and rs571221) risk alleles haplotype in this region was significantly higher (compared with other haplotypes) in frail older adults compared with non-frail older adults (29.7 vs. 20.8%, p = 0.0005, respectively). Functional analyses using in silico approaches placed rs518054 in the CTCF binding site as well as DNase hypersensitive region. Furthermore, rs518054 was found to be in an enhancer site of NFIB gene located downstream. NFIB is a transcription factor that promotes cell differentiation during development, has antiapoptotic effect, maintains stem cell populations in adult tissues, and also acts as epigenetic regulators. Our study found novel association of SNPs in the regulatory region in the 9p21-23 region with the frailty phenotype; signifying the importance of this locus in aging.			WGS				NFIB
29765866	chr6	31572670	31574670	TNF	These results suggest that the endosulfan isomers have some capacity to alter inflammatory responses differentially, particularly with IFN-γ stimulation.	mouse	lymphoid tissue	High+Lowthroughput	Effects of endosulfan isomers on cytokine and nitric oxide production by differentially activated RAW 264.7 cells	否	无	inflammation	RAW 264.7 CELLS	E_02_0306	Cytotoxicity assays,Nitrite assays,ELISAs	These results suggest that the endosulfan isomers have some capacity to alter inflammatory responses differentially, particularly with IFN-γ stimulation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that the endosulfan isomers have some capacity to alter inflammatory responses differentially, particularly with IFN-γ stimulation.		These results suggest that the endosulfan isomers have some capacity to alter inflammatory responses differentially, particularly with IFN-γ stimulation.	Immunohistochemical staining	These results suggest that the endosulfan isomers have some capacity to alter inflammatory responses differentially, particularly with IFN-γ stimulation.			Cytotoxicity assays,Nitrite assays,ELISAs				TNF
29765516	chr21	40003867	40015913	GFI1B	Collectively, the selective separation of LSD1 from GFI1B by NCD38 restores the ERG super-enhancer activation and consequently upregulates ERG expression, inducing the transdifferentiation linked to the anti-leukemia effect.	human	connective tissue	Low+High throughput	Selective dissociation between LSD1 and GFI1B by a LSD1 inhibitor NCD38 induces the activation of ERG super-enhancer in erythroleukemia cells	否	--	Leukemia	HEL cell 	E_02_0307	ChIP-qPCR,ChIP-seq	Chromatin-immunoprecipitation followed by quantitative PCR (ChIP-qPCR) analysis for GFI1B and RUNX1 was performed at highly conserved noncoding areas including upstream, promotor, 3’ UTR, and SE regions.	Super-Enhancer	--	ChIP-qPCR	Furthermore,ChIP-qPCR analysis for H3K27ac revealed that the level of H3K27ac was elevated only at the SE region after the NCD38 treatment.	erg-3,p55	--	--	--	GFI1B,RUNX1,KDM1A	BDPLT17,ZNF163B,AML1, AML1-EVI-1, AMLCR1, CBF2alpha, CBFA2, EVI-1, PEBP2aB, PEBP2alpha,AOF2, BHC110, CPRF, KDM1, LSD1	ChIP-qPCR	ChIP-qPCR analysis for GFI1B, RUNX1, or control IgG in the conserved non-coding regions at the ERG locus in HEL cells.ChIP-qPCR analysis for GFI1B (C), LSD1 (D), and CoREST (E) at the ERG-SE locus in HEL cells treated with DMSO or NCD38 for 24 hours. All ChIP-qPCR assays were performed independently twice and the means are displayed.	--	--	ERG
29765516	chr21	40003867	40015913	RUNX1	Collectively, the selective separation of LSD1 from GFI1B by NCD38 restores the ERG super-enhancer activation and consequently upregulates ERG expression, inducing the transdifferentiation linked to the anti-leukemia effect.	human	connective tissue	Low+High throughput	Selective dissociation between LSD1 and GFI1B by a LSD1 inhibitor NCD38 induces the activation of ERG super-enhancer in erythroleukemia cells	否	--	Leukemia	HEL cell 	E_02_0307	ChIP-qPCR,ChIP-seq	Chromatin-immunoprecipitation followed by quantitative PCR (ChIP-qPCR) analysis for GFI1B and RUNX1 was performed at highly conserved noncoding areas including upstream, promotor, 3’ UTR, and SE regions.	Super-Enhancer	--	ChIP-qPCR	Furthermore,ChIP-qPCR analysis for H3K27ac revealed that the level of H3K27ac was elevated only at the SE region after the NCD38 treatment.	erg-3,p55	--	--	--	GFI1B,RUNX1,KDM1A	BDPLT17,ZNF163B,AML1, AML1-EVI-1, AMLCR1, CBF2alpha, CBFA2, EVI-1, PEBP2aB, PEBP2alpha,AOF2, BHC110, CPRF, KDM1, LSD1	ChIP-qPCR	ChIP-qPCR analysis for GFI1B, RUNX1, or control IgG in the conserved non-coding regions at the ERG locus in HEL cells.ChIP-qPCR analysis for GFI1B (C), LSD1 (D), and CoREST (E) at the ERG-SE locus in HEL cells treated with DMSO or NCD38 for 24 hours. All ChIP-qPCR assays were performed independently twice and the means are displayed.	--	--	ERG
29765516	chr21	40003867	40015913	HDAC1	Collectively, the selective separation of LSD1 from GFI1B by NCD38 restores the ERG super-enhancer activation and consequently upregulates ERG expression, inducing the transdifferentiation linked to the anti-leukemia effect.	human	connective tissue	Low+High throughput	Selective dissociation between LSD1 and GFI1B by a LSD1 inhibitor NCD38 induces the activation of ERG super-enhancer in erythroleukemia cells	否	--	Leukemia	HEL cell 	E_02_0307	ChIP-qPCR,ChIP-seq	Chromatin-immunoprecipitation followed by quantitative PCR (ChIP-qPCR) analysis for GFI1B and RUNX1 was performed at highly conserved noncoding areas including upstream, promotor, 3’ UTR, and SE regions.	Super-Enhancer	--	ChIP-qPCR	Furthermore,ChIP-qPCR analysis for H3K27ac revealed that the level of H3K27ac was elevated only at the SE region after the NCD38 treatment.	erg-3,p55	--	--	--	GFI1B,RUNX1,KDM1A	BDPLT17,ZNF163B,AML1, AML1-EVI-1, AMLCR1, CBF2alpha, CBFA2, EVI-1, PEBP2aB, PEBP2alpha,AOF2, BHC110, CPRF, KDM1, LSD1	ChIP-qPCR	ChIP-qPCR analysis for GFI1B, RUNX1, or control IgG in the conserved non-coding regions at the ERG locus in HEL cells.ChIP-qPCR analysis for GFI1B (C), LSD1 (D), and CoREST (E) at the ERG-SE locus in HEL cells treated with DMSO or NCD38 for 24 hours. All ChIP-qPCR assays were performed independently twice and the means are displayed.	--	--	ERG
29765516	chr21	40003867	40015913	HDAC2	Collectively, the selective separation of LSD1 from GFI1B by NCD38 restores the ERG super-enhancer activation and consequently upregulates ERG expression, inducing the transdifferentiation linked to the anti-leukemia effect.	human	connective tissue	Low+High throughput	Selective dissociation between LSD1 and GFI1B by a LSD1 inhibitor NCD38 induces the activation of ERG super-enhancer in erythroleukemia cells	否	--	Leukemia	HEL cell 	E_02_0307	ChIP-qPCR,ChIP-seq	Chromatin-immunoprecipitation followed by quantitative PCR (ChIP-qPCR) analysis for GFI1B and RUNX1 was performed at highly conserved noncoding areas including upstream, promotor, 3’ UTR, and SE regions.	Super-Enhancer	--	ChIP-qPCR	Furthermore,ChIP-qPCR analysis for H3K27ac revealed that the level of H3K27ac was elevated only at the SE region after the NCD38 treatment.	erg-3,p55	--	--	--	GFI1B,RUNX1,KDM1A	BDPLT17,ZNF163B,AML1, AML1-EVI-1, AMLCR1, CBF2alpha, CBFA2, EVI-1, PEBP2aB, PEBP2alpha,AOF2, BHC110, CPRF, KDM1, LSD1	ChIP-qPCR	ChIP-qPCR analysis for GFI1B, RUNX1, or control IgG in the conserved non-coding regions at the ERG locus in HEL cells.ChIP-qPCR analysis for GFI1B (C), LSD1 (D), and CoREST (E) at the ERG-SE locus in HEL cells treated with DMSO or NCD38 for 24 hours. All ChIP-qPCR assays were performed independently twice and the means are displayed.	--	--	ERG
29763375	chr12	56268405	56270405	CS	Thus, pre-pregnancy maternal obesity disrupts the placental hGH/CS gene locus chromosomal architecture. However, based on data from obese women who develop GDM, insulin treatment partially recapitulates the chromosomal architecture seen in lean women and positively affects hCS production, presumably facilitating prolactin receptor-related signaling by hCS.	human	Placental tissue	High+Lowthroughput	Chromosomal architecture and placental expression of the human growth hormone gene family are targeted by pre-pregnancy maternal obesity	否	无	Obesity		E_01_0478	Real-time reverse transcription-polymerase chain reaction,protein immunoblotting,Enzyme-linked immunosorbent assay (ELISA),Chromosome conformation capture (3C) assay,Amplicon sequencing,bioinformatics, Chromatin immunoprecipitation (ChIP) assay	Thus, pre-pregnancy maternal obesity disrupts the placental hGH/CS gene locus chromosomal architecture. However, based on data from obese women who develop GDM, insulin treatment partially recapitulates the chromosomal architecture seen in lean women and positively affects hCS production, presumably facilitating prolactin receptor-related signaling by hCS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, pre-pregnancy maternal obesity disrupts the placental hGH/CS gene locus chromosomal architecture. However, based on data from obese women who develop GDM, insulin treatment partially recapitulates the chromosomal architecture seen in lean women and positively affects hCS production, presumably facilitating prolactin receptor-related signaling by hCS.		Thus, pre-pregnancy maternal obesity disrupts the placental hGH/CS gene locus chromosomal architecture. However, based on data from obese women who develop GDM, insulin treatment partially recapitulates the chromosomal architecture seen in lean women and positively affects hCS production, presumably facilitating prolactin receptor-related signaling by hCS.	Immunohistochemical staining	Thus, pre-pregnancy maternal obesity disrupts the placental hGH/CS gene locus chromosomal architecture. However, based on data from obese women who develop GDM, insulin treatment partially recapitulates the chromosomal architecture seen in lean women and positively affects hCS production, presumably facilitating prolactin receptor-related signaling by hCS.			Real-time reverse transcription-polymerase chain reaction,protein immunoblotting,Enzyme-linked immunosorbent assay (ELISA),Chromosome conformation capture (3C) assay,Amplicon sequencing,bioinformatics, Chromatin immunoprecipitation (ChIP) assay				CS
29762844	chr9	117701608	117703608	TLR4	TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.	human	connective tissue	High+Lowthroughput	Free fatty acids mediates human umbilical vein endothelial cells inflammation through toll-like receptor-4	否	无	Inflammation in HUVECs	HEK293 cell	E_01_0479	Flow Cytometry,ELISA,qPCR,Western Blot,Cell Apoptosis Assay,Viability Assay	TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.	Immunohistochemical staining	TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.	TLR4		Flow Cytometry,ELISA,qPCR,Western Blot,Cell Apoptosis Assay,Viability Assay	TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.			
29762844	chr17	35868626	35870626	CCL5	TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.	human	connective tissue	High+Lowthroughput	Free fatty acids mediates human umbilical vein endothelial cells inflammation through toll-like receptor-4	否	无	Inflammation in HUVECs	HEK293 cell	E_01_0479	Flow Cytometry,ELISA,qPCR,Western Blot,Cell Apoptosis Assay,Viability Assay	TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.	Immunohistochemical staining	TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.	CCL5		Flow Cytometry,ELISA,qPCR,Western Blot,Cell Apoptosis Assay,Viability Assay	TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.			
29762844	chr4	76018879	76020879	CXCL10	TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.	human	connective tissue	High+Lowthroughput	Free fatty acids mediates human umbilical vein endothelial cells inflammation through toll-like receptor-4	否	无	Inflammation in HUVECs	HEK293 cell	E_01_0479	Flow Cytometry,ELISA,qPCR,Western Blot,Cell Apoptosis Assay,Viability Assay	TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.	Immunohistochemical staining	TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.	CXCL10		Flow Cytometry,ELISA,qPCR,Western Blot,Cell Apoptosis Assay,Viability Assay	TLR4 mediates FFAs induced inflammatory responses in HUVECs. TLR4 interference in HUVECs significantly reduces the inflammatory cytokines expression, decreases the cell apoptosis rate and increases cell viability.			
29761871	chr18	63121195	63123195	BCL2	Autophagy was suppressed in the PNALD model, which was demonstrated by less light chain 3 fluorescence (LC3) puncta and lower LC3II expression. Rapamycin effectively induced hepatic autophagy in PN rats. The PN + Rapa group presented improved hepatic function, decreased pathology scores, and less steatosis than the PN group. In addition, rapamycin treatment decreased terminal deoxynucleotidyl transferase dUTP nick end labeling and cleaved-caspase 3 expression, indicating a lower level of hepatocyte apoptosis. Compared with the PN group, the PN + Rapa group had lower levels of ROS and reduced expression of ER stress-related protein markers, such as BIP, sXBP1 and CHOP.	mouse	Liver tissue	High+Lowthroughput	Autophagy May Protect Against Parenteral Nutrition-Associated Liver Disease by Suppressing Endoplasmic Reticulum Stress	否	无	Parenteral nutrition (PN) - associated liver disease (PNALD)	LC3 cell 	E_02_0308	Immunofluorescence staining,Oil red staining,Immunohistochemistry,TUNEL staining,Western blot	Autophagy was suppressed in the PNALD model, which was demonstrated by less light chain 3 fluorescence (LC3) puncta and lower LC3II expression. Rapamycin effectively induced hepatic autophagy in PN rats. The PN + Rapa group presented improved hepatic function, decreased pathology scores, and less steatosis than the PN group. In addition, rapamycin treatment decreased terminal deoxynucleotidyl transferase dUTP nick end labeling and cleaved-caspase 3 expression, indicating a lower level of hepatocyte apoptosis. Compared with the PN group, the PN + Rapa group had lower levels of ROS and reduced expression of ER stress-related protein markers, such as BIP, sXBP1 and CHOP.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Autophagy was suppressed in the PNALD model, which was demonstrated by less light chain 3 fluorescence (LC3) puncta and lower LC3II expression. Rapamycin effectively induced hepatic autophagy in PN rats. The PN + Rapa group presented improved hepatic function, decreased pathology scores, and less steatosis than the PN group. In addition, rapamycin treatment decreased terminal deoxynucleotidyl transferase dUTP nick end labeling and cleaved-caspase 3 expression, indicating a lower level of hepatocyte apoptosis. Compared with the PN group, the PN + Rapa group had lower levels of ROS and reduced expression of ER stress-related protein markers, such as BIP, sXBP1 and CHOP.		Autophagy was suppressed in the PNALD model, which was demonstrated by less light chain 3 fluorescence (LC3) puncta and lower LC3II expression. Rapamycin effectively induced hepatic autophagy in PN rats. The PN + Rapa group presented improved hepatic function, decreased pathology scores, and less steatosis than the PN group. In addition, rapamycin treatment decreased terminal deoxynucleotidyl transferase dUTP nick end labeling and cleaved-caspase 3 expression, indicating a lower level of hepatocyte apoptosis. Compared with the PN group, the PN + Rapa group had lower levels of ROS and reduced expression of ER stress-related protein markers, such as BIP, sXBP1 and CHOP.	Immunohistochemical staining	Autophagy was suppressed in the PNALD model, which was demonstrated by less light chain 3 fluorescence (LC3) puncta and lower LC3II expression. Rapamycin effectively induced hepatic autophagy in PN rats. The PN + Rapa group presented improved hepatic function, decreased pathology scores, and less steatosis than the PN group. In addition, rapamycin treatment decreased terminal deoxynucleotidyl transferase dUTP nick end labeling and cleaved-caspase 3 expression, indicating a lower level of hepatocyte apoptosis. Compared with the PN group, the PN + Rapa group had lower levels of ROS and reduced expression of ER stress-related protein markers, such as BIP, sXBP1 and CHOP.			Immunofluorescence staining,Oil red staining,Immunohistochemistry,TUNEL staining,Western blot				BCL2
29761425	chr3	133743127	133745127	TF	All the results suggested that genistein has the function of alleviating and treating LPS-induced DIC by anti-inflammatory and anticoagulation effects. We tentatively propose that genistein is a potential drug for auxiliary treatment of DIC.	human	lymphoid tissue	High+Lowthroughput	Genistein has the function of alleviating and treating disseminated intravascular coagulation caused by lipopolysaccharide	否	无	Disseminated intravascular coagulation (DIC)	 RAW 264.7	E_01_0480	Western blot, H&E staining,PTAH staining,MTT	All the results suggested that genistein has the function of alleviating and treating LPS-induced DIC by anti-inflammatory and anticoagulation effects. We tentatively propose that genistein is a potential drug for auxiliary treatment of DIC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	All the results suggested that genistein has the function of alleviating and treating LPS-induced DIC by anti-inflammatory and anticoagulation effects. We tentatively propose that genistein is a potential drug for auxiliary treatment of DIC.		All the results suggested that genistein has the function of alleviating and treating LPS-induced DIC by anti-inflammatory and anticoagulation effects. We tentatively propose that genistein is a potential drug for auxiliary treatment of DIC.	Immunohistochemical staining	All the results suggested that genistein has the function of alleviating and treating LPS-induced DIC by anti-inflammatory and anticoagulation effects. We tentatively propose that genistein is a potential drug for auxiliary treatment of DIC.			Western blot, H&E staining,PTAH staining,MTT				TF
29761173	chr20	22578409	22580409	FOXA2	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	human	Liver tissue	High+Lowthroughput	Liver-enriched transcription factor expression relates to chronic hepatic failure in humans	否	无	Liver metastasis, primary hepatocellular carcinoma, decompensated cirrhosis	hepatocyte	E_01_0481	qRT-PCR,immunohistochemistry	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	Immunohistochemical staining	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	FOXA2		qRT-PCR,immunohistochemistry	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 			
29761173	chrX	38349842	38351842	OTC	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	human	Liver tissue	High+Lowthroughput	Liver-enriched transcription factor expression relates to chronic hepatic failure in humans	否	无	Liver metastasis, primary hepatocellular carcinoma, decompensated cirrhosis	hepatocyte	E_01_0481	qRT-PCR,immunohistochemistry	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 		HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	Immunohistochemical staining	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 			qRT-PCR,immunohistochemistry				OTC
29761173	chr7	99753931	99755931	CYP3A4	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	human	Liver tissue	High+Lowthroughput	Liver-enriched transcription factor expression relates to chronic hepatic failure in humans	否	无	Liver metastasis, primary hepatocellular carcinoma, decompensated cirrhosis	hepatocyte	E_01_0481	qRT-PCR,immunohistochemistry	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 		HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	Immunohistochemical staining	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 			qRT-PCR,immunohistochemistry				CYP3A4
29761173	chr13	113102930	113104930	F7	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	human	Liver tissue	High+Lowthroughput	Liver-enriched transcription factor expression relates to chronic hepatic failure in humans	否	无	Liver metastasis, primary hepatocellular carcinoma, decompensated cirrhosis	hepatocyte	E_01_0481	qRT-PCR,immunohistochemistry	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 		HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	Immunohistochemical staining	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 			qRT-PCR,immunohistochemistry				F7
29761173	chr12	57125468	57127468	LRP1	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	human	Liver tissue	High+Lowthroughput	Liver-enriched transcription factor expression relates to chronic hepatic failure in humans	否	无	Liver metastasis, primary hepatocellular carcinoma, decompensated cirrhosis	hepatocyte	E_01_0481	qRT-PCR,immunohistochemistry	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 		HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 	Immunohistochemical staining	HNF4α and other members of the LETFs appear to be important regulators of hepatocyte function in patients with chronic hepatic failure. 			qRT-PCR,immunohistochemistry				LRP1
29760797	chr11	8221840	8223840	LMO1	In summary, the current study confirmed that the potentially functional LMO1 rs2168101 G>T and rs3750952 G>C polymorphisms were associated with neuroblastoma susceptibility. This research requires further validation with larger sample sizes and inclusion of different ethnicities.	human	lymphoid tissue	High+Lowthroughput	LMO1 super-enhancer polymorphism rs2168101 G>T correlates with decreased neuroblastoma risk in Chinese children	是	rs2168101,rs3750952	Neuroblastoma	lymphocyte	E_01_0482	RNA-seq	In summary, the current study confirmed that the potentially functional LMO1 rs2168101 G>T and rs3750952 G>C polymorphisms were associated with neuroblastoma susceptibility. This research requires further validation with larger sample sizes and inclusion of different ethnicities.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In summary, the current study confirmed that the potentially functional LMO1 rs2168101 G>T and rs3750952 G>C polymorphisms were associated with neuroblastoma susceptibility. This research requires further validation with larger sample sizes and inclusion of different ethnicities.	Immunohistochemical staining	In summary, the current study confirmed that the potentially functional LMO1 rs2168101 G>T and rs3750952 G>C polymorphisms were associated with neuroblastoma susceptibility. This research requires further validation with larger sample sizes and inclusion of different ethnicities.	LMO1		RNA-seq	In summary, the current study confirmed that the potentially functional LMO1 rs2168101 G>T and rs3750952 G>C polymorphisms were associated with neuroblastoma susceptibility. This research requires further validation with larger sample sizes and inclusion of different ethnicities.			
29760797	chr10	88950867	88952867	FAS	In summary, the current study confirmed that the potentially functional LMO1 rs2168101 G>T and rs3750952 G>C polymorphisms were associated with neuroblastoma susceptibility. This research requires further validation with larger sample sizes and inclusion of different ethnicities.	human	lymphoid tissue	High+Lowthroughput	LMO1 super-enhancer polymorphism rs2168101 G>T correlates with decreased neuroblastoma risk in Chinese children	是	rs2168101,rs3750952	Neuroblastoma	lymphocyte	E_01_0482	RNA-seq	In summary, the current study confirmed that the potentially functional LMO1 rs2168101 G>T and rs3750952 G>C polymorphisms were associated with neuroblastoma susceptibility. This research requires further validation with larger sample sizes and inclusion of different ethnicities.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In summary, the current study confirmed that the potentially functional LMO1 rs2168101 G>T and rs3750952 G>C polymorphisms were associated with neuroblastoma susceptibility. This research requires further validation with larger sample sizes and inclusion of different ethnicities.	Immunohistochemical staining	In summary, the current study confirmed that the potentially functional LMO1 rs2168101 G>T and rs3750952 G>C polymorphisms were associated with neuroblastoma susceptibility. This research requires further validation with larger sample sizes and inclusion of different ethnicities.	FAS		RNA-seq	In summary, the current study confirmed that the potentially functional LMO1 rs2168101 G>T and rs3750952 G>C polymorphisms were associated with neuroblastoma susceptibility. This research requires further validation with larger sample sizes and inclusion of different ethnicities.			
29760677	chr22	39516870	39518870	ATF4	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	mouse	adipose tissue	High+Lowthroughput	One-Week Exposure to a Free-Choice High-Fat High-Sugar Diet Does Not Interfere With the Lipopolysaccharide-Induced Acute Phase Response in the Hypothalamus of Male Rats	否	无	Obesity, low-grade hypothalamic inflammation	fat cell	E_02_0309	Western blot,RT-PCR,	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.		Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	Immunohistochemical staining	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.			Western blot,RT-PCR,				ATF4
29760677	chr12	55533292	55535292	Nfkbia	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	mouse	adipose tissue	High+Lowthroughput	One-Week Exposure to a Free-Choice High-Fat High-Sugar Diet Does Not Interfere With the Lipopolysaccharide-Induced Acute Phase Response in the Hypothalamus of Male Rats	否	无	Obesity, low-grade hypothalamic inflammation	fat cell	E_02_0309	Western blot,RT-PCR,	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.		Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	Immunohistochemical staining	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.			Western blot,RT-PCR,				Nfkbia
29760677	chr9	117701291	117703291	TLR4	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	mouse	adipose tissue	High+Lowthroughput	One-Week Exposure to a Free-Choice High-Fat High-Sugar Diet Does Not Interfere With the Lipopolysaccharide-Induced Acute Phase Response in the Hypothalamus of Male Rats	否	无	Obesity, low-grade hypothalamic inflammation	fat cell	E_02_0309	Western blot,RT-PCR,	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.		Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	Immunohistochemical staining	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.			Western blot,RT-PCR,				TLR4
29760677	chr11	117853920	117855920	Socs3	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	mouse	adipose tissue	High+Lowthroughput	One-Week Exposure to a Free-Choice High-Fat High-Sugar Diet Does Not Interfere With the Lipopolysaccharide-Induced Acute Phase Response in the Hypothalamus of Male Rats	否	无	Obesity, low-grade hypothalamic inflammation	fat cell	E_02_0309	Western blot,RT-PCR,	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.		Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	Immunohistochemical staining	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.			Western blot,RT-PCR,				Socs3
29760677	chr14	35398907	35400907	NFKBIA	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	mouse	adipose tissue	High+Lowthroughput	One-Week Exposure to a Free-Choice High-Fat High-Sugar Diet Does Not Interfere With the Lipopolysaccharide-Induced Acute Phase Response in the Hypothalamus of Male Rats	否	无	Obesity, low-grade hypothalamic inflammation	fat cell	E_02_0309	Western blot,RT-PCR,	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.		Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.	Immunohistochemical staining	Our study does not support a role for diet-induced mild hypothalamic inflammation in the increased susceptibility to infection despite altered Nfkbia and Socs3 mRNA expression after the diet. Additional factors, related to increased fat mass, might be involved.			Western blot,RT-PCR,				NFKBIA
29760402	chr15	39606417	39608417	Dcstamp	Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.	human	Nervous tissue	High+Lowthroughput	Roles of Enhancer RNAs in RANKL-induced Osteoclast Differentiation Identified by Genome-wide Cap-analysis of Gene Expression using CRISPR/Cas9	否	无	nothing		E_01_0483	qRT-PCR,TRAP staining,CRISPR/Cas9,Retroviral gene transfer,shRNA  transfection,CAGE,	Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.		Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.	Immunohistochemical staining	Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.			qRT-PCR,TRAP staining,CRISPR/Cas9,Retroviral gene transfer,shRNA  transfection,CAGE,				Dcstamp
29760402	chr18	80646704	80648704	Nfatc1	Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.	human	Nervous tissue	High+Lowthroughput	Roles of Enhancer RNAs in RANKL-induced Osteoclast Differentiation Identified by Genome-wide Cap-analysis of Gene Expression using CRISPR/Cas9	否	无	nothing		E_01_0483	qRT-PCR,TRAP staining,CRISPR/Cas9,Retroviral gene transfer,shRNA  transfection,CAGE,	Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.		Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.	Immunohistochemical staining	Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.			qRT-PCR,TRAP staining,CRISPR/Cas9,Retroviral gene transfer,shRNA  transfection,CAGE,				Nfatc1
29760402	chr1	62739677	62741677	Nrp2	Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.	human	Nervous tissue	High+Lowthroughput	Roles of Enhancer RNAs in RANKL-induced Osteoclast Differentiation Identified by Genome-wide Cap-analysis of Gene Expression using CRISPR/Cas9	否	无	nothing		E_01_0483	qRT-PCR,TRAP staining,CRISPR/Cas9,Retroviral gene transfer,shRNA  transfection,CAGE,	Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.		Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.	Immunohistochemical staining	Furthermore, osteoclast differentiation was impaired by targeted deletion of bidirectional eRNA regions. The combined results show that eRNAs play important roles in osteoclastogenic gene regulation, and may therefore provide novel insights to elucidate the transcriptional mechanisms that control osteoclast differentiation.			qRT-PCR,TRAP staining,CRISPR/Cas9,Retroviral gene transfer,shRNA  transfection,CAGE,				Nrp2
29760161	chr16	67559664	67561664	CTCF	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	human	connective tissue	High+Lowthroughput	CTCF boundary remodels chromatin domain and drives aberrant HOX gene transcription in acute myeloid leukemia	否	无	Acute myeloid leukemia (AML)	AML cell lines	E_01_0484	RNA,qRT-PCR,RNA-seq,ChIP,ChIP-seq,ATAC-seq,4C-seq,CRISPR/Cas9,	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	Immunohistochemical staining	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	CTCF		RNA,qRT-PCR,RNA-seq,ChIP,ChIP-seq,ATAC-seq,4C-seq,CRISPR/Cas9,	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.			
29760161	chr7	27150805	27152805	HOXA7	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	human	connective tissue	High+Lowthroughput	CTCF boundary remodels chromatin domain and drives aberrant HOX gene transcription in acute myeloid leukemia	否	无	Acute myeloid leukemia (AML)	AML cell lines	E_01_0484	RNA,qRT-PCR,RNA-seq,ChIP,ChIP-seq,ATAC-seq,4C-seq,CRISPR/Cas9,	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	Immunohistochemical staining	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	HOXA7		RNA,qRT-PCR,RNA-seq,ChIP,ChIP-seq,ATAC-seq,4C-seq,CRISPR/Cas9,	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.			
29760161	chr7	27159921	27161921	HOXA9	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	human	connective tissue	High+Lowthroughput	CTCF boundary remodels chromatin domain and drives aberrant HOX gene transcription in acute myeloid leukemia	否	无	Acute myeloid leukemia (AML)	AML cell lines	E_01_0484	RNA,qRT-PCR,RNA-seq,ChIP,ChIP-seq,ATAC-seq,4C-seq,CRISPR/Cas9,	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	Immunohistochemical staining	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	HOXA9		RNA,qRT-PCR,RNA-seq,ChIP,ChIP-seq,ATAC-seq,4C-seq,CRISPR/Cas9,	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.			
29760161	chr7	27190669	27192669	HOXA13	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	human	connective tissue	High+Lowthroughput	CTCF boundary remodels chromatin domain and drives aberrant HOX gene transcription in acute myeloid leukemia	否	无	Acute myeloid leukemia (AML)	AML cell lines	E_01_0484	RNA,qRT-PCR,RNA-seq,ChIP,ChIP-seq,ATAC-seq,4C-seq,CRISPR/Cas9,	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	Immunohistochemical staining	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.	HOXA13		RNA,qRT-PCR,RNA-seq,ChIP,ChIP-seq,ATAC-seq,4C-seq,CRISPR/Cas9,	Thus, the CTCF boundary constrains the normal gene-expression program, as well as plays a role in maintaining the oncogenic transcription program for leukemic transformation. The CTCF boundaries may serve as novel therapeutic targets for the treatment of myeloid malignancies.			
29759640	chr7	148804547	148806547	EZH2	The current study demonstrated that high EZH2 expression was associated with activation of tumor angiogenesis, and activation of the EZH2-mediated angiogenesis pathway predicted the prognosis of patients with ICC.	human	Epithelial tissues	High+Lowthroughput	Enhancer of zeste homolog 2 (EZH2) regulates tumor angiogenesis and predicts recurrence and prognosis of intrahepatic cholangiocarcinoma	否	无	Intrahepatic cholangiocarcinoma (ICC)	cholangiocarcinoma RBE cell	E_01_0485	Immunohistochemical staining and scoring,qRT-PCR,small interfering RNAs (siRNAs),qRT-PCR,Western blot,Bioinformatics analysis,	The current study demonstrated that high EZH2 expression was associated with activation of tumor angiogenesis, and activation of the EZH2-mediated angiogenesis pathway predicted the prognosis of patients with ICC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The current study demonstrated that high EZH2 expression was associated with activation of tumor angiogenesis, and activation of the EZH2-mediated angiogenesis pathway predicted the prognosis of patients with ICC.	Immunohistochemical staining	The current study demonstrated that high EZH2 expression was associated with activation of tumor angiogenesis, and activation of the EZH2-mediated angiogenesis pathway predicted the prognosis of patients with ICC.	EZH2		Immunohistochemical staining and scoring,qRT-PCR,small interfering RNAs (siRNAs),qRT-PCR,Western blot,Bioinformatics analysis,	The current study demonstrated that high EZH2 expression was associated with activation of tumor angiogenesis, and activation of the EZH2-mediated angiogenesis pathway predicted the prognosis of patients with ICC.			
29759640	chr14	76758674	76760674	VASH1	The current study demonstrated that high EZH2 expression was associated with activation of tumor angiogenesis, and activation of the EZH2-mediated angiogenesis pathway predicted the prognosis of patients with ICC.	human	Epithelial tissues	High+Lowthroughput	Enhancer of zeste homolog 2 (EZH2) regulates tumor angiogenesis and predicts recurrence and prognosis of intrahepatic cholangiocarcinoma	否	无	Intrahepatic cholangiocarcinoma (ICC)	cholangiocarcinoma RBE cell	E_01_0485	Immunohistochemical staining and scoring,qRT-PCR,small interfering RNAs (siRNAs),qRT-PCR,Western blot,Bioinformatics analysis,	The current study demonstrated that high EZH2 expression was associated with activation of tumor angiogenesis, and activation of the EZH2-mediated angiogenesis pathway predicted the prognosis of patients with ICC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The current study demonstrated that high EZH2 expression was associated with activation of tumor angiogenesis, and activation of the EZH2-mediated angiogenesis pathway predicted the prognosis of patients with ICC.		The current study demonstrated that high EZH2 expression was associated with activation of tumor angiogenesis, and activation of the EZH2-mediated angiogenesis pathway predicted the prognosis of patients with ICC.	Immunohistochemical staining	The current study demonstrated that high EZH2 expression was associated with activation of tumor angiogenesis, and activation of the EZH2-mediated angiogenesis pathway predicted the prognosis of patients with ICC.			Immunohistochemical staining and scoring,qRT-PCR,small interfering RNAs (siRNAs),qRT-PCR,Western blot,Bioinformatics analysis,				VASH1
29758293	chr9	81580468	81582468	TLE1	Using trio-based exome sequencing, we identified a homozygous missense mutation in the Transducin-like enhancer of split-1 (TLE1) gene, encoding for a non DNA-binding transcriptional corepressor, highly expressed in the postnatal brain. The regulation of the post-mitotic neural survival activity of TLE1 depends critically on an interaction with FOXG1, a gene shown to be involved in a postnatal microcephaly syndrome. Functional analysis on affected dermal fibroblasts showed a significant decrease in mitotic and proliferative index, indicating a lengthening of the cell cycle and a delay in mitosis, supporting that this gene could be a new candidate for postnatal microcephaly.	human	Nervous tissue	High+Lowthroughput	TLE1, a key player in neurogenesis, a new candidate gene for autosomal recessive postnatal microcephaly	是	rs201140985	Postnatal microcephaly	neural progenitor cell	E_01_0486	Immunostaining	Using trio-based exome sequencing, we identified a homozygous missense mutation in the Transducin-like enhancer of split-1 (TLE1) gene, encoding for a non DNA-binding transcriptional corepressor, highly expressed in the postnatal brain. The regulation of the post-mitotic neural survival activity of TLE1 depends critically on an interaction with FOXG1, a gene shown to be involved in a postnatal microcephaly syndrome. Functional analysis on affected dermal fibroblasts showed a significant decrease in mitotic and proliferative index, indicating a lengthening of the cell cycle and a delay in mitosis, supporting that this gene could be a new candidate for postnatal microcephaly.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Using trio-based exome sequencing, we identified a homozygous missense mutation in the Transducin-like enhancer of split-1 (TLE1) gene, encoding for a non DNA-binding transcriptional corepressor, highly expressed in the postnatal brain. The regulation of the post-mitotic neural survival activity of TLE1 depends critically on an interaction with FOXG1, a gene shown to be involved in a postnatal microcephaly syndrome. Functional analysis on affected dermal fibroblasts showed a significant decrease in mitotic and proliferative index, indicating a lengthening of the cell cycle and a delay in mitosis, supporting that this gene could be a new candidate for postnatal microcephaly.	Immunohistochemical staining	Using trio-based exome sequencing, we identified a homozygous missense mutation in the Transducin-like enhancer of split-1 (TLE1) gene, encoding for a non DNA-binding transcriptional corepressor, highly expressed in the postnatal brain. The regulation of the post-mitotic neural survival activity of TLE1 depends critically on an interaction with FOXG1, a gene shown to be involved in a postnatal microcephaly syndrome. Functional analysis on affected dermal fibroblasts showed a significant decrease in mitotic and proliferative index, indicating a lengthening of the cell cycle and a delay in mitosis, supporting that this gene could be a new candidate for postnatal microcephaly.	TLE1		Immunostaining	Using trio-based exome sequencing, we identified a homozygous missense mutation in the Transducin-like enhancer of split-1 (TLE1) gene, encoding for a non DNA-binding transcriptional corepressor, highly expressed in the postnatal brain. The regulation of the post-mitotic neural survival activity of TLE1 depends critically on an interaction with FOXG1, a gene shown to be involved in a postnatal microcephaly syndrome. Functional analysis on affected dermal fibroblasts showed a significant decrease in mitotic and proliferative index, indicating a lengthening of the cell cycle and a delay in mitosis, supporting that this gene could be a new candidate for postnatal microcephaly.			
29758293	chr14	28763995	28765995	FOXG1	Using trio-based exome sequencing, we identified a homozygous missense mutation in the Transducin-like enhancer of split-1 (TLE1) gene, encoding for a non DNA-binding transcriptional corepressor, highly expressed in the postnatal brain. The regulation of the post-mitotic neural survival activity of TLE1 depends critically on an interaction with FOXG1, a gene shown to be involved in a postnatal microcephaly syndrome. Functional analysis on affected dermal fibroblasts showed a significant decrease in mitotic and proliferative index, indicating a lengthening of the cell cycle and a delay in mitosis, supporting that this gene could be a new candidate for postnatal microcephaly.	human	Nervous tissue	High+Lowthroughput	TLE1, a key player in neurogenesis, a new candidate gene for autosomal recessive postnatal microcephaly	是	rs201140985	Postnatal microcephaly	neural progenitor cell	E_01_0486	Immunostaining	Using trio-based exome sequencing, we identified a homozygous missense mutation in the Transducin-like enhancer of split-1 (TLE1) gene, encoding for a non DNA-binding transcriptional corepressor, highly expressed in the postnatal brain. The regulation of the post-mitotic neural survival activity of TLE1 depends critically on an interaction with FOXG1, a gene shown to be involved in a postnatal microcephaly syndrome. Functional analysis on affected dermal fibroblasts showed a significant decrease in mitotic and proliferative index, indicating a lengthening of the cell cycle and a delay in mitosis, supporting that this gene could be a new candidate for postnatal microcephaly.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Using trio-based exome sequencing, we identified a homozygous missense mutation in the Transducin-like enhancer of split-1 (TLE1) gene, encoding for a non DNA-binding transcriptional corepressor, highly expressed in the postnatal brain. The regulation of the post-mitotic neural survival activity of TLE1 depends critically on an interaction with FOXG1, a gene shown to be involved in a postnatal microcephaly syndrome. Functional analysis on affected dermal fibroblasts showed a significant decrease in mitotic and proliferative index, indicating a lengthening of the cell cycle and a delay in mitosis, supporting that this gene could be a new candidate for postnatal microcephaly.		Using trio-based exome sequencing, we identified a homozygous missense mutation in the Transducin-like enhancer of split-1 (TLE1) gene, encoding for a non DNA-binding transcriptional corepressor, highly expressed in the postnatal brain. The regulation of the post-mitotic neural survival activity of TLE1 depends critically on an interaction with FOXG1, a gene shown to be involved in a postnatal microcephaly syndrome. Functional analysis on affected dermal fibroblasts showed a significant decrease in mitotic and proliferative index, indicating a lengthening of the cell cycle and a delay in mitosis, supporting that this gene could be a new candidate for postnatal microcephaly.	Immunohistochemical staining	Using trio-based exome sequencing, we identified a homozygous missense mutation in the Transducin-like enhancer of split-1 (TLE1) gene, encoding for a non DNA-binding transcriptional corepressor, highly expressed in the postnatal brain. The regulation of the post-mitotic neural survival activity of TLE1 depends critically on an interaction with FOXG1, a gene shown to be involved in a postnatal microcephaly syndrome. Functional analysis on affected dermal fibroblasts showed a significant decrease in mitotic and proliferative index, indicating a lengthening of the cell cycle and a delay in mitosis, supporting that this gene could be a new candidate for postnatal microcephaly.			Immunostaining				FOXG1
29757144	chr16	67559951	67561951	CTCF	These findings elucidate the role of intra-TAD cohesin-and-CTCF binding in nuclear organization associated with widespread insulation of distal enhancer activity.	mouse	Liver tissue	High+Lowthroughput	Computational prediction of CTCF/cohesin-based intra-TAD loops that insulate chromatin contacts and gene expression in mouse liver	否	无	nothing	CH12 cell	E_02_0310	ChIP,qPCR,PCR,4C-seq,Motif analysis,ChIP-seq,Sonication,CAC sites and score,Intra-TAD loop prediction method,RNA-seq,Hi-C,Alternative loop anchor analysis,ChIA-PET,	These findings elucidate the role of intra-TAD cohesin-and-CTCF binding in nuclear organization associated with widespread insulation of distal enhancer activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings elucidate the role of intra-TAD cohesin-and-CTCF binding in nuclear organization associated with widespread insulation of distal enhancer activity.		These findings elucidate the role of intra-TAD cohesin-and-CTCF binding in nuclear organization associated with widespread insulation of distal enhancer activity.	Immunohistochemical staining	These findings elucidate the role of intra-TAD cohesin-and-CTCF binding in nuclear organization associated with widespread insulation of distal enhancer activity.			ChIP,qPCR,PCR,4C-seq,Motif analysis,ChIP-seq,Sonication,CAC sites and score,Intra-TAD loop prediction method,RNA-seq,Hi-C,Alternative loop anchor analysis,ChIA-PET,				CTCF
29757144	chr3	133743302	133745302	TF	These findings elucidate the role of intra-TAD cohesin-and-CTCF binding in nuclear organization associated with widespread insulation of distal enhancer activity.	mouse	Liver tissue	High+Lowthroughput	Computational prediction of CTCF/cohesin-based intra-TAD loops that insulate chromatin contacts and gene expression in mouse liver	否	无	nothing	CH12 cell	E_02_0310	ChIP,qPCR,PCR,4C-seq,Motif analysis,ChIP-seq,Sonication,CAC sites and score,Intra-TAD loop prediction method,RNA-seq,Hi-C,Alternative loop anchor analysis,ChIA-PET,	These findings elucidate the role of intra-TAD cohesin-and-CTCF binding in nuclear organization associated with widespread insulation of distal enhancer activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings elucidate the role of intra-TAD cohesin-and-CTCF binding in nuclear organization associated with widespread insulation of distal enhancer activity.		These findings elucidate the role of intra-TAD cohesin-and-CTCF binding in nuclear organization associated with widespread insulation of distal enhancer activity.	Immunohistochemical staining	These findings elucidate the role of intra-TAD cohesin-and-CTCF binding in nuclear organization associated with widespread insulation of distal enhancer activity.			ChIP,qPCR,PCR,4C-seq,Motif analysis,ChIP-seq,Sonication,CAC sites and score,Intra-TAD loop prediction method,RNA-seq,Hi-C,Alternative loop anchor analysis,ChIA-PET,				TF
29755131	chr7	152132016	152134016	KMT2C	From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ERα, displaying ongoing sensitivity to ERα antagonists. We conclude that KMT2C is a key regulator of ERα activity whose loss uncouples breast cancer proliferation from hormone abundance.	human	Epithelial tissues	High+Lowthroughput	KMT2C mediates the estrogen dependence of breast cancer through regulation of ERα enhancer function	否	无	mammary cancer	SKBR3 cell	E_01_0487	CRISPR/Cas9,next-generation sequencing (IMPACT) assay,Proliferation assays,Immunoblotting,Lentiviral Infections,Quantitative RT-PCR,Chromatin Immunoprecipitation,Immunohistochemistry,Rapid immunoprecipitation mass spectrometry of endogenous proteins (RIME),Chromatin Immunoprecipitation followed by sequencing,	From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ERα, displaying ongoing sensitivity to ERα antagonists. We conclude that KMT2C is a key regulator of ERα activity whose loss uncouples breast cancer proliferation from hormone abundance.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ERα, displaying ongoing sensitivity to ERα antagonists. We conclude that KMT2C is a key regulator of ERα activity whose loss uncouples breast cancer proliferation from hormone abundance.	Immunohistochemical staining	From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ERα, displaying ongoing sensitivity to ERα antagonists. We conclude that KMT2C is a key regulator of ERα activity whose loss uncouples breast cancer proliferation from hormone abundance.	KMT2C		CRISPR/Cas9,next-generation sequencing (IMPACT) assay,Proliferation assays,Immunoblotting,Lentiviral Infections,Quantitative RT-PCR,Chromatin Immunoprecipitation,Immunohistochemistry,Rapid immunoprecipitation mass spectrometry of endogenous proteins (RIME),Chromatin Immunoprecipitation followed by sequencing,	From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ERα, displaying ongoing sensitivity to ERα antagonists. We conclude that KMT2C is a key regulator of ERα activity whose loss uncouples breast cancer proliferation from hormone abundance.			
29755131	chr14	37586788	37588788	FOXA1	From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ERα, displaying ongoing sensitivity to ERα antagonists. We conclude that KMT2C is a key regulator of ERα activity whose loss uncouples breast cancer proliferation from hormone abundance.	human	Epithelial tissues	High+Lowthroughput	KMT2C mediates the estrogen dependence of breast cancer through regulation of ERα enhancer function	否	无	mammary cancer	SKBR3 cell	E_01_0487	CRISPR/Cas9,next-generation sequencing (IMPACT) assay,Proliferation assays,Immunoblotting,Lentiviral Infections,Quantitative RT-PCR,Chromatin Immunoprecipitation,Immunohistochemistry,Rapid immunoprecipitation mass spectrometry of endogenous proteins (RIME),Chromatin Immunoprecipitation followed by sequencing,	From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ERα, displaying ongoing sensitivity to ERα antagonists. We conclude that KMT2C is a key regulator of ERα activity whose loss uncouples breast cancer proliferation from hormone abundance.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ERα, displaying ongoing sensitivity to ERα antagonists. We conclude that KMT2C is a key regulator of ERα activity whose loss uncouples breast cancer proliferation from hormone abundance.	Immunohistochemical staining	From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ERα, displaying ongoing sensitivity to ERα antagonists. We conclude that KMT2C is a key regulator of ERα activity whose loss uncouples breast cancer proliferation from hormone abundance.	FOXA1		CRISPR/Cas9,next-generation sequencing (IMPACT) assay,Proliferation assays,Immunoblotting,Lentiviral Infections,Quantitative RT-PCR,Chromatin Immunoprecipitation,Immunohistochemistry,Rapid immunoprecipitation mass spectrometry of endogenous proteins (RIME),Chromatin Immunoprecipitation followed by sequencing,	From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ERα, displaying ongoing sensitivity to ERα antagonists. We conclude that KMT2C is a key regulator of ERα activity whose loss uncouples breast cancer proliferation from hormone abundance.			
29755129	chr13	27063070	27065070	USP12	Consequently, USP12 levels are predictive not only of cancer development but also of patient's therapy resistance, relapse and survival. Therefore, our findings suggest that USP12 could serve as a promising therapeutic target in currently incurable castrate-resistant prostate cancer.	human	connective tissue	High+Lowthroughput	Molecular mechanism of the TP53-MDM2-AR-AKT signalling network regulation by USP12	否	无	prostatic cancer	LNCaP	E_01_0488	transfection,siRNA gene silencing,Immunoprecipitation (IP),Immunohistochemistry,Colony formation,Chromatin immunoprecipitation (ChIP),qPCR,	Consequently, USP12 levels are predictive not only of cancer development but also of patient's therapy resistance, relapse and survival. Therefore, our findings suggest that USP12 could serve as a promising therapeutic target in currently incurable castrate-resistant prostate cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consequently, USP12 levels are predictive not only of cancer development but also of patient's therapy resistance, relapse and survival. Therefore, our findings suggest that USP12 could serve as a promising therapeutic target in currently incurable castrate-resistant prostate cancer.		Consequently, USP12 levels are predictive not only of cancer development but also of patient's therapy resistance, relapse and survival. Therefore, our findings suggest that USP12 could serve as a promising therapeutic target in currently incurable castrate-resistant prostate cancer.	Immunohistochemical staining	Consequently, USP12 levels are predictive not only of cancer development but also of patient's therapy resistance, relapse and survival. Therefore, our findings suggest that USP12 could serve as a promising therapeutic target in currently incurable castrate-resistant prostate cancer.			transfection,siRNA gene silencing,Immunoprecipitation (IP),Immunohistochemistry,Colony formation,Chromatin immunoprecipitation (ChIP),qPCR,				USP12
29755129	chr17	7659073	7661073	TP53	Consequently, USP12 levels are predictive not only of cancer development but also of patient's therapy resistance, relapse and survival. Therefore, our findings suggest that USP12 could serve as a promising therapeutic target in currently incurable castrate-resistant prostate cancer.	human	connective tissue	High+Lowthroughput	Molecular mechanism of the TP53-MDM2-AR-AKT signalling network regulation by USP12	否	无	prostatic cancer	LNCaP	E_01_0488	transfection,siRNA gene silencing,Immunoprecipitation (IP),Immunohistochemistry,Colony formation,Chromatin immunoprecipitation (ChIP),qPCR,	Consequently, USP12 levels are predictive not only of cancer development but also of patient's therapy resistance, relapse and survival. Therefore, our findings suggest that USP12 could serve as a promising therapeutic target in currently incurable castrate-resistant prostate cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Consequently, USP12 levels are predictive not only of cancer development but also of patient's therapy resistance, relapse and survival. Therefore, our findings suggest that USP12 could serve as a promising therapeutic target in currently incurable castrate-resistant prostate cancer.	Immunohistochemical staining	Consequently, USP12 levels are predictive not only of cancer development but also of patient's therapy resistance, relapse and survival. Therefore, our findings suggest that USP12 could serve as a promising therapeutic target in currently incurable castrate-resistant prostate cancer.	TP53		transfection,siRNA gene silencing,Immunoprecipitation (IP),Immunohistochemistry,Colony formation,Chromatin immunoprecipitation (ChIP),qPCR,	Consequently, USP12 levels are predictive not only of cancer development but also of patient's therapy resistance, relapse and survival. Therefore, our findings suggest that USP12 could serve as a promising therapeutic target in currently incurable castrate-resistant prostate cancer.			
29754817	chr12	47838311	47840311	VDR	Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.	human	connective tissue	High+Lowthroughput	Vitamin D Switches BAF Complexes to Protect β Cells	否	无	Type 2 diabetes (T2D)	INS1 cell	E_01_0489	CRISPR screening,RNA-Seq,qPCR,H&E staining,Immunohistochemistry,immunofluorescence,Immunoprecipitation,siRNA knockdown,transfection,shRNA knockdown,FACS analysis,ELISA,Chromatin Immunoprecipitation,ChIP-Seq,ATAC-Seq,Transmission electronic microscopy,LC-MS Analysis,	Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.	Immunohistochemical staining	Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.	CYP27B1		CRISPR screening,RNA-Seq,qPCR,H&E staining,Immunohistochemistry,immunofluorescence,Immunoprecipitation,siRNA knockdown,transfection,shRNA knockdown,FACS analysis,ELISA,Chromatin Immunoprecipitation,ChIP-Seq,ATAC-Seq,Transmission electronic microscopy,LC-MS Analysis,	Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.			
29754817	chr16	50310919	50312919	BRD7	Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.	human	connective tissue	High+Lowthroughput	Vitamin D Switches BAF Complexes to Protect β Cells	否	无	Type 2 diabetes (T2D)	INS1 cell	E_01_0489	CRISPR screening,RNA-Seq,qPCR,H&E staining,Immunohistochemistry,immunofluorescence,Immunoprecipitation,siRNA knockdown,transfection,shRNA knockdown,FACS analysis,ELISA,Chromatin Immunoprecipitation,ChIP-Seq,ATAC-Seq,Transmission electronic microscopy,LC-MS Analysis,	Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.		Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.	Immunohistochemical staining	Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.			CRISPR screening,RNA-Seq,qPCR,H&E staining,Immunohistochemistry,immunofluorescence,Immunoprecipitation,siRNA knockdown,transfection,shRNA knockdown,FACS analysis,ELISA,Chromatin Immunoprecipitation,ChIP-Seq,ATAC-Seq,Transmission electronic microscopy,LC-MS Analysis,				BRD7
29754817	chr5	847663	849663	BRD9	Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.	human	connective tissue	High+Lowthroughput	Vitamin D Switches BAF Complexes to Protect β Cells	否	无	Type 2 diabetes (T2D)	INS1 cell	E_01_0489	CRISPR screening,RNA-Seq,qPCR,H&E staining,Immunohistochemistry,immunofluorescence,Immunoprecipitation,siRNA knockdown,transfection,shRNA knockdown,FACS analysis,ELISA,Chromatin Immunoprecipitation,ChIP-Seq,ATAC-Seq,Transmission electronic microscopy,LC-MS Analysis,	Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.		Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.	Immunohistochemical staining	Mechanistically, ligand promotes VDR association with PBAF to effect genome-wide changes in chromatin accessibility and enhancer landscape, resulting in an anti-inflammatory response. Importantly, pharmacological inhibition of BRD9 promotes PBAF-VDR association to restore β cell function and ameliorate hyperglycemia in murine T2D models. These studies reveal an unrecognized VDR-dependent transcriptional program underpinning β cell survival and identifies the VDR:PBAF/BAF association as a potential therapeutic target for T2D.			CRISPR screening,RNA-Seq,qPCR,H&E staining,Immunohistochemistry,immunofluorescence,Immunoprecipitation,siRNA knockdown,transfection,shRNA knockdown,FACS analysis,ELISA,Chromatin Immunoprecipitation,ChIP-Seq,ATAC-Seq,Transmission electronic microscopy,LC-MS Analysis,				BRD9
29754779	chr9	134132377	134134377	WDR5	In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.	human	Epithelial tissues	High+Lowthroughput	A Linc1405/Eomes Complex Promotes Cardiac Mesoderm Specification and Cardiogenesis	否	无	nothing	embryonic stem cell	E_01_0490	PCR,CRISPR,Fluorescence activated cell sorter analysis,Microarray analysis,Chromatin immunoprecipitation,Fluorescent in situ hybridization,Quantitative RT-PCR,Western blot,Immunostaining,RIP assay,RNA immunoprecipitation,Luciferase reporter assay,Co-immunoprecipitation,Echocardiography analysis,Hematoxylin and Eeosin staining,	In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.		In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.	Immunohistochemical staining	In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.			PCR,CRISPR,Fluorescence activated cell sorter analysis,Microarray analysis,Chromatin immunoprecipitation,Fluorescent in situ hybridization,Quantitative RT-PCR,Western blot,Immunostaining,RIP assay,RNA immunoprecipitation,Luciferase reporter assay,Co-immunoprecipitation,Echocardiography analysis,Hematoxylin and Eeosin staining,				WDR5
29754779	chr7	79439703	79441703	Mesp1	In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.	human	Epithelial tissues	High+Lowthroughput	A Linc1405/Eomes Complex Promotes Cardiac Mesoderm Specification and Cardiogenesis	否	无	nothing	embryonic stem cell	E_01_0490	PCR,CRISPR,Fluorescence activated cell sorter analysis,Microarray analysis,Chromatin immunoprecipitation,Fluorescent in situ hybridization,Quantitative RT-PCR,Western blot,Immunostaining,RIP assay,RNA immunoprecipitation,Luciferase reporter assay,Co-immunoprecipitation,Echocardiography analysis,Hematoxylin and Eeosin staining,	In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.		In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.	Immunohistochemical staining	In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.			PCR,CRISPR,Fluorescence activated cell sorter analysis,Microarray analysis,Chromatin immunoprecipitation,Fluorescent in situ hybridization,Quantitative RT-PCR,Western blot,Immunostaining,RIP assay,RNA immunoprecipitation,Luciferase reporter assay,Co-immunoprecipitation,Echocardiography analysis,Hematoxylin and Eeosin staining,				Mesp1
29754779	chr9	118304512	118306512	Eomes	In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.	human	Epithelial tissues	High+Lowthroughput	A Linc1405/Eomes Complex Promotes Cardiac Mesoderm Specification and Cardiogenesis	否	无	nothing	embryonic stem cell	E_01_0490	PCR,CRISPR,Fluorescence activated cell sorter analysis,Microarray analysis,Chromatin immunoprecipitation,Fluorescent in situ hybridization,Quantitative RT-PCR,Western blot,Immunostaining,RIP assay,RNA immunoprecipitation,Luciferase reporter assay,Co-immunoprecipitation,Echocardiography analysis,Hematoxylin and Eeosin staining,	In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.		In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.	Immunohistochemical staining	In summary, linc1405 mediates a Eomes/WDR5/GCN5 complex that contributes to cardiogenesis, highlighting the critical roles of lincRNA-based complexes in the epigenetic regulation of cardiogenesis in vitro and in vivo.			PCR,CRISPR,Fluorescence activated cell sorter analysis,Microarray analysis,Chromatin immunoprecipitation,Fluorescent in situ hybridization,Quantitative RT-PCR,Western blot,Immunostaining,RIP assay,RNA immunoprecipitation,Luciferase reporter assay,Co-immunoprecipitation,Echocardiography analysis,Hematoxylin and Eeosin staining,				Eomes
29754769	chr2	45385835	45387835	SRBD1	It also supports meta-analysis of multiple DNM studies, while adjusting for study-specific technical effects. We applied TADA-A to WGS data of _x0001_300 autism-affected family trios across five studies and discovered several autism risk genes.The software is freely available for all research uses.	human	/	High+Lowthroughput	A Statistical Framework for Mapping Risk Genes from De Novo Mutations in Whole-Genome-Sequencing Studies	否	无	autism		E_01_0491	WES,WGS,TADA-Annotations(TADA-A),	It also supports meta-analysis of multiple DNM studies, while adjusting for study-specific technical effects. We applied TADA-A to WGS data of _x0001_300 autism-affected family trios across five studies and discovered several autism risk genes.The software is freely available for all research uses.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	It also supports meta-analysis of multiple DNM studies, while adjusting for study-specific technical effects. We applied TADA-A to WGS data of _x0001_300 autism-affected family trios across five studies and discovered several autism risk genes.The software is freely available for all research uses.		It also supports meta-analysis of multiple DNM studies, while adjusting for study-specific technical effects. We applied TADA-A to WGS data of _x0001_300 autism-affected family trios across five studies and discovered several autism risk genes.The software is freely available for all research uses.	Immunohistochemical staining	It also supports meta-analysis of multiple DNM studies, while adjusting for study-specific technical effects. We applied TADA-A to WGS data of _x0001_300 autism-affected family trios across five studies and discovered several autism risk genes.The software is freely available for all research uses.			WES,WGS,TADA-Annotations(TADA-A),				SRBD1
29753018	chr7	30330197	30332197	Etv2	In Etv2-inhibited embryos and larvae, the number of lymphatic progenitors is greatly reduced, the major lymphatic vessel, the thoracic duct, is absent or severely fragmented, and lymphangiogenesis-associated marker expression, including lyve1b, prox1a, and vegfr3/flt4, is strongly downregulated. We also demonstrate that lymphatic progenitors in Etv2 deficient embryos fail to respond to Vegfc signaling. Chromatin immunoprecipitation and sequencing (ChIP-Seq) studies using differentiated mouse embryonic stem (ES) cells as well as luciferase reporter studies in the ES cells and in zebrafish embryos argue that Etv2 directly binds the promoter/enhancer regions of Vegfc receptor Vegfr3/Flt4 and lymphatic marker Lyve1, and promotes their expression. Together these data support a model where Etv2 initiates lymphangiogenesis by directly promoting the expression of flt4 within the posterior cardinal vein.	mouse	Nervous tissue	High+Lowthroughput	ETS transcription factor Etsrp / Etv2 is required for lymphangiogenesis and directly regulates vegfr3 / flt4 expression	否	无	nothing	murine embryonic stem (ES) cell	E_02_0311	Etv2 knockdown,In situ hybridization(ISH),Luciferase experiments,Chromatin immunoprecipitation and sequencing (ChIP-Seq),immunohistochemistry,Dual‐Luciferase Reporter Assay,PCR,	In Etv2-inhibited embryos and larvae, the number of lymphatic progenitors is greatly reduced, the major lymphatic vessel, the thoracic duct, is absent or severely fragmented, and lymphangiogenesis-associated marker expression, including lyve1b, prox1a, and vegfr3/flt4, is strongly downregulated. We also demonstrate that lymphatic progenitors in Etv2 deficient embryos fail to respond to Vegfc signaling. Chromatin immunoprecipitation and sequencing (ChIP-Seq) studies using differentiated mouse embryonic stem (ES) cells as well as luciferase reporter studies in the ES cells and in zebrafish embryos argue that Etv2 directly binds the promoter/enhancer regions of Vegfc receptor Vegfr3/Flt4 and lymphatic marker Lyve1, and promotes their expression. Together these data support a model where Etv2 initiates lymphangiogenesis by directly promoting the expression of flt4 within the posterior cardinal vein.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In Etv2-inhibited embryos and larvae, the number of lymphatic progenitors is greatly reduced, the major lymphatic vessel, the thoracic duct, is absent or severely fragmented, and lymphangiogenesis-associated marker expression, including lyve1b, prox1a, and vegfr3/flt4, is strongly downregulated. We also demonstrate that lymphatic progenitors in Etv2 deficient embryos fail to respond to Vegfc signaling. Chromatin immunoprecipitation and sequencing (ChIP-Seq) studies using differentiated mouse embryonic stem (ES) cells as well as luciferase reporter studies in the ES cells and in zebrafish embryos argue that Etv2 directly binds the promoter/enhancer regions of Vegfc receptor Vegfr3/Flt4 and lymphatic marker Lyve1, and promotes their expression. Together these data support a model where Etv2 initiates lymphangiogenesis by directly promoting the expression of flt4 within the posterior cardinal vein.		In Etv2-inhibited embryos and larvae, the number of lymphatic progenitors is greatly reduced, the major lymphatic vessel, the thoracic duct, is absent or severely fragmented, and lymphangiogenesis-associated marker expression, including lyve1b, prox1a, and vegfr3/flt4, is strongly downregulated. We also demonstrate that lymphatic progenitors in Etv2 deficient embryos fail to respond to Vegfc signaling. Chromatin immunoprecipitation and sequencing (ChIP-Seq) studies using differentiated mouse embryonic stem (ES) cells as well as luciferase reporter studies in the ES cells and in zebrafish embryos argue that Etv2 directly binds the promoter/enhancer regions of Vegfc receptor Vegfr3/Flt4 and lymphatic marker Lyve1, and promotes their expression. Together these data support a model where Etv2 initiates lymphangiogenesis by directly promoting the expression of flt4 within the posterior cardinal vein.	Immunohistochemical staining	In Etv2-inhibited embryos and larvae, the number of lymphatic progenitors is greatly reduced, the major lymphatic vessel, the thoracic duct, is absent or severely fragmented, and lymphangiogenesis-associated marker expression, including lyve1b, prox1a, and vegfr3/flt4, is strongly downregulated. We also demonstrate that lymphatic progenitors in Etv2 deficient embryos fail to respond to Vegfc signaling. Chromatin immunoprecipitation and sequencing (ChIP-Seq) studies using differentiated mouse embryonic stem (ES) cells as well as luciferase reporter studies in the ES cells and in zebrafish embryos argue that Etv2 directly binds the promoter/enhancer regions of Vegfc receptor Vegfr3/Flt4 and lymphatic marker Lyve1, and promotes their expression. Together these data support a model where Etv2 initiates lymphangiogenesis by directly promoting the expression of flt4 within the posterior cardinal vein.			Etv2 knockdown,In situ hybridization(ISH),Luciferase experiments,Chromatin immunoprecipitation and sequencing (ChIP-Seq),immunohistochemistry,Dual‐Luciferase Reporter Assay,PCR,				Etv2
29752714	chr6	64703439	64705439	Atoh1	In the present study, to address this issue, we examined in detail the behavior of post-crossing dI1 axons in mice, using the Atoh1 enhancer-based conditional expression system that enables selective and sparse labeling of individual dI1 axons, together with Hb9 and ChAT immunohistochemistry for precise identification of spinal motor neurons (MNs).Our findings thus reveal a previously unrecognized projection of dI1 commissural axons that may contribute directly to generating proper motor output.	mouse	Nervous tissue	High+Lowthroughput	Post-crossing segment of dI1 commissural axons forms collateral branches to motor neurons in the developing spinal cord	否	无	nothing		E_02_0312	Hb9 and ChAT immunohistochemistry,Whole-mount immunohistochemistry,Immunostaining,	In the present study, to address this issue, we examined in detail the behavior of post-crossing dI1 axons in mice, using the Atoh1 enhancer-based conditional expression system that enables selective and sparse labeling of individual dI1 axons, together with Hb9 and ChAT immunohistochemistry for precise identification of spinal motor neurons (MNs).Our findings thus reveal a previously unrecognized projection of dI1 commissural axons that may contribute directly to generating proper motor output.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, to address this issue, we examined in detail the behavior of post-crossing dI1 axons in mice, using the Atoh1 enhancer-based conditional expression system that enables selective and sparse labeling of individual dI1 axons, together with Hb9 and ChAT immunohistochemistry for precise identification of spinal motor neurons (MNs).Our findings thus reveal a previously unrecognized projection of dI1 commissural axons that may contribute directly to generating proper motor output.		In the present study, to address this issue, we examined in detail the behavior of post-crossing dI1 axons in mice, using the Atoh1 enhancer-based conditional expression system that enables selective and sparse labeling of individual dI1 axons, together with Hb9 and ChAT immunohistochemistry for precise identification of spinal motor neurons (MNs).Our findings thus reveal a previously unrecognized projection of dI1 commissural axons that may contribute directly to generating proper motor output.	Immunohistochemical staining	In the present study, to address this issue, we examined in detail the behavior of post-crossing dI1 axons in mice, using the Atoh1 enhancer-based conditional expression system that enables selective and sparse labeling of individual dI1 axons, together with Hb9 and ChAT immunohistochemistry for precise identification of spinal motor neurons (MNs).Our findings thus reveal a previously unrecognized projection of dI1 commissural axons that may contribute directly to generating proper motor output.			Hb9 and ChAT immunohistochemistry,Whole-mount immunohistochemistry,Immunostaining,				Atoh1
29752567	chr7	148804760	148806760	EZH2	EZH2 is upregulated, whereas inhibiting EZH2 exerted rescuing effect in anesthetics (bupivacaine)-induced spinal cord DRG. The possible downstream target of EZH2 inhibition may interact with caspase and TrkC signaling pathways.	mouse	Nervous tissue	High+Lowthroughput	Inhibiting EZH2 rescued bupivacaine-induced neuronal apoptosis in spinal cord dorsal root ganglia in mice	否	无	nothing		E_02_0313	Western blot,Quantitative real‑time polymerase chain reaction(qRT‑PCR),Caspase‑9 activity assay,TUNEL,siRNA 	EZH2 is upregulated, whereas inhibiting EZH2 exerted rescuing effect in anesthetics (bupivacaine)-induced spinal cord DRG. The possible downstream target of EZH2 inhibition may interact with caspase and TrkC signaling pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EZH2 is upregulated, whereas inhibiting EZH2 exerted rescuing effect in anesthetics (bupivacaine)-induced spinal cord DRG. The possible downstream target of EZH2 inhibition may interact with caspase and TrkC signaling pathways.		EZH2 is upregulated, whereas inhibiting EZH2 exerted rescuing effect in anesthetics (bupivacaine)-induced spinal cord DRG. The possible downstream target of EZH2 inhibition may interact with caspase and TrkC signaling pathways.	Immunohistochemical staining	EZH2 is upregulated, whereas inhibiting EZH2 exerted rescuing effect in anesthetics (bupivacaine)-induced spinal cord DRG. The possible downstream target of EZH2 inhibition may interact with caspase and TrkC signaling pathways.			Western blot,Quantitative real‑time polymerase chain reaction(qRT‑PCR),Caspase‑9 activity assay,TUNEL,siRNA 				EZH2
29751043	chr7	45108269	45110269	Bax	In addition, TUDCA suppressed gentamicin-induced endoplasmic reticulum stress as reflected by inversing the expression levels of Binding immunoglobulin protein (Bip), CCAAT/-enhancer-binding protein homologous protein (CHOP) and Caspase 3. TUDCA attenuated gentamicin-induced hair cell death by inhibiting protein nitration activation and ER stress, providing new insights into the new potential therapies for sensorineural deafness.	human	connective tissue	High+Lowthroughput	Tauroursodeoxycholic acid attenuates gentamicin-induced cochlear hair cell death in vitro	否	无	nothing	HEI-OC1 cell	E_01_0492	Quantitative real-time PCR,ELISA,Western blot,Cochlear hair cell staining,	In addition, TUDCA suppressed gentamicin-induced endoplasmic reticulum stress as reflected by inversing the expression levels of Binding immunoglobulin protein (Bip), CCAAT/-enhancer-binding protein homologous protein (CHOP) and Caspase 3. TUDCA attenuated gentamicin-induced hair cell death by inhibiting protein nitration activation and ER stress, providing new insights into the new potential therapies for sensorineural deafness.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, TUDCA suppressed gentamicin-induced endoplasmic reticulum stress as reflected by inversing the expression levels of Binding immunoglobulin protein (Bip), CCAAT/-enhancer-binding protein homologous protein (CHOP) and Caspase 3. TUDCA attenuated gentamicin-induced hair cell death by inhibiting protein nitration activation and ER stress, providing new insights into the new potential therapies for sensorineural deafness.		In addition, TUDCA suppressed gentamicin-induced endoplasmic reticulum stress as reflected by inversing the expression levels of Binding immunoglobulin protein (Bip), CCAAT/-enhancer-binding protein homologous protein (CHOP) and Caspase 3. TUDCA attenuated gentamicin-induced hair cell death by inhibiting protein nitration activation and ER stress, providing new insights into the new potential therapies for sensorineural deafness.	Immunohistochemical staining	In addition, TUDCA suppressed gentamicin-induced endoplasmic reticulum stress as reflected by inversing the expression levels of Binding immunoglobulin protein (Bip), CCAAT/-enhancer-binding protein homologous protein (CHOP) and Caspase 3. TUDCA attenuated gentamicin-induced hair cell death by inhibiting protein nitration activation and ER stress, providing new insights into the new potential therapies for sensorineural deafness.			Quantitative real-time PCR,ELISA,Western blot,Cochlear hair cell staining,				Bax
29751043	chr1	106462952	106464952	Bcl2	In addition, TUDCA suppressed gentamicin-induced endoplasmic reticulum stress as reflected by inversing the expression levels of Binding immunoglobulin protein (Bip), CCAAT/-enhancer-binding protein homologous protein (CHOP) and Caspase 3. TUDCA attenuated gentamicin-induced hair cell death by inhibiting protein nitration activation and ER stress, providing new insights into the new potential therapies for sensorineural deafness.	human	connective tissue	High+Lowthroughput	Tauroursodeoxycholic acid attenuates gentamicin-induced cochlear hair cell death in vitro	否	无	nothing	HEI-OC1 cell	E_01_0492	Quantitative real-time PCR,ELISA,Western blot,Cochlear hair cell staining,	In addition, TUDCA suppressed gentamicin-induced endoplasmic reticulum stress as reflected by inversing the expression levels of Binding immunoglobulin protein (Bip), CCAAT/-enhancer-binding protein homologous protein (CHOP) and Caspase 3. TUDCA attenuated gentamicin-induced hair cell death by inhibiting protein nitration activation and ER stress, providing new insights into the new potential therapies for sensorineural deafness.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, TUDCA suppressed gentamicin-induced endoplasmic reticulum stress as reflected by inversing the expression levels of Binding immunoglobulin protein (Bip), CCAAT/-enhancer-binding protein homologous protein (CHOP) and Caspase 3. TUDCA attenuated gentamicin-induced hair cell death by inhibiting protein nitration activation and ER stress, providing new insights into the new potential therapies for sensorineural deafness.		In addition, TUDCA suppressed gentamicin-induced endoplasmic reticulum stress as reflected by inversing the expression levels of Binding immunoglobulin protein (Bip), CCAAT/-enhancer-binding protein homologous protein (CHOP) and Caspase 3. TUDCA attenuated gentamicin-induced hair cell death by inhibiting protein nitration activation and ER stress, providing new insights into the new potential therapies for sensorineural deafness.	Immunohistochemical staining	In addition, TUDCA suppressed gentamicin-induced endoplasmic reticulum stress as reflected by inversing the expression levels of Binding immunoglobulin protein (Bip), CCAAT/-enhancer-binding protein homologous protein (CHOP) and Caspase 3. TUDCA attenuated gentamicin-induced hair cell death by inhibiting protein nitration activation and ER stress, providing new insights into the new potential therapies for sensorineural deafness.			Quantitative real-time PCR,ELISA,Western blot,Cochlear hair cell staining,				Bcl2
29750193	chr3	10290270	10292270	SEC13	mEAK-7 knockdown decreases cell proliferation and migration, whereas overexpression of mEAK-7 enhances these cellular effects. Constitutively activated S6K rescues mTOR signaling in mEAK-7-knocked down cells. Thus, mEAK-7 activates an alternative mTOR signaling pathway through S6K2 and 4E-BP1 to regulate cell proliferation and migration.	human	connective tissue	High+Lowthroughput	Mammalian EAK-7 activates alternative mTOR signaling to regulate cell proliferation and migration	否	无	nothing	H1299 cell	E_01_0493	siRNA,transfection,Immunoprecipitation analysis,mmunoblotting,immunofluorescence,	mEAK-7 knockdown decreases cell proliferation and migration, whereas overexpression of mEAK-7 enhances these cellular effects. Constitutively activated S6K rescues mTOR signaling in mEAK-7-knocked down cells. Thus, mEAK-7 activates an alternative mTOR signaling pathway through S6K2 and 4E-BP1 to regulate cell proliferation and migration.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	mEAK-7 knockdown decreases cell proliferation and migration, whereas overexpression of mEAK-7 enhances these cellular effects. Constitutively activated S6K rescues mTOR signaling in mEAK-7-knocked down cells. Thus, mEAK-7 activates an alternative mTOR signaling pathway through S6K2 and 4E-BP1 to regulate cell proliferation and migration.		mEAK-7 knockdown decreases cell proliferation and migration, whereas overexpression of mEAK-7 enhances these cellular effects. Constitutively activated S6K rescues mTOR signaling in mEAK-7-knocked down cells. Thus, mEAK-7 activates an alternative mTOR signaling pathway through S6K2 and 4E-BP1 to regulate cell proliferation and migration.	Immunohistochemical staining	mEAK-7 knockdown decreases cell proliferation and migration, whereas overexpression of mEAK-7 enhances these cellular effects. Constitutively activated S6K rescues mTOR signaling in mEAK-7-knocked down cells. Thus, mEAK-7 activates an alternative mTOR signaling pathway through S6K2 and 4E-BP1 to regulate cell proliferation and migration.			siRNA,transfection,Immunoprecipitation analysis,mmunoblotting,immunofluorescence,				SEC13
29749927	chr9	63857441	63859441	Smad6	Functional experiments prototypically validated the strongly epigenetically regulated inhibitors of TGFβ family signaling SMAD6 and SMAD7 as regulators of EC quiescence. These data establish the transcriptional and epigenetic landscape of vascular quiescence that will serve as a foundation for further mechanistic studies of vascular homeostasis and disease-associated activation.	human	Lung tissue	High+Lowthroughput	The transcriptomic and epigenetic map of vascular quiescence in the continuous lung endothelium	否	无	nothing	HUVECs cell 	E_01_0494	FACS,Immunofluorescence staining,Elisa,Immunoblot,qPCR,RNA-seq,T-WGBS,MassARRAY,Interactome analysis,	Functional experiments prototypically validated the strongly epigenetically regulated inhibitors of TGFβ family signaling SMAD6 and SMAD7 as regulators of EC quiescence. These data establish the transcriptional and epigenetic landscape of vascular quiescence that will serve as a foundation for further mechanistic studies of vascular homeostasis and disease-associated activation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Functional experiments prototypically validated the strongly epigenetically regulated inhibitors of TGFβ family signaling SMAD6 and SMAD7 as regulators of EC quiescence. These data establish the transcriptional and epigenetic landscape of vascular quiescence that will serve as a foundation for further mechanistic studies of vascular homeostasis and disease-associated activation.		Functional experiments prototypically validated the strongly epigenetically regulated inhibitors of TGFβ family signaling SMAD6 and SMAD7 as regulators of EC quiescence. These data establish the transcriptional and epigenetic landscape of vascular quiescence that will serve as a foundation for further mechanistic studies of vascular homeostasis and disease-associated activation.	Immunohistochemical staining	Functional experiments prototypically validated the strongly epigenetically regulated inhibitors of TGFβ family signaling SMAD6 and SMAD7 as regulators of EC quiescence. These data establish the transcriptional and epigenetic landscape of vascular quiescence that will serve as a foundation for further mechanistic studies of vascular homeostasis and disease-associated activation.			FACS,Immunofluorescence staining,Elisa,Immunoblot,qPCR,RNA-seq,T-WGBS,MassARRAY,Interactome analysis,				Smad6
29749927	chr18	75498083	75500083	Smad7	Functional experiments prototypically validated the strongly epigenetically regulated inhibitors of TGFβ family signaling SMAD6 and SMAD7 as regulators of EC quiescence. These data establish the transcriptional and epigenetic landscape of vascular quiescence that will serve as a foundation for further mechanistic studies of vascular homeostasis and disease-associated activation.	human	Lung tissue	High+Lowthroughput	The transcriptomic and epigenetic map of vascular quiescence in the continuous lung endothelium	否	无	nothing	HUVECs cell 	E_01_0494	FACS,Immunofluorescence staining,Elisa,Immunoblot,qPCR,RNA-seq,T-WGBS,MassARRAY,Interactome analysis,	Functional experiments prototypically validated the strongly epigenetically regulated inhibitors of TGFβ family signaling SMAD6 and SMAD7 as regulators of EC quiescence. These data establish the transcriptional and epigenetic landscape of vascular quiescence that will serve as a foundation for further mechanistic studies of vascular homeostasis and disease-associated activation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Functional experiments prototypically validated the strongly epigenetically regulated inhibitors of TGFβ family signaling SMAD6 and SMAD7 as regulators of EC quiescence. These data establish the transcriptional and epigenetic landscape of vascular quiescence that will serve as a foundation for further mechanistic studies of vascular homeostasis and disease-associated activation.		Functional experiments prototypically validated the strongly epigenetically regulated inhibitors of TGFβ family signaling SMAD6 and SMAD7 as regulators of EC quiescence. These data establish the transcriptional and epigenetic landscape of vascular quiescence that will serve as a foundation for further mechanistic studies of vascular homeostasis and disease-associated activation.	Immunohistochemical staining	Functional experiments prototypically validated the strongly epigenetically regulated inhibitors of TGFβ family signaling SMAD6 and SMAD7 as regulators of EC quiescence. These data establish the transcriptional and epigenetic landscape of vascular quiescence that will serve as a foundation for further mechanistic studies of vascular homeostasis and disease-associated activation.			FACS,Immunofluorescence staining,Elisa,Immunoblot,qPCR,RNA-seq,T-WGBS,MassARRAY,Interactome analysis,				Smad7
29749529	chr17	44900352	44902352	GFAP	In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.	human	connective tissue	High+Lowthroughput	α?synuclein induces apoptosis of astrocytes by causing dysfunction of the endoplasmic reticulum?Golgi compartment	否	无	Parkinson's disease (PD)	 293FT	E_01_0495	Immunofluorescence,Immunoassay,Western blot, CHOP Knockdown,transfection,Immunostaining,flow cytometry,RNA-seq,siRNA,	In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.	Immunohistochemical staining	In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.	GFAP		Immunofluorescence,Immunoassay,Western blot, CHOP Knockdown,transfection,Immunostaining,flow cytometry,RNA-seq,siRNA,	In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.			
29749529	chr2	209421660	209423660	MAP2	In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.	human	connective tissue	High+Lowthroughput	α?synuclein induces apoptosis of astrocytes by causing dysfunction of the endoplasmic reticulum?Golgi compartment	否	无	Parkinson's disease (PD)	 293FT	E_01_0495	Immunofluorescence,Immunoassay,Western blot, CHOP Knockdown,transfection,Immunostaining,flow cytometry,RNA-seq,siRNA,	In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.		In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.	Immunohistochemical staining	In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.			Immunofluorescence,Immunoassay,Western blot, CHOP Knockdown,transfection,Immunostaining,flow cytometry,RNA-seq,siRNA,				MAP2
29749529	chr5	37809714	37811714	GDNF	In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.	human	connective tissue	High+Lowthroughput	α?synuclein induces apoptosis of astrocytes by causing dysfunction of the endoplasmic reticulum?Golgi compartment	否	无	Parkinson's disease (PD)	 293FT	E_01_0495	Immunofluorescence,Immunoassay,Western blot, CHOP Knockdown,transfection,Immunostaining,flow cytometry,RNA-seq,siRNA,	In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.	Immunohistochemical staining	In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.	GDNF		Immunofluorescence,Immunoassay,Western blot, CHOP Knockdown,transfection,Immunostaining,flow cytometry,RNA-seq,siRNA,	In addition, Golgi fragmentation was observed in the process. On the other hand, it was also demonstrated, in a primary neuronal‑astroglial co‑culture system, that the overexpression of α‑syn significantly decreased the levels of glia‑derived neurotrophic factor (GDNF) and partly inhibited neurite outgrowth. Although direct evidence is currently lacking, it was proposed that dysfunction of the ER‑Golgi compartment in astrocytes overexpressing α‑syn may lead to a decline of GDNF levels, which in turn would suppress neurite outgrowth. Taken together, the results of the present study offer further insights into the pathogenesis of PD from the perspective of astrocytes, which may provide novel strategies for the diagnosis and treatment of PD in the future.			
29749505	chr1	52156183	52158183	Stat1	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	mouse	lymphoid tissue	High+Lowthroughput	Identification of genes and pathways associated with multiple organ dysfunction syndrome by microarray analysis	否	无	Multiple organ dysfunction syndrome (MODS)	T lymphocyte	E_02_0314	Pathway enrichment analysis	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.		A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	Immunohistochemical staining	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.			Pathway enrichment analysis				Stat1
29749505	chr2	167528617	167530617	Cebpb	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	mouse	lymphoid tissue	High+Lowthroughput	Identification of genes and pathways associated with multiple organ dysfunction syndrome by microarray analysis	否	无	Multiple organ dysfunction syndrome (MODS)	T lymphocyte	E_02_0314	Pathway enrichment analysis	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.		A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	Immunohistochemical staining	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.			Pathway enrichment analysis				Cebpb
29749505	chr7	107164112	107166112	Olfml1	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	mouse	lymphoid tissue	High+Lowthroughput	Identification of genes and pathways associated with multiple organ dysfunction syndrome by microarray analysis	否	无	Multiple organ dysfunction syndrome (MODS)	T lymphocyte	E_02_0314	Pathway enrichment analysis	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.		A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	Immunohistochemical staining	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.			Pathway enrichment analysis				Olfml1
29749505	chr5	91036572	91038572	Cxcl1	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	mouse	lymphoid tissue	High+Lowthroughput	Identification of genes and pathways associated with multiple organ dysfunction syndrome by microarray analysis	否	无	Multiple organ dysfunction syndrome (MODS)	T lymphocyte	E_02_0314	Pathway enrichment analysis	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.		A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	Immunohistochemical staining	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.			Pathway enrichment analysis				Cxcl1
29749505	chr5	92491797	92493797	Cxcl10	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	mouse	lymphoid tissue	High+Lowthroughput	Identification of genes and pathways associated with multiple organ dysfunction syndrome by microarray analysis	否	无	Multiple organ dysfunction syndrome (MODS)	T lymphocyte	E_02_0314	Pathway enrichment analysis	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.		A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.	Immunohistochemical staining	A total of 18 DEGs were common among lung, liver and kidney tissues, including CCAAT/enhancer binding protein β (Cebpb) and olfactomedin‑like 1 (Olfml1). Cebpb modulated various other DEGs, such as Cxcl1, and Olfml1 was regulated by Stat5A. These genes and pathways may serve roles in the progression of MODS and may be considered to be potential therapy targets for MODS.			Pathway enrichment analysis				Cxcl10
29749465	chrY	2784042	2786042	SRY	In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.	human	Mammary tissue	High+Lowthroughput	12(S)-HETE induces lymph endothelial cell retraction in?vitro by upregulation of SOX18	否	无	mammary cancer	MDA-MB231 breast cancer cell	E_01_0496	CCID assay,Transfection,RT-qPCR,Western blot,immunofluorescence,	In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.	Immunohistochemical staining	In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.	SRY		CCID assay,Transfection,RT-qPCR,Western blot,immunofluorescence,	In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.			
29749465	chr20	64044111	64046111	SOX18	In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.	human	Mammary tissue	High+Lowthroughput	12(S)-HETE induces lymph endothelial cell retraction in?vitro by upregulation of SOX18	否	无	mammary cancer	MDA-MB231 breast cancer cell	E_01_0496	CCID assay,Transfection,RT-qPCR,Western blot,immunofluorescence,	In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.	Immunohistochemical staining	In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.	SOX18		CCID assay,Transfection,RT-qPCR,Western blot,immunofluorescence,	In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.			
29749465	chr1	213980378	213982378	PROX1	In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.	human	Mammary tissue	High+Lowthroughput	12(S)-HETE induces lymph endothelial cell retraction in?vitro by upregulation of SOX18	否	无	mammary cancer	MDA-MB231 breast cancer cell	E_01_0496	CCID assay,Transfection,RT-qPCR,Western blot,immunofluorescence,	In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.		In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.	Immunohistochemical staining	In addition, the current findings indicate that there is crosstalk between SOX18 and nuclear factor κ-light-chain-enhancer of activated B cells, which was demonstrated to contribute to MDA-MB231/lymph endothelial intravasation. The present data demonstrate that the endothelial-specific and lymph endothelial-specific transcription factors SOX18 and PROX1 contribute to LEC retraction.			CCID assay,Transfection,RT-qPCR,Western blot,immunofluorescence,				PROX1
29749460	chr6	7878754	7880754	TXNDC5	These findings suggested that TXNDC5 functions as an important stress survival factor to maintain tumorigenesis of CRC cells under hypoxia by regulating hypoxia‑induced ROS/ER stress signaling. The present study provided novel insights into the role of TXNDC5 in the tumorigenesis of CRC.	human	Colon tissue	High+Lowthroughput	Role of TXNDC5 in tumorigenesis of colorectal cancer cells: In vivo and in vitro evidence	否	无	Colorectal cancer (CRC)	rKo cell	E_01_0497	Western blot,RT‑qPCR,Immunohistochemistry,MTT cell proliferation assay,Colony formation assay,Cell apoptosis assay,Transient transfection of small interfering (si)RNA,	These findings suggested that TXNDC5 functions as an important stress survival factor to maintain tumorigenesis of CRC cells under hypoxia by regulating hypoxia‑induced ROS/ER stress signaling. The present study provided novel insights into the role of TXNDC5 in the tumorigenesis of CRC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggested that TXNDC5 functions as an important stress survival factor to maintain tumorigenesis of CRC cells under hypoxia by regulating hypoxia‑induced ROS/ER stress signaling. The present study provided novel insights into the role of TXNDC5 in the tumorigenesis of CRC.		These findings suggested that TXNDC5 functions as an important stress survival factor to maintain tumorigenesis of CRC cells under hypoxia by regulating hypoxia‑induced ROS/ER stress signaling. The present study provided novel insights into the role of TXNDC5 in the tumorigenesis of CRC.	Immunohistochemical staining	These findings suggested that TXNDC5 functions as an important stress survival factor to maintain tumorigenesis of CRC cells under hypoxia by regulating hypoxia‑induced ROS/ER stress signaling. The present study provided novel insights into the role of TXNDC5 in the tumorigenesis of CRC.			Western blot,RT‑qPCR,Immunohistochemistry,MTT cell proliferation assay,Colony formation assay,Cell apoptosis assay,Transient transfection of small interfering (si)RNA,				TXNDC5
29749460	chr22	39517183	39519183	ATF4	These findings suggested that TXNDC5 functions as an important stress survival factor to maintain tumorigenesis of CRC cells under hypoxia by regulating hypoxia‑induced ROS/ER stress signaling. The present study provided novel insights into the role of TXNDC5 in the tumorigenesis of CRC.	human	Colon tissue	High+Lowthroughput	Role of TXNDC5 in tumorigenesis of colorectal cancer cells: In vivo and in vitro evidence	否	无	Colorectal cancer (CRC)	rKo cell	E_01_0497	Western blot,RT‑qPCR,Immunohistochemistry,MTT cell proliferation assay,Colony formation assay,Cell apoptosis assay,Transient transfection of small interfering (si)RNA,	These findings suggested that TXNDC5 functions as an important stress survival factor to maintain tumorigenesis of CRC cells under hypoxia by regulating hypoxia‑induced ROS/ER stress signaling. The present study provided novel insights into the role of TXNDC5 in the tumorigenesis of CRC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These findings suggested that TXNDC5 functions as an important stress survival factor to maintain tumorigenesis of CRC cells under hypoxia by regulating hypoxia‑induced ROS/ER stress signaling. The present study provided novel insights into the role of TXNDC5 in the tumorigenesis of CRC.	Immunohistochemical staining	These findings suggested that TXNDC5 functions as an important stress survival factor to maintain tumorigenesis of CRC cells under hypoxia by regulating hypoxia‑induced ROS/ER stress signaling. The present study provided novel insights into the role of TXNDC5 in the tumorigenesis of CRC.	ATF4		Western blot,RT‑qPCR,Immunohistochemistry,MTT cell proliferation assay,Colony formation assay,Cell apoptosis assay,Transient transfection of small interfering (si)RNA,	These findings suggested that TXNDC5 functions as an important stress survival factor to maintain tumorigenesis of CRC cells under hypoxia by regulating hypoxia‑induced ROS/ER stress signaling. The present study provided novel insights into the role of TXNDC5 in the tumorigenesis of CRC.			
29749452	chr2	192746411	192748411	PCGEM1	In conclusion, the present study demonstrated a positive regulatory association between MEF2 and PCGEM1, and a reciprocal negative regulatory association between PCGEM1 and miR‑148a that controls cell apoptosis. The present study, therefore, provides new insights into the mechanism of PCGEM1 function in prostate cancer development.	human	Prostate cancer tissues	High+Lowthroughput	MEF2?activated long non?coding RNA PCGEM1 promotes cell proliferation in hormone?refractory prostate cancer through downregulation of miR?148a	否	无	prostatic cancer	LNCaP	E_01_0498	RT‑qPCR,Western blot,Cell transfection,luciferase reporter assay,Chromatin immunoprecipitation (ChIP) assay,Apoptosis assay,flow cytometry,siRNA,	In conclusion, the present study demonstrated a positive regulatory association between MEF2 and PCGEM1, and a reciprocal negative regulatory association between PCGEM1 and miR‑148a that controls cell apoptosis. The present study, therefore, provides new insights into the mechanism of PCGEM1 function in prostate cancer development.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, the present study demonstrated a positive regulatory association between MEF2 and PCGEM1, and a reciprocal negative regulatory association between PCGEM1 and miR‑148a that controls cell apoptosis. The present study, therefore, provides new insights into the mechanism of PCGEM1 function in prostate cancer development.		In conclusion, the present study demonstrated a positive regulatory association between MEF2 and PCGEM1, and a reciprocal negative regulatory association between PCGEM1 and miR‑148a that controls cell apoptosis. The present study, therefore, provides new insights into the mechanism of PCGEM1 function in prostate cancer development.	Immunohistochemical staining	In conclusion, the present study demonstrated a positive regulatory association between MEF2 and PCGEM1, and a reciprocal negative regulatory association between PCGEM1 and miR‑148a that controls cell apoptosis. The present study, therefore, provides new insights into the mechanism of PCGEM1 function in prostate cancer development.			RT‑qPCR,Western blot,Cell transfection,luciferase reporter assay,Chromatin immunoprecipitation (ChIP) assay,Apoptosis assay,flow cytometry,siRNA,				PCGEM1
29748386	chr5	132437549	132439549	IRF1	In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.	human	Adrenal tissue	High+Lowthroughput	Frequent interferon regulatory factor 1 (IRF1) binding at remote elements without histone modification	否	无	nothing	SW13 cell	E_01_0499	ChIP–qPCR,qPCR,ChIP,ChIP-chip assays,	In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.	Immunohistochemical staining	In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.	IRF1		ChIP–qPCR,qPCR,ChIP,ChIP-chip assays,	In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.			
29748386	chr2	190905653	190907653	STAT1	In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.	human	Adrenal tissue	High+Lowthroughput	Frequent interferon regulatory factor 1 (IRF1) binding at remote elements without histone modification	否	无	nothing	SW13 cell	E_01_0499	ChIP–qPCR,qPCR,ChIP,ChIP-chip assays,	In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.	Immunohistochemical staining	In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.	STAT1		ChIP–qPCR,qPCR,ChIP,ChIP-chip assays,	In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.			
29748386	chr19	10958357	10960357	SMARCA4	In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.	human	Adrenal tissue	High+Lowthroughput	Frequent interferon regulatory factor 1 (IRF1) binding at remote elements without histone modification	否	无	nothing	SW13 cell	E_01_0499	ChIP–qPCR,qPCR,ChIP,ChIP-chip assays,	In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.	Immunohistochemical staining	In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.	SMARCA4		ChIP–qPCR,qPCR,ChIP,ChIP-chip assays,	In conclusion, although IRF1 can trigger enhanceosome formation independently of STAT1, its ability to do so depends on local chromatin cues.			
29748098	chr7	148804691	148806691	EZH2	Increased EZH2 expression is associated with adverse pathologic features and inferior oncologic outcomes in patients with high-grade UTUC. The role of EZH2 biology in UTUC pathogenesis remains to be further elucidated.	human	Epithelial tissues	High+Lowthroughput	Multi-institutional evaluation of the prognostic significance of EZH2 expression in high-grade upper tract urothelial carcinoma	否	无	Upper urothelial carcinoma (utuc)	epithelial cell	E_01_0500	immunohistochemical staining (IHC),	Increased EZH2 expression is associated with adverse pathologic features and inferior oncologic outcomes in patients with high-grade UTUC. The role of EZH2 biology in UTUC pathogenesis remains to be further elucidated.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Increased EZH2 expression is associated with adverse pathologic features and inferior oncologic outcomes in patients with high-grade UTUC. The role of EZH2 biology in UTUC pathogenesis remains to be further elucidated.	Immunohistochemical staining	Increased EZH2 expression is associated with adverse pathologic features and inferior oncologic outcomes in patients with high-grade UTUC. The role of EZH2 biology in UTUC pathogenesis remains to be further elucidated.	EZH2		immunohistochemical staining (IHC),	Increased EZH2 expression is associated with adverse pathologic features and inferior oncologic outcomes in patients with high-grade UTUC. The role of EZH2 biology in UTUC pathogenesis remains to be further elucidated.			
29743187	chr12	100470925	100472925	NR1H4	In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases.	human	Liver tissue	High+Lowthroughput	Effects of Farnesoid X Receptor Activation on Arachidonic Acid Metabolism, NF-kB Signaling, and Hepatic Inflammation	否	无	Non alcoholic fatty liver disease (NAFLD), inflammation	THP-1 cells	E_01_0501	Migration assay,Transient transfection,gene expression analysis,immunostaining,	In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases.	Immunohistochemical staining	In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases.	NR1H4		Migration assay,Transient transfection,gene expression analysis,immunostaining,	In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases.			
29743187	chr6	31577761	31579761	LTB	In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases.	human	Liver tissue	High+Lowthroughput	Effects of Farnesoid X Receptor Activation on Arachidonic Acid Metabolism, NF-kB Signaling, and Hepatic Inflammation	否	无	Non alcoholic fatty liver disease (NAFLD), inflammation	THP-1 cells	E_01_0501	Migration assay,Transient transfection,gene expression analysis,immunostaining,	In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases.		In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases.	Immunohistochemical staining	In summary, NAFLD was characterized by an imbalance in arachidonate metabolism. FXR activation reprogramed arachidonate metabolism by inducing P450 epoxygenase expression and EET production. In vitro, FXR-mediated NF-kB inhibition required active P450 epoxygenases.			Migration assay,Transient transfection,gene expression analysis,immunostaining,				LTB
29742982	chr9	21137636	21139636	Keap1	Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.	human	Epithelial tissues	High+Lowthroughput	NFE2-Related Transcription Factor 2 Coordinates Antioxidant Defense with Thyroglobulin Production and Iodination in the Thyroid Gland	否	无	nothing	PCCL3 cell	E_01_0502	real-time PCR,Protein isolation,Western immunoblotting,immunohistochemistry,analysis of protein oxidation,RNA interference,Chromatin immunoprecip,Cell transfections,reporter assay,CRISPR/Cas9,	Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.		Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.	Immunohistochemical staining	Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.			real-time PCR,Protein isolation,Western immunoblotting,immunohistochemistry,analysis of protein oxidation,RNA interference,Chromatin immunoprecip,Cell transfections,reporter assay,CRISPR/Cas9,				Keap1
29742982	chr12	54289031	54291031	NFE2	Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.	human	Epithelial tissues	High+Lowthroughput	NFE2-Related Transcription Factor 2 Coordinates Antioxidant Defense with Thyroglobulin Production and Iodination in the Thyroid Gland	否	无	nothing	PCCL3 cell	E_01_0502	real-time PCR,Protein isolation,Western immunoblotting,immunohistochemistry,analysis of protein oxidation,RNA interference,Chromatin immunoprecip,Cell transfections,reporter assay,CRISPR/Cas9,	Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.	Immunohistochemical staining	Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.	NFE2		real-time PCR,Protein isolation,Western immunoblotting,immunohistochemistry,analysis of protein oxidation,RNA interference,Chromatin immunoprecip,Cell transfections,reporter assay,CRISPR/Cas9,	Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.			
29742982	chr15	66539822	66541822	Tg	Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.	human	Epithelial tissues	High+Lowthroughput	NFE2-Related Transcription Factor 2 Coordinates Antioxidant Defense with Thyroglobulin Production and Iodination in the Thyroid Gland	否	无	nothing	PCCL3 cell	E_01_0502	real-time PCR,Protein isolation,Western immunoblotting,immunohistochemistry,analysis of protein oxidation,RNA interference,Chromatin immunoprecip,Cell transfections,reporter assay,CRISPR/Cas9,	Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.		Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.	Immunohistochemical staining	Nrf2 exerts pleiotropic roles in the thyroid gland to couple cell stress defense mechanisms to iodide metabolism and the thyroid hormone synthesis machinery, both under basal conditions and in response to excess iodide.			real-time PCR,Protein isolation,Western immunoblotting,immunohistochemistry,analysis of protein oxidation,RNA interference,Chromatin immunoprecip,Cell transfections,reporter assay,CRISPR/Cas9,				Tg
29740349	chr22	28791734	28793734	XBP1	The levels of p-PI3K(Ser191), p-PI3K(Ser262), p-AKT(Ser473), and p-mTOR were decreased postburn, suggesting that autophagy-related PI3K/AKT/mTOR pathway is involved in the intestinal epithelial barrier dysfunction following severe burn. In summary, severe burn injury induces the ER stress and autophagy in intestinal epithelia, leading to the disruption of intestinal barrier.	human	Epithelial tissues	High+Lowthroughput	Severe Burn-Induced Intestinal Epithelial Barrier Dysfunction Is Associated With Endoplasmic Reticulum Stress and Autophagy in Mice	否	无	Intestinal barrier dysfunction	epithelial cell	E_01_0503	histological,immunofluorescent,Western blot,Immunofluorescent Staining,Microscopy,Image Analysis,	The levels of p-PI3K(Ser191), p-PI3K(Ser262), p-AKT(Ser473), and p-mTOR were decreased postburn, suggesting that autophagy-related PI3K/AKT/mTOR pathway is involved in the intestinal epithelial barrier dysfunction following severe burn. In summary, severe burn injury induces the ER stress and autophagy in intestinal epithelia, leading to the disruption of intestinal barrier.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The levels of p-PI3K(Ser191), p-PI3K(Ser262), p-AKT(Ser473), and p-mTOR were decreased postburn, suggesting that autophagy-related PI3K/AKT/mTOR pathway is involved in the intestinal epithelial barrier dysfunction following severe burn. In summary, severe burn injury induces the ER stress and autophagy in intestinal epithelia, leading to the disruption of intestinal barrier.	Immunohistochemical staining	The levels of p-PI3K(Ser191), p-PI3K(Ser262), p-AKT(Ser473), and p-mTOR were decreased postburn, suggesting that autophagy-related PI3K/AKT/mTOR pathway is involved in the intestinal epithelial barrier dysfunction following severe burn. In summary, severe burn injury induces the ER stress and autophagy in intestinal epithelia, leading to the disruption of intestinal barrier.	XBP1		histological,immunofluorescent,Western blot,Immunofluorescent Staining,Microscopy,Image Analysis,	The levels of p-PI3K(Ser191), p-PI3K(Ser262), p-AKT(Ser473), and p-mTOR were decreased postburn, suggesting that autophagy-related PI3K/AKT/mTOR pathway is involved in the intestinal epithelial barrier dysfunction following severe burn. In summary, severe burn injury induces the ER stress and autophagy in intestinal epithelia, leading to the disruption of intestinal barrier.			
29740349	chr6	106042654	106044654	ATG5	The levels of p-PI3K(Ser191), p-PI3K(Ser262), p-AKT(Ser473), and p-mTOR were decreased postburn, suggesting that autophagy-related PI3K/AKT/mTOR pathway is involved in the intestinal epithelial barrier dysfunction following severe burn. In summary, severe burn injury induces the ER stress and autophagy in intestinal epithelia, leading to the disruption of intestinal barrier.	human	Epithelial tissues	High+Lowthroughput	Severe Burn-Induced Intestinal Epithelial Barrier Dysfunction Is Associated With Endoplasmic Reticulum Stress and Autophagy in Mice	否	无	Intestinal barrier dysfunction	epithelial cell	E_01_0503	histological,immunofluorescent,Western blot,Immunofluorescent Staining,Microscopy,Image Analysis,	The levels of p-PI3K(Ser191), p-PI3K(Ser262), p-AKT(Ser473), and p-mTOR were decreased postburn, suggesting that autophagy-related PI3K/AKT/mTOR pathway is involved in the intestinal epithelial barrier dysfunction following severe burn. In summary, severe burn injury induces the ER stress and autophagy in intestinal epithelia, leading to the disruption of intestinal barrier.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The levels of p-PI3K(Ser191), p-PI3K(Ser262), p-AKT(Ser473), and p-mTOR were decreased postburn, suggesting that autophagy-related PI3K/AKT/mTOR pathway is involved in the intestinal epithelial barrier dysfunction following severe burn. In summary, severe burn injury induces the ER stress and autophagy in intestinal epithelia, leading to the disruption of intestinal barrier.		The levels of p-PI3K(Ser191), p-PI3K(Ser262), p-AKT(Ser473), and p-mTOR were decreased postburn, suggesting that autophagy-related PI3K/AKT/mTOR pathway is involved in the intestinal epithelial barrier dysfunction following severe burn. In summary, severe burn injury induces the ER stress and autophagy in intestinal epithelia, leading to the disruption of intestinal barrier.	Immunohistochemical staining	The levels of p-PI3K(Ser191), p-PI3K(Ser262), p-AKT(Ser473), and p-mTOR were decreased postburn, suggesting that autophagy-related PI3K/AKT/mTOR pathway is involved in the intestinal epithelial barrier dysfunction following severe burn. In summary, severe burn injury induces the ER stress and autophagy in intestinal epithelia, leading to the disruption of intestinal barrier.			histological,immunofluorescent,Western blot,Immunofluorescent Staining,Microscopy,Image Analysis,				ATG5
29740122	chr1	150643764	150645764	GOLPH3L	Furthermore, we identify genetic variants affecting expression of 927 enhancers, which we refer to as enhancer expression quantitative loci or eeQTLs. Enhancer expression patterns are consistent across studies, including differentially expressed eRNAs and eeQTLs. Combining eeQTLs with a genome-wide association study of schizophrenia identifies a genetic variant that alters enhancer function and expression of its target gene, GOLPH3L. Our novel approach to analyzing enhancer transcription is adaptable to other large-scale, non-poly-A depleted, RNA-seq studies.	human	Nervous tissue	High+Lowthroughput	Differential activity of transcribed enhancers in the prefrontal cortex of 537 cases with schizophrenia and controls	否	无	Schizophrenia	neuronal cell	E_01_0504	RNA-seq,Gene co-expression analyses,ATACseq,	Furthermore, we identify genetic variants affecting expression of 927 enhancers, which we refer to as enhancer expression quantitative loci or eeQTLs. Enhancer expression patterns are consistent across studies, including differentially expressed eRNAs and eeQTLs. Combining eeQTLs with a genome-wide association study of schizophrenia identifies a genetic variant that alters enhancer function and expression of its target gene, GOLPH3L. Our novel approach to analyzing enhancer transcription is adaptable to other large-scale, non-poly-A depleted, RNA-seq studies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, we identify genetic variants affecting expression of 927 enhancers, which we refer to as enhancer expression quantitative loci or eeQTLs. Enhancer expression patterns are consistent across studies, including differentially expressed eRNAs and eeQTLs. Combining eeQTLs with a genome-wide association study of schizophrenia identifies a genetic variant that alters enhancer function and expression of its target gene, GOLPH3L. Our novel approach to analyzing enhancer transcription is adaptable to other large-scale, non-poly-A depleted, RNA-seq studies.		Furthermore, we identify genetic variants affecting expression of 927 enhancers, which we refer to as enhancer expression quantitative loci or eeQTLs. Enhancer expression patterns are consistent across studies, including differentially expressed eRNAs and eeQTLs. Combining eeQTLs with a genome-wide association study of schizophrenia identifies a genetic variant that alters enhancer function and expression of its target gene, GOLPH3L. Our novel approach to analyzing enhancer transcription is adaptable to other large-scale, non-poly-A depleted, RNA-seq studies.	Immunohistochemical staining	Furthermore, we identify genetic variants affecting expression of 927 enhancers, which we refer to as enhancer expression quantitative loci or eeQTLs. Enhancer expression patterns are consistent across studies, including differentially expressed eRNAs and eeQTLs. Combining eeQTLs with a genome-wide association study of schizophrenia identifies a genetic variant that alters enhancer function and expression of its target gene, GOLPH3L. Our novel approach to analyzing enhancer transcription is adaptable to other large-scale, non-poly-A depleted, RNA-seq studies.			RNA-seq,Gene co-expression analyses,ATACseq,				GOLPH3L
29739060	chr1	206764791	206766791	IL10	Our findings suggested a potential role of miR-10a in the inflammatory process underlying atherosclerosis; however, more studies are needed to support these finding.	human	Nervous tissue	High+Lowthroughput	Lower Expression of miR-10a in Coronary Artery Disease and its Association with Pro/Anti-Inflammatory Cytokines	否	无	Coronary artery disease (CAD), atherosclerosis	peripheral blood mononuclear cell	E_01_0505	Quantitative real-time PCR,ELISA,	Our findings suggested a potential role of miR-10a in the inflammatory process underlying atherosclerosis; however, more studies are needed to support these finding.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our findings suggested a potential role of miR-10a in the inflammatory process underlying atherosclerosis; however, more studies are needed to support these finding.	Immunohistochemical staining	Our findings suggested a potential role of miR-10a in the inflammatory process underlying atherosclerosis; however, more studies are needed to support these finding.	IL10		Quantitative real-time PCR,ELISA,	Our findings suggested a potential role of miR-10a in the inflammatory process underlying atherosclerosis; however, more studies are needed to support these finding.			
29738565	chr4	71739247	71741247	GC	Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5. Furthermore blocked GBR are in a closed conformation prior to Hic-5 depletion, and require Hic-5 depletion and glucocorticoid treatment to create an open conformation necessary for GR occupancy. A transcription factor binding motif characteristic of the ETS family was enriched near blocked GBR and blocked genes but not near non-blocked GBR or non-blocked GR target genes. Thus, we identify specific differences in chromatin conformation, chromatin remodeler requirements, and local DNA sequence motifs that contribute to gene-specific actions of transcription factors and coregulators. These findings shed light on mechanisms that contribute to binding site selection by transcription factors, which vary in a cell type-specific manner.	human	Osteosarcoma tissues	High+Lowthroughput	Different chromatin and DNA sequence characteristics define glucocorticoid receptor binding sites that are blocked or not blocked by coregulator Hic-5	否	无	nothing	U2OS osteosarcoma cells 	E_01_0506	siRNA transfection,ChIP,Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq),	Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5. Furthermore blocked GBR are in a closed conformation prior to Hic-5 depletion, and require Hic-5 depletion and glucocorticoid treatment to create an open conformation necessary for GR occupancy. A transcription factor binding motif characteristic of the ETS family was enriched near blocked GBR and blocked genes but not near non-blocked GBR or non-blocked GR target genes. Thus, we identify specific differences in chromatin conformation, chromatin remodeler requirements, and local DNA sequence motifs that contribute to gene-specific actions of transcription factors and coregulators. These findings shed light on mechanisms that contribute to binding site selection by transcription factors, which vary in a cell type-specific manner.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5. Furthermore blocked GBR are in a closed conformation prior to Hic-5 depletion, and require Hic-5 depletion and glucocorticoid treatment to create an open conformation necessary for GR occupancy. A transcription factor binding motif characteristic of the ETS family was enriched near blocked GBR and blocked genes but not near non-blocked GBR or non-blocked GR target genes. Thus, we identify specific differences in chromatin conformation, chromatin remodeler requirements, and local DNA sequence motifs that contribute to gene-specific actions of transcription factors and coregulators. These findings shed light on mechanisms that contribute to binding site selection by transcription factors, which vary in a cell type-specific manner.		Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5. Furthermore blocked GBR are in a closed conformation prior to Hic-5 depletion, and require Hic-5 depletion and glucocorticoid treatment to create an open conformation necessary for GR occupancy. A transcription factor binding motif characteristic of the ETS family was enriched near blocked GBR and blocked genes but not near non-blocked GBR or non-blocked GR target genes. Thus, we identify specific differences in chromatin conformation, chromatin remodeler requirements, and local DNA sequence motifs that contribute to gene-specific actions of transcription factors and coregulators. These findings shed light on mechanisms that contribute to binding site selection by transcription factors, which vary in a cell type-specific manner.	Immunohistochemical staining	Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5. Furthermore blocked GBR are in a closed conformation prior to Hic-5 depletion, and require Hic-5 depletion and glucocorticoid treatment to create an open conformation necessary for GR occupancy. A transcription factor binding motif characteristic of the ETS family was enriched near blocked GBR and blocked genes but not near non-blocked GBR or non-blocked GR target genes. Thus, we identify specific differences in chromatin conformation, chromatin remodeler requirements, and local DNA sequence motifs that contribute to gene-specific actions of transcription factors and coregulators. These findings shed light on mechanisms that contribute to binding site selection by transcription factors, which vary in a cell type-specific manner.			siRNA transfection,ChIP,Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq),				GC
29738565	chr16	53051758	53053758	CHD9	Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5. Furthermore blocked GBR are in a closed conformation prior to Hic-5 depletion, and require Hic-5 depletion and glucocorticoid treatment to create an open conformation necessary for GR occupancy. A transcription factor binding motif characteristic of the ETS family was enriched near blocked GBR and blocked genes but not near non-blocked GBR or non-blocked GR target genes. Thus, we identify specific differences in chromatin conformation, chromatin remodeler requirements, and local DNA sequence motifs that contribute to gene-specific actions of transcription factors and coregulators. These findings shed light on mechanisms that contribute to binding site selection by transcription factors, which vary in a cell type-specific manner.	human	Osteosarcoma tissues	High+Lowthroughput	Different chromatin and DNA sequence characteristics define glucocorticoid receptor binding sites that are blocked or not blocked by coregulator Hic-5	否	无	nothing	U2OS osteosarcoma cells 	E_01_0506	siRNA transfection,ChIP,Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq),	Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5. Furthermore blocked GBR are in a closed conformation prior to Hic-5 depletion, and require Hic-5 depletion and glucocorticoid treatment to create an open conformation necessary for GR occupancy. A transcription factor binding motif characteristic of the ETS family was enriched near blocked GBR and blocked genes but not near non-blocked GBR or non-blocked GR target genes. Thus, we identify specific differences in chromatin conformation, chromatin remodeler requirements, and local DNA sequence motifs that contribute to gene-specific actions of transcription factors and coregulators. These findings shed light on mechanisms that contribute to binding site selection by transcription factors, which vary in a cell type-specific manner.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5. Furthermore blocked GBR are in a closed conformation prior to Hic-5 depletion, and require Hic-5 depletion and glucocorticoid treatment to create an open conformation necessary for GR occupancy. A transcription factor binding motif characteristic of the ETS family was enriched near blocked GBR and blocked genes but not near non-blocked GBR or non-blocked GR target genes. Thus, we identify specific differences in chromatin conformation, chromatin remodeler requirements, and local DNA sequence motifs that contribute to gene-specific actions of transcription factors and coregulators. These findings shed light on mechanisms that contribute to binding site selection by transcription factors, which vary in a cell type-specific manner.		Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5. Furthermore blocked GBR are in a closed conformation prior to Hic-5 depletion, and require Hic-5 depletion and glucocorticoid treatment to create an open conformation necessary for GR occupancy. A transcription factor binding motif characteristic of the ETS family was enriched near blocked GBR and blocked genes but not near non-blocked GBR or non-blocked GR target genes. Thus, we identify specific differences in chromatin conformation, chromatin remodeler requirements, and local DNA sequence motifs that contribute to gene-specific actions of transcription factors and coregulators. These findings shed light on mechanisms that contribute to binding site selection by transcription factors, which vary in a cell type-specific manner.	Immunohistochemical staining	Here we show genome-wide that blocked GBR generally require CHD9 and BRM for GR occupancy in contrast to GBR that are not blocked by Hic-5. Hic-5 blocked GBR are enriched near Hic-5 blocked GR target genes but not near GR target genes that are not blocked by Hic-5. Furthermore blocked GBR are in a closed conformation prior to Hic-5 depletion, and require Hic-5 depletion and glucocorticoid treatment to create an open conformation necessary for GR occupancy. A transcription factor binding motif characteristic of the ETS family was enriched near blocked GBR and blocked genes but not near non-blocked GBR or non-blocked GR target genes. Thus, we identify specific differences in chromatin conformation, chromatin remodeler requirements, and local DNA sequence motifs that contribute to gene-specific actions of transcription factors and coregulators. These findings shed light on mechanisms that contribute to binding site selection by transcription factors, which vary in a cell type-specific manner.			siRNA transfection,ChIP,Assay for Transposase-Accessible Chromatin using sequencing (ATAC-seq),				CHD9
29738494	chr19	41216765	41218765	AXL	Using the first X-ray structure of the hYAP50⁻71-hTEAD1209⁻426 complex (PDB 3KYS) published in 2010, a protein-protein interaction inhibitors-enriched library (175,000 chemical compounds) was screened against this hydrophobic pocket of TEAD. Four different chemical families have been identified and evaluated using biophysical techniques (thermal shift assay, microscale thermophoresis) and in cellulo assays (luciferase activity in transfected HEK293 cells, RTqPCR in MDA-MB231 cells). A first promising hit with micromolar inhibition in the luciferase gene reporter assay was discovered. This hit also decreased mRNA levels of TEAD target genes.	human	connective tissue	High+Lowthroughput	Toward the Discovery of a Novel Class of YAP?TEAD Interaction Inhibitors by Virtual Screening Approach Targeting YAP?TEAD Protein?Protein Interface	否	无	cancer	HEK293 cell	E_01_0507	RT-qPCR,luciferase gene reporter assay,Microscale Thermophoresis,	Using the first X-ray structure of the hYAP50⁻71-hTEAD1209⁻426 complex (PDB 3KYS) published in 2010, a protein-protein interaction inhibitors-enriched library (175,000 chemical compounds) was screened against this hydrophobic pocket of TEAD. Four different chemical families have been identified and evaluated using biophysical techniques (thermal shift assay, microscale thermophoresis) and in cellulo assays (luciferase activity in transfected HEK293 cells, RTqPCR in MDA-MB231 cells). A first promising hit with micromolar inhibition in the luciferase gene reporter assay was discovered. This hit also decreased mRNA levels of TEAD target genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Using the first X-ray structure of the hYAP50⁻71-hTEAD1209⁻426 complex (PDB 3KYS) published in 2010, a protein-protein interaction inhibitors-enriched library (175,000 chemical compounds) was screened against this hydrophobic pocket of TEAD. Four different chemical families have been identified and evaluated using biophysical techniques (thermal shift assay, microscale thermophoresis) and in cellulo assays (luciferase activity in transfected HEK293 cells, RTqPCR in MDA-MB231 cells). A first promising hit with micromolar inhibition in the luciferase gene reporter assay was discovered. This hit also decreased mRNA levels of TEAD target genes.		Using the first X-ray structure of the hYAP50⁻71-hTEAD1209⁻426 complex (PDB 3KYS) published in 2010, a protein-protein interaction inhibitors-enriched library (175,000 chemical compounds) was screened against this hydrophobic pocket of TEAD. Four different chemical families have been identified and evaluated using biophysical techniques (thermal shift assay, microscale thermophoresis) and in cellulo assays (luciferase activity in transfected HEK293 cells, RTqPCR in MDA-MB231 cells). A first promising hit with micromolar inhibition in the luciferase gene reporter assay was discovered. This hit also decreased mRNA levels of TEAD target genes.	Immunohistochemical staining	Using the first X-ray structure of the hYAP50⁻71-hTEAD1209⁻426 complex (PDB 3KYS) published in 2010, a protein-protein interaction inhibitors-enriched library (175,000 chemical compounds) was screened against this hydrophobic pocket of TEAD. Four different chemical families have been identified and evaluated using biophysical techniques (thermal shift assay, microscale thermophoresis) and in cellulo assays (luciferase activity in transfected HEK293 cells, RTqPCR in MDA-MB231 cells). A first promising hit with micromolar inhibition in the luciferase gene reporter assay was discovered. This hit also decreased mRNA levels of TEAD target genes.			RT-qPCR,luciferase gene reporter assay,Microscale Thermophoresis,				AXL
29737550	chr7	45108306	45110306	Bax	In-silico analysis revealed new enhancer and silencer motifs for mutant alleles of CASP-3rs4647602 and rs4647610 polymorphisms. In conclusion, placental CASP-3rs4647602 and rs4647610 polymorphisms were not associated with PE. Further studies with higher sample size are necessary to confirm or refute these findings.	human	Placental tissue	High+Lowthroughput	The association of the placental CASPASE-3 gene polymorphisms and preeclampsia susceptibility and in-silico analysis	是	rs4647602,rs4647610	Preeclampsia		E_01_0508	PCR-RFLP,Bioinformatics analysis,	In-silico analysis revealed new enhancer and silencer motifs for mutant alleles of CASP-3rs4647602 and rs4647610 polymorphisms. In conclusion, placental CASP-3rs4647602 and rs4647610 polymorphisms were not associated with PE. Further studies with higher sample size are necessary to confirm or refute these findings.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In-silico analysis revealed new enhancer and silencer motifs for mutant alleles of CASP-3rs4647602 and rs4647610 polymorphisms. In conclusion, placental CASP-3rs4647602 and rs4647610 polymorphisms were not associated with PE. Further studies with higher sample size are necessary to confirm or refute these findings.		In-silico analysis revealed new enhancer and silencer motifs for mutant alleles of CASP-3rs4647602 and rs4647610 polymorphisms. In conclusion, placental CASP-3rs4647602 and rs4647610 polymorphisms were not associated with PE. Further studies with higher sample size are necessary to confirm or refute these findings.	Immunohistochemical staining	In-silico analysis revealed new enhancer and silencer motifs for mutant alleles of CASP-3rs4647602 and rs4647610 polymorphisms. In conclusion, placental CASP-3rs4647602 and rs4647610 polymorphisms were not associated with PE. Further studies with higher sample size are necessary to confirm or refute these findings.			PCR-RFLP,Bioinformatics analysis,				Bax
29736797	chr3	41192441	41194441	CTNNB1	We examined three SN-GPCs by immunohistochemistry and CTNNB1 mutation analysis. All cases expressed nuclear β-catenin. We identified CTNNB1 exon 3 mutations in two analyzable cases. Lymphoid enhancer-binding factor 1 (LEF1), a protein downstream from β-catenin, was also expressed in all cases. Our results further characterized the activation of the Wnt signaling pathway caused by CTNNB1 exon 3 mutation and suggest the utility of LEF1 immunohistochemistry in the differential diagnosis of SN-GPC.	human	/	High+Lowthroughput	β-catenin (CTNNB1) mutation and LEF1 expression in sinonasal glomangiopericytoma (sinonasal-type hemangiopericytoma)	否	无	Sinonasal tubular cell tumor (sn-gpc)		E_01_0509	Immunohistochemistry,PCR,Sanger sequencing,	We examined three SN-GPCs by immunohistochemistry and CTNNB1 mutation analysis. All cases expressed nuclear β-catenin. We identified CTNNB1 exon 3 mutations in two analyzable cases. Lymphoid enhancer-binding factor 1 (LEF1), a protein downstream from β-catenin, was also expressed in all cases. Our results further characterized the activation of the Wnt signaling pathway caused by CTNNB1 exon 3 mutation and suggest the utility of LEF1 immunohistochemistry in the differential diagnosis of SN-GPC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We examined three SN-GPCs by immunohistochemistry and CTNNB1 mutation analysis. All cases expressed nuclear β-catenin. We identified CTNNB1 exon 3 mutations in two analyzable cases. Lymphoid enhancer-binding factor 1 (LEF1), a protein downstream from β-catenin, was also expressed in all cases. Our results further characterized the activation of the Wnt signaling pathway caused by CTNNB1 exon 3 mutation and suggest the utility of LEF1 immunohistochemistry in the differential diagnosis of SN-GPC.	Immunohistochemical staining	We examined three SN-GPCs by immunohistochemistry and CTNNB1 mutation analysis. All cases expressed nuclear β-catenin. We identified CTNNB1 exon 3 mutations in two analyzable cases. Lymphoid enhancer-binding factor 1 (LEF1), a protein downstream from β-catenin, was also expressed in all cases. Our results further characterized the activation of the Wnt signaling pathway caused by CTNNB1 exon 3 mutation and suggest the utility of LEF1 immunohistochemistry in the differential diagnosis of SN-GPC.	CTNNB1		Immunohistochemistry,PCR,Sanger sequencing,	We examined three SN-GPCs by immunohistochemistry and CTNNB1 mutation analysis. All cases expressed nuclear β-catenin. We identified CTNNB1 exon 3 mutations in two analyzable cases. Lymphoid enhancer-binding factor 1 (LEF1), a protein downstream from β-catenin, was also expressed in all cases. Our results further characterized the activation of the Wnt signaling pathway caused by CTNNB1 exon 3 mutation and suggest the utility of LEF1 immunohistochemistry in the differential diagnosis of SN-GPC.			
29736797	chr4	108044785	108046785	LEF1	We examined three SN-GPCs by immunohistochemistry and CTNNB1 mutation analysis. All cases expressed nuclear β-catenin. We identified CTNNB1 exon 3 mutations in two analyzable cases. Lymphoid enhancer-binding factor 1 (LEF1), a protein downstream from β-catenin, was also expressed in all cases. Our results further characterized the activation of the Wnt signaling pathway caused by CTNNB1 exon 3 mutation and suggest the utility of LEF1 immunohistochemistry in the differential diagnosis of SN-GPC.	human	/	High+Lowthroughput	β-catenin (CTNNB1) mutation and LEF1 expression in sinonasal glomangiopericytoma (sinonasal-type hemangiopericytoma)	否	无	Sinonasal tubular cell tumor (sn-gpc)		E_01_0509	Immunohistochemistry,PCR,Sanger sequencing,	We examined three SN-GPCs by immunohistochemistry and CTNNB1 mutation analysis. All cases expressed nuclear β-catenin. We identified CTNNB1 exon 3 mutations in two analyzable cases. Lymphoid enhancer-binding factor 1 (LEF1), a protein downstream from β-catenin, was also expressed in all cases. Our results further characterized the activation of the Wnt signaling pathway caused by CTNNB1 exon 3 mutation and suggest the utility of LEF1 immunohistochemistry in the differential diagnosis of SN-GPC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We examined three SN-GPCs by immunohistochemistry and CTNNB1 mutation analysis. All cases expressed nuclear β-catenin. We identified CTNNB1 exon 3 mutations in two analyzable cases. Lymphoid enhancer-binding factor 1 (LEF1), a protein downstream from β-catenin, was also expressed in all cases. Our results further characterized the activation of the Wnt signaling pathway caused by CTNNB1 exon 3 mutation and suggest the utility of LEF1 immunohistochemistry in the differential diagnosis of SN-GPC.	Immunohistochemical staining	We examined three SN-GPCs by immunohistochemistry and CTNNB1 mutation analysis. All cases expressed nuclear β-catenin. We identified CTNNB1 exon 3 mutations in two analyzable cases. Lymphoid enhancer-binding factor 1 (LEF1), a protein downstream from β-catenin, was also expressed in all cases. Our results further characterized the activation of the Wnt signaling pathway caused by CTNNB1 exon 3 mutation and suggest the utility of LEF1 immunohistochemistry in the differential diagnosis of SN-GPC.	LEF1		Immunohistochemistry,PCR,Sanger sequencing,	We examined three SN-GPCs by immunohistochemistry and CTNNB1 mutation analysis. All cases expressed nuclear β-catenin. We identified CTNNB1 exon 3 mutations in two analyzable cases. Lymphoid enhancer-binding factor 1 (LEF1), a protein downstream from β-catenin, was also expressed in all cases. Our results further characterized the activation of the Wnt signaling pathway caused by CTNNB1 exon 3 mutation and suggest the utility of LEF1 immunohistochemistry in the differential diagnosis of SN-GPC.			
29736028	chr1	205825403	205827403	PM20D1	We find that PM20D1 is a methylation and expression quantitative trait locus coupled to an AD-risk associated haplotype, which displays enhancer-like characteristics and contacts the PM20D1 promoter via a haplotype-dependent, CCCTC-binding-factor-mediated chromatin loop. Furthermore, PM20D1 is increased following AD-related neurotoxic insults at symptomatic stages in the APP/PS1 mouse model of AD and in human patients with AD who are carriers of the non-risk haplotype. In line, genetically increasing or decreasing the expression of PM20D1 reduces and aggravates AD-related pathologies, respectively. These findings suggest that in a particular genetic background, PM20D1 contributes to neuroprotection against AD.	human	lymphoid tissue	High+Lowthroughput	PM20D1 is a?quantitative trait locus associated with Alzheimer's disease	是	rs708727,s960603	Alzheimer's disease (AD)	Immortalized B cells	E_01_0510	GWAS,EWAS,RT–PCR,quantitative real-time PCR,DNA methylation,RNA expression,Chromatin conformation capture (3C) protocol,Chromatin immunoprecipitation (ChIP) assays,Cloning,Immunohistochemistry (IHC),Western blot,Luciferase assays,Cell viability assays,Lentivirus production,Amyloid plaques,Amyloid-β assays,	We find that PM20D1 is a methylation and expression quantitative trait locus coupled to an AD-risk associated haplotype, which displays enhancer-like characteristics and contacts the PM20D1 promoter via a haplotype-dependent, CCCTC-binding-factor-mediated chromatin loop. Furthermore, PM20D1 is increased following AD-related neurotoxic insults at symptomatic stages in the APP/PS1 mouse model of AD and in human patients with AD who are carriers of the non-risk haplotype. In line, genetically increasing or decreasing the expression of PM20D1 reduces and aggravates AD-related pathologies, respectively. These findings suggest that in a particular genetic background, PM20D1 contributes to neuroprotection against AD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that PM20D1 is a methylation and expression quantitative trait locus coupled to an AD-risk associated haplotype, which displays enhancer-like characteristics and contacts the PM20D1 promoter via a haplotype-dependent, CCCTC-binding-factor-mediated chromatin loop. Furthermore, PM20D1 is increased following AD-related neurotoxic insults at symptomatic stages in the APP/PS1 mouse model of AD and in human patients with AD who are carriers of the non-risk haplotype. In line, genetically increasing or decreasing the expression of PM20D1 reduces and aggravates AD-related pathologies, respectively. These findings suggest that in a particular genetic background, PM20D1 contributes to neuroprotection against AD.		We find that PM20D1 is a methylation and expression quantitative trait locus coupled to an AD-risk associated haplotype, which displays enhancer-like characteristics and contacts the PM20D1 promoter via a haplotype-dependent, CCCTC-binding-factor-mediated chromatin loop. Furthermore, PM20D1 is increased following AD-related neurotoxic insults at symptomatic stages in the APP/PS1 mouse model of AD and in human patients with AD who are carriers of the non-risk haplotype. In line, genetically increasing or decreasing the expression of PM20D1 reduces and aggravates AD-related pathologies, respectively. These findings suggest that in a particular genetic background, PM20D1 contributes to neuroprotection against AD.	Immunohistochemical staining	We find that PM20D1 is a methylation and expression quantitative trait locus coupled to an AD-risk associated haplotype, which displays enhancer-like characteristics and contacts the PM20D1 promoter via a haplotype-dependent, CCCTC-binding-factor-mediated chromatin loop. Furthermore, PM20D1 is increased following AD-related neurotoxic insults at symptomatic stages in the APP/PS1 mouse model of AD and in human patients with AD who are carriers of the non-risk haplotype. In line, genetically increasing or decreasing the expression of PM20D1 reduces and aggravates AD-related pathologies, respectively. These findings suggest that in a particular genetic background, PM20D1 contributes to neuroprotection against AD.			GWAS,EWAS,RT–PCR,quantitative real-time PCR,DNA methylation,RNA expression,Chromatin conformation capture (3C) protocol,Chromatin immunoprecipitation (ChIP) assays,Cloning,Immunohistochemistry (IHC),Western blot,Luciferase assays,Cell viability assays,Lentivirus production,Amyloid plaques,Amyloid-β assays,				PM20D1
29736013	chrX	44870832	44872832	KDM6A	Collectively, our findings identify a dual role for UTX in suppressing acute myeloid leukemia via repression of oncogenic ETS and upregulation of tumor-suppressive GATA programs.	human	connective tissue	High+Lowthroughput	UTX-mediated enhancer and chromatin remodeling suppresses myeloid leukemogenesis through noncatalytic inverse regulation of ETS and GATA programs	否	无	Acute myeloid leukemia		E_01_0511	PCR,qRT–PCR,cDNA synthesis,Flow cytometry,Protein extraction,immunoblotting,coimmunoprecipitation,Proliferation assays,Plasmids,cloning,Histological analysis of mouse tissue,RNA extraction,RNA-seq,ChIP–seq,ChIP–qPCR,ATAC–seq,Chip–seq,motif analysis,GSEA,data visualization,LC–MS/MS analysis,Exome sequencing,Exome data analysis,	Collectively, our findings identify a dual role for UTX in suppressing acute myeloid leukemia via repression of oncogenic ETS and upregulation of tumor-suppressive GATA programs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Collectively, our findings identify a dual role for UTX in suppressing acute myeloid leukemia via repression of oncogenic ETS and upregulation of tumor-suppressive GATA programs.		Collectively, our findings identify a dual role for UTX in suppressing acute myeloid leukemia via repression of oncogenic ETS and upregulation of tumor-suppressive GATA programs.	Immunohistochemical staining	Collectively, our findings identify a dual role for UTX in suppressing acute myeloid leukemia via repression of oncogenic ETS and upregulation of tumor-suppressive GATA programs.			PCR,qRT–PCR,cDNA synthesis,Flow cytometry,Protein extraction,immunoblotting,coimmunoprecipitation,Proliferation assays,Plasmids,cloning,Histological analysis of mouse tissue,RNA extraction,RNA-seq,ChIP–seq,ChIP–qPCR,ATAC–seq,Chip–seq,motif analysis,GSEA,data visualization,LC–MS/MS analysis,Exome sequencing,Exome data analysis,				KDM6A
29735004	chr13	40553262	40555262	FOXO1	EPAC2 knockdown markedly reduced Phe-stimulated C/EBPβ and C/EBPδ mRNA levels, as well as forkhead box O1 (FOXO1) protein levels. These results suggest that EPAC signalling enhances PKA-mediated dPRL expression in ESCs by acting on C/EBP response elements in the promoter region of the gene.	human	Epithelial tissues	High+Lowthroughput	Exchange protein directly activated by cAMP (EPAC) promotes transcriptional activation of the decidual prolactin gene via CCAAT/enhancer-binding protein in human endometrial stromal cells	否	无	nothing	endometrial stromal cell	E_01_0512	Luciferase assay,Treatment with siRNAs,RT-qPCR,Immunoblotting,Immunofluorescence,transfection,	EPAC2 knockdown markedly reduced Phe-stimulated C/EBPβ and C/EBPδ mRNA levels, as well as forkhead box O1 (FOXO1) protein levels. These results suggest that EPAC signalling enhances PKA-mediated dPRL expression in ESCs by acting on C/EBP response elements in the promoter region of the gene.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EPAC2 knockdown markedly reduced Phe-stimulated C/EBPβ and C/EBPδ mRNA levels, as well as forkhead box O1 (FOXO1) protein levels. These results suggest that EPAC signalling enhances PKA-mediated dPRL expression in ESCs by acting on C/EBP response elements in the promoter region of the gene.	Immunohistochemical staining	EPAC2 knockdown markedly reduced Phe-stimulated C/EBPβ and C/EBPδ mRNA levels, as well as forkhead box O1 (FOXO1) protein levels. These results suggest that EPAC signalling enhances PKA-mediated dPRL expression in ESCs by acting on C/EBP response elements in the promoter region of the gene.	FOXO1		Luciferase assay,Treatment with siRNAs,RT-qPCR,Immunoblotting,Immunofluorescence,transfection,	EPAC2 knockdown markedly reduced Phe-stimulated C/EBPβ and C/EBPδ mRNA levels, as well as forkhead box O1 (FOXO1) protein levels. These results suggest that EPAC signalling enhances PKA-mediated dPRL expression in ESCs by acting on C/EBP response elements in the promoter region of the gene.			
29734115	chr7	18083808	18085808	HDAC9	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	mouse	lymphoid tissue	High+Lowthroughput	Transcriptional and posttranscriptional repression of histone deacetylases by docosahexaenoic acid in macrophages	否	无	nothing	RAW 264.7 macrophages	E_02_0315	HDAC9 knockdown by small interfering RNA (siRNA),RT-qPCR,Western blot,	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.		Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	Immunohistochemical staining	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.			HDAC9 knockdown by small interfering RNA (siRNA),RT-qPCR,Western blot,				HDAC9
29734115	chr1	32289320	32291320	HDAC1	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	mouse	lymphoid tissue	High+Lowthroughput	Transcriptional and posttranscriptional repression of histone deacetylases by docosahexaenoic acid in macrophages	否	无	nothing	RAW 264.7 macrophages	E_02_0315	HDAC9 knockdown by small interfering RNA (siRNA),RT-qPCR,Western blot,	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.		Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	Immunohistochemical staining	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.			HDAC9 knockdown by small interfering RNA (siRNA),RT-qPCR,Western blot,				HDAC1
29734115	chr5	141618350	141620350	HDAC3	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	mouse	lymphoid tissue	High+Lowthroughput	Transcriptional and posttranscriptional repression of histone deacetylases by docosahexaenoic acid in macrophages	否	无	nothing	RAW 264.7 macrophages	E_02_0315	HDAC9 knockdown by small interfering RNA (siRNA),RT-qPCR,Western blot,	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.		Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	Immunohistochemical staining	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.			HDAC9 knockdown by small interfering RNA (siRNA),RT-qPCR,Western blot,				HDAC3
29734115	chr6	113930609	113932609	HDAC2	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	mouse	lymphoid tissue	High+Lowthroughput	Transcriptional and posttranscriptional repression of histone deacetylases by docosahexaenoic acid in macrophages	否	无	nothing	RAW 264.7 macrophages	E_02_0315	HDAC9 knockdown by small interfering RNA (siRNA),RT-qPCR,Western blot,	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.		Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	Immunohistochemical staining	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.			HDAC9 knockdown by small interfering RNA (siRNA),RT-qPCR,Western blot,				HDAC2
29734115	chr2	239045401	239047401	HDAC4	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	mouse	lymphoid tissue	High+Lowthroughput	Transcriptional and posttranscriptional repression of histone deacetylases by docosahexaenoic acid in macrophages	否	无	nothing	RAW 264.7 macrophages	E_02_0315	HDAC9 knockdown by small interfering RNA (siRNA),RT-qPCR,Western blot,	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.		Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.	Immunohistochemical staining	Our results demonstrate that DHA represses the expression of HDAC3, 4 and 9 at the transcriptional or posttranscriptional levels in murine macrophages. This suggests that the anti-inflammatory effect of DHA may be mediated by the reduction of HDACs.			HDAC9 knockdown by small interfering RNA (siRNA),RT-qPCR,Western blot,				HDAC4
29733381	chr6	108557419	108559419	FOXO3	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	human	connective tissue	High+Lowthroughput	The longevity SNP rs2802292 uncovered: HSF1 activates stress-dependent expression of FOXO3 through an intronic enhancer	是	rs2802292	nothing		E_01_0513	CRISPR/Cas9,Quantitative real-time PCR,Immunoblotting,Cell transfection,RNA interference,Cloning,ChIP,Luciferase assay,ChIP-loop assay,Cellular glutathione assay,DNA damage assay,Cell proliferation assay,	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	Immunohistochemical staining	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	FOXO3		CRISPR/Cas9,Quantitative real-time PCR,Immunoblotting,Cell transfection,RNA interference,Cloning,ChIP,Luciferase assay,ChIP-loop assay,Cellular glutathione assay,DNA damage assay,Cell proliferation assay,	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.			
29733381	chr8	144289380	144291380	HSF1	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	human	connective tissue	High+Lowthroughput	The longevity SNP rs2802292 uncovered: HSF1 activates stress-dependent expression of FOXO3 through an intronic enhancer	是	rs2802292	nothing		E_01_0513	CRISPR/Cas9,Quantitative real-time PCR,Immunoblotting,Cell transfection,RNA interference,Cloning,ChIP,Luciferase assay,ChIP-loop assay,Cellular glutathione assay,DNA damage assay,Cell proliferation assay,	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	Immunohistochemical staining	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	HSF1		CRISPR/Cas9,Quantitative real-time PCR,Immunoblotting,Cell transfection,RNA interference,Cloning,ChIP,Luciferase assay,ChIP-loop assay,Cellular glutathione assay,DNA damage assay,Cell proliferation assay,	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.			
29733381	chr6	159666205	159668205	SOD2	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	human	connective tissue	High+Lowthroughput	The longevity SNP rs2802292 uncovered: HSF1 activates stress-dependent expression of FOXO3 through an intronic enhancer	是	rs2802292	nothing		E_01_0513	CRISPR/Cas9,Quantitative real-time PCR,Immunoblotting,Cell transfection,RNA interference,Cloning,ChIP,Luciferase assay,ChIP-loop assay,Cellular glutathione assay,DNA damage assay,Cell proliferation assay,	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.		Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	Immunohistochemical staining	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.			CRISPR/Cas9,Quantitative real-time PCR,Immunoblotting,Cell transfection,RNA interference,Cloning,ChIP,Luciferase assay,ChIP-loop assay,Cellular glutathione assay,DNA damage assay,Cell proliferation assay,				SOD2
29733381	chr1	67682158	67684158	GADD45A	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	human	connective tissue	High+Lowthroughput	The longevity SNP rs2802292 uncovered: HSF1 activates stress-dependent expression of FOXO3 through an intronic enhancer	是	rs2802292	nothing		E_01_0513	CRISPR/Cas9,Quantitative real-time PCR,Immunoblotting,Cell transfection,RNA interference,Cloning,ChIP,Luciferase assay,ChIP-loop assay,Cellular glutathione assay,DNA damage assay,Cell proliferation assay,	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	Immunohistochemical staining	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.	GADD45A		CRISPR/Cas9,Quantitative real-time PCR,Immunoblotting,Cell transfection,RNA interference,Cloning,ChIP,Luciferase assay,ChIP-loop assay,Cellular glutathione assay,DNA damage assay,Cell proliferation assay,	Our functional studies highlighted the importance of the HSF1-FOXO3-SOD2/CAT/GADD45A cascade in cellular stress response and survival by promoting ROS detoxification, redox balance and DNA repair. Our findings suggest the existence of an HSF1-FOXO3 axis in human cells that could be involved in stress response pathways functionally regulating lifespan and disease susceptibility.			
29732557	chr7	148804423	148806423	EZH2	Our results indicate that elevated levels of EZH2 are relevant to CM tumourigenesis and progression, and that EZH2 may become a potential therapeutic target for patients with CM.	human	connective tissue	High+Lowthroughput	Overexpression of EZH2 in conjunctival melanoma offers a new therapeutic target	否	无	Conjunctival malignant melanoma (CM)		E_01_0514	Immunohistochemistry (IHC) staining,Immunoblotting,Cell proliferation,colony assay,Flow cytometry,RNA isolation,cDNA synthesis,quantitative PCR,	Our results indicate that elevated levels of EZH2 are relevant to CM tumourigenesis and progression, and that EZH2 may become a potential therapeutic target for patients with CM.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our results indicate that elevated levels of EZH2 are relevant to CM tumourigenesis and progression, and that EZH2 may become a potential therapeutic target for patients with CM.	Immunohistochemical staining	Our results indicate that elevated levels of EZH2 are relevant to CM tumourigenesis and progression, and that EZH2 may become a potential therapeutic target for patients with CM.	EZH2		Immunohistochemistry (IHC) staining,Immunoblotting,Cell proliferation,colony assay,Flow cytometry,RNA isolation,cDNA synthesis,quantitative PCR,	Our results indicate that elevated levels of EZH2 are relevant to CM tumourigenesis and progression, and that EZH2 may become a potential therapeutic target for patients with CM.			
29732557	chr6	36673567	36675567	CDKN1A	Our results indicate that elevated levels of EZH2 are relevant to CM tumourigenesis and progression, and that EZH2 may become a potential therapeutic target for patients with CM.	human	connective tissue	High+Lowthroughput	Overexpression of EZH2 in conjunctival melanoma offers a new therapeutic target	否	无	Conjunctival malignant melanoma (CM)		E_01_0514	Immunohistochemistry (IHC) staining,Immunoblotting,Cell proliferation,colony assay,Flow cytometry,RNA isolation,cDNA synthesis,quantitative PCR,	Our results indicate that elevated levels of EZH2 are relevant to CM tumourigenesis and progression, and that EZH2 may become a potential therapeutic target for patients with CM.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our results indicate that elevated levels of EZH2 are relevant to CM tumourigenesis and progression, and that EZH2 may become a potential therapeutic target for patients with CM.	Immunohistochemical staining	Our results indicate that elevated levels of EZH2 are relevant to CM tumourigenesis and progression, and that EZH2 may become a potential therapeutic target for patients with CM.	CDKN1A		Immunohistochemistry (IHC) staining,Immunoblotting,Cell proliferation,colony assay,Flow cytometry,RNA isolation,cDNA synthesis,quantitative PCR,	Our results indicate that elevated levels of EZH2 are relevant to CM tumourigenesis and progression, and that EZH2 may become a potential therapeutic target for patients with CM.			
29731896	chr20	10635162	10637162	JAG1	Together, these results indicated that miR-124 suppressed gastric cancer progression, partly through inhibiting JAG1 and EZH2. Thus, lentivirus-mediated overexpression of miR-124 may be a potential therapeutic strategy against gastric cancer.	human	Gastric cancer tissues	High+Lowthroughput	Lentivirus-mediated overexpression of miR-124 suppresses growth and invasion by targeting JAG1 and EZH2 in gastric cancer	否	无	gastric cancer	GC cell	E_01_0515	siRNA transfection,RT‑qPCR,Methylation analysis,Cell proliferation assay,Western blot,Cell migration,cell invasion assays,	Together, these results indicated that miR-124 suppressed gastric cancer progression, partly through inhibiting JAG1 and EZH2. Thus, lentivirus-mediated overexpression of miR-124 may be a potential therapeutic strategy against gastric cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Together, these results indicated that miR-124 suppressed gastric cancer progression, partly through inhibiting JAG1 and EZH2. Thus, lentivirus-mediated overexpression of miR-124 may be a potential therapeutic strategy against gastric cancer.		Together, these results indicated that miR-124 suppressed gastric cancer progression, partly through inhibiting JAG1 and EZH2. Thus, lentivirus-mediated overexpression of miR-124 may be a potential therapeutic strategy against gastric cancer.	Immunohistochemical staining	Together, these results indicated that miR-124 suppressed gastric cancer progression, partly through inhibiting JAG1 and EZH2. Thus, lentivirus-mediated overexpression of miR-124 may be a potential therapeutic strategy against gastric cancer.			siRNA transfection,RT‑qPCR,Methylation analysis,Cell proliferation assay,Western blot,Cell migration,cell invasion assays,				JAG1
29731896	chr7	148804261	148806261	EZH2	Together, these results indicated that miR-124 suppressed gastric cancer progression, partly through inhibiting JAG1 and EZH2. Thus, lentivirus-mediated overexpression of miR-124 may be a potential therapeutic strategy against gastric cancer.	human	Gastric cancer tissues	High+Lowthroughput	Lentivirus-mediated overexpression of miR-124 suppresses growth and invasion by targeting JAG1 and EZH2 in gastric cancer	否	无	gastric cancer	GC cell	E_01_0515	siRNA transfection,RT‑qPCR,Methylation analysis,Cell proliferation assay,Western blot,Cell migration,cell invasion assays,	Together, these results indicated that miR-124 suppressed gastric cancer progression, partly through inhibiting JAG1 and EZH2. Thus, lentivirus-mediated overexpression of miR-124 may be a potential therapeutic strategy against gastric cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Together, these results indicated that miR-124 suppressed gastric cancer progression, partly through inhibiting JAG1 and EZH2. Thus, lentivirus-mediated overexpression of miR-124 may be a potential therapeutic strategy against gastric cancer.	Immunohistochemical staining	Together, these results indicated that miR-124 suppressed gastric cancer progression, partly through inhibiting JAG1 and EZH2. Thus, lentivirus-mediated overexpression of miR-124 may be a potential therapeutic strategy against gastric cancer.	EZH2		siRNA transfection,RT‑qPCR,Methylation analysis,Cell proliferation assay,Western blot,Cell migration,cell invasion assays,	Together, these results indicated that miR-124 suppressed gastric cancer progression, partly through inhibiting JAG1 and EZH2. Thus, lentivirus-mediated overexpression of miR-124 may be a potential therapeutic strategy against gastric cancer.			
29731818	chr18	59217032	59219032	GRP	Furthermore, levels of ERS-associated proteins, including caspase-3, activating transcription factor 6, serine/threonine-protein kinase/endoribonuclease inositol-requiring enzyme 1 α, eukaryotic initiation factor 2 α and GRP78, were significantly increased following SCI; however, administration of MTX for 7 days significantly reversed this effect (P<0.05, P<0.01 and P<0.001). Therefore, MTX may improve SCI by suppressing ERS-induced apoptosis in vitro and in vivo.	mouse	connective tissue	High+Lowthroughput	Methotrexate remediates spinal cord injury in vivo and in vitro via suppression of endoplasmic reticulum stress-induced apoptosis	否	无	Spinal cord injury (SCI)	PC12 cell	E_02_0316	Basso, Beattie and Bresnahan (BBB) scoring,MTT colorimetric assay,Western blot,Apoptosis assay,Terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end (TUNEL),ELISA,flow cytometry,	Furthermore, levels of ERS-associated proteins, including caspase-3, activating transcription factor 6, serine/threonine-protein kinase/endoribonuclease inositol-requiring enzyme 1 α, eukaryotic initiation factor 2 α and GRP78, were significantly increased following SCI; however, administration of MTX for 7 days significantly reversed this effect (P<0.05, P<0.01 and P<0.001). Therefore, MTX may improve SCI by suppressing ERS-induced apoptosis in vitro and in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, levels of ERS-associated proteins, including caspase-3, activating transcription factor 6, serine/threonine-protein kinase/endoribonuclease inositol-requiring enzyme 1 α, eukaryotic initiation factor 2 α and GRP78, were significantly increased following SCI; however, administration of MTX for 7 days significantly reversed this effect (P<0.05, P<0.01 and P<0.001). Therefore, MTX may improve SCI by suppressing ERS-induced apoptosis in vitro and in vivo.		Furthermore, levels of ERS-associated proteins, including caspase-3, activating transcription factor 6, serine/threonine-protein kinase/endoribonuclease inositol-requiring enzyme 1 α, eukaryotic initiation factor 2 α and GRP78, were significantly increased following SCI; however, administration of MTX for 7 days significantly reversed this effect (P<0.05, P<0.01 and P<0.001). Therefore, MTX may improve SCI by suppressing ERS-induced apoptosis in vitro and in vivo.	Immunohistochemical staining	Furthermore, levels of ERS-associated proteins, including caspase-3, activating transcription factor 6, serine/threonine-protein kinase/endoribonuclease inositol-requiring enzyme 1 α, eukaryotic initiation factor 2 α and GRP78, were significantly increased following SCI; however, administration of MTX for 7 days significantly reversed this effect (P<0.05, P<0.01 and P<0.001). Therefore, MTX may improve SCI by suppressing ERS-induced apoptosis in vitro and in vivo.			Basso, Beattie and Bresnahan (BBB) scoring,MTT colorimetric assay,Western blot,Apoptosis assay,Terminal deoxynucleotidyl‑transferase‑mediated dUTP nick end (TUNEL),ELISA,flow cytometry,				GRP
29731168	chr8	127791607	127793607	PVT1	Cancer genome sequencing identifies recurrent mutations encompassing the human PVT1 promoter, and genome editing verified that PVT1 promoter mutation promotes cancer cell growth. These results highlight regulatory sequences of lncRNA genes as potential disease-associated DNA elements.	human	connective tissue	High+Lowthroughput	Promoter of lncRNA Gene PVT1 Is a Tumor-Suppressor DNA Boundary Element	否	无	mammary cancer	HEK293T	E_01_0516	RNA-seq,Rearrangement analysis,Hi-ChIP,UMI-4C,4C-Seq,Luciferase reporter assay,CRISPR/Cas9,4sU-labeling,JQ1 treatment,ChIP,ATAC-seq,Northern blot,Cell growth competition assay,Western blot,qRT-PCR,siRNA,ASO,	Cancer genome sequencing identifies recurrent mutations encompassing the human PVT1 promoter, and genome editing verified that PVT1 promoter mutation promotes cancer cell growth. These results highlight regulatory sequences of lncRNA genes as potential disease-associated DNA elements.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cancer genome sequencing identifies recurrent mutations encompassing the human PVT1 promoter, and genome editing verified that PVT1 promoter mutation promotes cancer cell growth. These results highlight regulatory sequences of lncRNA genes as potential disease-associated DNA elements.		Cancer genome sequencing identifies recurrent mutations encompassing the human PVT1 promoter, and genome editing verified that PVT1 promoter mutation promotes cancer cell growth. These results highlight regulatory sequences of lncRNA genes as potential disease-associated DNA elements.	Immunohistochemical staining	Cancer genome sequencing identifies recurrent mutations encompassing the human PVT1 promoter, and genome editing verified that PVT1 promoter mutation promotes cancer cell growth. These results highlight regulatory sequences of lncRNA genes as potential disease-associated DNA elements.			RNA-seq,Rearrangement analysis,Hi-ChIP,UMI-4C,4C-Seq,Luciferase reporter assay,CRISPR/Cas9,4sU-labeling,JQ1 treatment,ChIP,ATAC-seq,Northern blot,Cell growth competition assay,Western blot,qRT-PCR,siRNA,ASO,				PVT1
29730385	chr19	6658582	6660582	TNFSF14	To explore signaling in melanocytes treated with TNFSF14, we performed RNA-seq and found that nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) signaling is activated by TNFSF14. Further, we observed that inhibition of NF-kB effectively blocks the hypopigmentation induced by TNFSF14. We conclude that TNFSF14 inhibits melanogenesis in melanocytes via NF-κB signaling and could be applied in the treatment of cutaneous pigment disorders.	human	Epithelial tissues	High+Lowthroughput	TNFSF14 inhibits melanogenesis via NF-kB signaling in melanocytes	否	无	Skin pigmentation disturbances	Normal human epidermal melanocytes	E_01_0517	RNA-seq,transfection,RT-qPCR,Cell proliferation assay,Western blot,	To explore signaling in melanocytes treated with TNFSF14, we performed RNA-seq and found that nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) signaling is activated by TNFSF14. Further, we observed that inhibition of NF-kB effectively blocks the hypopigmentation induced by TNFSF14. We conclude that TNFSF14 inhibits melanogenesis in melanocytes via NF-κB signaling and could be applied in the treatment of cutaneous pigment disorders.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To explore signaling in melanocytes treated with TNFSF14, we performed RNA-seq and found that nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) signaling is activated by TNFSF14. Further, we observed that inhibition of NF-kB effectively blocks the hypopigmentation induced by TNFSF14. We conclude that TNFSF14 inhibits melanogenesis in melanocytes via NF-κB signaling and could be applied in the treatment of cutaneous pigment disorders.		To explore signaling in melanocytes treated with TNFSF14, we performed RNA-seq and found that nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) signaling is activated by TNFSF14. Further, we observed that inhibition of NF-kB effectively blocks the hypopigmentation induced by TNFSF14. We conclude that TNFSF14 inhibits melanogenesis in melanocytes via NF-κB signaling and could be applied in the treatment of cutaneous pigment disorders.	Immunohistochemical staining	To explore signaling in melanocytes treated with TNFSF14, we performed RNA-seq and found that nuclear factor κ-light-chain-enhancer of activated B cells (NF-κB) signaling is activated by TNFSF14. Further, we observed that inhibition of NF-kB effectively blocks the hypopigmentation induced by TNFSF14. We conclude that TNFSF14 inhibits melanogenesis in melanocytes via NF-κB signaling and could be applied in the treatment of cutaneous pigment disorders.			RNA-seq,transfection,RT-qPCR,Cell proliferation assay,Western blot,				TNFSF14
29729398	chr13	15635141	15637141	Gli3	Absent anterior skeletal elements in the Ezh2 mutant background were not rescued by either reduction of Gli activator or forced expression of Gli repressor. The data imply that Ezh2 is epistatic to Gli3 and suggest the possibility that hedghehog activation is repressed by the recruitment of polycomb repressive complex 2.	mouse	/	High+Lowthroughput	Genetic interaction between Gli3 and Ezh2 during limb pattern formation	否	无	nothing		E_02_0317	Whole mount in situ hybridisation,staining,	Absent anterior skeletal elements in the Ezh2 mutant background were not rescued by either reduction of Gli activator or forced expression of Gli repressor. The data imply that Ezh2 is epistatic to Gli3 and suggest the possibility that hedghehog activation is repressed by the recruitment of polycomb repressive complex 2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Absent anterior skeletal elements in the Ezh2 mutant background were not rescued by either reduction of Gli activator or forced expression of Gli repressor. The data imply that Ezh2 is epistatic to Gli3 and suggest the possibility that hedghehog activation is repressed by the recruitment of polycomb repressive complex 2.		Absent anterior skeletal elements in the Ezh2 mutant background were not rescued by either reduction of Gli activator or forced expression of Gli repressor. The data imply that Ezh2 is epistatic to Gli3 and suggest the possibility that hedghehog activation is repressed by the recruitment of polycomb repressive complex 2.	Immunohistochemical staining	Absent anterior skeletal elements in the Ezh2 mutant background were not rescued by either reduction of Gli activator or forced expression of Gli repressor. The data imply that Ezh2 is epistatic to Gli3 and suggest the possibility that hedghehog activation is repressed by the recruitment of polycomb repressive complex 2.			Whole mount in situ hybridisation,staining,				Gli3
29729398	chr6	47504143	47506143	Ezh2	Absent anterior skeletal elements in the Ezh2 mutant background were not rescued by either reduction of Gli activator or forced expression of Gli repressor. The data imply that Ezh2 is epistatic to Gli3 and suggest the possibility that hedghehog activation is repressed by the recruitment of polycomb repressive complex 2.	mouse	/	High+Lowthroughput	Genetic interaction between Gli3 and Ezh2 during limb pattern formation	否	无	nothing		E_02_0317	Whole mount in situ hybridisation,staining,	Absent anterior skeletal elements in the Ezh2 mutant background were not rescued by either reduction of Gli activator or forced expression of Gli repressor. The data imply that Ezh2 is epistatic to Gli3 and suggest the possibility that hedghehog activation is repressed by the recruitment of polycomb repressive complex 2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Absent anterior skeletal elements in the Ezh2 mutant background were not rescued by either reduction of Gli activator or forced expression of Gli repressor. The data imply that Ezh2 is epistatic to Gli3 and suggest the possibility that hedghehog activation is repressed by the recruitment of polycomb repressive complex 2.		Absent anterior skeletal elements in the Ezh2 mutant background were not rescued by either reduction of Gli activator or forced expression of Gli repressor. The data imply that Ezh2 is epistatic to Gli3 and suggest the possibility that hedghehog activation is repressed by the recruitment of polycomb repressive complex 2.	Immunohistochemical staining	Absent anterior skeletal elements in the Ezh2 mutant background were not rescued by either reduction of Gli activator or forced expression of Gli repressor. The data imply that Ezh2 is epistatic to Gli3 and suggest the possibility that hedghehog activation is repressed by the recruitment of polycomb repressive complex 2.			Whole mount in situ hybridisation,staining,				Ezh2
29728367	chr6	43180135	43182135	CUL9	We conclude that our proposed method is potentially useful and is complementary to TWAS and other standard gene- and pathway-based methods.	human		High+Lowthroughput	Integration of Enhancer-Promoter Interactions with GWAS Summary Results Identifies Novel Schizophrenia-Associated Genes and Pathways	是	无	Schizophrenia (SCZ)	MCF-7 cell	E_01_0518	ChIA-PET,RNA-seq,GWAS,TWAS,	We conclude that our proposed method is potentially useful and is complementary to TWAS and other standard gene- and pathway-based methods.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We conclude that our proposed method is potentially useful and is complementary to TWAS and other standard gene- and pathway-based methods.		We conclude that our proposed method is potentially useful and is complementary to TWAS and other standard gene- and pathway-based methods.	Immunohistochemical staining	We conclude that our proposed method is potentially useful and is complementary to TWAS and other standard gene- and pathway-based methods.			ChIA-PET,RNA-seq,GWAS,TWAS,				CUL9
29728367	chr2	27768990	27770990	MRPL33	We conclude that our proposed method is potentially useful and is complementary to TWAS and other standard gene- and pathway-based methods.	human		High+Lowthroughput	Integration of Enhancer-Promoter Interactions with GWAS Summary Results Identifies Novel Schizophrenia-Associated Genes and Pathways	是	无	Schizophrenia (SCZ)	MCF-7 cell	E_01_0518	ChIA-PET,RNA-seq,GWAS,TWAS,	We conclude that our proposed method is potentially useful and is complementary to TWAS and other standard gene- and pathway-based methods.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We conclude that our proposed method is potentially useful and is complementary to TWAS and other standard gene- and pathway-based methods.		We conclude that our proposed method is potentially useful and is complementary to TWAS and other standard gene- and pathway-based methods.	Immunohistochemical staining	We conclude that our proposed method is potentially useful and is complementary to TWAS and other standard gene- and pathway-based methods.			ChIA-PET,RNA-seq,GWAS,TWAS,				MRPL33
29726894	chr1	56491946	56493946	PLPP3	DNA methylation of a MIR-based enhancer downregulates the expression of PLPP3 and promotes the mineralization of the AV.	human		High+Lowthroughput	DNA methylation of a PLPP3 MIR transposon-based enhancer promotes an osteogenic programme in calcific aortic valve disease	否	无	Calcific aortic valve disease (cavd)	HEK293T	E_01_0519	Real-time PCR,Western blot,Whole-genome gene expression,DNA methylation,Pyrosequencing,ChIP,Cell Transfection,Luciferase reporter assay,Determination of alkaline phosphatase activity,	DNA methylation of a MIR-based enhancer downregulates the expression of PLPP3 and promotes the mineralization of the AV.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			DNA methylation of a MIR-based enhancer downregulates the expression of PLPP3 and promotes the mineralization of the AV.	Immunohistochemical staining	DNA methylation of a MIR-based enhancer downregulates the expression of PLPP3 and promotes the mineralization of the AV.	PLPP3		Real-time PCR,Western blot,Whole-genome gene expression,DNA methylation,Pyrosequencing,ChIP,Cell Transfection,Luciferase reporter assay,Determination of alkaline phosphatase activity,	DNA methylation of a MIR-based enhancer downregulates the expression of PLPP3 and promotes the mineralization of the AV.			
29725441	chr17	28503593	28505593	FOXN1	In conclusion, the present study demonstrated that FOXN1 served major roles in NSCLC proliferation and invasion by directly repressing EZH2 and β-catenin, which suggested that FOXN1 may function as a tumor suppressor in NSCLC.	human	Epithelial tissues	High+Lowthroughput	Forkhead box N1 inhibits the progression of non-small cell lung cancer and serves as a tumor suppressor	否	无	Non small cell lung cancer (NSCLC)	Normal human bronchial epithelial cell	E_01_0520	Transfection,Western blot,RNA extraction,RT‑qPCR,Invasion assay,MTT,Quantitative chromatin immunoprecipitation (qChIP),Dual‑luciferase reporter assay,	In conclusion, the present study demonstrated that FOXN1 served major roles in NSCLC proliferation and invasion by directly repressing EZH2 and β-catenin, which suggested that FOXN1 may function as a tumor suppressor in NSCLC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, the present study demonstrated that FOXN1 served major roles in NSCLC proliferation and invasion by directly repressing EZH2 and β-catenin, which suggested that FOXN1 may function as a tumor suppressor in NSCLC.		In conclusion, the present study demonstrated that FOXN1 served major roles in NSCLC proliferation and invasion by directly repressing EZH2 and β-catenin, which suggested that FOXN1 may function as a tumor suppressor in NSCLC.	Immunohistochemical staining	In conclusion, the present study demonstrated that FOXN1 served major roles in NSCLC proliferation and invasion by directly repressing EZH2 and β-catenin, which suggested that FOXN1 may function as a tumor suppressor in NSCLC.			Transfection,Western blot,RNA extraction,RT‑qPCR,Invasion assay,MTT,Quantitative chromatin immunoprecipitation (qChIP),Dual‑luciferase reporter assay,				FOXN1
29725441	chr7	148804538	148806538	EZH2	In conclusion, the present study demonstrated that FOXN1 served major roles in NSCLC proliferation and invasion by directly repressing EZH2 and β-catenin, which suggested that FOXN1 may function as a tumor suppressor in NSCLC.	human	Epithelial tissues	High+Lowthroughput	Forkhead box N1 inhibits the progression of non-small cell lung cancer and serves as a tumor suppressor	否	无	Non small cell lung cancer (NSCLC)	Normal human bronchial epithelial cell	E_01_0520	Transfection,Western blot,RNA extraction,RT‑qPCR,Invasion assay,MTT,Quantitative chromatin immunoprecipitation (qChIP),Dual‑luciferase reporter assay,	In conclusion, the present study demonstrated that FOXN1 served major roles in NSCLC proliferation and invasion by directly repressing EZH2 and β-catenin, which suggested that FOXN1 may function as a tumor suppressor in NSCLC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In conclusion, the present study demonstrated that FOXN1 served major roles in NSCLC proliferation and invasion by directly repressing EZH2 and β-catenin, which suggested that FOXN1 may function as a tumor suppressor in NSCLC.	Immunohistochemical staining	In conclusion, the present study demonstrated that FOXN1 served major roles in NSCLC proliferation and invasion by directly repressing EZH2 and β-catenin, which suggested that FOXN1 may function as a tumor suppressor in NSCLC.	EZH2		Transfection,Western blot,RNA extraction,RT‑qPCR,Invasion assay,MTT,Quantitative chromatin immunoprecipitation (qChIP),Dual‑luciferase reporter assay,	In conclusion, the present study demonstrated that FOXN1 served major roles in NSCLC proliferation and invasion by directly repressing EZH2 and β-catenin, which suggested that FOXN1 may function as a tumor suppressor in NSCLC.			
29725411	chr7	148804870	148806870	EZH2	The results of the present study suggested that COE prevents migration and invasion by suppressing the EZH2/ROCK1 signaling pathway in NPC cells. On the basis of the results of the present study, COE may be a novel anticancer agent for the treatment of metastasis in NPC.	human	NPC tissues	High+Lowthroughput	Efficacy of extracts of Celastrus orbiculatus in suppressing migration and invasion by inhibiting the EZH2/ROCK1 signaling pathway in human nasopharyngeal carcinoma	否	无	Nasopharyngeal carcinoma (NPC)	human NPC cell line 5-8F	E_01_0521	Western blot,flow cytometry,MTS cytotoxicity assay,RT‑qPCR,	The results of the present study suggested that COE prevents migration and invasion by suppressing the EZH2/ROCK1 signaling pathway in NPC cells. On the basis of the results of the present study, COE may be a novel anticancer agent for the treatment of metastasis in NPC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The results of the present study suggested that COE prevents migration and invasion by suppressing the EZH2/ROCK1 signaling pathway in NPC cells. On the basis of the results of the present study, COE may be a novel anticancer agent for the treatment of metastasis in NPC.	Immunohistochemical staining	The results of the present study suggested that COE prevents migration and invasion by suppressing the EZH2/ROCK1 signaling pathway in NPC cells. On the basis of the results of the present study, COE may be a novel anticancer agent for the treatment of metastasis in NPC.	EZH2		Western blot,flow cytometry,MTS cytotoxicity assay,RT‑qPCR,	The results of the present study suggested that COE prevents migration and invasion by suppressing the EZH2/ROCK1 signaling pathway in NPC cells. On the basis of the results of the present study, COE may be a novel anticancer agent for the treatment of metastasis in NPC.			
29725411	chr18	20944510	20946510	ROCK1	The results of the present study suggested that COE prevents migration and invasion by suppressing the EZH2/ROCK1 signaling pathway in NPC cells. On the basis of the results of the present study, COE may be a novel anticancer agent for the treatment of metastasis in NPC.	human	NPC tissues	High+Lowthroughput	Efficacy of extracts of Celastrus orbiculatus in suppressing migration and invasion by inhibiting the EZH2/ROCK1 signaling pathway in human nasopharyngeal carcinoma	否	无	Nasopharyngeal carcinoma (NPC)	human NPC cell line 5-8F	E_01_0521	Western blot,flow cytometry,MTS cytotoxicity assay,RT‑qPCR,	The results of the present study suggested that COE prevents migration and invasion by suppressing the EZH2/ROCK1 signaling pathway in NPC cells. On the basis of the results of the present study, COE may be a novel anticancer agent for the treatment of metastasis in NPC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The results of the present study suggested that COE prevents migration and invasion by suppressing the EZH2/ROCK1 signaling pathway in NPC cells. On the basis of the results of the present study, COE may be a novel anticancer agent for the treatment of metastasis in NPC.		The results of the present study suggested that COE prevents migration and invasion by suppressing the EZH2/ROCK1 signaling pathway in NPC cells. On the basis of the results of the present study, COE may be a novel anticancer agent for the treatment of metastasis in NPC.	Immunohistochemical staining	The results of the present study suggested that COE prevents migration and invasion by suppressing the EZH2/ROCK1 signaling pathway in NPC cells. On the basis of the results of the present study, COE may be a novel anticancer agent for the treatment of metastasis in NPC.			Western blot,flow cytometry,MTS cytotoxicity assay,RT‑qPCR,				ROCK1
29725368	chr7	45108303	45110303	Bax	In the present study, diabetes complicated by MI promoted ST-segment elevation and myocardial apoptosis, increased infarct size, induced pathological changes and elevated LVEDP, CK-MB, cTnT, GRP78, CHOP, Bax, Ero1α, Ero1β and PDI; however, it decreased heart rate, LVSP and Bcl-2. Additionally, high glucose combined with hypoxic treatment reduced cell viability, induced cell cycle arrest at G1 phase, promoted cell apoptosis, and activated the GRP78/CHOP and Ero1/PDI signaling pathways, which were reversed by CHOP knockdown. Thus, CHOP may be an effective therapeutic target for the treatment of diabetes complicated by MI.	human	Myocardial tissue	High+Lowthroughput	CCAAT/enhancer binding protein homologous protein knockdown alleviates hypoxia-induced myocardial injury in rat cardiomyocytes exposed to high glucose	否	无	Diabetes complicating myocardial infarction	H9c2 cell	E_01_0522	H&E staining,TUNEL assay,Western blot,ELISA,Triphenyltetrazolium chloride (TTC) staining,Hoechst 33258 staining,Cell Counting Kit‑8 (CCK‑8) assay,	In the present study, diabetes complicated by MI promoted ST-segment elevation and myocardial apoptosis, increased infarct size, induced pathological changes and elevated LVEDP, CK-MB, cTnT, GRP78, CHOP, Bax, Ero1α, Ero1β and PDI; however, it decreased heart rate, LVSP and Bcl-2. Additionally, high glucose combined with hypoxic treatment reduced cell viability, induced cell cycle arrest at G1 phase, promoted cell apoptosis, and activated the GRP78/CHOP and Ero1/PDI signaling pathways, which were reversed by CHOP knockdown. Thus, CHOP may be an effective therapeutic target for the treatment of diabetes complicated by MI.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, diabetes complicated by MI promoted ST-segment elevation and myocardial apoptosis, increased infarct size, induced pathological changes and elevated LVEDP, CK-MB, cTnT, GRP78, CHOP, Bax, Ero1α, Ero1β and PDI; however, it decreased heart rate, LVSP and Bcl-2. Additionally, high glucose combined with hypoxic treatment reduced cell viability, induced cell cycle arrest at G1 phase, promoted cell apoptosis, and activated the GRP78/CHOP and Ero1/PDI signaling pathways, which were reversed by CHOP knockdown. Thus, CHOP may be an effective therapeutic target for the treatment of diabetes complicated by MI.		In the present study, diabetes complicated by MI promoted ST-segment elevation and myocardial apoptosis, increased infarct size, induced pathological changes and elevated LVEDP, CK-MB, cTnT, GRP78, CHOP, Bax, Ero1α, Ero1β and PDI; however, it decreased heart rate, LVSP and Bcl-2. Additionally, high glucose combined with hypoxic treatment reduced cell viability, induced cell cycle arrest at G1 phase, promoted cell apoptosis, and activated the GRP78/CHOP and Ero1/PDI signaling pathways, which were reversed by CHOP knockdown. Thus, CHOP may be an effective therapeutic target for the treatment of diabetes complicated by MI.	Immunohistochemical staining	In the present study, diabetes complicated by MI promoted ST-segment elevation and myocardial apoptosis, increased infarct size, induced pathological changes and elevated LVEDP, CK-MB, cTnT, GRP78, CHOP, Bax, Ero1α, Ero1β and PDI; however, it decreased heart rate, LVSP and Bcl-2. Additionally, high glucose combined with hypoxic treatment reduced cell viability, induced cell cycle arrest at G1 phase, promoted cell apoptosis, and activated the GRP78/CHOP and Ero1/PDI signaling pathways, which were reversed by CHOP knockdown. Thus, CHOP may be an effective therapeutic target for the treatment of diabetes complicated by MI.			H&E staining,TUNEL assay,Western blot,ELISA,Triphenyltetrazolium chloride (TTC) staining,Hoechst 33258 staining,Cell Counting Kit‑8 (CCK‑8) assay,				Bax
29725115	chr8	17024798	17026798	MICU3	We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.	human	connective tissue	High+Lowthroughput	MICU3 is a tissue-specific enhancer of mitochondrial calcium uptake	否	无	nothing		E_01_0523	transfection,Co-immunoprecipitation,Aequorin measurements,SDS-PAGE,western blot,RNA extraction,reverse transcription PCR,quantitative real-time PCR,RNA-seq,bioinformatics,	We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.		We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.	Immunohistochemical staining	We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.			transfection,Co-immunoprecipitation,Aequorin measurements,SDS-PAGE,western blot,RNA extraction,reverse transcription PCR,quantitative real-time PCR,RNA-seq,bioinformatics,				MICU3
29725115	chr10	72364869	72366869	MICU1	We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.	human	connective tissue	High+Lowthroughput	MICU3 is a tissue-specific enhancer of mitochondrial calcium uptake	否	无	nothing		E_01_0523	transfection,Co-immunoprecipitation,Aequorin measurements,SDS-PAGE,western blot,RNA extraction,reverse transcription PCR,quantitative real-time PCR,RNA-seq,bioinformatics,	We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.		We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.	Immunohistochemical staining	We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.			transfection,Co-immunoprecipitation,Aequorin measurements,SDS-PAGE,western blot,RNA extraction,reverse transcription PCR,quantitative real-time PCR,RNA-seq,bioinformatics,				MICU1
29725115	chr13	21489948	21491948	MICU2	We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.	human	connective tissue	High+Lowthroughput	MICU3 is a tissue-specific enhancer of mitochondrial calcium uptake	否	无	nothing		E_01_0523	transfection,Co-immunoprecipitation,Aequorin measurements,SDS-PAGE,western blot,RNA extraction,reverse transcription PCR,quantitative real-time PCR,RNA-seq,bioinformatics,	We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.		We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.	Immunohistochemical staining	We here investigate the role of MICU3, an EF-hand containing protein expressed at high levels, especially in brain. We show that MICU3 forms a disulfide bond-mediated dimer with MICU1, but not with MICU2, and it acts as enhancer of MCU-dependent mitochondrial Ca2+ uptake. Silencing of MICU3 in primary cortical neurons impairs Ca2+ signals elicited by synaptic activity, thus suggesting a specific role in regulating neuronal function.			transfection,Co-immunoprecipitation,Aequorin measurements,SDS-PAGE,western blot,RNA extraction,reverse transcription PCR,quantitative real-time PCR,RNA-seq,bioinformatics,				MICU2
29721194	chr10	32265166	32267166	EPC1	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	human		High+Lowthroughput	Identification of an EPC2-PHF1 fusion transcript in low-grade endometrial stromal sarcoma	否	无	Endometrial stromal sarcoma (lg-ess)		E_01_0524	Fluorescence in situ hybridization (FISH),Molecular genetic analyses,PCR,RT-PCR,RNA-seq,	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.		Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	Immunohistochemical staining	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.			Fluorescence in situ hybridization (FISH),Molecular genetic analyses,PCR,RT-PCR,RNA-seq,				EPC1
29721194	chr2	148641473	148643473	EPC2	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	human		High+Lowthroughput	Identification of an EPC2-PHF1 fusion transcript in low-grade endometrial stromal sarcoma	否	无	Endometrial stromal sarcoma (lg-ess)		E_01_0524	Fluorescence in situ hybridization (FISH),Molecular genetic analyses,PCR,RT-PCR,RNA-seq,	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.		Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	Immunohistochemical staining	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.			Fluorescence in situ hybridization (FISH),Molecular genetic analyses,PCR,RT-PCR,RNA-seq,				EPC2
29721194	chr6	33407576	33409576	PHF1	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	human		High+Lowthroughput	Identification of an EPC2-PHF1 fusion transcript in low-grade endometrial stromal sarcoma	否	无	Endometrial stromal sarcoma (lg-ess)		E_01_0524	Fluorescence in situ hybridization (FISH),Molecular genetic analyses,PCR,RT-PCR,RNA-seq,	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.		Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	Immunohistochemical staining	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.			Fluorescence in situ hybridization (FISH),Molecular genetic analyses,PCR,RT-PCR,RNA-seq,				PHF1
29721194	chr7	27827645	27829645	JAZF1	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	human		High+Lowthroughput	Identification of an EPC2-PHF1 fusion transcript in low-grade endometrial stromal sarcoma	否	无	Endometrial stromal sarcoma (lg-ess)		E_01_0524	Fluorescence in situ hybridization (FISH),Molecular genetic analyses,PCR,RT-PCR,RNA-seq,	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.		Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	Immunohistochemical staining	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.			Fluorescence in situ hybridization (FISH),Molecular genetic analyses,PCR,RT-PCR,RNA-seq,				JAZF1
29721194	chr1	37487175	37489175	MEAF6	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	human		High+Lowthroughput	Identification of an EPC2-PHF1 fusion transcript in low-grade endometrial stromal sarcoma	否	无	Endometrial stromal sarcoma (lg-ess)		E_01_0524	Fluorescence in situ hybridization (FISH),Molecular genetic analyses,PCR,RT-PCR,RNA-seq,	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.		Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	Immunohistochemical staining	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.			Fluorescence in situ hybridization (FISH),Molecular genetic analyses,PCR,RT-PCR,RNA-seq,				MEAF6
29721194	chr5	138137040	138139040	BRD8	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	human		High+Lowthroughput	Identification of an EPC2-PHF1 fusion transcript in low-grade endometrial stromal sarcoma	否	无	Endometrial stromal sarcoma (lg-ess)		E_01_0524	Fluorescence in situ hybridization (FISH),Molecular genetic analyses,PCR,RT-PCR,RNA-seq,	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.		Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.	Immunohistochemical staining	Involvement of the PHF1 gene in chromosomal rearrangements targeting band 6p21 has been found in LG-ESS with different partners from JAZF1 mapping in 7p15, to EPC1 from 10p11, MEAF6 from 1p34, and BRD8 from 5q31.In the present study, RNA sequencing of a LG-ESS showed a novel recombination of PHF1 with the Enhancer of Polycomb homolog 2 (EPC2). RT-PCR followed by Sanger sequencing and FISH analysis confirmed the EPC2-PHF1 fusion transcript.			Fluorescence in situ hybridization (FISH),Molecular genetic analyses,PCR,RT-PCR,RNA-seq,				BRD8
29720835	chr10	88951288	88953288	FAS	PE and GE efficiently inhibited adipocyte differentiation by suppressing the expression of adipogenic transcription factor CEBP-α and PPAR-γ.PE and GE significantly decreased the expression of adipogenic enzyme FAS.PE and GE increased the expression of lipid degrading enzyme HSL.Mixture of PE and GE exhibited additive or moderately synergistic effect on adipocyte differentiation and lipid accumulation. 	human	adipose tissue	High+Lowthroughput	Combination of Garcinia cambogia Extract and Pear Pomace Extract Additively Suppresses Adipogenesis and Enhances Lipolysis in 3T3-L1 Cells	否	无	Obesity, diabetes, hypertension, atherosclerosis, cancer	3T3-L1 cell	E_01_0525	MTS‑PMS assay,Oil Red O staining,Immunocytochemistry,	PE and GE efficiently inhibited adipocyte differentiation by suppressing the expression of adipogenic transcription factor CEBP-α and PPAR-γ.PE and GE significantly decreased the expression of adipogenic enzyme FAS.PE and GE increased the expression of lipid degrading enzyme HSL.Mixture of PE and GE exhibited additive or moderately synergistic effect on adipocyte differentiation and lipid accumulation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			PE and GE efficiently inhibited adipocyte differentiation by suppressing the expression of adipogenic transcription factor CEBP-α and PPAR-γ.PE and GE significantly decreased the expression of adipogenic enzyme FAS.PE and GE increased the expression of lipid degrading enzyme HSL.Mixture of PE and GE exhibited additive or moderately synergistic effect on adipocyte differentiation and lipid accumulation. 	Immunohistochemical staining	PE and GE efficiently inhibited adipocyte differentiation by suppressing the expression of adipogenic transcription factor CEBP-α and PPAR-γ.PE and GE significantly decreased the expression of adipogenic enzyme FAS.PE and GE increased the expression of lipid degrading enzyme HSL.Mixture of PE and GE exhibited additive or moderately synergistic effect on adipocyte differentiation and lipid accumulation. 	FAS		MTS‑PMS assay,Oil Red O staining,Immunocytochemistry,	PE and GE efficiently inhibited adipocyte differentiation by suppressing the expression of adipogenic transcription factor CEBP-α and PPAR-γ.PE and GE significantly decreased the expression of adipogenic enzyme FAS.PE and GE increased the expression of lipid degrading enzyme HSL.Mixture of PE and GE exhibited additive or moderately synergistic effect on adipocyte differentiation and lipid accumulation. 			
29719267	chr17	43751286	43753286	SOST	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	human	Embryonic craniofacial tissues	High+Lowthroughput	High-Resolution Epigenomic Atlas of Human Embryonic Craniofacial Development	否	无	Cleft lip, cleft palate	cranial neural crest cell	E_01_0526	ChIP-Seq,ChIP	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 		We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	Immunohistochemical staining	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 			ChIP-Seq,ChIP				SOST
29719267	chr17	72118287	72120287	SOX9	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	human	Embryonic craniofacial tissues	High+Lowthroughput	High-Resolution Epigenomic Atlas of Human Embryonic Craniofacial Development	否	无	Cleft lip, cleft palate	cranial neural crest cell	E_01_0526	ChIP-Seq,ChIP	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	Immunohistochemical staining	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	SOX9		ChIP-Seq,ChIP	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 			
29719267	chr1	3066882	3068882	PRDM16	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	human	Embryonic craniofacial tissues	High+Lowthroughput	High-Resolution Epigenomic Atlas of Human Embryonic Craniofacial Development	否	无	Cleft lip, cleft palate	cranial neural crest cell	E_01_0526	ChIP-Seq,ChIP	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 		We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	Immunohistochemical staining	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 			ChIP-Seq,ChIP				PRDM16
29719267	chr8	127732417	127734417	MYC	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	human	Embryonic craniofacial tissues	High+Lowthroughput	High-Resolution Epigenomic Atlas of Human Embryonic Craniofacial Development	否	无	Cleft lip, cleft palate	cranial neural crest cell	E_01_0526	ChIP-Seq,ChIP	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	Immunohistochemical staining	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 	MYC		ChIP-Seq,ChIP	We demonstrate significant enrichment of common variants associated with orofacial clefting in enhancers active early in embryonic development, while those associated with normal facial variation are enriched near the end of the embryonic period. 			
29718709	chr5	75333700	75335700	HMGCR	The effects of GCs on cholesterol metabolism and epigenetic regulation were verified using the L02 cell line. The results showed that PCE induced hypercholesterolemia in adult offspring, which manifested as significantly higher levels of serum total cholesterol and LDL cholesterol (LDL-C) as well as higher ratios of LDL-C/HDL cholesterol. We further found that the cholesterol levels were increased in fetal livers but were decreased in fetal blood, accompanied by increased maternal blood cholesterol levels and reduced placental cholesterol transport. Furthermore, analysis of PCE offspring in the uterus and in a postnatal basal/chronic stress state and the results of in vitro experiments showed that hepatic cholesterol metabolism underwent GC-dependent changes and was associated with cholesterol synthase via abnormalities in 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) histone acetylation. We concluded that, to compensate for intrauterine placentally derived decreases in fetal blood cholesterol levels, high intrauterine GC levels activated fetal hepatic CCAAT enhancer binding protein α signaling and down-regulated Sirtuin1 expression, which mediated the high levels of histone acetylation ( via H3K9ac and H3K14ac) and expression of HMGCR.	mouse		High+Lowthroughput	Intrauterine programming mechanism for hypercholesterolemia in prenatal caffeine-exposed female adult rat offspring	否	无	Hypercholesterolemia	L02	E_02_0318	small interfering RNA,ELISA, quantitative RT-PCR,Sulforhodamine B assay,Chromatin immunoprecipitation assay,Western blot,	The effects of GCs on cholesterol metabolism and epigenetic regulation were verified using the L02 cell line. The results showed that PCE induced hypercholesterolemia in adult offspring, which manifested as significantly higher levels of serum total cholesterol and LDL cholesterol (LDL-C) as well as higher ratios of LDL-C/HDL cholesterol. We further found that the cholesterol levels were increased in fetal livers but were decreased in fetal blood, accompanied by increased maternal blood cholesterol levels and reduced placental cholesterol transport. Furthermore, analysis of PCE offspring in the uterus and in a postnatal basal/chronic stress state and the results of in vitro experiments showed that hepatic cholesterol metabolism underwent GC-dependent changes and was associated with cholesterol synthase via abnormalities in 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) histone acetylation. We concluded that, to compensate for intrauterine placentally derived decreases in fetal blood cholesterol levels, high intrauterine GC levels activated fetal hepatic CCAAT enhancer binding protein α signaling and down-regulated Sirtuin1 expression, which mediated the high levels of histone acetylation ( via H3K9ac and H3K14ac) and expression of HMGCR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The effects of GCs on cholesterol metabolism and epigenetic regulation were verified using the L02 cell line. The results showed that PCE induced hypercholesterolemia in adult offspring, which manifested as significantly higher levels of serum total cholesterol and LDL cholesterol (LDL-C) as well as higher ratios of LDL-C/HDL cholesterol. We further found that the cholesterol levels were increased in fetal livers but were decreased in fetal blood, accompanied by increased maternal blood cholesterol levels and reduced placental cholesterol transport. Furthermore, analysis of PCE offspring in the uterus and in a postnatal basal/chronic stress state and the results of in vitro experiments showed that hepatic cholesterol metabolism underwent GC-dependent changes and was associated with cholesterol synthase via abnormalities in 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) histone acetylation. We concluded that, to compensate for intrauterine placentally derived decreases in fetal blood cholesterol levels, high intrauterine GC levels activated fetal hepatic CCAAT enhancer binding protein α signaling and down-regulated Sirtuin1 expression, which mediated the high levels of histone acetylation ( via H3K9ac and H3K14ac) and expression of HMGCR.		The effects of GCs on cholesterol metabolism and epigenetic regulation were verified using the L02 cell line. The results showed that PCE induced hypercholesterolemia in adult offspring, which manifested as significantly higher levels of serum total cholesterol and LDL cholesterol (LDL-C) as well as higher ratios of LDL-C/HDL cholesterol. We further found that the cholesterol levels were increased in fetal livers but were decreased in fetal blood, accompanied by increased maternal blood cholesterol levels and reduced placental cholesterol transport. Furthermore, analysis of PCE offspring in the uterus and in a postnatal basal/chronic stress state and the results of in vitro experiments showed that hepatic cholesterol metabolism underwent GC-dependent changes and was associated with cholesterol synthase via abnormalities in 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) histone acetylation. We concluded that, to compensate for intrauterine placentally derived decreases in fetal blood cholesterol levels, high intrauterine GC levels activated fetal hepatic CCAAT enhancer binding protein α signaling and down-regulated Sirtuin1 expression, which mediated the high levels of histone acetylation ( via H3K9ac and H3K14ac) and expression of HMGCR.	Immunohistochemical staining	The effects of GCs on cholesterol metabolism and epigenetic regulation were verified using the L02 cell line. The results showed that PCE induced hypercholesterolemia in adult offspring, which manifested as significantly higher levels of serum total cholesterol and LDL cholesterol (LDL-C) as well as higher ratios of LDL-C/HDL cholesterol. We further found that the cholesterol levels were increased in fetal livers but were decreased in fetal blood, accompanied by increased maternal blood cholesterol levels and reduced placental cholesterol transport. Furthermore, analysis of PCE offspring in the uterus and in a postnatal basal/chronic stress state and the results of in vitro experiments showed that hepatic cholesterol metabolism underwent GC-dependent changes and was associated with cholesterol synthase via abnormalities in 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) histone acetylation. We concluded that, to compensate for intrauterine placentally derived decreases in fetal blood cholesterol levels, high intrauterine GC levels activated fetal hepatic CCAAT enhancer binding protein α signaling and down-regulated Sirtuin1 expression, which mediated the high levels of histone acetylation ( via H3K9ac and H3K14ac) and expression of HMGCR.			small interfering RNA,ELISA, quantitative RT-PCR,Sulforhodamine B assay,Chromatin immunoprecipitation assay,Western blot,				HMGCR
29718709	chr4	71738716	71740716	GC	The effects of GCs on cholesterol metabolism and epigenetic regulation were verified using the L02 cell line. The results showed that PCE induced hypercholesterolemia in adult offspring, which manifested as significantly higher levels of serum total cholesterol and LDL cholesterol (LDL-C) as well as higher ratios of LDL-C/HDL cholesterol. We further found that the cholesterol levels were increased in fetal livers but were decreased in fetal blood, accompanied by increased maternal blood cholesterol levels and reduced placental cholesterol transport. Furthermore, analysis of PCE offspring in the uterus and in a postnatal basal/chronic stress state and the results of in vitro experiments showed that hepatic cholesterol metabolism underwent GC-dependent changes and was associated with cholesterol synthase via abnormalities in 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) histone acetylation. We concluded that, to compensate for intrauterine placentally derived decreases in fetal blood cholesterol levels, high intrauterine GC levels activated fetal hepatic CCAAT enhancer binding protein α signaling and down-regulated Sirtuin1 expression, which mediated the high levels of histone acetylation ( via H3K9ac and H3K14ac) and expression of HMGCR.	mouse		High+Lowthroughput	Intrauterine programming mechanism for hypercholesterolemia in prenatal caffeine-exposed female adult rat offspring	否	无	Hypercholesterolemia	L02	E_02_0318	small interfering RNA,ELISA, quantitative RT-PCR,Sulforhodamine B assay,Chromatin immunoprecipitation assay,Western blot,	The effects of GCs on cholesterol metabolism and epigenetic regulation were verified using the L02 cell line. The results showed that PCE induced hypercholesterolemia in adult offspring, which manifested as significantly higher levels of serum total cholesterol and LDL cholesterol (LDL-C) as well as higher ratios of LDL-C/HDL cholesterol. We further found that the cholesterol levels were increased in fetal livers but were decreased in fetal blood, accompanied by increased maternal blood cholesterol levels and reduced placental cholesterol transport. Furthermore, analysis of PCE offspring in the uterus and in a postnatal basal/chronic stress state and the results of in vitro experiments showed that hepatic cholesterol metabolism underwent GC-dependent changes and was associated with cholesterol synthase via abnormalities in 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) histone acetylation. We concluded that, to compensate for intrauterine placentally derived decreases in fetal blood cholesterol levels, high intrauterine GC levels activated fetal hepatic CCAAT enhancer binding protein α signaling and down-regulated Sirtuin1 expression, which mediated the high levels of histone acetylation ( via H3K9ac and H3K14ac) and expression of HMGCR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The effects of GCs on cholesterol metabolism and epigenetic regulation were verified using the L02 cell line. The results showed that PCE induced hypercholesterolemia in adult offspring, which manifested as significantly higher levels of serum total cholesterol and LDL cholesterol (LDL-C) as well as higher ratios of LDL-C/HDL cholesterol. We further found that the cholesterol levels were increased in fetal livers but were decreased in fetal blood, accompanied by increased maternal blood cholesterol levels and reduced placental cholesterol transport. Furthermore, analysis of PCE offspring in the uterus and in a postnatal basal/chronic stress state and the results of in vitro experiments showed that hepatic cholesterol metabolism underwent GC-dependent changes and was associated with cholesterol synthase via abnormalities in 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) histone acetylation. We concluded that, to compensate for intrauterine placentally derived decreases in fetal blood cholesterol levels, high intrauterine GC levels activated fetal hepatic CCAAT enhancer binding protein α signaling and down-regulated Sirtuin1 expression, which mediated the high levels of histone acetylation ( via H3K9ac and H3K14ac) and expression of HMGCR.		The effects of GCs on cholesterol metabolism and epigenetic regulation were verified using the L02 cell line. The results showed that PCE induced hypercholesterolemia in adult offspring, which manifested as significantly higher levels of serum total cholesterol and LDL cholesterol (LDL-C) as well as higher ratios of LDL-C/HDL cholesterol. We further found that the cholesterol levels were increased in fetal livers but were decreased in fetal blood, accompanied by increased maternal blood cholesterol levels and reduced placental cholesterol transport. Furthermore, analysis of PCE offspring in the uterus and in a postnatal basal/chronic stress state and the results of in vitro experiments showed that hepatic cholesterol metabolism underwent GC-dependent changes and was associated with cholesterol synthase via abnormalities in 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) histone acetylation. We concluded that, to compensate for intrauterine placentally derived decreases in fetal blood cholesterol levels, high intrauterine GC levels activated fetal hepatic CCAAT enhancer binding protein α signaling and down-regulated Sirtuin1 expression, which mediated the high levels of histone acetylation ( via H3K9ac and H3K14ac) and expression of HMGCR.	Immunohistochemical staining	The effects of GCs on cholesterol metabolism and epigenetic regulation were verified using the L02 cell line. The results showed that PCE induced hypercholesterolemia in adult offspring, which manifested as significantly higher levels of serum total cholesterol and LDL cholesterol (LDL-C) as well as higher ratios of LDL-C/HDL cholesterol. We further found that the cholesterol levels were increased in fetal livers but were decreased in fetal blood, accompanied by increased maternal blood cholesterol levels and reduced placental cholesterol transport. Furthermore, analysis of PCE offspring in the uterus and in a postnatal basal/chronic stress state and the results of in vitro experiments showed that hepatic cholesterol metabolism underwent GC-dependent changes and was associated with cholesterol synthase via abnormalities in 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) histone acetylation. We concluded that, to compensate for intrauterine placentally derived decreases in fetal blood cholesterol levels, high intrauterine GC levels activated fetal hepatic CCAAT enhancer binding protein α signaling and down-regulated Sirtuin1 expression, which mediated the high levels of histone acetylation ( via H3K9ac and H3K14ac) and expression of HMGCR.			small interfering RNA,ELISA, quantitative RT-PCR,Sulforhodamine B assay,Chromatin immunoprecipitation assay,Western blot,				GC
29716548	chr6	3220562	3222562	TUBB2B	Our efforts provide insight into the utility of employing strict conservation for rSNP discovery. This strategy, combined with functional analyses, can yield candidate target genes. In support of this, our efforts suggest that investigating the role of Tubb2b in SOX10-positive cells may reveal novel biology within these cell populations.	mouse		High+Lowthroughput	A genome-wide assessment of conserved SNP alleles reveals a panel of regulatory SNPs relevant to the peripheral nerve	是	无	Neuropathy	immortalized rat Schwann (S16) cell	E_02_0319	PCR,transfection,TRANSFAC analysis,CRISPR/Cas9,RNA-Seq,RT-PCR,Digital droplet PCR,transgenic mice,Cap analysis gene expression (CAGE),ChIP-Seq,	Our efforts provide insight into the utility of employing strict conservation for rSNP discovery. This strategy, combined with functional analyses, can yield candidate target genes. In support of this, our efforts suggest that investigating the role of Tubb2b in SOX10-positive cells may reveal novel biology within these cell populations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our efforts provide insight into the utility of employing strict conservation for rSNP discovery. This strategy, combined with functional analyses, can yield candidate target genes. In support of this, our efforts suggest that investigating the role of Tubb2b in SOX10-positive cells may reveal novel biology within these cell populations.		Our efforts provide insight into the utility of employing strict conservation for rSNP discovery. This strategy, combined with functional analyses, can yield candidate target genes. In support of this, our efforts suggest that investigating the role of Tubb2b in SOX10-positive cells may reveal novel biology within these cell populations.	Immunohistochemical staining	Our efforts provide insight into the utility of employing strict conservation for rSNP discovery. This strategy, combined with functional analyses, can yield candidate target genes. In support of this, our efforts suggest that investigating the role of Tubb2b in SOX10-positive cells may reveal novel biology within these cell populations.			PCR,transfection,TRANSFAC analysis,CRISPR/Cas9,RNA-Seq,RT-PCR,Digital droplet PCR,transgenic mice,Cap analysis gene expression (CAGE),ChIP-Seq,				TUBB2B
29716548	chr22	37967991	37969991	SOX10	Our efforts provide insight into the utility of employing strict conservation for rSNP discovery. This strategy, combined with functional analyses, can yield candidate target genes. In support of this, our efforts suggest that investigating the role of Tubb2b in SOX10-positive cells may reveal novel biology within these cell populations.	mouse		High+Lowthroughput	A genome-wide assessment of conserved SNP alleles reveals a panel of regulatory SNPs relevant to the peripheral nerve	是	无	Neuropathy	immortalized rat Schwann (S16) cell	E_02_0319	PCR,transfection,TRANSFAC analysis,CRISPR/Cas9,RNA-Seq,RT-PCR,Digital droplet PCR,transgenic mice,Cap analysis gene expression (CAGE),ChIP-Seq,	Our efforts provide insight into the utility of employing strict conservation for rSNP discovery. This strategy, combined with functional analyses, can yield candidate target genes. In support of this, our efforts suggest that investigating the role of Tubb2b in SOX10-positive cells may reveal novel biology within these cell populations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our efforts provide insight into the utility of employing strict conservation for rSNP discovery. This strategy, combined with functional analyses, can yield candidate target genes. In support of this, our efforts suggest that investigating the role of Tubb2b in SOX10-positive cells may reveal novel biology within these cell populations.		Our efforts provide insight into the utility of employing strict conservation for rSNP discovery. This strategy, combined with functional analyses, can yield candidate target genes. In support of this, our efforts suggest that investigating the role of Tubb2b in SOX10-positive cells may reveal novel biology within these cell populations.	Immunohistochemical staining	Our efforts provide insight into the utility of employing strict conservation for rSNP discovery. This strategy, combined with functional analyses, can yield candidate target genes. In support of this, our efforts suggest that investigating the role of Tubb2b in SOX10-positive cells may reveal novel biology within these cell populations.			PCR,transfection,TRANSFAC analysis,CRISPR/Cas9,RNA-Seq,RT-PCR,Digital droplet PCR,transgenic mice,Cap analysis gene expression (CAGE),ChIP-Seq,				SOX10
29714661	chr5	88714300	88716300	MEF2C	Our study provides novel insight into the regulation mechanism of MIG6 and suggests potential implications for the therapeutic strategies of gefitinib resistance through inhibiting MEF2C in hepatic cancer cells.	human	Liver cancer tissues	High+Lowthroughput	MEF2C promotes gefitinib resistance in hepatic cancer cells through regulating MIG6 transcription	否	无	liver cancer	Hepatic cancer cell lines PHCC 	E_01_0527	 MEF2C knockdown,Chromatin immunoprecipitation assay,Dual luciferase assay,Western blot,Real-time quantitative PCR,CCK-8 method,	Our study provides novel insight into the regulation mechanism of MIG6 and suggests potential implications for the therapeutic strategies of gefitinib resistance through inhibiting MEF2C in hepatic cancer cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our study provides novel insight into the regulation mechanism of MIG6 and suggests potential implications for the therapeutic strategies of gefitinib resistance through inhibiting MEF2C in hepatic cancer cells.	Immunohistochemical staining	Our study provides novel insight into the regulation mechanism of MIG6 and suggests potential implications for the therapeutic strategies of gefitinib resistance through inhibiting MEF2C in hepatic cancer cells.	MEF2C		 MEF2C knockdown,Chromatin immunoprecipitation assay,Dual luciferase assay,Western blot,Real-time quantitative PCR,CCK-8 method,	Our study provides novel insight into the regulation mechanism of MIG6 and suggests potential implications for the therapeutic strategies of gefitinib resistance through inhibiting MEF2C in hepatic cancer cells.			
29714661	chr7	55016424	55018424	EGFR	Our study provides novel insight into the regulation mechanism of MIG6 and suggests potential implications for the therapeutic strategies of gefitinib resistance through inhibiting MEF2C in hepatic cancer cells.	human	Liver cancer tissues	High+Lowthroughput	MEF2C promotes gefitinib resistance in hepatic cancer cells through regulating MIG6 transcription	否	无	liver cancer	Hepatic cancer cell lines PHCC 	E_01_0527	 MEF2C knockdown,Chromatin immunoprecipitation assay,Dual luciferase assay,Western blot,Real-time quantitative PCR,CCK-8 method,	Our study provides novel insight into the regulation mechanism of MIG6 and suggests potential implications for the therapeutic strategies of gefitinib resistance through inhibiting MEF2C in hepatic cancer cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our study provides novel insight into the regulation mechanism of MIG6 and suggests potential implications for the therapeutic strategies of gefitinib resistance through inhibiting MEF2C in hepatic cancer cells.	Immunohistochemical staining	Our study provides novel insight into the regulation mechanism of MIG6 and suggests potential implications for the therapeutic strategies of gefitinib resistance through inhibiting MEF2C in hepatic cancer cells.	EGFR		 MEF2C knockdown,Chromatin immunoprecipitation assay,Dual luciferase assay,Western blot,Real-time quantitative PCR,CCK-8 method,	Our study provides novel insight into the regulation mechanism of MIG6 and suggests potential implications for the therapeutic strategies of gefitinib resistance through inhibiting MEF2C in hepatic cancer cells.			
29714127	chr14	104767057	104769057	AKT1	The present study is a novel finding of the possible role of AKT1 mutations which might help to identify gastric cancer patients.	human		High+Lowthroughput	Novel AKT1 mutations associated with cell-cycle abnormalities in gastric carcinoma	否	无	gastric cancer	gastric cancer cell	E_01_0528	PCR,cell-cycle analysis	The present study is a novel finding of the possible role of AKT1 mutations which might help to identify gastric cancer patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The present study is a novel finding of the possible role of AKT1 mutations which might help to identify gastric cancer patients.	Immunohistochemical staining	The present study is a novel finding of the possible role of AKT1 mutations which might help to identify gastric cancer patients.	AKT1		PCR,cell-cycle analysis	The present study is a novel finding of the possible role of AKT1 mutations which might help to identify gastric cancer patients.			
29712641	chr1	32289831	32291831	HDAC1	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	mouse		High+Lowthroughput	Histone deacetylases 1 and 2 regulate the transcriptional programs of nephron progenitors and renal vesicles	否	无	NPC, kidney development	293T cell	E_02_0320	ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.		Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Immunohistochemical staining	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.			ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,				HDAC1
29712641	chr6	113930310	113932310	HDAC2	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	mouse		High+Lowthroughput	Histone deacetylases 1 and 2 regulate the transcriptional programs of nephron progenitors and renal vesicles	否	无	NPC, kidney development	293T cell	E_02_0320	ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.		Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Immunohistochemical staining	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.			ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,				HDAC2
29712641	chr17	85989234	85991234	Six2	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	mouse		High+Lowthroughput	Histone deacetylases 1 and 2 regulate the transcriptional programs of nephron progenitors and renal vesicles	否	无	NPC, kidney development	293T cell	E_02_0320	ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.		Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Immunohistochemical staining	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.			ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,				Six2
29712641	chr12	9617813	9619813	Osr1	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	mouse		High+Lowthroughput	Histone deacetylases 1 and 2 regulate the transcriptional programs of nephron progenitors and renal vesicles	否	无	NPC, kidney development	293T cell	E_02_0320	ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.		Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Immunohistochemical staining	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.			ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,				Osr1
29712641	chr8	89751594	89753594	Sall1	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	mouse		High+Lowthroughput	Histone deacetylases 1 and 2 regulate the transcriptional programs of nephron progenitors and renal vesicles	否	无	NPC, kidney development	293T cell	E_02_0320	ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.		Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Immunohistochemical staining	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.			ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,				Sall1
29712641	chr11	84405982	84407982	Lhx1	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	mouse		High+Lowthroughput	Histone deacetylases 1 and 2 regulate the transcriptional programs of nephron progenitors and renal vesicles	否	无	NPC, kidney development	293T cell	E_02_0320	ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.		Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Immunohistochemical staining	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.			ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,				Lhx1
29712641	chr17	15584752	15586752	Dll1	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	mouse		High+Lowthroughput	Histone deacetylases 1 and 2 regulate the transcriptional programs of nephron progenitors and renal vesicles	否	无	NPC, kidney development	293T cell	E_02_0320	ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.		Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Immunohistochemical staining	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.			ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,				Dll1
29712641	chr11	69468671	69470671	Trp53	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	mouse		High+Lowthroughput	Histone deacetylases 1 and 2 regulate the transcriptional programs of nephron progenitors and renal vesicles	否	无	NPC, kidney development	293T cell	E_02_0320	ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.		Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.	Immunohistochemical staining	Here, we report that NPC-specific deletion of Hdac1 and Hdac2 genes in mice results in early postnatal lethality owing to renal hypodysplasia and loss of NPCs. HDAC1/2 interact with the NPC renewal regulators Six2, Osr1 and Sall1, and are co-bound along with Six2 on the Six2 enhancer. Although the mutant NPCs differentiate into renal vesicles (RVs), Hdac1/2 mutant kidneys lack nascent nephrons or mature glomeruli, a phenocopy of Lhx1 mutants. Transcriptional profiling and network analysis identified disrupted expression of Lhx1 and its downstream genes, Dll1 and Hnf1a/4a, as key mediators of the renal phenotype. Finally, although HDAC1/2-deficient NPCs and RVs overexpress hyperacetylated p53, Trp53 deletion failed to rescue the renal dysgenesis. We conclude that the epigenetic regulators HDAC1 and HDAC2 control nephrogenesis via interactions with the transcriptional programs of nephron progenitors and renal vesicles.			ChIP-PCR,droplet digital PCR (ddPCR),qPCR,RT-qPCR,PCR,Chromatin Immunoprecipitation (ChIP),Immunoprecipitation,Western blot,transfection,TUNEL Assay,Section in situ hybridization (ISH),Histology, immunohistochemistry,Genome-wide microarray analysis,transgenic mice,				Trp53
29710537	chr7	148804458	148806458	EZH2	These results demonstrated that the hsa_circ_0071589/miR-600/EZH2 axis may play critical regulatory roles in the pathogenesis of CRC and may serve as a novel therapy target in CRC.	human	Colon tissue	High+Lowthroughput	Hsa_circ_0071589 promotes carcinogenesis via the miR-600/EZH2 axis in colorectal cancer	否	无	Colorectal cancer (CRC)	colon cancer cell line HCT116	E_01_0529	Cell transfection, reverse transcription PCR,quantitative real-time PCR(qRT-PCR),wound-healing assay,Colony formation assay,Cell viability assay (MTT assay),Western blot,Plasmid construction,Dual luciferase activity assay,RNA immunoprecipitation (RIP) assay,	These results demonstrated that the hsa_circ_0071589/miR-600/EZH2 axis may play critical regulatory roles in the pathogenesis of CRC and may serve as a novel therapy target in CRC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These results demonstrated that the hsa_circ_0071589/miR-600/EZH2 axis may play critical regulatory roles in the pathogenesis of CRC and may serve as a novel therapy target in CRC.	Immunohistochemical staining	These results demonstrated that the hsa_circ_0071589/miR-600/EZH2 axis may play critical regulatory roles in the pathogenesis of CRC and may serve as a novel therapy target in CRC.	EZH2		Cell transfection, reverse transcription PCR,quantitative real-time PCR(qRT-PCR),wound-healing assay,Colony formation assay,Cell viability assay (MTT assay),Western blot,Plasmid construction,Dual luciferase activity assay,RNA immunoprecipitation (RIP) assay,	These results demonstrated that the hsa_circ_0071589/miR-600/EZH2 axis may play critical regulatory roles in the pathogenesis of CRC and may serve as a novel therapy target in CRC.			
29710475	chr1	60862803	60864803	NFIA	miR-200c repressed HBV replication by directly targeting NFIA, which might provide a novel therapeutic target for HBV infection.	human		High+Lowthroughput	miR-200c targets nuclear factor IA to suppress HBV replication and gene expression via repressing HBV Enhancer I activity	否	无	Hepatitis B virus (HBV) chronic infection, cirrhosis, hepatocellular carcinoma	293T cell	E_01_0530	qRT-PCR,Western blot,Dual-Luciferase Reporter assay,ELISA,qRCR,	miR-200c repressed HBV replication by directly targeting NFIA, which might provide a novel therapeutic target for HBV infection.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			miR-200c repressed HBV replication by directly targeting NFIA, which might provide a novel therapeutic target for HBV infection.	Immunohistochemical staining	miR-200c repressed HBV replication by directly targeting NFIA, which might provide a novel therapeutic target for HBV infection.	NFIA		qRT-PCR,Western blot,Dual-Luciferase Reporter assay,ELISA,qRCR,	miR-200c repressed HBV replication by directly targeting NFIA, which might provide a novel therapeutic target for HBV infection.			
29710033	chr10	88951091	88953091	FAS	CE dose-dependently decreased fat accumulation in 3T3-L1 cells without affecting cell viability. CE also dose-dependently decreased the protein and gene expression levels of two adipogenesis-related transcription factors, peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding proteins (C/EBPs). Moreover, CE decreased protein expression levels of sterol regulatory element-binding protein 1 (SREBP1) and its downstream fatty acid synthase (FAS), which was accompanied by the retained localization of SREBP1 in the cytoplasm of 3T3-L1 cells. After ICR mice were fed a diet containing 1% CE for 1 wk, their white adipose tissue weight was lower, whereas their brown adipose tissue weight was higher compared with those of control animals. Additionally, the protein expression levels of PPARγ, C/EBPs, SREBP1, and FAS in the white adipose tissue of these mice were also lower than those in control animals. In contrast, diet supplementation with CE induced higher levels of phosphorylated AMP-activated protein kinase (AMPK) and its downstream acetyl-CoA carboxylase. In conclusion, methylxanthine derivative-rich CE decreases fat accumulation in adipocytes by downregulating the expression of the adipocyte differentiation master regulators through the activation of AMPK.	mouse	adipose tissue	High+Lowthroughput	Methylxanthine Derivative-Rich Cacao Extract Suppresses Differentiation of Adipocytes through Downregulation of PPARγ and C/EBPs	否	无	Obesity	3T3-L1 preadipocytes	E_02_0321	Western blot,qPCR,Immunofluorescence,crystal violet staining assays,sudan II staining,	CE dose-dependently decreased fat accumulation in 3T3-L1 cells without affecting cell viability. CE also dose-dependently decreased the protein and gene expression levels of two adipogenesis-related transcription factors, peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding proteins (C/EBPs). Moreover, CE decreased protein expression levels of sterol regulatory element-binding protein 1 (SREBP1) and its downstream fatty acid synthase (FAS), which was accompanied by the retained localization of SREBP1 in the cytoplasm of 3T3-L1 cells. After ICR mice were fed a diet containing 1% CE for 1 wk, their white adipose tissue weight was lower, whereas their brown adipose tissue weight was higher compared with those of control animals. Additionally, the protein expression levels of PPARγ, C/EBPs, SREBP1, and FAS in the white adipose tissue of these mice were also lower than those in control animals. In contrast, diet supplementation with CE induced higher levels of phosphorylated AMP-activated protein kinase (AMPK) and its downstream acetyl-CoA carboxylase. In conclusion, methylxanthine derivative-rich CE decreases fat accumulation in adipocytes by downregulating the expression of the adipocyte differentiation master regulators through the activation of AMPK.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CE dose-dependently decreased fat accumulation in 3T3-L1 cells without affecting cell viability. CE also dose-dependently decreased the protein and gene expression levels of two adipogenesis-related transcription factors, peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding proteins (C/EBPs). Moreover, CE decreased protein expression levels of sterol regulatory element-binding protein 1 (SREBP1) and its downstream fatty acid synthase (FAS), which was accompanied by the retained localization of SREBP1 in the cytoplasm of 3T3-L1 cells. After ICR mice were fed a diet containing 1% CE for 1 wk, their white adipose tissue weight was lower, whereas their brown adipose tissue weight was higher compared with those of control animals. Additionally, the protein expression levels of PPARγ, C/EBPs, SREBP1, and FAS in the white adipose tissue of these mice were also lower than those in control animals. In contrast, diet supplementation with CE induced higher levels of phosphorylated AMP-activated protein kinase (AMPK) and its downstream acetyl-CoA carboxylase. In conclusion, methylxanthine derivative-rich CE decreases fat accumulation in adipocytes by downregulating the expression of the adipocyte differentiation master regulators through the activation of AMPK.		CE dose-dependently decreased fat accumulation in 3T3-L1 cells without affecting cell viability. CE also dose-dependently decreased the protein and gene expression levels of two adipogenesis-related transcription factors, peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding proteins (C/EBPs). Moreover, CE decreased protein expression levels of sterol regulatory element-binding protein 1 (SREBP1) and its downstream fatty acid synthase (FAS), which was accompanied by the retained localization of SREBP1 in the cytoplasm of 3T3-L1 cells. After ICR mice were fed a diet containing 1% CE for 1 wk, their white adipose tissue weight was lower, whereas their brown adipose tissue weight was higher compared with those of control animals. Additionally, the protein expression levels of PPARγ, C/EBPs, SREBP1, and FAS in the white adipose tissue of these mice were also lower than those in control animals. In contrast, diet supplementation with CE induced higher levels of phosphorylated AMP-activated protein kinase (AMPK) and its downstream acetyl-CoA carboxylase. In conclusion, methylxanthine derivative-rich CE decreases fat accumulation in adipocytes by downregulating the expression of the adipocyte differentiation master regulators through the activation of AMPK.	Immunohistochemical staining	CE dose-dependently decreased fat accumulation in 3T3-L1 cells without affecting cell viability. CE also dose-dependently decreased the protein and gene expression levels of two adipogenesis-related transcription factors, peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding proteins (C/EBPs). Moreover, CE decreased protein expression levels of sterol regulatory element-binding protein 1 (SREBP1) and its downstream fatty acid synthase (FAS), which was accompanied by the retained localization of SREBP1 in the cytoplasm of 3T3-L1 cells. After ICR mice were fed a diet containing 1% CE for 1 wk, their white adipose tissue weight was lower, whereas their brown adipose tissue weight was higher compared with those of control animals. Additionally, the protein expression levels of PPARγ, C/EBPs, SREBP1, and FAS in the white adipose tissue of these mice were also lower than those in control animals. In contrast, diet supplementation with CE induced higher levels of phosphorylated AMP-activated protein kinase (AMPK) and its downstream acetyl-CoA carboxylase. In conclusion, methylxanthine derivative-rich CE decreases fat accumulation in adipocytes by downregulating the expression of the adipocyte differentiation master regulators through the activation of AMPK.			Western blot,qPCR,Immunofluorescence,crystal violet staining assays,sudan II staining,				FAS
29709906	chr8	81476346	81478346	FABP4	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	human	adipose tissue	High+Lowthroughput	Dibenzoylmethane Suppresses Lipid Accumulation and Reactive Oxygen Species Production through Regulation of Nuclear Factor (Erythroid-Derived 2)-Like 2 and Insulin Signaling in Adipocytes	否	无	nothing	3T3-L1 preadipocytes	E_01_0531	ORO Staining,Western Blot,MTT Assay,Real Time PCR,immunoblotting,	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	Immunohistochemical staining	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	FABP4		ORO Staining,Western Blot,MTT Assay,Real Time PCR,immunoblotting,	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.			
29709906	chr19	16321898	16323898	KLF2	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	human	adipose tissue	High+Lowthroughput	Dibenzoylmethane Suppresses Lipid Accumulation and Reactive Oxygen Species Production through Regulation of Nuclear Factor (Erythroid-Derived 2)-Like 2 and Insulin Signaling in Adipocytes	否	无	nothing	3T3-L1 preadipocytes	E_01_0531	ORO Staining,Western Blot,MTT Assay,Real Time PCR,immunoblotting,	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	Immunohistochemical staining	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	KLF2		ORO Staining,Western Blot,MTT Assay,Real Time PCR,immunoblotting,	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.			
29709906	chr11	34436459	34438459	CAT	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	human	adipose tissue	High+Lowthroughput	Dibenzoylmethane Suppresses Lipid Accumulation and Reactive Oxygen Species Production through Regulation of Nuclear Factor (Erythroid-Derived 2)-Like 2 and Insulin Signaling in Adipocytes	否	无	nothing	3T3-L1 preadipocytes	E_01_0531	ORO Staining,Western Blot,MTT Assay,Real Time PCR,immunoblotting,	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.		DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	Immunohistochemical staining	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.			ORO Staining,Western Blot,MTT Assay,Real Time PCR,immunoblotting,				CAT
29709906	chr21	31656703	31658703	SOD1	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	human	adipose tissue	High+Lowthroughput	Dibenzoylmethane Suppresses Lipid Accumulation and Reactive Oxygen Species Production through Regulation of Nuclear Factor (Erythroid-Derived 2)-Like 2 and Insulin Signaling in Adipocytes	否	无	nothing	3T3-L1 preadipocytes	E_01_0531	ORO Staining,Western Blot,MTT Assay,Real Time PCR,immunoblotting,	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.		DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.	Immunohistochemical staining	DBM significantly increased the translocation of nuclear factor (erythroid-derived 2)-like 2(Nrf2) into the nucleus, promoting the protein expression of its target gene, heme oxygenase-1 (HO-1). DBM significantly suppressed the insulin-mediated activation of phosphoinositide 3-kinase (PI3K) and protein kinase B (Akt), which are components of insulin signaling. In addition, intracellular ROS production was effectively reduced by DBM treatment, which upregulated antioxidant genes such as glutathione peroxidase (Gpx), catalase (CAT), and superoxide dismutase 1 (SOD1). Furthermore, DBM significantly regulated the expression of the adipokines, resistin and adiponectin. This DBM-mediated regulation of lipid accumulation, ROS production, and adipokine production was shown to be involved in the regulation of the Nrf2 and insulin signaling.			ORO Staining,Western Blot,MTT Assay,Real Time PCR,immunoblotting,				SOD1
29707136	chr3	108040485	108042485	CD47	Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.	human		High+Lowthroughput	BNIP3 modulates the interface between B16-F10 melanoma cells and immune cells	否	无	Cancer, melanoma	B16-F10 cell 	E_01_0532	Flow Cytometry,Immunoblotting,ATP assay,In vitro phagocytosis assay,In vivo phagocytosis assay,western blot,	Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.	Immunohistochemical staining	Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.	CD47		Flow Cytometry,Immunoblotting,ATP assay,In vitro phagocytosis assay,In vivo phagocytosis assay,western blot,	Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.			
29707136	chr19	12935602	12937602	CALR	Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.	human		High+Lowthroughput	BNIP3 modulates the interface between B16-F10 melanoma cells and immune cells	否	无	Cancer, melanoma	B16-F10 cell 	E_01_0532	Flow Cytometry,Immunoblotting,ATP assay,In vitro phagocytosis assay,In vivo phagocytosis assay,western blot,	Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.		Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.	Immunohistochemical staining	Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.			Flow Cytometry,Immunoblotting,ATP assay,In vitro phagocytosis assay,In vivo phagocytosis assay,western blot,				CALR
29707136	chr10	131964518	131966518	BNIP3	Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.	human		High+Lowthroughput	BNIP3 modulates the interface between B16-F10 melanoma cells and immune cells	否	无	Cancer, melanoma	B16-F10 cell 	E_01_0532	Flow Cytometry,Immunoblotting,ATP assay,In vitro phagocytosis assay,In vivo phagocytosis assay,western blot,	Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.		Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.	Immunohistochemical staining	Thus, normoxic vs. hypoxic and live vs. dying cell contexts influence the ultimate immunomodulatory roles of melanoma cell-associated BNIP3.			Flow Cytometry,Immunoblotting,ATP assay,In vitro phagocytosis assay,In vivo phagocytosis assay,western blot,				BNIP3
29706346	chr1	22021633	22023633	LINC00339	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	human		High+Lowthroughput	An Osteoporosis Risk SNP at 1p36.12 Acts as an Allele-Specific Enhancer to Modulate LINC00339 Expression via Long-Range Loop Formation	是	rs6426749,rs34963268,rs6684375	Osteoporosis	The hFOB 1.19 cells 	E_01_0533	Motif Analysis,SMR analysis,Quantitative Real-Time PCR,siRNA knocdown,shRNA Knockdown,Chromatin Immunoprecipitation (ChIP) Assay,Dual-Luciferase Reporter Assays,Site-Directed Mutagenesis,Analysis of Shared Causal Genetic Variants,AseQTL Analysis,Genotyping,Association Analysis,cis-eQTL Analysis,Hi-C,TAD Analysis,Haplotype Analysis,GWAS,CRISPR/Cas9,	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."		"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	Immunohistochemical staining	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."			Motif Analysis,SMR analysis,Quantitative Real-Time PCR,siRNA knocdown,shRNA Knockdown,Chromatin Immunoprecipitation (ChIP) Assay,Dual-Luciferase Reporter Assays,Site-Directed Mutagenesis,Analysis of Shared Causal Genetic Variants,AseQTL Analysis,Genotyping,Association Analysis,cis-eQTL Analysis,Hi-C,TAD Analysis,Haplotype Analysis,GWAS,CRISPR/Cas9,				LINC00339
29706346	chr16	67559744	67561744	CTCF	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	human		High+Lowthroughput	An Osteoporosis Risk SNP at 1p36.12 Acts as an Allele-Specific Enhancer to Modulate LINC00339 Expression via Long-Range Loop Formation	是	rs6426749,rs34963268,rs6684375	Osteoporosis	The hFOB 1.19 cells 	E_01_0533	Motif Analysis,SMR analysis,Quantitative Real-Time PCR,siRNA knocdown,shRNA Knockdown,Chromatin Immunoprecipitation (ChIP) Assay,Dual-Luciferase Reporter Assays,Site-Directed Mutagenesis,Analysis of Shared Causal Genetic Variants,AseQTL Analysis,Genotyping,Association Analysis,cis-eQTL Analysis,Hi-C,TAD Analysis,Haplotype Analysis,GWAS,CRISPR/Cas9,	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	Immunohistochemical staining	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	CTCF		Motif Analysis,SMR analysis,Quantitative Real-Time PCR,siRNA knocdown,shRNA Knockdown,Chromatin Immunoprecipitation (ChIP) Assay,Dual-Luciferase Reporter Assays,Site-Directed Mutagenesis,Analysis of Shared Causal Genetic Variants,AseQTL Analysis,Genotyping,Association Analysis,cis-eQTL Analysis,Hi-C,TAD Analysis,Haplotype Analysis,GWAS,CRISPR/Cas9,	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."			
29706346	chr6	10390461	10392461	TFAP2A	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	human		High+Lowthroughput	An Osteoporosis Risk SNP at 1p36.12 Acts as an Allele-Specific Enhancer to Modulate LINC00339 Expression via Long-Range Loop Formation	是	rs6426749,rs34963268,rs6684375	Osteoporosis	The hFOB 1.19 cells 	E_01_0533	Motif Analysis,SMR analysis,Quantitative Real-Time PCR,siRNA knocdown,shRNA Knockdown,Chromatin Immunoprecipitation (ChIP) Assay,Dual-Luciferase Reporter Assays,Site-Directed Mutagenesis,Analysis of Shared Causal Genetic Variants,AseQTL Analysis,Genotyping,Association Analysis,cis-eQTL Analysis,Hi-C,TAD Analysis,Haplotype Analysis,GWAS,CRISPR/Cas9,	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	Immunohistochemical staining	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	TFAP2A		Motif Analysis,SMR analysis,Quantitative Real-Time PCR,siRNA knocdown,shRNA Knockdown,Chromatin Immunoprecipitation (ChIP) Assay,Dual-Luciferase Reporter Assays,Site-Directed Mutagenesis,Analysis of Shared Causal Genetic Variants,AseQTL Analysis,Genotyping,Association Analysis,cis-eQTL Analysis,Hi-C,TAD Analysis,Haplotype Analysis,GWAS,CRISPR/Cas9,	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."			
29706346	chr1	22049511	22051511	CDC42	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	human		High+Lowthroughput	An Osteoporosis Risk SNP at 1p36.12 Acts as an Allele-Specific Enhancer to Modulate LINC00339 Expression via Long-Range Loop Formation	是	rs6426749,rs34963268,rs6684375	Osteoporosis	The hFOB 1.19 cells 	E_01_0533	Motif Analysis,SMR analysis,Quantitative Real-Time PCR,siRNA knocdown,shRNA Knockdown,Chromatin Immunoprecipitation (ChIP) Assay,Dual-Luciferase Reporter Assays,Site-Directed Mutagenesis,Analysis of Shared Causal Genetic Variants,AseQTL Analysis,Genotyping,Association Analysis,cis-eQTL Analysis,Hi-C,TAD Analysis,Haplotype Analysis,GWAS,CRISPR/Cas9,	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."		"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."	Immunohistochemical staining	"Through an integrative functional genomic and epigenomic analyses, we prioritized rs6426749 as a potential causal SNP for osteoporosis at 1p36.12. Dual-luciferase assay and CRISPR/Cas9 experiments demonstrate that rs6426749 acts as a distal allele-specific enhancer regulating expression of a lncRNA (LINC00339)(_x0001_360 kb) via long-range chromatin loop formation and that this loop is mediated by CTCF occupied near rs6426749 and
LINC00339 promoter region. Specifically, rs6426749-G allele can bind transcription factor TFAP2A, which efficiently elevates the enhancer activity and increases LINC00339 expression. Downregulation of LINC00339 significantly increases the expression of CDC42 in osteoblast cells, which is a pivotal regulator involved in bone metabolism. Our study provides mechanistic insight into how a noncoding SNP affects osteoporosis by long-range interaction, a finding that could indicate promising therapeutic targets for osteoporosis."			Motif Analysis,SMR analysis,Quantitative Real-Time PCR,siRNA knocdown,shRNA Knockdown,Chromatin Immunoprecipitation (ChIP) Assay,Dual-Luciferase Reporter Assays,Site-Directed Mutagenesis,Analysis of Shared Causal Genetic Variants,AseQTL Analysis,Genotyping,Association Analysis,cis-eQTL Analysis,Hi-C,TAD Analysis,Haplotype Analysis,GWAS,CRISPR/Cas9,				CDC42
29706059	chr5	372500	376000	HOXA5	Our findings suggest that AHRR SM-DMR up-regulates AHRR mRNA in a monocyte-specific manner by activating the AHRR enhancer. Cell type-specific activation of enhancers at SM-DMRs may represent a mechanism driving smoking-related disease. 	human		Low+High throughput	Identification of Smoking-Associated Differentially Methylated Regions Using Reduced Representation Bisulfite Sequencing and Cell type-Specific Enhancer Activation and Gene Expression	是	--	Cardiovascular Cancer	CD14+ cell	E_02_0322	ChIP-seq,RNA-seq	We tested total RNA samples from a group of CRU-mRNA with available RNA (n=11smokers/10 nonsmokers) and observed three ofthe SM-DMR locations(AHRR, C5orf55-EXOC-AS, and SASH1) showedup-regulation of correspondinge RNA expression as well as mRNA.	Enhancer	--	RT-PCR	The Figure6C bar graph displays the significants moking-associated fold-change results for each RT-qPCR relative to their genome position in the AHRR region.	AHH,AHHR,bHLHe77	--	--	--	--	--	--	--	--	--	AHRR
29706059	chr5	372500	376000	PPP1R15A	Our findings suggest that AHRR SM-DMR up-regulates AHRR mRNA in a monocyte-specific manner by activating the AHRR enhancer. Cell type-specific activation of enhancers at SM-DMRs may represent a mechanism driving smoking-related disease. 	human		Low+High throughput	Identification of Smoking-Associated Differentially Methylated Regions Using Reduced Representation Bisulfite Sequencing and Cell type-Specific Enhancer Activation and Gene Expression	是	--	Cardiovascular Cancer	CD14+ cell	E_02_0322	ChIP-seq,RNA-seq	We tested total RNA samples from a group of CRU-mRNA with available RNA (n=11smokers/10 nonsmokers) and observed three ofthe SM-DMR locations(AHRR, C5orf55-EXOC-AS, and SASH1) showedup-regulation of correspondinge RNA expression as well as mRNA.	Enhancer	--	RT-PCR	The Figure6C bar graph displays the significants moking-associated fold-change results for each RT-qPCR relative to their genome position in the AHRR region.	AHH,AHHR,bHLHe77	--	--	--	--	--	--	--	--	--	AHRR
29706059	chr5	372500	376000	CPAMD8	Our findings suggest that AHRR SM-DMR up-regulates AHRR mRNA in a monocyte-specific manner by activating the AHRR enhancer. Cell type-specific activation of enhancers at SM-DMRs may represent a mechanism driving smoking-related disease. 	human		Low+High throughput	Identification of Smoking-Associated Differentially Methylated Regions Using Reduced Representation Bisulfite Sequencing and Cell type-Specific Enhancer Activation and Gene Expression	是	--	Cardiovascular Cancer	CD14+ cell	E_02_0322	ChIP-seq,RNA-seq	We tested total RNA samples from a group of CRU-mRNA with available RNA (n=11smokers/10 nonsmokers) and observed three ofthe SM-DMR locations(AHRR, C5orf55-EXOC-AS, and SASH1) showedup-regulation of correspondinge RNA expression as well as mRNA.	Enhancer	--	RT-PCR	The Figure6C bar graph displays the significants moking-associated fold-change results for each RT-qPCR relative to their genome position in the AHRR region.	AHH,AHHR,bHLHe77	--	--	--	--	--	--	--	--	--	AHRR
29706059	chr5	372500	376000	PZP	Our findings suggest that AHRR SM-DMR up-regulates AHRR mRNA in a monocyte-specific manner by activating the AHRR enhancer. Cell type-specific activation of enhancers at SM-DMRs may represent a mechanism driving smoking-related disease. 	human		Low+High throughput	Identification of Smoking-Associated Differentially Methylated Regions Using Reduced Representation Bisulfite Sequencing and Cell type-Specific Enhancer Activation and Gene Expression	是	--	Cardiovascular Cancer	CD14+ cell	E_02_0322	ChIP-seq,RNA-seq	We tested total RNA samples from a group of CRU-mRNA with available RNA (n=11smokers/10 nonsmokers) and observed three ofthe SM-DMR locations(AHRR, C5orf55-EXOC-AS, and SASH1) showedup-regulation of correspondinge RNA expression as well as mRNA.	Enhancer	--	RT-PCR	The Figure6C bar graph displays the significants moking-associated fold-change results for each RT-qPCR relative to their genome position in the AHRR region.	AHH,AHHR,bHLHe77	--	--	--	--	--	--	--	--	--	AHRR
29706059	chr5	372500	376000	F2RL3	Our findings suggest that AHRR SM-DMR up-regulates AHRR mRNA in a monocyte-specific manner by activating the AHRR enhancer. Cell type-specific activation of enhancers at SM-DMRs may represent a mechanism driving smoking-related disease. 	human		Low+High throughput	Identification of Smoking-Associated Differentially Methylated Regions Using Reduced Representation Bisulfite Sequencing and Cell type-Specific Enhancer Activation and Gene Expression	是	--	Cardiovascular Cancer	CD14+ cell	E_02_0322	ChIP-seq,RNA-seq	We tested total RNA samples from a group of CRU-mRNA with available RNA (n=11smokers/10 nonsmokers) and observed three ofthe SM-DMR locations(AHRR, C5orf55-EXOC-AS, and SASH1) showedup-regulation of correspondinge RNA expression as well as mRNA.	Enhancer	--	RT-PCR	The Figure6C bar graph displays the significants moking-associated fold-change results for each RT-qPCR relative to their genome position in the AHRR region.	AHH,AHHR,bHLHe77	--	--	--	--	--	--	--	--	--	AHRR
29706059	chr5	372500	376000	LRP5	Our findings suggest that AHRR SM-DMR up-regulates AHRR mRNA in a monocyte-specific manner by activating the AHRR enhancer. Cell type-specific activation of enhancers at SM-DMRs may represent a mechanism driving smoking-related disease. 	human		Low+High throughput	Identification of Smoking-Associated Differentially Methylated Regions Using Reduced Representation Bisulfite Sequencing and Cell type-Specific Enhancer Activation and Gene Expression	是	--	Cardiovascular Cancer	CD14+ cell	E_02_0322	ChIP-seq,RNA-seq	We tested total RNA samples from a group of CRU-mRNA with available RNA (n=11smokers/10 nonsmokers) and observed three ofthe SM-DMR locations(AHRR, C5orf55-EXOC-AS, and SASH1) showedup-regulation of correspondinge RNA expression as well as mRNA.	Enhancer	--	RT-PCR	The Figure6C bar graph displays the significants moking-associated fold-change results for each RT-qPCR relative to their genome position in the AHRR region.	AHH,AHHR,bHLHe77	--	--	--	--	--	--	--	--	--	AHRR
29706059	chr5	372500	376000	RDX	Our findings suggest that AHRR SM-DMR up-regulates AHRR mRNA in a monocyte-specific manner by activating the AHRR enhancer. Cell type-specific activation of enhancers at SM-DMRs may represent a mechanism driving smoking-related disease. 	human		Low+High throughput	Identification of Smoking-Associated Differentially Methylated Regions Using Reduced Representation Bisulfite Sequencing and Cell type-Specific Enhancer Activation and Gene Expression	是	--	Cardiovascular Cancer	CD14+ cell	E_02_0322	ChIP-seq,RNA-seq	We tested total RNA samples from a group of CRU-mRNA with available RNA (n=11smokers/10 nonsmokers) and observed three ofthe SM-DMR locations(AHRR, C5orf55-EXOC-AS, and SASH1) showedup-regulation of correspondinge RNA expression as well as mRNA.	Enhancer	--	RT-PCR	The Figure6C bar graph displays the significants moking-associated fold-change results for each RT-qPCR relative to their genome position in the AHRR region.	AHH,AHHR,bHLHe77	--	--	--	--	--	--	--	--	--	AHRR
29706059	chr5	372500	376000	AHRR	Our findings suggest that AHRR SM-DMR up-regulates AHRR mRNA in a monocyte-specific manner by activating the AHRR enhancer. Cell type-specific activation of enhancers at SM-DMRs may represent a mechanism driving smoking-related disease. 	human		Low+High throughput	Identification of Smoking-Associated Differentially Methylated Regions Using Reduced Representation Bisulfite Sequencing and Cell type-Specific Enhancer Activation and Gene Expression	是	--	Cardiovascular Cancer	CD14+ cell	E_02_0322	ChIP-seq,RNA-seq	We tested total RNA samples from a group of CRU-mRNA with available RNA (n=11smokers/10 nonsmokers) and observed three ofthe SM-DMR locations(AHRR, C5orf55-EXOC-AS, and SASH1) showedup-regulation of correspondinge RNA expression as well as mRNA.	Enhancer	--	RT-PCR	The Figure6C bar graph displays the significants moking-associated fold-change results for each RT-qPCR relative to their genome position in the AHRR region.	AHH,AHHR,bHLHe77	--	--	--	--	--	--	--	--	--	AHRR
29706059	chr5	372500	376000	SASH1	Our findings suggest that AHRR SM-DMR up-regulates AHRR mRNA in a monocyte-specific manner by activating the AHRR enhancer. Cell type-specific activation of enhancers at SM-DMRs may represent a mechanism driving smoking-related disease. 	human		Low+High throughput	Identification of Smoking-Associated Differentially Methylated Regions Using Reduced Representation Bisulfite Sequencing and Cell type-Specific Enhancer Activation and Gene Expression	是	--	Cardiovascular Cancer	CD14+ cell	E_02_0322	ChIP-seq,RNA-seq	We tested total RNA samples from a group of CRU-mRNA with available RNA (n=11smokers/10 nonsmokers) and observed three ofthe SM-DMR locations(AHRR, C5orf55-EXOC-AS, and SASH1) showedup-regulation of correspondinge RNA expression as well as mRNA.	Enhancer	--	RT-PCR	The Figure6C bar graph displays the significants moking-associated fold-change results for each RT-qPCR relative to their genome position in the AHRR region.	AHH,AHHR,bHLHe77	--	--	--	--	--	--	--	--	--	AHRR
29704115	chr11	27652286	27654286	BDNF	Taken together, our results suggest that BDNF/TrkB pathway plays an important mediatory role in the antidepressant-like action of H2S in CUMS-exposed rats, which is by suppression of hippocampal ER stress. These data provide a novel mechanism underlying the protection of H2S against CUMS-induced depressive-like behaviors.	human	/	High+Lowthroughput	BDNF/TrkB Pathway Mediates the Antidepressant-Like Role of H(2)S in CUMS-Exposed Rats by Inhibition of Hippocampal ER Stress	否	无	depression		E_01_0534	Western Blot,BCA assay,	Taken together, our results suggest that BDNF/TrkB pathway plays an important mediatory role in the antidepressant-like action of H2S in CUMS-exposed rats, which is by suppression of hippocampal ER stress. These data provide a novel mechanism underlying the protection of H2S against CUMS-induced depressive-like behaviors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Taken together, our results suggest that BDNF/TrkB pathway plays an important mediatory role in the antidepressant-like action of H2S in CUMS-exposed rats, which is by suppression of hippocampal ER stress. These data provide a novel mechanism underlying the protection of H2S against CUMS-induced depressive-like behaviors.	Immunohistochemical staining	Taken together, our results suggest that BDNF/TrkB pathway plays an important mediatory role in the antidepressant-like action of H2S in CUMS-exposed rats, which is by suppression of hippocampal ER stress. These data provide a novel mechanism underlying the protection of H2S against CUMS-induced depressive-like behaviors.	BDNF		Western Blot,BCA assay,	Taken together, our results suggest that BDNF/TrkB pathway plays an important mediatory role in the antidepressant-like action of H2S in CUMS-exposed rats, which is by suppression of hippocampal ER stress. These data provide a novel mechanism underlying the protection of H2S against CUMS-induced depressive-like behaviors.			
29702085	chr17	42310982	42312982	STAT3	STAT3 contributed to TNF-α induced nuclear translocation of phospho-NFκB in pericytes. TNF-α-induced IL-6 release in astrocytes was mediated by NFκB but not by STAT3. The presence of pericytes amplified TNF-α-induced iNOS mRNA expression in BV-2 microglia. This effect was blocked by a neutralizing antibody for IL-6. These findings indicated that crosstalk between the IκB-NFκB and JAK-STAT3 pathways is a pericyte specific mechanism, not occurring in astrocytes, for TNF-α-induced IL-6 release. IL-6 derived from pericytes enhanced microglial activation. Our findings increase understanding of the role of pericyte-microglia crosstalk in the brain under neuroinflammatory conditions and suggest a potentially attractive therapeutic target for brain inflammation.	human	Nervous tissue	High+Lowthroughput	TNF-α-sensitive brain pericytes activate microglia by releasing IL-6 through cooperation between IκB-NFκB and JAK-STAT3 pathways	否	无	Neuroinflammation	brain pericyte	E_01_0535	Western blot,RT-PCR,	STAT3 contributed to TNF-α induced nuclear translocation of phospho-NFκB in pericytes. TNF-α-induced IL-6 release in astrocytes was mediated by NFκB but not by STAT3. The presence of pericytes amplified TNF-α-induced iNOS mRNA expression in BV-2 microglia. This effect was blocked by a neutralizing antibody for IL-6. These findings indicated that crosstalk between the IκB-NFκB and JAK-STAT3 pathways is a pericyte specific mechanism, not occurring in astrocytes, for TNF-α-induced IL-6 release. IL-6 derived from pericytes enhanced microglial activation. Our findings increase understanding of the role of pericyte-microglia crosstalk in the brain under neuroinflammatory conditions and suggest a potentially attractive therapeutic target for brain inflammation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			STAT3 contributed to TNF-α induced nuclear translocation of phospho-NFκB in pericytes. TNF-α-induced IL-6 release in astrocytes was mediated by NFκB but not by STAT3. The presence of pericytes amplified TNF-α-induced iNOS mRNA expression in BV-2 microglia. This effect was blocked by a neutralizing antibody for IL-6. These findings indicated that crosstalk between the IκB-NFκB and JAK-STAT3 pathways is a pericyte specific mechanism, not occurring in astrocytes, for TNF-α-induced IL-6 release. IL-6 derived from pericytes enhanced microglial activation. Our findings increase understanding of the role of pericyte-microglia crosstalk in the brain under neuroinflammatory conditions and suggest a potentially attractive therapeutic target for brain inflammation.	Immunohistochemical staining	STAT3 contributed to TNF-α induced nuclear translocation of phospho-NFκB in pericytes. TNF-α-induced IL-6 release in astrocytes was mediated by NFκB but not by STAT3. The presence of pericytes amplified TNF-α-induced iNOS mRNA expression in BV-2 microglia. This effect was blocked by a neutralizing antibody for IL-6. These findings indicated that crosstalk between the IκB-NFκB and JAK-STAT3 pathways is a pericyte specific mechanism, not occurring in astrocytes, for TNF-α-induced IL-6 release. IL-6 derived from pericytes enhanced microglial activation. Our findings increase understanding of the role of pericyte-microglia crosstalk in the brain under neuroinflammatory conditions and suggest a potentially attractive therapeutic target for brain inflammation.	STAT3		Western blot,RT-PCR,	STAT3 contributed to TNF-α induced nuclear translocation of phospho-NFκB in pericytes. TNF-α-induced IL-6 release in astrocytes was mediated by NFκB but not by STAT3. The presence of pericytes amplified TNF-α-induced iNOS mRNA expression in BV-2 microglia. This effect was blocked by a neutralizing antibody for IL-6. These findings indicated that crosstalk between the IκB-NFκB and JAK-STAT3 pathways is a pericyte specific mechanism, not occurring in astrocytes, for TNF-α-induced IL-6 release. IL-6 derived from pericytes enhanced microglial activation. Our findings increase understanding of the role of pericyte-microglia crosstalk in the brain under neuroinflammatory conditions and suggest a potentially attractive therapeutic target for brain inflammation.			
29696026	chr16	23780812	23782812	Bcl6	The inhibitory functions of Bcl6 in MPT and MPTH2 cells attenuated allergic responses. Bcl6 is a critical regulator of IL-4 production by MPT and MPTH2 cells in TH2 immune responses related to the pathogenesis of allergies.	human	lymphoid tissue	High+Lowthroughput	Allergic T(H)2 Response Governed by B-Cell Lymphoma 6 Function in Naturally Occurring Memory Phenotype CD4(+) T Cells	否	无	asthma	cD4+ T cell	E_01_0536	Fluorescence-activated cell sorting(Facs) analysis,chromatin immunoprecipitation(ChIP),ELISA,retroviral Vectors With a d2EGFP reporter gene,Western Blot,OVA Challenge,Bronchoalveolar lavage (BAL),Histologic Examination,transgenic mice,	The inhibitory functions of Bcl6 in MPT and MPTH2 cells attenuated allergic responses. Bcl6 is a critical regulator of IL-4 production by MPT and MPTH2 cells in TH2 immune responses related to the pathogenesis of allergies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The inhibitory functions of Bcl6 in MPT and MPTH2 cells attenuated allergic responses. Bcl6 is a critical regulator of IL-4 production by MPT and MPTH2 cells in TH2 immune responses related to the pathogenesis of allergies.		The inhibitory functions of Bcl6 in MPT and MPTH2 cells attenuated allergic responses. Bcl6 is a critical regulator of IL-4 production by MPT and MPTH2 cells in TH2 immune responses related to the pathogenesis of allergies.	Immunohistochemical staining	The inhibitory functions of Bcl6 in MPT and MPTH2 cells attenuated allergic responses. Bcl6 is a critical regulator of IL-4 production by MPT and MPTH2 cells in TH2 immune responses related to the pathogenesis of allergies.			Fluorescence-activated cell sorting(Facs) analysis,chromatin immunoprecipitation(ChIP),ELISA,retroviral Vectors With a d2EGFP reporter gene,Western Blot,OVA Challenge,Bronchoalveolar lavage (BAL),Histologic Examination,transgenic mice,				Bcl6
29695955	chr1	231623949	231625949	DISC1	Our results suggest GLYX-13 as a candidate for schizophrenia treatment, and NR2B and DISC1 in the hippocampus may account for the molecular mechanisms of GLYX-13.	mouse	Nervous tissue	High+Lowthroughput	GLYX-13 Ameliorates Schizophrenia-Like Phenotype Induced by MK-801 in Mice: Role of Hippocampal NR2B and DISC1	否	无	Schizophrenia type 1 disorder, schizophrenia		E_02_0323	Western Blot,Immunohistochemistry Analysis,	Our results suggest GLYX-13 as a candidate for schizophrenia treatment, and NR2B and DISC1 in the hippocampus may account for the molecular mechanisms of GLYX-13.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results suggest GLYX-13 as a candidate for schizophrenia treatment, and NR2B and DISC1 in the hippocampus may account for the molecular mechanisms of GLYX-13.		Our results suggest GLYX-13 as a candidate for schizophrenia treatment, and NR2B and DISC1 in the hippocampus may account for the molecular mechanisms of GLYX-13.	Immunohistochemical staining	Our results suggest GLYX-13 as a candidate for schizophrenia treatment, and NR2B and DISC1 in the hippocampus may account for the molecular mechanisms of GLYX-13.			Western Blot,Immunohistochemistry Analysis,				DISC1
29695788	chr6	31137269	31137697	TFAP2C	To identify new transcription factors that differentially regulate the unique pluripotent stages, we mapped open chromatin using ATAC-seq and found enrichment of the activator protein-2 (AP2) transcription factor binding motif at naive-specific open chromatin. We determined that the AP2 family member TFAP2C is upregulated during primed to naive reversion and becomes widespread at naive-specific enhancers. TFAP2C functions to maintain pluripotency and repress neuroectodermal differentiation during the transition from primed to naive by facilitating the opening of enhancers proximal to pluripotency factors. Additionally, we identify a previously undiscovered naive-specific POU5F1 (OCT4) enhancer enriched for TFAP2C binding. Taken together, TFAP2C establishes and maintains naive human pluripotency and regulates OCT4 expression by mechanisms that are distinct from mouse.	human		Low+High throughput	TFAP2C regulates transcription in human naive pluripotency by opening enhancers	否	--	--	embryonic stem cell	E_02_0324	ATAC-seq,Luciferase Reporter Assay,ChIP-seq	In human pre-implantation blastocyst, however, neither enhancer appears open, whereas two putative enhancers appear downstream of the POU5F1 TSS. Each of these peaks contains a cluster of AP2 sites and a KLF site, indicating that they could be opened by the combinatorial activity of these transcription factors during preimplantation development.	Enhancer	CRISPR/Cas9	--	We found normal expression of OCT4 and self-renewal in the primed state, but a dramatic loss of OCT4 expression accompanied by differentiation upon reversion to the naive state. This indicates a potential direct role for TFAP2C in regulating the pluripotency master-regulator OCT4 by binding to a previously unknown enhancer, which in turn is likely to be important for preimplantation OCT4 expression.	OCT3, OCT4, OTF-3, OTF3, OTF4, Oct-3, Oct-4	TFAP2C functions to maintain pluripotency and repress neuroectodermal differentiation during the transition from primed to naive by facilitating the opening of enhancers proximal to pluripotency factors.	Luciferase Reporter Assay,CRISPR/Cas9	This indicates a potential direct role for TFAP2C in regulating the pluripotency master-regulator OCT4 by binding to a previously unknown Enhancer, which in turn is likely to be important for preimplantation OCT4 expression.	TFAP2C	AP2-GAMMA,ERF1,TFAP2G,hAP-2g	Luciferase Reporter Assay	Luciferase activity from a pGL3 construct in which WT or mutant Intron Element 1 had been cloned, normalized to signal from a pGL3 construct with no enhancer. Results are shown from two independent experiment, except for the ΔAP2 sample, for which there are n=3 replicates from two experiments. All signals were first normalized for Renilla signal.	--	--	POU5F1
29695788	chr6	31137269	31137697	POU5F1	To identify new transcription factors that differentially regulate the unique pluripotent stages, we mapped open chromatin using ATAC-seq and found enrichment of the activator protein-2 (AP2) transcription factor binding motif at naive-specific open chromatin. We determined that the AP2 family member TFAP2C is upregulated during primed to naive reversion and becomes widespread at naive-specific enhancers. TFAP2C functions to maintain pluripotency and repress neuroectodermal differentiation during the transition from primed to naive by facilitating the opening of enhancers proximal to pluripotency factors. Additionally, we identify a previously undiscovered naive-specific POU5F1 (OCT4) enhancer enriched for TFAP2C binding. Taken together, TFAP2C establishes and maintains naive human pluripotency and regulates OCT4 expression by mechanisms that are distinct from mouse.	human		Low+High throughput	TFAP2C regulates transcription in human naive pluripotency by opening enhancers	否	--	--	embryonic stem cell	E_02_0324	ATAC-seq,Luciferase Reporter Assay,ChIP-seq	In human pre-implantation blastocyst, however, neither enhancer appears open, whereas two putative enhancers appear downstream of the POU5F1 TSS. Each of these peaks contains a cluster of AP2 sites and a KLF site, indicating that they could be opened by the combinatorial activity of these transcription factors during preimplantation development.	Enhancer	CRISPR/Cas9	--	We found normal expression of OCT4 and self-renewal in the primed state, but a dramatic loss of OCT4 expression accompanied by differentiation upon reversion to the naive state. This indicates a potential direct role for TFAP2C in regulating the pluripotency master-regulator OCT4 by binding to a previously unknown enhancer, which in turn is likely to be important for preimplantation OCT4 expression.	OCT3, OCT4, OTF-3, OTF3, OTF4, Oct-3, Oct-4	TFAP2C functions to maintain pluripotency and repress neuroectodermal differentiation during the transition from primed to naive by facilitating the opening of enhancers proximal to pluripotency factors.	Luciferase Reporter Assay,CRISPR/Cas9	This indicates a potential direct role for TFAP2C in regulating the pluripotency master-regulator OCT4 by binding to a previously unknown Enhancer, which in turn is likely to be important for preimplantation OCT4 expression.	TFAP2C	AP2-GAMMA,ERF1,TFAP2G,hAP-2g	Luciferase Reporter Assay	Luciferase activity from a pGL3 construct in which WT or mutant Intron Element 1 had been cloned, normalized to signal from a pGL3 construct with no enhancer. Results are shown from two independent experiment, except for the ΔAP2 sample, for which there are n=3 replicates from two experiments. All signals were first normalized for Renilla signal.	--	--	POU5F1
29695774	chr8	7052292	7054292	DEFA5	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				DEFA5
29695774	chr8	6922235	6924235	DEFA6	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				DEFA6
29695774	chr2	79117802	79119802	REG1A	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				REG1A
29695774	chr2	79082390	79084390	REG1B	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				REG1B
29695774	chr2	79154511	79156511	REG3A	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				REG3A
29695774	chr3	190302823	190304823	CLDN1	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	CLDN1		CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			
29695774	chrX	106897354	106899354	CLDN2	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				CLDN2
29695774	chr13	95431053	95433053	CLDN10	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				CLDN10
29695774	chr21	36457908	36459908	CLDN14	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				CLDN14
29695774	chr3	137995503	137997503	CLDN18	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				CLDN18
29695774	chr3	186927501	186929501	ST6GAL1	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				ST6GAL1
29695774	chr4	73737783	73739783	CXCL8	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	CXCL8		CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			
29695774	chr4	73833876	73835876	CXCL6	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	CXCL6		CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			
29695774	chr4	73850235	73852235	PF4V1	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				PF4V1
29695774	chr4	73866918	73868918	CXCL1	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				CXCL1
29695774	chr4	73978159	73980159	PF4	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				PF4
29695774	chr4	73983469	73985469	PPBP	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				PPBP
29695774	chr4	73993410	73995410	CXCL5	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				CXCL5
29695774	chr4	74033547	74035547	CXCL3	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	CXCL3		CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			
29695774	chr4	74051398	74053398	PPBPP2	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				PPBPP2
29695774	chr4	74093762	74095762	CXCL2	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	human	Colon tissue	High+Lowthroughput	Characterization of the enhancer and promoter landscape of inflammatory bowel disease from human colon biopsies	是	rs11676348	Inflammatory bowel disease (IBD)	monocyte cells	E_01_0537	CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.		We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.	Immunohistochemical staining	We find that as few as 35 TSSs can distinguish active CD, UC, and controls with 85% accuracy in an independent cohort. Our data constitute a foundation for understanding the molecular pathology, gene regulation, and genetics of IBD.			CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,				CXCL2
29694926	chr1	207878058	207880058	CD34	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	human	connective tissue	High+Lowthroughput	GH prevents adipogenic differentiation of mesenchymal stromal stem cells derived from human trabecular bone via canonical Wnt signaling	否	无	Osteoporosis		E_01_0538	FACS analysis, Staining assay,Reverse transcription PCR,semi-quantitative real time PCR,Western blot,Nuclear fractionation,ELISA,siRNA-mediated β-catenin gene silencing,	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.		In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	Immunohistochemical staining	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.			FACS analysis, Staining assay,Reverse transcription PCR,semi-quantitative real time PCR,Western blot,Nuclear fractionation,ELISA,siRNA-mediated β-catenin gene silencing,				CD34
29694926	chr8	19899572	19901572	LPL	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	human	connective tissue	High+Lowthroughput	GH prevents adipogenic differentiation of mesenchymal stromal stem cells derived from human trabecular bone via canonical Wnt signaling	否	无	Osteoporosis		E_01_0538	FACS analysis, Staining assay,Reverse transcription PCR,semi-quantitative real time PCR,Western blot,Nuclear fractionation,ELISA,siRNA-mediated β-catenin gene silencing,	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	Immunohistochemical staining	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	LPL		FACS analysis, Staining assay,Reverse transcription PCR,semi-quantitative real time PCR,Western blot,Nuclear fractionation,ELISA,siRNA-mediated β-catenin gene silencing,	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.			
29694926	chr17	37082220	37084220	ACACA	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	human	connective tissue	High+Lowthroughput	GH prevents adipogenic differentiation of mesenchymal stromal stem cells derived from human trabecular bone via canonical Wnt signaling	否	无	Osteoporosis		E_01_0538	FACS analysis, Staining assay,Reverse transcription PCR,semi-quantitative real time PCR,Western blot,Nuclear fractionation,ELISA,siRNA-mediated β-catenin gene silencing,	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.		In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	Immunohistochemical staining	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.			FACS analysis, Staining assay,Reverse transcription PCR,semi-quantitative real time PCR,Western blot,Nuclear fractionation,ELISA,siRNA-mediated β-catenin gene silencing,				ACACA
29694926	chr10	52311147	52313147	DKK1	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	human	connective tissue	High+Lowthroughput	GH prevents adipogenic differentiation of mesenchymal stromal stem cells derived from human trabecular bone via canonical Wnt signaling	否	无	Osteoporosis		E_01_0538	FACS analysis, Staining assay,Reverse transcription PCR,semi-quantitative real time PCR,Western blot,Nuclear fractionation,ELISA,siRNA-mediated β-catenin gene silencing,	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.		In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	Immunohistochemical staining	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.			FACS analysis, Staining assay,Reverse transcription PCR,semi-quantitative real time PCR,Western blot,Nuclear fractionation,ELISA,siRNA-mediated β-catenin gene silencing,				DKK1
29694926	chr4	153777800	153779800	SFRP2	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	human	connective tissue	High+Lowthroughput	GH prevents adipogenic differentiation of mesenchymal stromal stem cells derived from human trabecular bone via canonical Wnt signaling	否	无	Osteoporosis		E_01_0538	FACS analysis, Staining assay,Reverse transcription PCR,semi-quantitative real time PCR,Western blot,Nuclear fractionation,ELISA,siRNA-mediated β-catenin gene silencing,	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.		In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.	Immunohistochemical staining	In the present study, using primary human mesenchymal stromal cells (hMSCs) isolated from trabecular bone, we assessed the possible effect of GH on hMSC differentiation potential into adipocytes. GH (5 ng/ml) significantly inhibited the lipid accumulation in hMSCs cultured for 14 days in lipogenic medium. GH decreased the expression of the adipogenic genes, CCAAT/enhancer-binding protein alpha (C/EBPα) and adiponectin (ADN) as well as the expression of two lipogenesis-related enzymes, lipoprotein lipase (LPL) and acethylCoA carboxylase (ACACA). In parallel, GH induced an increase in the gene expression and protein levels of osterix (OSX) and osteoprotegerin (OPG). These effects were ascribed to enhanced Wnt signaling as GH significantly reduced Wnt inhibitors, Dickkopf 1 (DKK1) and the secreted frizzled protein 2 (SFRP2), and increased the expression of an activator of Wnt, Wnt3. Accordingly, the expression of β-catenin and its nuclear levels were raised. Wnt involvement in GH anti-adipogenic effect was further confirmed by the silencing of β-catenin. In silenced hMSC, both the inhibitory effect of GH on the expression of the adipogenic genes, ADN and C/EBPα and the lipogenesis enzymes LPL and ACACA, were prevented together with the stimulatory effect of GH on the osteogenic genes OSX and OPG. The present study supports the hypothesis that when GH secretion declines as in aging, the fat in the bone-marrow cavities increases and the osteogenic capacity of the MSC pool is reduced due to a decrease in Wnt signaling.			FACS analysis, Staining assay,Reverse transcription PCR,semi-quantitative real time PCR,Western blot,Nuclear fractionation,ELISA,siRNA-mediated β-catenin gene silencing,				SFRP2
29693178	chr7	79765210	79767210	GNAI1	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	human	Epithelial tissues	High+Lowthroughput	Identifying genes as potential prognostic indicators in patients with serous ovarian cancer resistant to carboplatin using integrated bioinformatics analysis	否	无	Serous ovarian cancer (SOC)	normal ovarian surface epithelial cells	E_01_0539	Gene Ontology (GO) analysis,Immunohistochemistry (IHC) analysis,Kaplan‑Meier survival analysis,Protein‑protein interaction (PPI) network,	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	Immunohistochemical staining	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	GNAI1		Gene Ontology (GO) analysis,Immunohistochemistry (IHC) analysis,Kaplan‑Meier survival analysis,Protein‑protein interaction (PPI) network,	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.			
29693178	chr2	96332647	96334647	NCAPH	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	human	Epithelial tissues	High+Lowthroughput	Identifying genes as potential prognostic indicators in patients with serous ovarian cancer resistant to carboplatin using integrated bioinformatics analysis	否	无	Serous ovarian cancer (SOC)	normal ovarian surface epithelial cells	E_01_0539	Gene Ontology (GO) analysis,Immunohistochemistry (IHC) analysis,Kaplan‑Meier survival analysis,Protein‑protein interaction (PPI) network,	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.		Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	Immunohistochemical staining	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.			Gene Ontology (GO) analysis,Immunohistochemistry (IHC) analysis,Kaplan‑Meier survival analysis,Protein‑protein interaction (PPI) network,				NCAPH
29693178	chr20	46006178	46008178	MMP9	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	human	Epithelial tissues	High+Lowthroughput	Identifying genes as potential prognostic indicators in patients with serous ovarian cancer resistant to carboplatin using integrated bioinformatics analysis	否	无	Serous ovarian cancer (SOC)	normal ovarian surface epithelial cells	E_01_0539	Gene Ontology (GO) analysis,Immunohistochemistry (IHC) analysis,Kaplan‑Meier survival analysis,Protein‑protein interaction (PPI) network,	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	Immunohistochemical staining	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	MMP9		Gene Ontology (GO) analysis,Immunohistochemistry (IHC) analysis,Kaplan‑Meier survival analysis,Protein‑protein interaction (PPI) network,	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.			
29693178	chr20	56366570	56368570	AURKA	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	human	Epithelial tissues	High+Lowthroughput	Identifying genes as potential prognostic indicators in patients with serous ovarian cancer resistant to carboplatin using integrated bioinformatics analysis	否	无	Serous ovarian cancer (SOC)	normal ovarian surface epithelial cells	E_01_0539	Gene Ontology (GO) analysis,Immunohistochemistry (IHC) analysis,Kaplan‑Meier survival analysis,Protein‑protein interaction (PPI) network,	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.		Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	Immunohistochemical staining	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.			Gene Ontology (GO) analysis,Immunohistochemistry (IHC) analysis,Kaplan‑Meier survival analysis,Protein‑protein interaction (PPI) network,				AURKA
29693178	chr7	148805000	148807000	EZH2	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	human	Epithelial tissues	High+Lowthroughput	Identifying genes as potential prognostic indicators in patients with serous ovarian cancer resistant to carboplatin using integrated bioinformatics analysis	否	无	Serous ovarian cancer (SOC)	normal ovarian surface epithelial cells	E_01_0539	Gene Ontology (GO) analysis,Immunohistochemistry (IHC) analysis,Kaplan‑Meier survival analysis,Protein‑protein interaction (PPI) network,	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	Immunohistochemical staining	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.	EZH2		Gene Ontology (GO) analysis,Immunohistochemistry (IHC) analysis,Kaplan‑Meier survival analysis,Protein‑protein interaction (PPI) network,	Through survival analysis, comparison of genes across numerous analyses, and immunohistochemistry, GNAI1, non‑structural maintenance of chromosomes (non‑SMC) condensin I complex subunit H (NCAPH), matrix metallopeptidase 9 (MMP9), aurora kinase A (AURKA) and enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) were identified as the key molecules that may be involved in the carcinogenesis and carboplatin resistance of SOC. In conclusion, GNAI1, NCAPH, MMP9, AURKA and EZH2 should be examined in further studies for the possibility of their participation in the carcinogenesis and carboplatin response of SOC.			
29691190	chr11	2161549	2163549	TH	NFJ increased Con A-induced lymphocyte proliferation, IL-2 and IFN-γ production, and p-ERK1/2 expression both in vitro and in vivo. In in vivo NFJ-treated old rats, lymph node lymphocytes showed increased expression of p-TH and Akt, nitric oxide production and decreased expression of p-NF-κB p65 and p50.	mouse	lymphoid tissue	High+Lowthroughput	Noni (Morinda citrifolia L.) fruit juice delays immunosenescence in the lymphocytes in lymph nodes of old F344 rats	否	无	Immunosenescence, inflammation	lymphocyte	E_02_0325	MTT assays,Western blot,NO production,Assays for antioxidant enzymes,assays for lipid peroxidation,ELISA,	NFJ increased Con A-induced lymphocyte proliferation, IL-2 and IFN-γ production, and p-ERK1/2 expression both in vitro and in vivo. In in vivo NFJ-treated old rats, lymph node lymphocytes showed increased expression of p-TH and Akt, nitric oxide production and decreased expression of p-NF-κB p65 and p50.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	NFJ increased Con A-induced lymphocyte proliferation, IL-2 and IFN-γ production, and p-ERK1/2 expression both in vitro and in vivo. In in vivo NFJ-treated old rats, lymph node lymphocytes showed increased expression of p-TH and Akt, nitric oxide production and decreased expression of p-NF-κB p65 and p50.		NFJ increased Con A-induced lymphocyte proliferation, IL-2 and IFN-γ production, and p-ERK1/2 expression both in vitro and in vivo. In in vivo NFJ-treated old rats, lymph node lymphocytes showed increased expression of p-TH and Akt, nitric oxide production and decreased expression of p-NF-κB p65 and p50.	Immunohistochemical staining	NFJ increased Con A-induced lymphocyte proliferation, IL-2 and IFN-γ production, and p-ERK1/2 expression both in vitro and in vivo. In in vivo NFJ-treated old rats, lymph node lymphocytes showed increased expression of p-TH and Akt, nitric oxide production and decreased expression of p-NF-κB p65 and p50.			MTT assays,Western blot,NO production,Assays for antioxidant enzymes,assays for lipid peroxidation,ELISA,				TH
29689351	chr17	42310380	42312380	STAT3	GFE inhibits lipogenesis by negative regulation of adipogenic transcription factors, which is associated with GFE-mediated cell cycle arrest and STAT3 inhibition.	mouse	adipose tissue	High+Lowthroughput	The fruits of Gleditsia sinensis Lam. inhibits adipogenesis through modulation of mitotic clonal expansion and STAT3 activation in 3T3-L1 cells	否	无	Neoplasms, thrombosis, inflammation related disorders, obesity	3T3-L1 cell	E_02_0326	MTT,Oil Red O staining,crystal violet staining,flow cytometry,ELISA,Quantitative Real-time PCR, Immunofluorescence,western blot,Immunoblotting,	GFE inhibits lipogenesis by negative regulation of adipogenic transcription factors, which is associated with GFE-mediated cell cycle arrest and STAT3 inhibition.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	GFE inhibits lipogenesis by negative regulation of adipogenic transcription factors, which is associated with GFE-mediated cell cycle arrest and STAT3 inhibition.		GFE inhibits lipogenesis by negative regulation of adipogenic transcription factors, which is associated with GFE-mediated cell cycle arrest and STAT3 inhibition.	Immunohistochemical staining	GFE inhibits lipogenesis by negative regulation of adipogenic transcription factors, which is associated with GFE-mediated cell cycle arrest and STAT3 inhibition.			MTT,Oil Red O staining,crystal violet staining,flow cytometry,ELISA,Quantitative Real-time PCR, Immunofluorescence,western blot,Immunoblotting,				STAT3
29685965	chr7	148804465	148806465	EZH2	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	human		High+Lowthroughput	Pyrazole-based inhibitors of enhancer of zeste homologue 2 induce apoptosis and autophagy in cancer cells	否	无	nothing	MDA-MB-231	E_01_0540	western blot,MTS,	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	Immunohistochemical staining	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	EZH2		western blot,MTS,	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.			
29685965	chr17	31934321	31936321	SUZ12	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	human		High+Lowthroughput	Pyrazole-based inhibitors of enhancer of zeste homologue 2 induce apoptosis and autophagy in cancer cells	否	无	nothing	MDA-MB-231	E_01_0540	western blot,MTS,	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	Immunohistochemical staining	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	SUZ12		western blot,MTS,	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.			
29685965	chr12	19401282	19403282	AEBP2	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	human		High+Lowthroughput	Pyrazole-based inhibitors of enhancer of zeste homologue 2 induce apoptosis and autophagy in cancer cells	否	无	nothing	MDA-MB-231	E_01_0540	western blot,MTS,	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.		Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	Immunohistochemical staining	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.			western blot,MTS,				AEBP2
29685965	chr19	49673356	49675356	PRMT1	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	human		High+Lowthroughput	Pyrazole-based inhibitors of enhancer of zeste homologue 2 induce apoptosis and autophagy in cancer cells	否	无	nothing	MDA-MB-231	E_01_0540	western blot,MTS,	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.		Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	Immunohistochemical staining	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.			western blot,MTS,				PRMT1
29685965	chr19	10130545	10132545	DNMT1	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	human		High+Lowthroughput	Pyrazole-based inhibitors of enhancer of zeste homologue 2 induce apoptosis and autophagy in cancer cells	否	无	nothing	MDA-MB-231	E_01_0540	western blot,MTS,	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	Immunohistochemical staining	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	DNMT1		western blot,MTS,	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.			
29685965	chr19	2161241	2163241	DOT1L	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	human		High+Lowthroughput	Pyrazole-based inhibitors of enhancer of zeste homologue 2 induce apoptosis and autophagy in cancer cells	否	无	nothing	MDA-MB-231	E_01_0540	western blot,MTS,	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.		Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.	Immunohistochemical staining	Novel pyrazole-based EZH2 inhibitors have been prepared through a molecular pruning approach from known inhibitors bearing a bicyclic moiety as a central scaffold. The hit compound 1o (N-((4,6-dimethyl-2-oxo-1,2-dihydropyridin-3-yl)methyl)-5-methyl-1-phenyl-1H-pyrazole-4-carboxamide) showed low micromolar EZH2/PRC2 inhibition and high selectivity towards a panel of other methyltransferases. Moreover, 1o displayed cell growth arrest in breast MDA-MB231, leukaemia K562, and neuroblastoma SK-N-BE cancer cells joined to reduction of H3K27me3 levels and induction of apoptosis and autophagy.This article is part of a discussion meeting issue 'Frontiers in epigenetic chemical biology'.			western blot,MTS,				DOT1L
32161797	chr1	51574533	51576533	OSBPL9	OSBPL9 is a novel ER stress-responsive gene and we confirmed that endogenous mRNA expression of OSBPL9 is upregulated by thapsigargin, and is repressed by IRE1α inhibitors, 4μ8C and toyocamycin, but not significantly by a PERK inhibitor, GSK2656157. These results demonstrate that this approach can be used to discover novel genes regulated by any stimuli without the need for microarray analysis, and that it can concomitantly produce reporter cells without identification of stimuli-responsive promoter/enhancer elements. Therefore, this system has a variety of benefits for basic and clinical research.	mouse		High+Lowthroughput	A highly sensitive trap vector system for isolating reporter cells and identification of responsive genes	否	无	nothing	NMuMG cell	E_02_0327	Luciferase assay,Immunoblotting,Real-time PCR,Splinkerette PCR,Fluorescence-activated cell sorting,transfection,	OSBPL9 is a novel ER stress-responsive gene and we confirmed that endogenous mRNA expression of OSBPL9 is upregulated by thapsigargin, and is repressed by IRE1α inhibitors, 4μ8C and toyocamycin, but not significantly by a PERK inhibitor, GSK2656157. These results demonstrate that this approach can be used to discover novel genes regulated by any stimuli without the need for microarray analysis, and that it can concomitantly produce reporter cells without identification of stimuli-responsive promoter/enhancer elements. Therefore, this system has a variety of benefits for basic and clinical research.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	OSBPL9 is a novel ER stress-responsive gene and we confirmed that endogenous mRNA expression of OSBPL9 is upregulated by thapsigargin, and is repressed by IRE1α inhibitors, 4μ8C and toyocamycin, but not significantly by a PERK inhibitor, GSK2656157. These results demonstrate that this approach can be used to discover novel genes regulated by any stimuli without the need for microarray analysis, and that it can concomitantly produce reporter cells without identification of stimuli-responsive promoter/enhancer elements. Therefore, this system has a variety of benefits for basic and clinical research.		OSBPL9 is a novel ER stress-responsive gene and we confirmed that endogenous mRNA expression of OSBPL9 is upregulated by thapsigargin, and is repressed by IRE1α inhibitors, 4μ8C and toyocamycin, but not significantly by a PERK inhibitor, GSK2656157. These results demonstrate that this approach can be used to discover novel genes regulated by any stimuli without the need for microarray analysis, and that it can concomitantly produce reporter cells without identification of stimuli-responsive promoter/enhancer elements. Therefore, this system has a variety of benefits for basic and clinical research.	Immunohistochemical staining	OSBPL9 is a novel ER stress-responsive gene and we confirmed that endogenous mRNA expression of OSBPL9 is upregulated by thapsigargin, and is repressed by IRE1α inhibitors, 4μ8C and toyocamycin, but not significantly by a PERK inhibitor, GSK2656157. These results demonstrate that this approach can be used to discover novel genes regulated by any stimuli without the need for microarray analysis, and that it can concomitantly produce reporter cells without identification of stimuli-responsive promoter/enhancer elements. Therefore, this system has a variety of benefits for basic and clinical research.			Luciferase assay,Immunoblotting,Real-time PCR,Splinkerette PCR,Fluorescence-activated cell sorting,transfection,				OSBPL9
32161797	chr8	127732371	127734371	MYC	OSBPL9 is a novel ER stress-responsive gene and we confirmed that endogenous mRNA expression of OSBPL9 is upregulated by thapsigargin, and is repressed by IRE1α inhibitors, 4μ8C and toyocamycin, but not significantly by a PERK inhibitor, GSK2656157. These results demonstrate that this approach can be used to discover novel genes regulated by any stimuli without the need for microarray analysis, and that it can concomitantly produce reporter cells without identification of stimuli-responsive promoter/enhancer elements. Therefore, this system has a variety of benefits for basic and clinical research.	mouse		High+Lowthroughput	A highly sensitive trap vector system for isolating reporter cells and identification of responsive genes	否	无	nothing	NMuMG cell	E_02_0327	Luciferase assay,Immunoblotting,Real-time PCR,Splinkerette PCR,Fluorescence-activated cell sorting,transfection,	OSBPL9 is a novel ER stress-responsive gene and we confirmed that endogenous mRNA expression of OSBPL9 is upregulated by thapsigargin, and is repressed by IRE1α inhibitors, 4μ8C and toyocamycin, but not significantly by a PERK inhibitor, GSK2656157. These results demonstrate that this approach can be used to discover novel genes regulated by any stimuli without the need for microarray analysis, and that it can concomitantly produce reporter cells without identification of stimuli-responsive promoter/enhancer elements. Therefore, this system has a variety of benefits for basic and clinical research.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	OSBPL9 is a novel ER stress-responsive gene and we confirmed that endogenous mRNA expression of OSBPL9 is upregulated by thapsigargin, and is repressed by IRE1α inhibitors, 4μ8C and toyocamycin, but not significantly by a PERK inhibitor, GSK2656157. These results demonstrate that this approach can be used to discover novel genes regulated by any stimuli without the need for microarray analysis, and that it can concomitantly produce reporter cells without identification of stimuli-responsive promoter/enhancer elements. Therefore, this system has a variety of benefits for basic and clinical research.		OSBPL9 is a novel ER stress-responsive gene and we confirmed that endogenous mRNA expression of OSBPL9 is upregulated by thapsigargin, and is repressed by IRE1α inhibitors, 4μ8C and toyocamycin, but not significantly by a PERK inhibitor, GSK2656157. These results demonstrate that this approach can be used to discover novel genes regulated by any stimuli without the need for microarray analysis, and that it can concomitantly produce reporter cells without identification of stimuli-responsive promoter/enhancer elements. Therefore, this system has a variety of benefits for basic and clinical research.	Immunohistochemical staining	OSBPL9 is a novel ER stress-responsive gene and we confirmed that endogenous mRNA expression of OSBPL9 is upregulated by thapsigargin, and is repressed by IRE1α inhibitors, 4μ8C and toyocamycin, but not significantly by a PERK inhibitor, GSK2656157. These results demonstrate that this approach can be used to discover novel genes regulated by any stimuli without the need for microarray analysis, and that it can concomitantly produce reporter cells without identification of stimuli-responsive promoter/enhancer elements. Therefore, this system has a variety of benefits for basic and clinical research.			Luciferase assay,Immunoblotting,Real-time PCR,Splinkerette PCR,Fluorescence-activated cell sorting,transfection,				MYC
29684535	chr1	45691360	45693360	IPP	In conclusion, there was a reduction in the hypotensive effects of IPP and LKP in SHRs when intestinal PepT1 was inhibited by Gly-Sar, but C10 may circumvent this by enhancing paracellular permeability.	mouse		High+Lowthroughput	Sodium caprate enables the blood pressure-lowering effect of Ile-Pro-Pro and Leu-Lys-Pro in spontaneously hypertensive rats by indirectly overcoming PepT1 inhibition	否	无	nothing	Caco-2 cell	E_02_0328	Immunofluorescence, Histology,In vivo rat studies,	In conclusion, there was a reduction in the hypotensive effects of IPP and LKP in SHRs when intestinal PepT1 was inhibited by Gly-Sar, but C10 may circumvent this by enhancing paracellular permeability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, there was a reduction in the hypotensive effects of IPP and LKP in SHRs when intestinal PepT1 was inhibited by Gly-Sar, but C10 may circumvent this by enhancing paracellular permeability.		In conclusion, there was a reduction in the hypotensive effects of IPP and LKP in SHRs when intestinal PepT1 was inhibited by Gly-Sar, but C10 may circumvent this by enhancing paracellular permeability.	Immunohistochemical staining	In conclusion, there was a reduction in the hypotensive effects of IPP and LKP in SHRs when intestinal PepT1 was inhibited by Gly-Sar, but C10 may circumvent this by enhancing paracellular permeability.			Immunofluorescence, Histology,In vivo rat studies,				IPP
29684535	chr17	63474258	63476258	ACE	In conclusion, there was a reduction in the hypotensive effects of IPP and LKP in SHRs when intestinal PepT1 was inhibited by Gly-Sar, but C10 may circumvent this by enhancing paracellular permeability.	mouse		High+Lowthroughput	Sodium caprate enables the blood pressure-lowering effect of Ile-Pro-Pro and Leu-Lys-Pro in spontaneously hypertensive rats by indirectly overcoming PepT1 inhibition	否	无	nothing	Caco-2 cell	E_02_0328	Immunofluorescence, Histology,In vivo rat studies,	In conclusion, there was a reduction in the hypotensive effects of IPP and LKP in SHRs when intestinal PepT1 was inhibited by Gly-Sar, but C10 may circumvent this by enhancing paracellular permeability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, there was a reduction in the hypotensive effects of IPP and LKP in SHRs when intestinal PepT1 was inhibited by Gly-Sar, but C10 may circumvent this by enhancing paracellular permeability.		In conclusion, there was a reduction in the hypotensive effects of IPP and LKP in SHRs when intestinal PepT1 was inhibited by Gly-Sar, but C10 may circumvent this by enhancing paracellular permeability.	Immunohistochemical staining	In conclusion, there was a reduction in the hypotensive effects of IPP and LKP in SHRs when intestinal PepT1 was inhibited by Gly-Sar, but C10 may circumvent this by enhancing paracellular permeability.			Immunofluorescence, Histology,In vivo rat studies,				ACE
29683870	chr4	153680698	153682698	TLR2	Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.	mouse	/	High+Lowthroughput	Isosteviol sodium injection improves outcomes by modulating TLRs/NF-κB-dependent inflammatory responses following experimental traumatic brain injury in rats	否	无	inflammatory reaction 		E_02_0329	Nissl staining,Immunohistochemical assays,qRT-PCR,Enzyme-linked immunosorbent assay(ELISA),Western blot,	Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.		Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.	Immunohistochemical staining	Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.			Nissl staining,Immunohistochemical assays,qRT-PCR,Enzyme-linked immunosorbent assay(ELISA),Western blot,				TLR2
29683870	chr9	117701301	117703301	TLR4	Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.	mouse	/	High+Lowthroughput	Isosteviol sodium injection improves outcomes by modulating TLRs/NF-κB-dependent inflammatory responses following experimental traumatic brain injury in rats	否	无	inflammatory reaction 		E_02_0329	Nissl staining,Immunohistochemical assays,qRT-PCR,Enzyme-linked immunosorbent assay(ELISA),Western blot,	Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.		Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.	Immunohistochemical staining	Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.			Nissl staining,Immunohistochemical assays,qRT-PCR,Enzyme-linked immunosorbent assay(ELISA),Western blot,				TLR4
29683870	chr17	44900356	44902356	GFAP	Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.	mouse	/	High+Lowthroughput	Isosteviol sodium injection improves outcomes by modulating TLRs/NF-κB-dependent inflammatory responses following experimental traumatic brain injury in rats	否	无	inflammatory reaction 		E_02_0329	Nissl staining,Immunohistochemical assays,qRT-PCR,Enzyme-linked immunosorbent assay(ELISA),Western blot,	Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.		Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.	Immunohistochemical staining	Results from quantitative real-time-PCR and western blotting also show that the mRNA and protein expression levels of TLR2, TLR4, and NF-κB were significantly lower in STVNa-treated rats compared with the vehicle-treated rats. The administration of STVNa attenuates the TLR/NF-κB signaling pathway-mediated inflammatory responses in the injured rat brain, and this may be the mechanism by which STVNa improves the outcome following TBI.			Nissl staining,Immunohistochemical assays,qRT-PCR,Enzyme-linked immunosorbent assay(ELISA),Western blot,				GFAP
29683207	chrX	103771498	103773498	PLP1	These results demonstrate for the first time that the wmN1 enhancer region: (1) is functional in hPLP1; (2) works in collaboration with its native promoter-not just a basal heterologous promoter; (3) is required for high levels of hPLP1 gene activity; (4) has a broader effect, both spatially and temporally, than originally projected with mPlp1.	mouse		High+Lowthroughput	The wmN1 enhancer region in intron 1 is required for expression of human PLP1	否	无	Human X-linked inherited disorders	Oli-neu cell	E_02_0330	Transgenic mice,qRT-PCR, b-galactosidase histochemistry,b-galactosidase enzyme assay,Combined X-gal staining,immunohistochemistry,Southern blot,	These results demonstrate for the first time that the wmN1 enhancer region: (1) is functional in hPLP1; (2) works in collaboration with its native promoter-not just a basal heterologous promoter; (3) is required for high levels of hPLP1 gene activity; (4) has a broader effect, both spatially and temporally, than originally projected with mPlp1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results demonstrate for the first time that the wmN1 enhancer region: (1) is functional in hPLP1; (2) works in collaboration with its native promoter-not just a basal heterologous promoter; (3) is required for high levels of hPLP1 gene activity; (4) has a broader effect, both spatially and temporally, than originally projected with mPlp1.		These results demonstrate for the first time that the wmN1 enhancer region: (1) is functional in hPLP1; (2) works in collaboration with its native promoter-not just a basal heterologous promoter; (3) is required for high levels of hPLP1 gene activity; (4) has a broader effect, both spatially and temporally, than originally projected with mPlp1.	Immunohistochemical staining	These results demonstrate for the first time that the wmN1 enhancer region: (1) is functional in hPLP1; (2) works in collaboration with its native promoter-not just a basal heterologous promoter; (3) is required for high levels of hPLP1 gene activity; (4) has a broader effect, both spatially and temporally, than originally projected with mPlp1.			Transgenic mice,qRT-PCR, b-galactosidase histochemistry,b-galactosidase enzyme assay,Combined X-gal staining,immunohistochemistry,Southern blot,				PLP1
29680697	chr16	29880079	29882079	Hes1	Therefore, PLGA-NP-mediated delivery of siHes1 to the cochlea represents a promising pharmacologic approach to regenerate functional and sustainable mammalian HCs in vivo.	mouse		High+Lowthroughput	Regeneration of Cochlear Hair Cells and Hearing Recovery through Hes1 Modulation with siRNA Nanoparticles in Adult Guinea Pigs	否	无	Acute acoustic trauma		E_02_0331	RT-qPCR,Auditory brainstem response (ABR) measurements,siRNA,Immunohistology,Scanning electron microscopy,	Therefore, PLGA-NP-mediated delivery of siHes1 to the cochlea represents a promising pharmacologic approach to regenerate functional and sustainable mammalian HCs in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, PLGA-NP-mediated delivery of siHes1 to the cochlea represents a promising pharmacologic approach to regenerate functional and sustainable mammalian HCs in vivo.		Therefore, PLGA-NP-mediated delivery of siHes1 to the cochlea represents a promising pharmacologic approach to regenerate functional and sustainable mammalian HCs in vivo.	Immunohistochemical staining	Therefore, PLGA-NP-mediated delivery of siHes1 to the cochlea represents a promising pharmacologic approach to regenerate functional and sustainable mammalian HCs in vivo.			RT-qPCR,Auditory brainstem response (ABR) measurements,siRNA,Immunohistology,Scanning electron microscopy,				Hes1
29678838	chr17	34252627	34254627	CCL2	Treatment of human retinal Müller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK ½, p-NF-κB and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina.	mouse	Nervous tissue	High+Lowthroughput	Rho-Associated Protein Kinase-1 Mediates the Regulation of Inflammatory Markers in Diabetic Retina and in Retinal Müller Cells	否	无	Diabetic retinopathy, inflammation	MIO-M1 cell	E_02_0332	Enzyme-linked immunosorbent assay(ELISA),Western blot,Immunofluorescence,	Treatment of human retinal Müller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK ½, p-NF-κB and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Treatment of human retinal Müller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK ½, p-NF-κB and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina.		Treatment of human retinal Müller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK ½, p-NF-κB and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina.	Immunohistochemical staining	Treatment of human retinal Müller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK ½, p-NF-κB and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina.			Enzyme-linked immunosorbent assay(ELISA),Western blot,Immunofluorescence,				CCL2
29678838	chr6	115906088	115908088	Rho	Treatment of human retinal Müller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK ½, p-NF-κB and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina.	mouse	Nervous tissue	High+Lowthroughput	Rho-Associated Protein Kinase-1 Mediates the Regulation of Inflammatory Markers in Diabetic Retina and in Retinal Müller Cells	否	无	Diabetic retinopathy, inflammation	MIO-M1 cell	E_02_0332	Enzyme-linked immunosorbent assay(ELISA),Western blot,Immunofluorescence,	Treatment of human retinal Müller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK ½, p-NF-κB and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Treatment of human retinal Müller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK ½, p-NF-κB and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina.		Treatment of human retinal Müller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK ½, p-NF-κB and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina.	Immunohistochemical staining	Treatment of human retinal Müller cells with high-glucose induced significant upregulation of ROCK-1, VEGF, and MCP-1/CCL2. Fasudil co-treatment normalized the high-glucose-induced upregulation of these mediators. Similarly, fasudil attenuated high-glucose-induced enhanced immunoreactivity for ROCK-1 and VEGF. Diabetes induced upregulation of ROCK-1, p-ERK ½, p-NF-κB and iNOS expression in retinas of mice. Constant fasudil intake from the onset of diabetes did not affect the metabolic status of diabetic mice but it attenuated diabetes-induced upregulation of these inflammatory signaling pathways.Our finding suggests that Rho-associated protein kinase-1 activation mediates regulation of inflammatory signaling pathways in diabetic retina.			Enzyme-linked immunosorbent assay(ELISA),Western blot,Immunofluorescence,				Rho
29678826	chr3	38545384	38547384	SCN5A	In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.	human	Myotome	High+Lowthroughput	RNA Binding Protein, HuR, Regulates SCN5A Expression Through Stabilizing MEF2C transcription factor mRNA	否	无	nothing	 RL14	E_01_0541	Transfection,Real-Time PCR Quantification,Western Blot,Ribonucleoprotein Immunoprecipitation,Electrophoretic Mobility Shift Assay(EMSA),Chromatin Immunoprecipitation–qPCR,	In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.		In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.	Immunohistochemical staining	In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.			Transfection,Real-Time PCR Quantification,Western Blot,Ribonucleoprotein Immunoprecipitation,Electrophoretic Mobility Shift Assay(EMSA),Chromatin Immunoprecipitation–qPCR,				SCN5A
29678826	chr5	88714350	88716350	MEF2C	In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.	human	Myotome	High+Lowthroughput	RNA Binding Protein, HuR, Regulates SCN5A Expression Through Stabilizing MEF2C transcription factor mRNA	否	无	nothing	 RL14	E_01_0541	Transfection,Real-Time PCR Quantification,Western Blot,Ribonucleoprotein Immunoprecipitation,Electrophoretic Mobility Shift Assay(EMSA),Chromatin Immunoprecipitation–qPCR,	In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.	Immunohistochemical staining	In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.	MEF2C		Transfection,Real-Time PCR Quantification,Western Blot,Ribonucleoprotein Immunoprecipitation,Electrophoretic Mobility Shift Assay(EMSA),Chromatin Immunoprecipitation–qPCR,	In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.			
29678826	chr19	7955547	7957547	ELAVL1	In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.	human	Myotome	High+Lowthroughput	RNA Binding Protein, HuR, Regulates SCN5A Expression Through Stabilizing MEF2C transcription factor mRNA	否	无	nothing	 RL14	E_01_0541	Transfection,Real-Time PCR Quantification,Western Blot,Ribonucleoprotein Immunoprecipitation,Electrophoretic Mobility Shift Assay(EMSA),Chromatin Immunoprecipitation–qPCR,	In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.	Immunohistochemical staining	In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.	ELAVL1		Transfection,Real-Time PCR Quantification,Western Blot,Ribonucleoprotein Immunoprecipitation,Electrophoretic Mobility Shift Assay(EMSA),Chromatin Immunoprecipitation–qPCR,	In conclusion, our results suggested that HuR participates in a combined network at the DNA and RNA levels that regulates SCN5A mRNA expression. HuR upregulates MEF2C mRNA expression by protecting MEF2C mRNA from degradation, and consequently, the elevated MEF2C enhances SCN5A mRNA transcription.			
29676032	chr12	6784508	6786508	CD4	Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.	mouse		High+Lowthroughput	Use of two gRNAs for CRISPR/Cas9 improves bi-allelic homologous recombination efficiency in mouse embryonic stem cells	否	无	nothing		E_02_0333	CRISPR/Cas9,transfection,Immunofluorescence,PCR,Flow Cytometry,T7E1 cleavage assay,	Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.		Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.	Immunohistochemical staining	Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.			CRISPR/Cas9,transfection,Immunofluorescence,PCR,Flow Cytometry,T7E1 cleavage assay,				CD4
29676032	chr18	66058520	66060520	Rax	Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.	mouse		High+Lowthroughput	Use of two gRNAs for CRISPR/Cas9 improves bi-allelic homologous recombination efficiency in mouse embryonic stem cells	否	无	nothing		E_02_0333	CRISPR/Cas9,transfection,Immunofluorescence,PCR,Flow Cytometry,T7E1 cleavage assay,	Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.		Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.	Immunohistochemical staining	Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.			CRISPR/Cas9,transfection,Immunofluorescence,PCR,Flow Cytometry,T7E1 cleavage assay,				Rax
29676032	chr8	22111738	22113738	HR	Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.	mouse		High+Lowthroughput	Use of two gRNAs for CRISPR/Cas9 improves bi-allelic homologous recombination efficiency in mouse embryonic stem cells	否	无	nothing		E_02_0333	CRISPR/Cas9,transfection,Immunofluorescence,PCR,Flow Cytometry,T7E1 cleavage assay,	Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.		Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.	Immunohistochemical staining	Here we describe an improved protocol that uses two gRNAs flanking the selected targeted region, leading to highly efficient homologous recombination in mouse ESCs. The bi-allelic recombination targeting efficiency is over 90% when using two gRNAs together with the inhibition of non-homologous end-joint repair. Moreover, this technique is compatible with the generation of knocked-in mice and the use of ESC-derived differentiation protocols, therefore facilitating and accelerating the gene targeting in mice and ESCs.			CRISPR/Cas9,transfection,Immunofluorescence,PCR,Flow Cytometry,T7E1 cleavage assay,				HR
29673286	chr9	117701285	117703285	TLR4	Among the different organs studied, the lungs and intestines exhibited significant differences among LPS alone, LPS combined with 3-MA and LPS combined with rapamycin. LPS combined with 3-MA attenuated the inflammatory damages of these organs as compared with LPS alone. In contrast, LPS combined with rapamycin increased damage in these organs. Consistently, serum inflammatory mediators TNF-α and IL-6 were decreased by the treatment of LPS combined with 3-MA as compared with LPS alone, while administration of LPS combined with rapamycin increased the serum TNF-α and IL-6 levels. Similar results were found in mouse bone marrow-derived macrophages exposed to LPS. Moreover, the regulatory effect of autophagy to endotoxic shock is dependent on the TLR4 signaling pathway. Our results demonstrate the central role of autophagy in the regulation of endotoxic shock and its potential modulation for endotoxic shock treatment.	mouse		High+Lowthroughput	Inhibition of autophagy with 3-methyladenine is protective in a lethal model of murine endotoxemia and polymicrobial sepsis	否	无	Endotoxic shock		E_02_0334	ELISA,immunohistochemical analysis,Western blot,	Among the different organs studied, the lungs and intestines exhibited significant differences among LPS alone, LPS combined with 3-MA and LPS combined with rapamycin. LPS combined with 3-MA attenuated the inflammatory damages of these organs as compared with LPS alone. In contrast, LPS combined with rapamycin increased damage in these organs. Consistently, serum inflammatory mediators TNF-α and IL-6 were decreased by the treatment of LPS combined with 3-MA as compared with LPS alone, while administration of LPS combined with rapamycin increased the serum TNF-α and IL-6 levels. Similar results were found in mouse bone marrow-derived macrophages exposed to LPS. Moreover, the regulatory effect of autophagy to endotoxic shock is dependent on the TLR4 signaling pathway. Our results demonstrate the central role of autophagy in the regulation of endotoxic shock and its potential modulation for endotoxic shock treatment.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Among the different organs studied, the lungs and intestines exhibited significant differences among LPS alone, LPS combined with 3-MA and LPS combined with rapamycin. LPS combined with 3-MA attenuated the inflammatory damages of these organs as compared with LPS alone. In contrast, LPS combined with rapamycin increased damage in these organs. Consistently, serum inflammatory mediators TNF-α and IL-6 were decreased by the treatment of LPS combined with 3-MA as compared with LPS alone, while administration of LPS combined with rapamycin increased the serum TNF-α and IL-6 levels. Similar results were found in mouse bone marrow-derived macrophages exposed to LPS. Moreover, the regulatory effect of autophagy to endotoxic shock is dependent on the TLR4 signaling pathway. Our results demonstrate the central role of autophagy in the regulation of endotoxic shock and its potential modulation for endotoxic shock treatment.		Among the different organs studied, the lungs and intestines exhibited significant differences among LPS alone, LPS combined with 3-MA and LPS combined with rapamycin. LPS combined with 3-MA attenuated the inflammatory damages of these organs as compared with LPS alone. In contrast, LPS combined with rapamycin increased damage in these organs. Consistently, serum inflammatory mediators TNF-α and IL-6 were decreased by the treatment of LPS combined with 3-MA as compared with LPS alone, while administration of LPS combined with rapamycin increased the serum TNF-α and IL-6 levels. Similar results were found in mouse bone marrow-derived macrophages exposed to LPS. Moreover, the regulatory effect of autophagy to endotoxic shock is dependent on the TLR4 signaling pathway. Our results demonstrate the central role of autophagy in the regulation of endotoxic shock and its potential modulation for endotoxic shock treatment.	Immunohistochemical staining	Among the different organs studied, the lungs and intestines exhibited significant differences among LPS alone, LPS combined with 3-MA and LPS combined with rapamycin. LPS combined with 3-MA attenuated the inflammatory damages of these organs as compared with LPS alone. In contrast, LPS combined with rapamycin increased damage in these organs. Consistently, serum inflammatory mediators TNF-α and IL-6 were decreased by the treatment of LPS combined with 3-MA as compared with LPS alone, while administration of LPS combined with rapamycin increased the serum TNF-α and IL-6 levels. Similar results were found in mouse bone marrow-derived macrophages exposed to LPS. Moreover, the regulatory effect of autophagy to endotoxic shock is dependent on the TLR4 signaling pathway. Our results demonstrate the central role of autophagy in the regulation of endotoxic shock and its potential modulation for endotoxic shock treatment.			ELISA,immunohistochemical analysis,Western blot,				TLR4
29670286	chr8	116843661	116845661	RAD21	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	human		High+Lowthroughput	Pluripotency factors functionally premark cell-type-restricted enhancers in ES cells	否	无	nothing	 ES cell	E_01_0542	ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.		Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Immunohistochemical staining	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.			ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,				RAD21
29670286	chr14	76308013	76310013	ESRRB	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	human		High+Lowthroughput	Pluripotency factors functionally premark cell-type-restricted enhancers in ES cells	否	无	nothing	 ES cell	E_01_0542	ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.		Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Immunohistochemical staining	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.			ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,				ESRRB
29670286	chr12	7785298	7787298	NANOG	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	human		High+Lowthroughput	Pluripotency factors functionally premark cell-type-restricted enhancers in ES cells	否	无	nothing	 ES cell	E_01_0542	ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.		Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Immunohistochemical staining	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.			ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,				NANOG
29670286	chr3	181709216	181711216	SOX2	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	human		High+Lowthroughput	Pluripotency factors functionally premark cell-type-restricted enhancers in ES cells	否	无	nothing	 ES cell	E_01_0542	ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Immunohistochemical staining	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	SOX2		ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.			
29670286	chr4	145478124	145480124	SMAD1	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	human		High+Lowthroughput	Pluripotency factors functionally premark cell-type-restricted enhancers in ES cells	否	无	nothing	 ES cell	E_01_0542	ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Immunohistochemical staining	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	SMAD1		ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.			
29670286	chr20	33672341	33674341	E2F1	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	human		High+Lowthroughput	Pluripotency factors functionally premark cell-type-restricted enhancers in ES cells	否	无	nothing	 ES cell	E_01_0542	ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Immunohistochemical staining	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	E2F1		ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.			
29670286	chrX	24146480	24148480	ZFX	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	human		High+Lowthroughput	Pluripotency factors functionally premark cell-type-restricted enhancers in ES cells	否	无	nothing	 ES cell	E_01_0542	ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.		Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Immunohistochemical staining	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.			ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,				ZFX
29670286	chr17	42310299	42312299	STAT3	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	human		High+Lowthroughput	Pluripotency factors functionally premark cell-type-restricted enhancers in ES cells	否	无	nothing	 ES cell	E_01_0542	ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Immunohistochemical staining	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	STAT3		ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.			
29670286	chr9	107482207	107484207	KLF4	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	human		High+Lowthroughput	Pluripotency factors functionally premark cell-type-restricted enhancers in ES cells	否	无	nothing	 ES cell	E_01_0542	ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	Immunohistochemical staining	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.	KLF4		ChIP,ChIP–seq,PRO-cap,Enhancer reporter assay,CRSIPR/Cas9,qRT–PCR,RNA-seq,MeDIP–seq,4C–seq,ATAC-seq,Deep sequencing,Bioinformatic characterization of enhancers,western blot,	Here we show that cell-type-restricted enhancers are 'premarked' and activated as transcription units by the binding of one or two ES cell transcription factors, although they do not exhibit traditional enhancer epigenetic marks in ES cells, thus uncovering the initial temporal origins of cell-type-restricted enhancers. This premarking is required for future cell-type-restricted enhancer activity in the differentiated cells, with the strength of the ES cell signature being functionally important for the subsequent robustness of cell-type-restricted enhancer activation. We have experimentally validated this model in macrophage-restricted enhancers and neural precursor cell (NPC)-restricted enhancers using ES cell-derived macrophages or NPCs, edited to contain specific ES cell transcription factor motif deletions. DNA hydroxyl-methylation of enhancers in ES cells, determined by ES cell transcription factors, may serve as a potential molecular memory for subsequent enhancer activation in mature macrophages. These findings suggest that the massive repertoire of cell-type-restricted enhancers are essentially hierarchically and obligatorily premarked by binding of a defining ES cell transcription factor in ES cells, dictating the robustness of enhancer activation in mature cells.			
29669761	chr2	29190441	29192441	ALK	Here we investigated the dynamic changes in the transcriptome and enhancer landscape during development of acquired resistance to ALK inhibitors. Histone H3 lysine 27 acetylation (H3K27ac) was profoundly altered during acquisition of resistance, and enhancer remodeling induced expression changes in both miRNAs and mRNAs. Decreased H3K27ac levels and reduced miR-34a expression associated with the activation of target genes such as AXL. Panobinostat, a pan-histone deacetylase inhibitor, altered the H3K27ac profile and activated tumor suppressor miRNAs such as miR-449,another member of the miR-34 family, and synergistically induced anti-proliferative effects with ALK inhibitors on resistant cells, xenografts, and EML4-ALK transgenic mice. Paired analysis of patient samples before and after treatment with ALK inhibitors revealed that repression of miR-34a or miR-449a and activation of AXL were mutually exclusive of secondary mutations in ALK. Our findings indicate that enhancer remodeling and altered expression of miRNAs play key roles in cancer drug resistance and suggest that strategies targeting epigenetic pathways represent a potentially effective method for overcoming acquired resistance to cancer therapy.	mouse		High+Lowthroughput	Enhancer Remodeling and MicroRNA Alterations Are Associated with Acquired Resistance to ALK Inhibitors	否	无	Positive lung cancer	H3122 cell	E_02_0335	transgenic mice,ChIP-seq,RNA-seq,small RNA-seq,microarray analysis,qRT-PCR,western blot,immunohistochemical staining,	Here we investigated the dynamic changes in the transcriptome and enhancer landscape during development of acquired resistance to ALK inhibitors. Histone H3 lysine 27 acetylation (H3K27ac) was profoundly altered during acquisition of resistance, and enhancer remodeling induced expression changes in both miRNAs and mRNAs. Decreased H3K27ac levels and reduced miR-34a expression associated with the activation of target genes such as AXL. Panobinostat, a pan-histone deacetylase inhibitor, altered the H3K27ac profile and activated tumor suppressor miRNAs such as miR-449,another member of the miR-34 family, and synergistically induced anti-proliferative effects with ALK inhibitors on resistant cells, xenografts, and EML4-ALK transgenic mice. Paired analysis of patient samples before and after treatment with ALK inhibitors revealed that repression of miR-34a or miR-449a and activation of AXL were mutually exclusive of secondary mutations in ALK. Our findings indicate that enhancer remodeling and altered expression of miRNAs play key roles in cancer drug resistance and suggest that strategies targeting epigenetic pathways represent a potentially effective method for overcoming acquired resistance to cancer therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we investigated the dynamic changes in the transcriptome and enhancer landscape during development of acquired resistance to ALK inhibitors. Histone H3 lysine 27 acetylation (H3K27ac) was profoundly altered during acquisition of resistance, and enhancer remodeling induced expression changes in both miRNAs and mRNAs. Decreased H3K27ac levels and reduced miR-34a expression associated with the activation of target genes such as AXL. Panobinostat, a pan-histone deacetylase inhibitor, altered the H3K27ac profile and activated tumor suppressor miRNAs such as miR-449,another member of the miR-34 family, and synergistically induced anti-proliferative effects with ALK inhibitors on resistant cells, xenografts, and EML4-ALK transgenic mice. Paired analysis of patient samples before and after treatment with ALK inhibitors revealed that repression of miR-34a or miR-449a and activation of AXL were mutually exclusive of secondary mutations in ALK. Our findings indicate that enhancer remodeling and altered expression of miRNAs play key roles in cancer drug resistance and suggest that strategies targeting epigenetic pathways represent a potentially effective method for overcoming acquired resistance to cancer therapy.		Here we investigated the dynamic changes in the transcriptome and enhancer landscape during development of acquired resistance to ALK inhibitors. Histone H3 lysine 27 acetylation (H3K27ac) was profoundly altered during acquisition of resistance, and enhancer remodeling induced expression changes in both miRNAs and mRNAs. Decreased H3K27ac levels and reduced miR-34a expression associated with the activation of target genes such as AXL. Panobinostat, a pan-histone deacetylase inhibitor, altered the H3K27ac profile and activated tumor suppressor miRNAs such as miR-449,another member of the miR-34 family, and synergistically induced anti-proliferative effects with ALK inhibitors on resistant cells, xenografts, and EML4-ALK transgenic mice. Paired analysis of patient samples before and after treatment with ALK inhibitors revealed that repression of miR-34a or miR-449a and activation of AXL were mutually exclusive of secondary mutations in ALK. Our findings indicate that enhancer remodeling and altered expression of miRNAs play key roles in cancer drug resistance and suggest that strategies targeting epigenetic pathways represent a potentially effective method for overcoming acquired resistance to cancer therapy.	Immunohistochemical staining	Here we investigated the dynamic changes in the transcriptome and enhancer landscape during development of acquired resistance to ALK inhibitors. Histone H3 lysine 27 acetylation (H3K27ac) was profoundly altered during acquisition of resistance, and enhancer remodeling induced expression changes in both miRNAs and mRNAs. Decreased H3K27ac levels and reduced miR-34a expression associated with the activation of target genes such as AXL. Panobinostat, a pan-histone deacetylase inhibitor, altered the H3K27ac profile and activated tumor suppressor miRNAs such as miR-449,another member of the miR-34 family, and synergistically induced anti-proliferative effects with ALK inhibitors on resistant cells, xenografts, and EML4-ALK transgenic mice. Paired analysis of patient samples before and after treatment with ALK inhibitors revealed that repression of miR-34a or miR-449a and activation of AXL were mutually exclusive of secondary mutations in ALK. Our findings indicate that enhancer remodeling and altered expression of miRNAs play key roles in cancer drug resistance and suggest that strategies targeting epigenetic pathways represent a potentially effective method for overcoming acquired resistance to cancer therapy.			transgenic mice,ChIP-seq,RNA-seq,small RNA-seq,microarray analysis,qRT-PCR,western blot,immunohistochemical staining,				ALK
29669022	chr14	37586703	37588703	FOXA1	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	human		High+Lowthroughput	DNA-mediated dimerization on a compact sequence signature controls enhancer engagement and regulation by FOXA1	是	rs541455835	nothing	MCF7 cell	E_01_0543	DNA binding domain (DBD),EMSA (electrophoretic mobility shift assays),Fluorescence-Activated Cell Sorting (FACS),Luciferase assay,Bioinformatics analysis,ChIP-seq,	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	Immunohistochemical staining	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	FOXA1		DNA binding domain (DBD),EMSA (electrophoretic mobility shift assays),Fluorescence-Activated Cell Sorting (FACS),Luciferase assay,Bioinformatics analysis,ChIP-seq,	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.			
29669022	chr10	8042658	8044658	GATA3	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	human		High+Lowthroughput	DNA-mediated dimerization on a compact sequence signature controls enhancer engagement and regulation by FOXA1	是	rs541455835	nothing	MCF7 cell	E_01_0543	DNA binding domain (DBD),EMSA (electrophoretic mobility shift assays),Fluorescence-Activated Cell Sorting (FACS),Luciferase assay,Bioinformatics analysis,ChIP-seq,	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	Immunohistochemical staining	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	GATA3		DNA binding domain (DBD),EMSA (electrophoretic mobility shift assays),Fluorescence-Activated Cell Sorting (FACS),Luciferase assay,Bioinformatics analysis,ChIP-seq,	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.			
29669022	chr16	67559243	67561243	CTCF	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	human		High+Lowthroughput	DNA-mediated dimerization on a compact sequence signature controls enhancer engagement and regulation by FOXA1	是	rs541455835	nothing	MCF7 cell	E_01_0543	DNA binding domain (DBD),EMSA (electrophoretic mobility shift assays),Fluorescence-Activated Cell Sorting (FACS),Luciferase assay,Bioinformatics analysis,ChIP-seq,	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	Immunohistochemical staining	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	CTCF		DNA binding domain (DBD),EMSA (electrophoretic mobility shift assays),Fluorescence-Activated Cell Sorting (FACS),Luciferase assay,Bioinformatics analysis,ChIP-seq,	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.			
29669022	chr17	45891764	45893764	MAPT	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	human		High+Lowthroughput	DNA-mediated dimerization on a compact sequence signature controls enhancer engagement and regulation by FOXA1	是	rs541455835	nothing	MCF7 cell	E_01_0543	DNA binding domain (DBD),EMSA (electrophoretic mobility shift assays),Fluorescence-Activated Cell Sorting (FACS),Luciferase assay,Bioinformatics analysis,ChIP-seq,	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.		Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	Immunohistochemical staining	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.			DNA binding domain (DBD),EMSA (electrophoretic mobility shift assays),Fluorescence-Activated Cell Sorting (FACS),Luciferase assay,Bioinformatics analysis,ChIP-seq,				MAPT
29669022	chr8	127792179	127794179	PVT1	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	human		High+Lowthroughput	DNA-mediated dimerization on a compact sequence signature controls enhancer engagement and regulation by FOXA1	是	rs541455835	nothing	MCF7 cell	E_01_0543	DNA binding domain (DBD),EMSA (electrophoretic mobility shift assays),Fluorescence-Activated Cell Sorting (FACS),Luciferase assay,Bioinformatics analysis,ChIP-seq,	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.		Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	Immunohistochemical staining	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.			DNA binding domain (DBD),EMSA (electrophoretic mobility shift assays),Fluorescence-Activated Cell Sorting (FACS),Luciferase assay,Bioinformatics analysis,ChIP-seq,				PVT1
29669022	chr8	127732985	127734985	MYC	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	human		High+Lowthroughput	DNA-mediated dimerization on a compact sequence signature controls enhancer engagement and regulation by FOXA1	是	rs541455835	nothing	MCF7 cell	E_01_0543	DNA binding domain (DBD),EMSA (electrophoretic mobility shift assays),Fluorescence-Activated Cell Sorting (FACS),Luciferase assay,Bioinformatics analysis,ChIP-seq,	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	Immunohistochemical staining	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.	MYC		DNA binding domain (DBD),EMSA (electrophoretic mobility shift assays),Fluorescence-Activated Cell Sorting (FACS),Luciferase assay,Bioinformatics analysis,ChIP-seq,	Reporter assays show that FOXA1-dependent transcriptional activity declines when homodimeric binding is disrupted. In response to phosphatidylinositol-3 kinase inhibition DIV sites pre-bound by FOXA1 such as at the PVT1/MYC locus exhibit a strong increase in accessibility suggesting a role of the DIV configuration in the chromatin closed-open dynamics. Moreover, several disease-associated single nucleotide polymorphisms map to DIV elements and show allelic differences in FOXA1 homodimerization, reporter gene expression and are annotated as quantitative trait loci. This includes the rs541455835 variant at the MAPT locus encoding the Tau protein associated with Parkinson's disease. Collectively, the DIV guides chromatin engagement and regulation by FOXA1 and its perturbation could be linked to disease etiologies.			
29667772	chr12	2956550	2958550	TEAD4	Both the mRNA and protein levels of TEAD4 were increased in LAD tissues than those in adjacent nontumourous tissues. Besides, database search indicated a poorer clinical outcome in LAD patients with higher TEAD4 expression, revealing its potential tumour-promoting role. Therefore, we conducted cellular experiments to further investigate its effect on tumour phenotypes. Accordingly, TEAD4 showed little impact on LAD cell cycle, proliferation, or apoptosis. However, silencing TEAD4 remarkably attenuated cell migration and invasion capacities. Consistently, several important epithelial-mesenchymal transition (EMT) markers such as E-cadherin and Slug were consequently altered by silencing TEAD4. Furthermore, we identified a novel TEAD4-targeted microRNA, namely miR6839-3p, and confirmed its function in suppressing TEAD4 expression. Finally, the impact of overexpressing miR6839-3p mimics on LAD progression was validated, which showed a similar pattern with TEAD4 knockdown cells. Taken together, our data not only revealed the significant role of TEAD4 in promoting LAD progression and predicting clinical outcome but also distinguished miR6839-3p mimics as a promising therapeutic direction.	human		High+Lowthroughput	TEAD4 exerts pro-metastatic effects and is negatively regulated by miR6839-3p in lung adenocarcinoma progression	否	无	Lung adenocarcinoma (LAD)		E_01_0544	Tissue microarray (TMA),immunohistochemical (IHC) staining, small interfering RNA(siRNA) transfection,Quantitative reverse transcription-PCR,MTT,Transwell assays,Western blot, Flow cytometric analyses,Luciferase activity assays,	Both the mRNA and protein levels of TEAD4 were increased in LAD tissues than those in adjacent nontumourous tissues. Besides, database search indicated a poorer clinical outcome in LAD patients with higher TEAD4 expression, revealing its potential tumour-promoting role. Therefore, we conducted cellular experiments to further investigate its effect on tumour phenotypes. Accordingly, TEAD4 showed little impact on LAD cell cycle, proliferation, or apoptosis. However, silencing TEAD4 remarkably attenuated cell migration and invasion capacities. Consistently, several important epithelial-mesenchymal transition (EMT) markers such as E-cadherin and Slug were consequently altered by silencing TEAD4. Furthermore, we identified a novel TEAD4-targeted microRNA, namely miR6839-3p, and confirmed its function in suppressing TEAD4 expression. Finally, the impact of overexpressing miR6839-3p mimics on LAD progression was validated, which showed a similar pattern with TEAD4 knockdown cells. Taken together, our data not only revealed the significant role of TEAD4 in promoting LAD progression and predicting clinical outcome but also distinguished miR6839-3p mimics as a promising therapeutic direction.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Both the mRNA and protein levels of TEAD4 were increased in LAD tissues than those in adjacent nontumourous tissues. Besides, database search indicated a poorer clinical outcome in LAD patients with higher TEAD4 expression, revealing its potential tumour-promoting role. Therefore, we conducted cellular experiments to further investigate its effect on tumour phenotypes. Accordingly, TEAD4 showed little impact on LAD cell cycle, proliferation, or apoptosis. However, silencing TEAD4 remarkably attenuated cell migration and invasion capacities. Consistently, several important epithelial-mesenchymal transition (EMT) markers such as E-cadherin and Slug were consequently altered by silencing TEAD4. Furthermore, we identified a novel TEAD4-targeted microRNA, namely miR6839-3p, and confirmed its function in suppressing TEAD4 expression. Finally, the impact of overexpressing miR6839-3p mimics on LAD progression was validated, which showed a similar pattern with TEAD4 knockdown cells. Taken together, our data not only revealed the significant role of TEAD4 in promoting LAD progression and predicting clinical outcome but also distinguished miR6839-3p mimics as a promising therapeutic direction.	Immunohistochemical staining	Both the mRNA and protein levels of TEAD4 were increased in LAD tissues than those in adjacent nontumourous tissues. Besides, database search indicated a poorer clinical outcome in LAD patients with higher TEAD4 expression, revealing its potential tumour-promoting role. Therefore, we conducted cellular experiments to further investigate its effect on tumour phenotypes. Accordingly, TEAD4 showed little impact on LAD cell cycle, proliferation, or apoptosis. However, silencing TEAD4 remarkably attenuated cell migration and invasion capacities. Consistently, several important epithelial-mesenchymal transition (EMT) markers such as E-cadherin and Slug were consequently altered by silencing TEAD4. Furthermore, we identified a novel TEAD4-targeted microRNA, namely miR6839-3p, and confirmed its function in suppressing TEAD4 expression. Finally, the impact of overexpressing miR6839-3p mimics on LAD progression was validated, which showed a similar pattern with TEAD4 knockdown cells. Taken together, our data not only revealed the significant role of TEAD4 in promoting LAD progression and predicting clinical outcome but also distinguished miR6839-3p mimics as a promising therapeutic direction.	TEAD4		Tissue microarray (TMA),immunohistochemical (IHC) staining, small interfering RNA(siRNA) transfection,Quantitative reverse transcription-PCR,MTT,Transwell assays,Western blot, Flow cytometric analyses,Luciferase activity assays,	Both the mRNA and protein levels of TEAD4 were increased in LAD tissues than those in adjacent nontumourous tissues. Besides, database search indicated a poorer clinical outcome in LAD patients with higher TEAD4 expression, revealing its potential tumour-promoting role. Therefore, we conducted cellular experiments to further investigate its effect on tumour phenotypes. Accordingly, TEAD4 showed little impact on LAD cell cycle, proliferation, or apoptosis. However, silencing TEAD4 remarkably attenuated cell migration and invasion capacities. Consistently, several important epithelial-mesenchymal transition (EMT) markers such as E-cadherin and Slug were consequently altered by silencing TEAD4. Furthermore, we identified a novel TEAD4-targeted microRNA, namely miR6839-3p, and confirmed its function in suppressing TEAD4 expression. Finally, the impact of overexpressing miR6839-3p mimics on LAD progression was validated, which showed a similar pattern with TEAD4 knockdown cells. Taken together, our data not only revealed the significant role of TEAD4 in promoting LAD progression and predicting clinical outcome but also distinguished miR6839-3p mimics as a promising therapeutic direction.			
29664056	chr1	161763600	161765600	ATF6	Exposure of HUVECs to ox-LDL also markedly induced caspase-3 activity together with increased CHOP mRNA level; these effects were inhibited by simvastatin treatment.	human	Epithelial tissues	High+Lowthroughput	Inhibitory Effects of Simvastatin on Oxidized Low-Density Lipoprotein-Induced Endoplasmic Reticulum Stress and Apoptosis in Vascular Endothelial Cells	否	无	nothing	HUVECs	E_01_0545	Western blot,Real‑time quantitative reverse transcription polymerase chain reaction,Caspase‑3 activity assay,	Exposure of HUVECs to ox-LDL also markedly induced caspase-3 activity together with increased CHOP mRNA level; these effects were inhibited by simvastatin treatment.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Exposure of HUVECs to ox-LDL also markedly induced caspase-3 activity together with increased CHOP mRNA level; these effects were inhibited by simvastatin treatment.	Immunohistochemical staining	Exposure of HUVECs to ox-LDL also markedly induced caspase-3 activity together with increased CHOP mRNA level; these effects were inhibited by simvastatin treatment.	ATF6		Western blot,Real‑time quantitative reverse transcription polymerase chain reaction,Caspase‑3 activity assay,	Exposure of HUVECs to ox-LDL also markedly induced caspase-3 activity together with increased CHOP mRNA level; these effects were inhibited by simvastatin treatment.			
29662163	chr2	221415351	221417351	EPHA4	Here we present a polymer-physics-based approach (PRISMR) to model 3D chromatin folding and to predict enhancer-promoter contacts. PRISMR predicts higher-order chromatin structure from genome-wide chromosome conformation capture (Hi-C) data. Using the EPHA4 locus as a model, the effects of pathogenic SVs are predicted in silico and compared to Hi-C data generated from mouse limb buds and patient-derived fibroblasts. PRISMR deconvolves the folding complexity of the EPHA4 locus and identifies SV-induced ectopic contacts and alterations of 3D genome organization in homozygous or heterozygous states. We show that SVs can reconfigure topologically associating domains, thereby producing extensive rewiring of regulatory interactions and causing disease by gene misexpression. PRISMR can be used to predict interactions in silico, thereby providing a tool for analyzing the disease-causing potential of SVs.	mouse		High+Lowthroughput	Polymer physics predicts the effects of structural variants on chromatin architecture	否	无	Structural variation (SV)	CH12-LX cell	E_02_0336	The PRISMR algorithm,Analyses of the model binding domains,Hi-C,cHi-C,	Here we present a polymer-physics-based approach (PRISMR) to model 3D chromatin folding and to predict enhancer-promoter contacts. PRISMR predicts higher-order chromatin structure from genome-wide chromosome conformation capture (Hi-C) data. Using the EPHA4 locus as a model, the effects of pathogenic SVs are predicted in silico and compared to Hi-C data generated from mouse limb buds and patient-derived fibroblasts. PRISMR deconvolves the folding complexity of the EPHA4 locus and identifies SV-induced ectopic contacts and alterations of 3D genome organization in homozygous or heterozygous states. We show that SVs can reconfigure topologically associating domains, thereby producing extensive rewiring of regulatory interactions and causing disease by gene misexpression. PRISMR can be used to predict interactions in silico, thereby providing a tool for analyzing the disease-causing potential of SVs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we present a polymer-physics-based approach (PRISMR) to model 3D chromatin folding and to predict enhancer-promoter contacts. PRISMR predicts higher-order chromatin structure from genome-wide chromosome conformation capture (Hi-C) data. Using the EPHA4 locus as a model, the effects of pathogenic SVs are predicted in silico and compared to Hi-C data generated from mouse limb buds and patient-derived fibroblasts. PRISMR deconvolves the folding complexity of the EPHA4 locus and identifies SV-induced ectopic contacts and alterations of 3D genome organization in homozygous or heterozygous states. We show that SVs can reconfigure topologically associating domains, thereby producing extensive rewiring of regulatory interactions and causing disease by gene misexpression. PRISMR can be used to predict interactions in silico, thereby providing a tool for analyzing the disease-causing potential of SVs.		Here we present a polymer-physics-based approach (PRISMR) to model 3D chromatin folding and to predict enhancer-promoter contacts. PRISMR predicts higher-order chromatin structure from genome-wide chromosome conformation capture (Hi-C) data. Using the EPHA4 locus as a model, the effects of pathogenic SVs are predicted in silico and compared to Hi-C data generated from mouse limb buds and patient-derived fibroblasts. PRISMR deconvolves the folding complexity of the EPHA4 locus and identifies SV-induced ectopic contacts and alterations of 3D genome organization in homozygous or heterozygous states. We show that SVs can reconfigure topologically associating domains, thereby producing extensive rewiring of regulatory interactions and causing disease by gene misexpression. PRISMR can be used to predict interactions in silico, thereby providing a tool for analyzing the disease-causing potential of SVs.	Immunohistochemical staining	Here we present a polymer-physics-based approach (PRISMR) to model 3D chromatin folding and to predict enhancer-promoter contacts. PRISMR predicts higher-order chromatin structure from genome-wide chromosome conformation capture (Hi-C) data. Using the EPHA4 locus as a model, the effects of pathogenic SVs are predicted in silico and compared to Hi-C data generated from mouse limb buds and patient-derived fibroblasts. PRISMR deconvolves the folding complexity of the EPHA4 locus and identifies SV-induced ectopic contacts and alterations of 3D genome organization in homozygous or heterozygous states. We show that SVs can reconfigure topologically associating domains, thereby producing extensive rewiring of regulatory interactions and causing disease by gene misexpression. PRISMR can be used to predict interactions in silico, thereby providing a tool for analyzing the disease-causing potential of SVs.			The PRISMR algorithm,Analyses of the model binding domains,Hi-C,cHi-C,				EPHA4
29662163	chr16	67560379	67562379	CTCF	Here we present a polymer-physics-based approach (PRISMR) to model 3D chromatin folding and to predict enhancer-promoter contacts. PRISMR predicts higher-order chromatin structure from genome-wide chromosome conformation capture (Hi-C) data. Using the EPHA4 locus as a model, the effects of pathogenic SVs are predicted in silico and compared to Hi-C data generated from mouse limb buds and patient-derived fibroblasts. PRISMR deconvolves the folding complexity of the EPHA4 locus and identifies SV-induced ectopic contacts and alterations of 3D genome organization in homozygous or heterozygous states. We show that SVs can reconfigure topologically associating domains, thereby producing extensive rewiring of regulatory interactions and causing disease by gene misexpression. PRISMR can be used to predict interactions in silico, thereby providing a tool for analyzing the disease-causing potential of SVs.	mouse		High+Lowthroughput	Polymer physics predicts the effects of structural variants on chromatin architecture	否	无	Structural variation (SV)	CH12-LX cell	E_02_0336	The PRISMR algorithm,Analyses of the model binding domains,Hi-C,cHi-C,	Here we present a polymer-physics-based approach (PRISMR) to model 3D chromatin folding and to predict enhancer-promoter contacts. PRISMR predicts higher-order chromatin structure from genome-wide chromosome conformation capture (Hi-C) data. Using the EPHA4 locus as a model, the effects of pathogenic SVs are predicted in silico and compared to Hi-C data generated from mouse limb buds and patient-derived fibroblasts. PRISMR deconvolves the folding complexity of the EPHA4 locus and identifies SV-induced ectopic contacts and alterations of 3D genome organization in homozygous or heterozygous states. We show that SVs can reconfigure topologically associating domains, thereby producing extensive rewiring of regulatory interactions and causing disease by gene misexpression. PRISMR can be used to predict interactions in silico, thereby providing a tool for analyzing the disease-causing potential of SVs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we present a polymer-physics-based approach (PRISMR) to model 3D chromatin folding and to predict enhancer-promoter contacts. PRISMR predicts higher-order chromatin structure from genome-wide chromosome conformation capture (Hi-C) data. Using the EPHA4 locus as a model, the effects of pathogenic SVs are predicted in silico and compared to Hi-C data generated from mouse limb buds and patient-derived fibroblasts. PRISMR deconvolves the folding complexity of the EPHA4 locus and identifies SV-induced ectopic contacts and alterations of 3D genome organization in homozygous or heterozygous states. We show that SVs can reconfigure topologically associating domains, thereby producing extensive rewiring of regulatory interactions and causing disease by gene misexpression. PRISMR can be used to predict interactions in silico, thereby providing a tool for analyzing the disease-causing potential of SVs.		Here we present a polymer-physics-based approach (PRISMR) to model 3D chromatin folding and to predict enhancer-promoter contacts. PRISMR predicts higher-order chromatin structure from genome-wide chromosome conformation capture (Hi-C) data. Using the EPHA4 locus as a model, the effects of pathogenic SVs are predicted in silico and compared to Hi-C data generated from mouse limb buds and patient-derived fibroblasts. PRISMR deconvolves the folding complexity of the EPHA4 locus and identifies SV-induced ectopic contacts and alterations of 3D genome organization in homozygous or heterozygous states. We show that SVs can reconfigure topologically associating domains, thereby producing extensive rewiring of regulatory interactions and causing disease by gene misexpression. PRISMR can be used to predict interactions in silico, thereby providing a tool for analyzing the disease-causing potential of SVs.	Immunohistochemical staining	Here we present a polymer-physics-based approach (PRISMR) to model 3D chromatin folding and to predict enhancer-promoter contacts. PRISMR predicts higher-order chromatin structure from genome-wide chromosome conformation capture (Hi-C) data. Using the EPHA4 locus as a model, the effects of pathogenic SVs are predicted in silico and compared to Hi-C data generated from mouse limb buds and patient-derived fibroblasts. PRISMR deconvolves the folding complexity of the EPHA4 locus and identifies SV-induced ectopic contacts and alterations of 3D genome organization in homozygous or heterozygous states. We show that SVs can reconfigure topologically associating domains, thereby producing extensive rewiring of regulatory interactions and causing disease by gene misexpression. PRISMR can be used to predict interactions in silico, thereby providing a tool for analyzing the disease-causing potential of SVs.			The PRISMR algorithm,Analyses of the model binding domains,Hi-C,cHi-C,				CTCF
29654753	chr6	47504283	47506283	Ezh2	We found that GSK126 treatment reduced body fat, improved glucose tolerance, increased lipolysis and improved cold tolerance in mice by promoting the differentiation of thermogenic beige adipocytes. Moreover, we discovered that GSK126 inhibited the differentiation of white adipocytes, and the decrease of Ezh2 enzymatic activity and H3K27me3 also changed the morphology of brown adipocytes but did not alter the expression of thermogenic genes in these cells. Our results indicated that GSK126 was a novel chemical inducer of beige adipocytes and may be a potential therapeutic agent for the management of obesity. Furthermore, they also prompted that Ezh2 and H3K27me3 play different roles in the differentiation of the white, brown, and beige adipocytes in vivo.	mouse	adipose tissue	High+Lowthroughput	GSK126 alleviates the obesity phenotype by promoting the differentiation of thermogenic beige adipocytes in diet-induced obese mice	否	无	Obesity	beige adipocytes	E_02_0337	Western blot,ELISAs,RT-qPCR, Immunohistochemistry,Histological analysis,	We found that GSK126 treatment reduced body fat, improved glucose tolerance, increased lipolysis and improved cold tolerance in mice by promoting the differentiation of thermogenic beige adipocytes. Moreover, we discovered that GSK126 inhibited the differentiation of white adipocytes, and the decrease of Ezh2 enzymatic activity and H3K27me3 also changed the morphology of brown adipocytes but did not alter the expression of thermogenic genes in these cells. Our results indicated that GSK126 was a novel chemical inducer of beige adipocytes and may be a potential therapeutic agent for the management of obesity. Furthermore, they also prompted that Ezh2 and H3K27me3 play different roles in the differentiation of the white, brown, and beige adipocytes in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found that GSK126 treatment reduced body fat, improved glucose tolerance, increased lipolysis and improved cold tolerance in mice by promoting the differentiation of thermogenic beige adipocytes. Moreover, we discovered that GSK126 inhibited the differentiation of white adipocytes, and the decrease of Ezh2 enzymatic activity and H3K27me3 also changed the morphology of brown adipocytes but did not alter the expression of thermogenic genes in these cells. Our results indicated that GSK126 was a novel chemical inducer of beige adipocytes and may be a potential therapeutic agent for the management of obesity. Furthermore, they also prompted that Ezh2 and H3K27me3 play different roles in the differentiation of the white, brown, and beige adipocytes in vivo.		We found that GSK126 treatment reduced body fat, improved glucose tolerance, increased lipolysis and improved cold tolerance in mice by promoting the differentiation of thermogenic beige adipocytes. Moreover, we discovered that GSK126 inhibited the differentiation of white adipocytes, and the decrease of Ezh2 enzymatic activity and H3K27me3 also changed the morphology of brown adipocytes but did not alter the expression of thermogenic genes in these cells. Our results indicated that GSK126 was a novel chemical inducer of beige adipocytes and may be a potential therapeutic agent for the management of obesity. Furthermore, they also prompted that Ezh2 and H3K27me3 play different roles in the differentiation of the white, brown, and beige adipocytes in vivo.	Immunohistochemical staining	We found that GSK126 treatment reduced body fat, improved glucose tolerance, increased lipolysis and improved cold tolerance in mice by promoting the differentiation of thermogenic beige adipocytes. Moreover, we discovered that GSK126 inhibited the differentiation of white adipocytes, and the decrease of Ezh2 enzymatic activity and H3K27me3 also changed the morphology of brown adipocytes but did not alter the expression of thermogenic genes in these cells. Our results indicated that GSK126 was a novel chemical inducer of beige adipocytes and may be a potential therapeutic agent for the management of obesity. Furthermore, they also prompted that Ezh2 and H3K27me3 play different roles in the differentiation of the white, brown, and beige adipocytes in vivo.			Western blot,ELISAs,RT-qPCR, Immunohistochemistry,Histological analysis,				Ezh2
29654271	chr9	36830631	36832631	PAX5	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	human	/	High+Lowthroughput	Whole-genome sequencing of multiple myeloma reveals oncogenic pathways are targeted somatically through multiple mechanisms	否	无	Multiple myeloma (mm)		E_01_0546	WGS,WES,Hi-C,	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	Immunohistochemical staining	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	PAX5		WGS,WES,Hi-C,	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.			
29654271	chr6	388985	390985	IRF4	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	human	/	High+Lowthroughput	Whole-genome sequencing of multiple myeloma reveals oncogenic pathways are targeted somatically through multiple mechanisms	否	无	Multiple myeloma (mm)		E_01_0546	WGS,WES,Hi-C,	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	Immunohistochemical staining	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	IRF4		WGS,WES,Hi-C,	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.			
29654271	chr6	105990201	105992201	PRDM1	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	human	/	High+Lowthroughput	Whole-genome sequencing of multiple myeloma reveals oncogenic pathways are targeted somatically through multiple mechanisms	否	无	Multiple myeloma (mm)		E_01_0546	WGS,WES,Hi-C,	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	Immunohistochemical staining	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	PRDM1		WGS,WES,Hi-C,	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.			
29654271	chr3	187718617	187720617	BCL6	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	human	/	High+Lowthroughput	Whole-genome sequencing of multiple myeloma reveals oncogenic pathways are targeted somatically through multiple mechanisms	否	无	Multiple myeloma (mm)		E_01_0546	WGS,WES,Hi-C,	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	Immunohistochemical staining	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.	BCL6		WGS,WES,Hi-C,	By employing promoter capture Hi-C in naïve B-cells, we identify cis-regulatory elements (CREs) that represent a highly enriched subset of the non-coding genome in which to search for driver mutations. We identify regulatory regions whose mutation significantly alters the expression of genes as candidate non-coding drivers, including copy number variation (CNV) at CREs of MYC and single-nucleotide variants (SNVs) in a PAX5 enhancer. To better inform the interplay between non-coding driver mutations with other driver mechanisms, and their respective roles in oncogenic pathways, we extended our analysis identifying coding drivers in 40 genes, including 11 novel candidates. We demonstrate the same pathways can be targeted by coding and non-coding mutations; exemplified by IRF4 and PRDM1, along with BCL6 and PAX5, genes that are central to plasma cell differentiation. This study reveals new insights into the complex genetic alterations driving MM development and an enhanced understanding of oncogenic pathways.			
29650362	chr7	148804787	148806787	EZH2	Tazemetostat showed a favourable safety profile and antitumour activity in patients with refractory B-cell non-Hodgkin lymphoma and advanced solid tumours, including epithelioid sarcoma. Further clinical investigation of tazemetostat monotherapy is ongoing in phase 2 studies in adults and a phase 1 study for children, which are currently enrolling patients who have B-cell non-Hodgkin lymphoma and INI1-negative or SMARCA4-negative tumours.	human		High+Lowthroughput	Tazemetostat, an EZH2 inhibitor, in relapsed or refractory B-cell non-Hodgkin lymphoma and advanced solid tumours: a first-in-human, open-label, phase 1 study	否	无	Refractory B-cell non Hodgkin lymphoma, advanced solid tumor, epithelioid sarcoma	malignant rhabdoid tumour cells	E_01_0547	RNA-seq,immunohistochemistry,PCR,	Tazemetostat showed a favourable safety profile and antitumour activity in patients with refractory B-cell non-Hodgkin lymphoma and advanced solid tumours, including epithelioid sarcoma. Further clinical investigation of tazemetostat monotherapy is ongoing in phase 2 studies in adults and a phase 1 study for children, which are currently enrolling patients who have B-cell non-Hodgkin lymphoma and INI1-negative or SMARCA4-negative tumours.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Tazemetostat showed a favourable safety profile and antitumour activity in patients with refractory B-cell non-Hodgkin lymphoma and advanced solid tumours, including epithelioid sarcoma. Further clinical investigation of tazemetostat monotherapy is ongoing in phase 2 studies in adults and a phase 1 study for children, which are currently enrolling patients who have B-cell non-Hodgkin lymphoma and INI1-negative or SMARCA4-negative tumours.	Immunohistochemical staining	Tazemetostat showed a favourable safety profile and antitumour activity in patients with refractory B-cell non-Hodgkin lymphoma and advanced solid tumours, including epithelioid sarcoma. Further clinical investigation of tazemetostat monotherapy is ongoing in phase 2 studies in adults and a phase 1 study for children, which are currently enrolling patients who have B-cell non-Hodgkin lymphoma and INI1-negative or SMARCA4-negative tumours.	EZH2		RNA-seq,immunohistochemistry,PCR,	Tazemetostat showed a favourable safety profile and antitumour activity in patients with refractory B-cell non-Hodgkin lymphoma and advanced solid tumours, including epithelioid sarcoma. Further clinical investigation of tazemetostat monotherapy is ongoing in phase 2 studies in adults and a phase 1 study for children, which are currently enrolling patients who have B-cell non-Hodgkin lymphoma and INI1-negative or SMARCA4-negative tumours.			
29650362	chr19	10957975	10959975	SMARCA4	Tazemetostat showed a favourable safety profile and antitumour activity in patients with refractory B-cell non-Hodgkin lymphoma and advanced solid tumours, including epithelioid sarcoma. Further clinical investigation of tazemetostat monotherapy is ongoing in phase 2 studies in adults and a phase 1 study for children, which are currently enrolling patients who have B-cell non-Hodgkin lymphoma and INI1-negative or SMARCA4-negative tumours.	human		High+Lowthroughput	Tazemetostat, an EZH2 inhibitor, in relapsed or refractory B-cell non-Hodgkin lymphoma and advanced solid tumours: a first-in-human, open-label, phase 1 study	否	无	Refractory B-cell non Hodgkin lymphoma, advanced solid tumor, epithelioid sarcoma	malignant rhabdoid tumour cells	E_01_0547	RNA-seq,immunohistochemistry,PCR,	Tazemetostat showed a favourable safety profile and antitumour activity in patients with refractory B-cell non-Hodgkin lymphoma and advanced solid tumours, including epithelioid sarcoma. Further clinical investigation of tazemetostat monotherapy is ongoing in phase 2 studies in adults and a phase 1 study for children, which are currently enrolling patients who have B-cell non-Hodgkin lymphoma and INI1-negative or SMARCA4-negative tumours.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Tazemetostat showed a favourable safety profile and antitumour activity in patients with refractory B-cell non-Hodgkin lymphoma and advanced solid tumours, including epithelioid sarcoma. Further clinical investigation of tazemetostat monotherapy is ongoing in phase 2 studies in adults and a phase 1 study for children, which are currently enrolling patients who have B-cell non-Hodgkin lymphoma and INI1-negative or SMARCA4-negative tumours.	Immunohistochemical staining	Tazemetostat showed a favourable safety profile and antitumour activity in patients with refractory B-cell non-Hodgkin lymphoma and advanced solid tumours, including epithelioid sarcoma. Further clinical investigation of tazemetostat monotherapy is ongoing in phase 2 studies in adults and a phase 1 study for children, which are currently enrolling patients who have B-cell non-Hodgkin lymphoma and INI1-negative or SMARCA4-negative tumours.	SMARCA4		RNA-seq,immunohistochemistry,PCR,	Tazemetostat showed a favourable safety profile and antitumour activity in patients with refractory B-cell non-Hodgkin lymphoma and advanced solid tumours, including epithelioid sarcoma. Further clinical investigation of tazemetostat monotherapy is ongoing in phase 2 studies in adults and a phase 1 study for children, which are currently enrolling patients who have B-cell non-Hodgkin lymphoma and INI1-negative or SMARCA4-negative tumours.			
29648668	chr20	22578409	22580409	FOXA2	Conditional uterine deletion of ERα, but not the pioneer transcription factors FOXA2 or FOXO1, prevented the majority of DES-mediated changes in gene expression and H3K27ac signal at target enhancers. An ERα dependent super-enhancer was located at the Padi gene locus and a topological connection to the Padi1 TSS was documented using 3C-PCR. Chromosome looping at this site was independent of ERα and DES exposure, indicating that the interaction is established prior to ligand signaling. However, enrichment of H3K27ac and transcriptional activation at this locus was both DES and ERα-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ERα binding sites near estrogen-regulated genes.	mouse		High+Lowthroughput	Widespread enhancer activation via ERα mediates estrogen response in vivo during uterine development	否	无	nothing	ES cell	E_02_0338	RNA-seq,microarray analysis,PCR,real time RT-PCR,RNA isolation,Chromatin immunoprecipitation for analysis,Histone purification,immunoblotting,Chromatin conformation capture assay (3C PCR),ChIP-seq,	Conditional uterine deletion of ERα, but not the pioneer transcription factors FOXA2 or FOXO1, prevented the majority of DES-mediated changes in gene expression and H3K27ac signal at target enhancers. An ERα dependent super-enhancer was located at the Padi gene locus and a topological connection to the Padi1 TSS was documented using 3C-PCR. Chromosome looping at this site was independent of ERα and DES exposure, indicating that the interaction is established prior to ligand signaling. However, enrichment of H3K27ac and transcriptional activation at this locus was both DES and ERα-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ERα binding sites near estrogen-regulated genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Conditional uterine deletion of ERα, but not the pioneer transcription factors FOXA2 or FOXO1, prevented the majority of DES-mediated changes in gene expression and H3K27ac signal at target enhancers. An ERα dependent super-enhancer was located at the Padi gene locus and a topological connection to the Padi1 TSS was documented using 3C-PCR. Chromosome looping at this site was independent of ERα and DES exposure, indicating that the interaction is established prior to ligand signaling. However, enrichment of H3K27ac and transcriptional activation at this locus was both DES and ERα-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ERα binding sites near estrogen-regulated genes.		Conditional uterine deletion of ERα, but not the pioneer transcription factors FOXA2 or FOXO1, prevented the majority of DES-mediated changes in gene expression and H3K27ac signal at target enhancers. An ERα dependent super-enhancer was located at the Padi gene locus and a topological connection to the Padi1 TSS was documented using 3C-PCR. Chromosome looping at this site was independent of ERα and DES exposure, indicating that the interaction is established prior to ligand signaling. However, enrichment of H3K27ac and transcriptional activation at this locus was both DES and ERα-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ERα binding sites near estrogen-regulated genes.	Immunohistochemical staining	Conditional uterine deletion of ERα, but not the pioneer transcription factors FOXA2 or FOXO1, prevented the majority of DES-mediated changes in gene expression and H3K27ac signal at target enhancers. An ERα dependent super-enhancer was located at the Padi gene locus and a topological connection to the Padi1 TSS was documented using 3C-PCR. Chromosome looping at this site was independent of ERα and DES exposure, indicating that the interaction is established prior to ligand signaling. However, enrichment of H3K27ac and transcriptional activation at this locus was both DES and ERα-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ERα binding sites near estrogen-regulated genes.			RNA-seq,microarray analysis,PCR,real time RT-PCR,RNA isolation,Chromatin immunoprecipitation for analysis,Histone purification,immunoblotting,Chromatin conformation capture assay (3C PCR),ChIP-seq,				FOXA2
29648668	chr13	40552817	40554817	FOXO1	Conditional uterine deletion of ERα, but not the pioneer transcription factors FOXA2 or FOXO1, prevented the majority of DES-mediated changes in gene expression and H3K27ac signal at target enhancers. An ERα dependent super-enhancer was located at the Padi gene locus and a topological connection to the Padi1 TSS was documented using 3C-PCR. Chromosome looping at this site was independent of ERα and DES exposure, indicating that the interaction is established prior to ligand signaling. However, enrichment of H3K27ac and transcriptional activation at this locus was both DES and ERα-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ERα binding sites near estrogen-regulated genes.	mouse		High+Lowthroughput	Widespread enhancer activation via ERα mediates estrogen response in vivo during uterine development	否	无	nothing	ES cell	E_02_0338	RNA-seq,microarray analysis,PCR,real time RT-PCR,RNA isolation,Chromatin immunoprecipitation for analysis,Histone purification,immunoblotting,Chromatin conformation capture assay (3C PCR),ChIP-seq,	Conditional uterine deletion of ERα, but not the pioneer transcription factors FOXA2 or FOXO1, prevented the majority of DES-mediated changes in gene expression and H3K27ac signal at target enhancers. An ERα dependent super-enhancer was located at the Padi gene locus and a topological connection to the Padi1 TSS was documented using 3C-PCR. Chromosome looping at this site was independent of ERα and DES exposure, indicating that the interaction is established prior to ligand signaling. However, enrichment of H3K27ac and transcriptional activation at this locus was both DES and ERα-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ERα binding sites near estrogen-regulated genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Conditional uterine deletion of ERα, but not the pioneer transcription factors FOXA2 or FOXO1, prevented the majority of DES-mediated changes in gene expression and H3K27ac signal at target enhancers. An ERα dependent super-enhancer was located at the Padi gene locus and a topological connection to the Padi1 TSS was documented using 3C-PCR. Chromosome looping at this site was independent of ERα and DES exposure, indicating that the interaction is established prior to ligand signaling. However, enrichment of H3K27ac and transcriptional activation at this locus was both DES and ERα-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ERα binding sites near estrogen-regulated genes.		Conditional uterine deletion of ERα, but not the pioneer transcription factors FOXA2 or FOXO1, prevented the majority of DES-mediated changes in gene expression and H3K27ac signal at target enhancers. An ERα dependent super-enhancer was located at the Padi gene locus and a topological connection to the Padi1 TSS was documented using 3C-PCR. Chromosome looping at this site was independent of ERα and DES exposure, indicating that the interaction is established prior to ligand signaling. However, enrichment of H3K27ac and transcriptional activation at this locus was both DES and ERα-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ERα binding sites near estrogen-regulated genes.	Immunohistochemical staining	Conditional uterine deletion of ERα, but not the pioneer transcription factors FOXA2 or FOXO1, prevented the majority of DES-mediated changes in gene expression and H3K27ac signal at target enhancers. An ERα dependent super-enhancer was located at the Padi gene locus and a topological connection to the Padi1 TSS was documented using 3C-PCR. Chromosome looping at this site was independent of ERα and DES exposure, indicating that the interaction is established prior to ligand signaling. However, enrichment of H3K27ac and transcriptional activation at this locus was both DES and ERα-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ERα binding sites near estrogen-regulated genes.			RNA-seq,microarray analysis,PCR,real time RT-PCR,RNA isolation,Chromatin immunoprecipitation for analysis,Histone purification,immunoblotting,Chromatin conformation capture assay (3C PCR),ChIP-seq,				FOXO1
29648621	chr19	45766891	45768891	DMPK	Our data indicate that MEF2-induced loss of sarcomeres is mediated by DMPK via a decrease in sarcomeric gene expression by interfering with SRF transcriptional activity. Together, these results demonstrate an unexpected role for DMPK as a direct mediator of adverse cardiomyocyte remodelling and heart failure.	mouse		High+Lowthroughput	The MEF2 transcriptional target DMPK induces loss of sarcomere structure and cardiomyopathy	否	无	heart failure	NRCM cell	E_02_0339	transfection,Gene expression profiling,Immunofluorescence,confocal microscopy,Histology,Electron microscopy,Western blot,Reverse-transcription PCR,Real-Time PCR,Chromatin immunoprecipitation,	Our data indicate that MEF2-induced loss of sarcomeres is mediated by DMPK via a decrease in sarcomeric gene expression by interfering with SRF transcriptional activity. Together, these results demonstrate an unexpected role for DMPK as a direct mediator of adverse cardiomyocyte remodelling and heart failure.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data indicate that MEF2-induced loss of sarcomeres is mediated by DMPK via a decrease in sarcomeric gene expression by interfering with SRF transcriptional activity. Together, these results demonstrate an unexpected role for DMPK as a direct mediator of adverse cardiomyocyte remodelling and heart failure.		Our data indicate that MEF2-induced loss of sarcomeres is mediated by DMPK via a decrease in sarcomeric gene expression by interfering with SRF transcriptional activity. Together, these results demonstrate an unexpected role for DMPK as a direct mediator of adverse cardiomyocyte remodelling and heart failure.	Immunohistochemical staining	Our data indicate that MEF2-induced loss of sarcomeres is mediated by DMPK via a decrease in sarcomeric gene expression by interfering with SRF transcriptional activity. Together, these results demonstrate an unexpected role for DMPK as a direct mediator of adverse cardiomyocyte remodelling and heart failure.			transfection,Gene expression profiling,Immunofluorescence,confocal microscopy,Histology,Electron microscopy,Western blot,Reverse-transcription PCR,Real-Time PCR,Chromatin immunoprecipitation,				DMPK
29648621	chr6	43168450	43170450	SRF	Our data indicate that MEF2-induced loss of sarcomeres is mediated by DMPK via a decrease in sarcomeric gene expression by interfering with SRF transcriptional activity. Together, these results demonstrate an unexpected role for DMPK as a direct mediator of adverse cardiomyocyte remodelling and heart failure.	mouse		High+Lowthroughput	The MEF2 transcriptional target DMPK induces loss of sarcomere structure and cardiomyopathy	否	无	heart failure	NRCM cell	E_02_0339	transfection,Gene expression profiling,Immunofluorescence,confocal microscopy,Histology,Electron microscopy,Western blot,Reverse-transcription PCR,Real-Time PCR,Chromatin immunoprecipitation,	Our data indicate that MEF2-induced loss of sarcomeres is mediated by DMPK via a decrease in sarcomeric gene expression by interfering with SRF transcriptional activity. Together, these results demonstrate an unexpected role for DMPK as a direct mediator of adverse cardiomyocyte remodelling and heart failure.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data indicate that MEF2-induced loss of sarcomeres is mediated by DMPK via a decrease in sarcomeric gene expression by interfering with SRF transcriptional activity. Together, these results demonstrate an unexpected role for DMPK as a direct mediator of adverse cardiomyocyte remodelling and heart failure.		Our data indicate that MEF2-induced loss of sarcomeres is mediated by DMPK via a decrease in sarcomeric gene expression by interfering with SRF transcriptional activity. Together, these results demonstrate an unexpected role for DMPK as a direct mediator of adverse cardiomyocyte remodelling and heart failure.	Immunohistochemical staining	Our data indicate that MEF2-induced loss of sarcomeres is mediated by DMPK via a decrease in sarcomeric gene expression by interfering with SRF transcriptional activity. Together, these results demonstrate an unexpected role for DMPK as a direct mediator of adverse cardiomyocyte remodelling and heart failure.			transfection,Gene expression profiling,Immunofluorescence,confocal microscopy,Histology,Electron microscopy,Western blot,Reverse-transcription PCR,Real-Time PCR,Chromatin immunoprecipitation,				SRF
29648516	chr16	69704436	69706436	NQO1	These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.	human		High+Lowthroughput	The phosphodiesterase-4 inhibitor roflumilast reverts proteolysis in skeletal muscle cells of patients with COPD cachexia	否	无	Severe chronic obstructive pulmonary disease (COPD)	Myogenic Precursor Cell	E_01_0548	multi-exonic gene assay,RT-PCR,immunoblotting,	These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.		These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.	Immunohistochemical staining	These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.			multi-exonic gene assay,RT-PCR,immunoblotting,				NQO1
29648516	chr6	53494801	53496801	GCLC	These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.	human		High+Lowthroughput	The phosphodiesterase-4 inhibitor roflumilast reverts proteolysis in skeletal muscle cells of patients with COPD cachexia	否	无	Severe chronic obstructive pulmonary disease (COPD)	Myogenic Precursor Cell	E_01_0548	multi-exonic gene assay,RT-PCR,immunoblotting,	These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.		These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.	Immunohistochemical staining	These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.			multi-exonic gene assay,RT-PCR,immunoblotting,				GCLC
29648516	chr1	93882524	93884524	GCLM	These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.	human		High+Lowthroughput	The phosphodiesterase-4 inhibitor roflumilast reverts proteolysis in skeletal muscle cells of patients with COPD cachexia	否	无	Severe chronic obstructive pulmonary disease (COPD)	Myogenic Precursor Cell	E_01_0548	multi-exonic gene assay,RT-PCR,immunoblotting,	These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.		These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.	Immunohistochemical staining	These results have potential therapeutic implications, as this PDE-4 inhibitor is currently available for the treatment of systemic inflammation and exacerbations in patients with severe COPD. NEW & NOTEWORTHY In myotubes of cachectic chronic obstructive pulmonary disease (COPD) patients, cAMP signaling exerted beneficial effects by targeting muscle proteolysis and reducing gene expression of proteolytic markers of the ubiquitin-proteasome system and that of myostatin. In myotubes of patients and controls, roflumilast also favored antioxidant defense through upregulation of the nuclear factor (erythroid-derived 2)-like 2 pathway, of sirtuin-1, and of gene expression of slow- and fast-twitch isoforms. These findings have potential clinical implications for the treatment of muscle wasting in patients with COPD and cachexia.			multi-exonic gene assay,RT-PCR,immunoblotting,				GCLM
29644902	chr11	1155170	1157170	MUC5AC	IL-36 gamma induced MUC5AC expression and activated the phosphorylation of extracellular signal regulated kinase (ERK) 1 and 2, p38, and nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-kappa B). IL-36 receptor antagonist significantly attenuated these effects. The specific inhibitor and siRNA of ERK1, ERK2, p38, and NF-kappa B significantly attenuated IL-36 gamma induced MUC5AC expression.These results indicated that IL-36 gamma induced MUC5AC expression via the IL-36 receptor-mediated ERK1/2 and p38/NF-kappa B pathway in human airway epithelial cells.	human	Epithelial tissues	High+Lowthroughput	Interleukin (IL) 36 gamma induces mucin 5AC, oligomeric mucus/gel-forming expression via IL-36 receptor-extracellular signal regulated kinase 1 and 2, and p38-nuclear factor kappa-light-chain-enhancer of activated B cells in human airway epithelial cells	否	无	Allergic and inflammatory airway disease	NCI-H292 cell	E_01_0549	RT-PCR,Real-Time PCR,Enzyme-Linked Immunosorbent Assay(ELISA),Western Blot,Cell Transfection with siRNA,Immunofluorescence Staining,	IL-36 gamma induced MUC5AC expression and activated the phosphorylation of extracellular signal regulated kinase (ERK) 1 and 2, p38, and nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-kappa B). IL-36 receptor antagonist significantly attenuated these effects. The specific inhibitor and siRNA of ERK1, ERK2, p38, and NF-kappa B significantly attenuated IL-36 gamma induced MUC5AC expression.These results indicated that IL-36 gamma induced MUC5AC expression via the IL-36 receptor-mediated ERK1/2 and p38/NF-kappa B pathway in human airway epithelial cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	IL-36 gamma induced MUC5AC expression and activated the phosphorylation of extracellular signal regulated kinase (ERK) 1 and 2, p38, and nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-kappa B). IL-36 receptor antagonist significantly attenuated these effects. The specific inhibitor and siRNA of ERK1, ERK2, p38, and NF-kappa B significantly attenuated IL-36 gamma induced MUC5AC expression.These results indicated that IL-36 gamma induced MUC5AC expression via the IL-36 receptor-mediated ERK1/2 and p38/NF-kappa B pathway in human airway epithelial cells.		IL-36 gamma induced MUC5AC expression and activated the phosphorylation of extracellular signal regulated kinase (ERK) 1 and 2, p38, and nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-kappa B). IL-36 receptor antagonist significantly attenuated these effects. The specific inhibitor and siRNA of ERK1, ERK2, p38, and NF-kappa B significantly attenuated IL-36 gamma induced MUC5AC expression.These results indicated that IL-36 gamma induced MUC5AC expression via the IL-36 receptor-mediated ERK1/2 and p38/NF-kappa B pathway in human airway epithelial cells.	Immunohistochemical staining	IL-36 gamma induced MUC5AC expression and activated the phosphorylation of extracellular signal regulated kinase (ERK) 1 and 2, p38, and nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-kappa B). IL-36 receptor antagonist significantly attenuated these effects. The specific inhibitor and siRNA of ERK1, ERK2, p38, and NF-kappa B significantly attenuated IL-36 gamma induced MUC5AC expression.These results indicated that IL-36 gamma induced MUC5AC expression via the IL-36 receptor-mediated ERK1/2 and p38/NF-kappa B pathway in human airway epithelial cells.			RT-PCR,Real-Time PCR,Enzyme-Linked Immunosorbent Assay(ELISA),Western Blot,Cell Transfection with siRNA,Immunofluorescence Staining,				MUC5AC
29644114	chr8	127732161	127734161	MYC	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	human		High+Lowthroughput	Super enhancer inhibitors suppress MYC driven transcriptional amplification and tumor progression in osteosarcoma	否	无	Osteosarcoma	 U2OS	E_01_0550	ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Immunohistochemical staining	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	MYC		ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.			
29644114	chr7	92602168	92604168	CDK6	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	human		High+Lowthroughput	Super enhancer inhibitors suppress MYC driven transcriptional amplification and tumor progression in osteosarcoma	否	无	Osteosarcoma	 U2OS	E_01_0550	ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.		THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Immunohistochemical staining	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.			ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,				CDK6
29644114	chr1	218342648	218344648	TGFB2	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	human		High+Lowthroughput	Super enhancer inhibitors suppress MYC driven transcriptional amplification and tumor progression in osteosarcoma	否	无	Osteosarcoma	 U2OS	E_01_0550	ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Immunohistochemical staining	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	TGFB2		ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.			
29644114	chr17	7658920	7660920	TP53	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	human		High+Lowthroughput	Super enhancer inhibitors suppress MYC driven transcriptional amplification and tumor progression in osteosarcoma	否	无	Osteosarcoma	 U2OS	E_01_0550	ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Immunohistochemical staining	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	TP53		ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.			
29644114	chr13	48300777	48302777	RB1	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	human		High+Lowthroughput	Super enhancer inhibitors suppress MYC driven transcriptional amplification and tumor progression in osteosarcoma	否	无	Osteosarcoma	 U2OS	E_01_0550	ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Immunohistochemical staining	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	RB1		ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.			
29644114	chr8	144508621	144510621	RECQL4	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	human		High+Lowthroughput	Super enhancer inhibitors suppress MYC driven transcriptional amplification and tumor progression in osteosarcoma	否	无	Osteosarcoma	 U2OS	E_01_0550	ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.		THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Immunohistochemical staining	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.			ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,				RECQL4
29644114	chr8	31031131	31033131	WRN	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	human		High+Lowthroughput	Super enhancer inhibitors suppress MYC driven transcriptional amplification and tumor progression in osteosarcoma	否	无	Osteosarcoma	 U2OS	E_01_0550	ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.		THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Immunohistochemical staining	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.			ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,				WRN
29644114	chr15	90714881	90716881	BLM	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	human		High+Lowthroughput	Super enhancer inhibitors suppress MYC driven transcriptional amplification and tumor progression in osteosarcoma	否	无	Osteosarcoma	 U2OS	E_01_0550	ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.		THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Immunohistochemical staining	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.			ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,				BLM
29644114	chr19	15232605	15234605	BRD4	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	human		High+Lowthroughput	Super enhancer inhibitors suppress MYC driven transcriptional amplification and tumor progression in osteosarcoma	否	无	Osteosarcoma	 U2OS	E_01_0550	ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	Immunohistochemical staining	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.	BRD4		ChIP-seq,Immunohistochemistry,western blot,High throughput RNA seq,MTS assay,	THZ1 and JQ1 effectively suppresses the proliferation, migration, and invasion of osteosarcoma cells. Mechanistically, THZ1 treatment suppresses a large group of super enhancer containing MYC target genes including CDK6 and TGFB2. These findings revealed that the MYC-driven super enhancer signaling is crucial for the osteosarcoma tumorigenesis and targeting the MYC/super enhancer axis represents as a promising therapeutic strategy for treatment of osteosarcoma patients.			
29642935	chr7	148804872	148806872	EZH2	SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.	human		High+Lowthroughput	SP1-induced upregulation of lncRNA SPRY4-IT1 exerts oncogenic properties by scaffolding EZH2/LSD1/DNMT1 and sponging miR-101-3p in cholangiocarcinoma	否	无	Cholangiocarcinoma (CCA)	RBE cell	E_01_0551	Cell transfection,RT-qPCR,Flow cytometry,TUNEL assay,Caspase-3/9 activity assay,CCK-8 assay,immunofluorescence staining,Luciferase reporter assay,RNA immunoprecipitation (RIP) assay,Chromatin immunoprecipitation (ChIP) assay,Western blotting,immunohistochemistry (IHC) assays,	SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.	Immunohistochemical staining	SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.	EZH2		Cell transfection,RT-qPCR,Flow cytometry,TUNEL assay,Caspase-3/9 activity assay,CCK-8 assay,immunofluorescence staining,Luciferase reporter assay,RNA immunoprecipitation (RIP) assay,Chromatin immunoprecipitation (ChIP) assay,Western blotting,immunohistochemistry (IHC) assays,	SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.			
29642935	chr19	10130306	10132306	DNMT1	SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.	human		High+Lowthroughput	SP1-induced upregulation of lncRNA SPRY4-IT1 exerts oncogenic properties by scaffolding EZH2/LSD1/DNMT1 and sponging miR-101-3p in cholangiocarcinoma	否	无	Cholangiocarcinoma (CCA)	RBE cell	E_01_0551	Cell transfection,RT-qPCR,Flow cytometry,TUNEL assay,Caspase-3/9 activity assay,CCK-8 assay,immunofluorescence staining,Luciferase reporter assay,RNA immunoprecipitation (RIP) assay,Chromatin immunoprecipitation (ChIP) assay,Western blotting,immunohistochemistry (IHC) assays,	SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.	Immunohistochemical staining	SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.	DNMT1		Cell transfection,RT-qPCR,Flow cytometry,TUNEL assay,Caspase-3/9 activity assay,CCK-8 assay,immunofluorescence staining,Luciferase reporter assay,RNA immunoprecipitation (RIP) assay,Chromatin immunoprecipitation (ChIP) assay,Western blotting,immunohistochemistry (IHC) assays,	SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.			
29642935	chr5	142307868	142309868	SPRY4	SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.	human		High+Lowthroughput	SP1-induced upregulation of lncRNA SPRY4-IT1 exerts oncogenic properties by scaffolding EZH2/LSD1/DNMT1 and sponging miR-101-3p in cholangiocarcinoma	否	无	Cholangiocarcinoma (CCA)	RBE cell	E_01_0551	Cell transfection,RT-qPCR,Flow cytometry,TUNEL assay,Caspase-3/9 activity assay,CCK-8 assay,immunofluorescence staining,Luciferase reporter assay,RNA immunoprecipitation (RIP) assay,Chromatin immunoprecipitation (ChIP) assay,Western blotting,immunohistochemistry (IHC) assays,	SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.		SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.	Immunohistochemical staining	SPRY4-IT1 was abnormally upregulated in CCA tissues and cells, and this upregulation was correlated with tumor stage and tumor node metastasis (TNM) stage in CCA patients. SPRY4-IT1 overexpression was also an unfavorable prognostic factor for patients with CCA. Additionally, SP1 could bind directly to the SPRY4-IT1 promoter region and activate its transcription. Furthermore, SPRY4-IT1 silencing caused tumor suppressive effects via reducing cell proliferation, migration and invasion; inducing cell apoptosis and reversing the epithelial-to-mesenchymal transition (EMT) process in CCA cells. Mechanistically, enhancer of zeste homolog 2 (EZH2) along with the lysine specific demethylase 1 (LSD1) or DNA methyltransferase 1 (DNMT1) were recruited by SPRY4-IT1, which functioned as a scaffold. Importantly, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p.Our data illustrate how SPRY4-IT1 plays an oncogenic role in CCA and may offer a potential therapeutic target for treating CCA.			Cell transfection,RT-qPCR,Flow cytometry,TUNEL assay,Caspase-3/9 activity assay,CCK-8 assay,immunofluorescence staining,Luciferase reporter assay,RNA immunoprecipitation (RIP) assay,Chromatin immunoprecipitation (ChIP) assay,Western blotting,immunohistochemistry (IHC) assays,				SPRY4
29641996	chr8	128206162	128314310	CTCF	We find that these diverse cancer-specific super-enhancers, differing in size and location, interact with the MYC gene through a common and conserved CTCF binding site located 2 kb upstream of the MYC promoter. Genetic perturbation of this enhancer-docking site in tumor cells reduces CTCF binding, super-enhancer interaction, MYC gene expression, and cell proliferation. CTCF binding is highly sensitive to DNA methylation, and this enhancer-docking site, which is hypomethylated in diverse cancers, can be inactivated through epigenetic editing with dCas9-DNMT. Similar enhancer-docking sites occur at other genes, including genes with prominent roles in multiple cancers, suggesting a mechanism by which tumor cell oncogenes can generally hijack enhancers. These results provide insights into mechanisms that allow a single target gene to be regulated by diverse enhancer elements in different cell types.	human		Low+High throughput	Transcriptional Dysregulation of MYC Reveals Common Enhancer-Docking Mechanism	否	--	--	K562 cell	E_02_0340	4C,ChIP-seq	Among the DNA loop structures observed in these datasets, a large 2.8 Mb DNA loop was evident in all four cell types. This loop connects CTCF sites encompassing the MYC gene and qualifies as an insulated neighborhood. The DNA anchor sites of this 2.8 Mb DNA loop occur at the boundaries of a TAD found in all cells.	Super-Enhancer	CRISPR/Cas9	ChIA-PET,ChIP-qPCR	CTCF chromatin immunoprecipitation quantative polymerase chain reaction (ChIP-qPCR) showed complete loss of CTCF binding to this site in K562 and HCT-116 cells and a 60%–70% reduction in CTCF binding at this site in Jurkat and MCF7 cells. RNA analysis revealed a 70%–80% reduction of endogenous MYC mRNA in the absence of the enhancer-docking site in all of these cell types.	MRTL,MYCC,bHLHe39,c-Myc	The CTCF site in the promoter-proximal region of MYC is important for optimal interaction with distal Enhancers and supports the idea that this CTCF site functions as an Enhancer-docking site.	4C,CRISPR/Cas9,ChIP-qPCR	Similar results were obtained in HCT-116 cells, where the viewpoint was centered on the super-Enhancer located -0.4 Mb upstream of the MYC gene	CTCF	MRD21	CRISPR/Cas9	An inducible CRISPR/Cas9 perturbation model showed reduced proliferation for these four cell types upon induction of CTCF-site deletions .These results indicate that the CTCF motif in the MYC Enhancer-docking site is necessary for CTCF binding, for high levels of MYC expression and for cellular proliferation.	--	--	MYC
29641996	chr8	128206162	128314310	MYC	We find that these diverse cancer-specific super-enhancers, differing in size and location, interact with the MYC gene through a common and conserved CTCF binding site located 2 kb upstream of the MYC promoter. Genetic perturbation of this enhancer-docking site in tumor cells reduces CTCF binding, super-enhancer interaction, MYC gene expression, and cell proliferation. CTCF binding is highly sensitive to DNA methylation, and this enhancer-docking site, which is hypomethylated in diverse cancers, can be inactivated through epigenetic editing with dCas9-DNMT. Similar enhancer-docking sites occur at other genes, including genes with prominent roles in multiple cancers, suggesting a mechanism by which tumor cell oncogenes can generally hijack enhancers. These results provide insights into mechanisms that allow a single target gene to be regulated by diverse enhancer elements in different cell types.	human		Low+High throughput	Transcriptional Dysregulation of MYC Reveals Common Enhancer-Docking Mechanism	否	--	--	K562 cell	E_02_0340	4C,ChIP-seq	Among the DNA loop structures observed in these datasets, a large 2.8 Mb DNA loop was evident in all four cell types. This loop connects CTCF sites encompassing the MYC gene and qualifies as an insulated neighborhood. The DNA anchor sites of this 2.8 Mb DNA loop occur at the boundaries of a TAD found in all cells.	Super-Enhancer	CRISPR/Cas9	ChIA-PET,ChIP-qPCR	CTCF chromatin immunoprecipitation quantative polymerase chain reaction (ChIP-qPCR) showed complete loss of CTCF binding to this site in K562 and HCT-116 cells and a 60%–70% reduction in CTCF binding at this site in Jurkat and MCF7 cells. RNA analysis revealed a 70%–80% reduction of endogenous MYC mRNA in the absence of the enhancer-docking site in all of these cell types.	MRTL,MYCC,bHLHe39,c-Myc	The CTCF site in the promoter-proximal region of MYC is important for optimal interaction with distal Enhancers and supports the idea that this CTCF site functions as an Enhancer-docking site.	4C,CRISPR/Cas9,ChIP-qPCR	Similar results were obtained in HCT-116 cells, where the viewpoint was centered on the super-Enhancer located -0.4 Mb upstream of the MYC gene	CTCF	MRD21	CRISPR/Cas9	An inducible CRISPR/Cas9 perturbation model showed reduced proliferation for these four cell types upon induction of CTCF-site deletions .These results indicate that the CTCF motif in the MYC Enhancer-docking site is necessary for CTCF binding, for high levels of MYC expression and for cellular proliferation.	--	--	MYC
29641253	chr3	41192092	41194092	CTNNB1	The novel bidirectional hypoxia-inducible shRNA expression vector may be efficient in colorectal cancer-specific gene therapy.	human		High+Lowthroughput	Constructing a Novel Hypoxia-Inducible Bidirectional shRNA Expression Vector for Simultaneous Gene Silencing in Colorectal Cancer Gene Therapy	否	无	colorectal cancer 	HT-29	E_01_0552	Transfection,GFP assay, qRT-PCR,Western blot,	The novel bidirectional hypoxia-inducible shRNA expression vector may be efficient in colorectal cancer-specific gene therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The novel bidirectional hypoxia-inducible shRNA expression vector may be efficient in colorectal cancer-specific gene therapy.	Immunohistochemical staining	The novel bidirectional hypoxia-inducible shRNA expression vector may be efficient in colorectal cancer-specific gene therapy.	CTNNB1		Transfection,GFP assay, qRT-PCR,Western blot,	The novel bidirectional hypoxia-inducible shRNA expression vector may be efficient in colorectal cancer-specific gene therapy.			
29637721	chr13	51928163	51930163	ATP7B	Our results suggest that aberrant exon skipping associated to putative splicing enhancer disruption and silencer creation is one previously unrecognized mechanism in Wilson disease. What is more, the multiplex ligation-dependent probe amplification assay for the detection of exon deletions may be valuable in individuals with clinical Wilson disease diagnosis where one or no mutation has been identified by sequencing.	human		High+Lowthroughput	Presumed missense and synonymous mutations in ATP7B gene cause exon skipping in Wilson disease	否	无	Wilson disease	HEK293T	E_01_0553	Transfection,RT-PCR,Bioinformatics predictions,MLPA analysis,	Our results suggest that aberrant exon skipping associated to putative splicing enhancer disruption and silencer creation is one previously unrecognized mechanism in Wilson disease. What is more, the multiplex ligation-dependent probe amplification assay for the detection of exon deletions may be valuable in individuals with clinical Wilson disease diagnosis where one or no mutation has been identified by sequencing.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results suggest that aberrant exon skipping associated to putative splicing enhancer disruption and silencer creation is one previously unrecognized mechanism in Wilson disease. What is more, the multiplex ligation-dependent probe amplification assay for the detection of exon deletions may be valuable in individuals with clinical Wilson disease diagnosis where one or no mutation has been identified by sequencing.		Our results suggest that aberrant exon skipping associated to putative splicing enhancer disruption and silencer creation is one previously unrecognized mechanism in Wilson disease. What is more, the multiplex ligation-dependent probe amplification assay for the detection of exon deletions may be valuable in individuals with clinical Wilson disease diagnosis where one or no mutation has been identified by sequencing.	Immunohistochemical staining	Our results suggest that aberrant exon skipping associated to putative splicing enhancer disruption and silencer creation is one previously unrecognized mechanism in Wilson disease. What is more, the multiplex ligation-dependent probe amplification assay for the detection of exon deletions may be valuable in individuals with clinical Wilson disease diagnosis where one or no mutation has been identified by sequencing.			Transfection,RT-PCR,Bioinformatics predictions,MLPA analysis,				ATP7B
29637561	chr10	126881148	126883148	Cyp27b1	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.	mouse		High+Lowthroughput	1,25-dihydroxyvitamin D deficiency accelerates alveolar bone loss independent of aging and extracellular calcium and phosphorus	否	无	Periodontal disease	 CD3+ T cell	E_02_0341	Computer-assisted Image Analysis,Quantitative Real-time PCR,Immunohistochemical Staining,Histochemical Staining,micro-computed tomography (micro-CT),	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.		1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.	Immunohistochemical staining	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.			Computer-assisted Image Analysis,Quantitative Real-time PCR,Immunohistochemical Staining,Histochemical Staining,micro-computed tomography (micro-CT),				Cyp27b1
29637561	chr12	47839117	47841117	VDR	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.	mouse		High+Lowthroughput	1,25-dihydroxyvitamin D deficiency accelerates alveolar bone loss independent of aging and extracellular calcium and phosphorus	否	无	Periodontal disease	 CD3+ T cell	E_02_0341	Computer-assisted Image Analysis,Quantitative Real-time PCR,Immunohistochemical Staining,Histochemical Staining,micro-computed tomography (micro-CT),	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.		1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.	Immunohistochemical staining	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.			Computer-assisted Image Analysis,Quantitative Real-time PCR,Immunohistochemical Staining,Histochemical Staining,micro-computed tomography (micro-CT),				VDR
29637561	chr11	102832638	102834638	MMP3	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.	mouse		High+Lowthroughput	1,25-dihydroxyvitamin D deficiency accelerates alveolar bone loss independent of aging and extracellular calcium and phosphorus	否	无	Periodontal disease	 CD3+ T cell	E_02_0341	Computer-assisted Image Analysis,Quantitative Real-time PCR,Immunohistochemical Staining,Histochemical Staining,micro-computed tomography (micro-CT),	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.		1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.	Immunohistochemical staining	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.			Computer-assisted Image Analysis,Quantitative Real-time PCR,Immunohistochemical Staining,Histochemical Staining,micro-computed tomography (micro-CT),				MMP3
29637561	chr11	102709305	102711305	MMP8	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.	mouse		High+Lowthroughput	1,25-dihydroxyvitamin D deficiency accelerates alveolar bone loss independent of aging and extracellular calcium and phosphorus	否	无	Periodontal disease	 CD3+ T cell	E_02_0341	Computer-assisted Image Analysis,Quantitative Real-time PCR,Immunohistochemical Staining,Histochemical Staining,micro-computed tomography (micro-CT),	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.		1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.	Immunohistochemical staining	1,25(OH)2 D deficiency in the 1α(OH)ase mice accelerated alveolar bone loss by inhibiting osteoblastic bone formation and enhancing periodontal tissue degeneration in a calcium- and phosphorus- as well as an age-independent manner.			Computer-assisted Image Analysis,Quantitative Real-time PCR,Immunohistochemical Staining,Histochemical Staining,micro-computed tomography (micro-CT),				MMP8
29637005	chr14	100235409	100237409	YY1	In the current study, we identify the role of p38 in osteogenic differentiation from a MAPK antibody array screen and investigate the mechanisms underlying its transcriptional regulation. Our data show that YY1, a ubiquitously expressed transcription factor, and HDAC9c coordinate p38 transcriptional activity to promote its expression to facilitate the osteogenic potential of MSCs. Our results show that p38 mediates osteogenic differentiation, and this has significant implications in bone-related diseases, bone tissue engineering, and regenerative medicine.	human		High+Lowthroughput	YY1 and HDAC9c transcriptionally regulate p38-mediated mesenchymal stem cell differentiation into osteoblasts	否	无	nothing		E_01_0554	Real-time RT-PCR,Reporter gene assay,Western blot,coimmunoprecipitation (CoIP),qChIP,Lentiviral infection,	In the current study, we identify the role of p38 in osteogenic differentiation from a MAPK antibody array screen and investigate the mechanisms underlying its transcriptional regulation. Our data show that YY1, a ubiquitously expressed transcription factor, and HDAC9c coordinate p38 transcriptional activity to promote its expression to facilitate the osteogenic potential of MSCs. Our results show that p38 mediates osteogenic differentiation, and this has significant implications in bone-related diseases, bone tissue engineering, and regenerative medicine.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In the current study, we identify the role of p38 in osteogenic differentiation from a MAPK antibody array screen and investigate the mechanisms underlying its transcriptional regulation. Our data show that YY1, a ubiquitously expressed transcription factor, and HDAC9c coordinate p38 transcriptional activity to promote its expression to facilitate the osteogenic potential of MSCs. Our results show that p38 mediates osteogenic differentiation, and this has significant implications in bone-related diseases, bone tissue engineering, and regenerative medicine.	Immunohistochemical staining	In the current study, we identify the role of p38 in osteogenic differentiation from a MAPK antibody array screen and investigate the mechanisms underlying its transcriptional regulation. Our data show that YY1, a ubiquitously expressed transcription factor, and HDAC9c coordinate p38 transcriptional activity to promote its expression to facilitate the osteogenic potential of MSCs. Our results show that p38 mediates osteogenic differentiation, and this has significant implications in bone-related diseases, bone tissue engineering, and regenerative medicine.	YY1		Real-time RT-PCR,Reporter gene assay,Western blot,coimmunoprecipitation (CoIP),qChIP,Lentiviral infection,	In the current study, we identify the role of p38 in osteogenic differentiation from a MAPK antibody array screen and investigate the mechanisms underlying its transcriptional regulation. Our data show that YY1, a ubiquitously expressed transcription factor, and HDAC9c coordinate p38 transcriptional activity to promote its expression to facilitate the osteogenic potential of MSCs. Our results show that p38 mediates osteogenic differentiation, and this has significant implications in bone-related diseases, bone tissue engineering, and regenerative medicine.			
29637005	chr7	148804617	148806617	EZH2	In the current study, we identify the role of p38 in osteogenic differentiation from a MAPK antibody array screen and investigate the mechanisms underlying its transcriptional regulation. Our data show that YY1, a ubiquitously expressed transcription factor, and HDAC9c coordinate p38 transcriptional activity to promote its expression to facilitate the osteogenic potential of MSCs. Our results show that p38 mediates osteogenic differentiation, and this has significant implications in bone-related diseases, bone tissue engineering, and regenerative medicine.	human		High+Lowthroughput	YY1 and HDAC9c transcriptionally regulate p38-mediated mesenchymal stem cell differentiation into osteoblasts	否	无	nothing		E_01_0554	Real-time RT-PCR,Reporter gene assay,Western blot,coimmunoprecipitation (CoIP),qChIP,Lentiviral infection,	In the current study, we identify the role of p38 in osteogenic differentiation from a MAPK antibody array screen and investigate the mechanisms underlying its transcriptional regulation. Our data show that YY1, a ubiquitously expressed transcription factor, and HDAC9c coordinate p38 transcriptional activity to promote its expression to facilitate the osteogenic potential of MSCs. Our results show that p38 mediates osteogenic differentiation, and this has significant implications in bone-related diseases, bone tissue engineering, and regenerative medicine.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In the current study, we identify the role of p38 in osteogenic differentiation from a MAPK antibody array screen and investigate the mechanisms underlying its transcriptional regulation. Our data show that YY1, a ubiquitously expressed transcription factor, and HDAC9c coordinate p38 transcriptional activity to promote its expression to facilitate the osteogenic potential of MSCs. Our results show that p38 mediates osteogenic differentiation, and this has significant implications in bone-related diseases, bone tissue engineering, and regenerative medicine.	Immunohistochemical staining	In the current study, we identify the role of p38 in osteogenic differentiation from a MAPK antibody array screen and investigate the mechanisms underlying its transcriptional regulation. Our data show that YY1, a ubiquitously expressed transcription factor, and HDAC9c coordinate p38 transcriptional activity to promote its expression to facilitate the osteogenic potential of MSCs. Our results show that p38 mediates osteogenic differentiation, and this has significant implications in bone-related diseases, bone tissue engineering, and regenerative medicine.	EZH2		Real-time RT-PCR,Reporter gene assay,Western blot,coimmunoprecipitation (CoIP),qChIP,Lentiviral infection,	In the current study, we identify the role of p38 in osteogenic differentiation from a MAPK antibody array screen and investigate the mechanisms underlying its transcriptional regulation. Our data show that YY1, a ubiquitously expressed transcription factor, and HDAC9c coordinate p38 transcriptional activity to promote its expression to facilitate the osteogenic potential of MSCs. Our results show that p38 mediates osteogenic differentiation, and this has significant implications in bone-related diseases, bone tissue engineering, and regenerative medicine.			
29636998	chr7	148804486	148806486	EZH2	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	human		High+Lowthroughput	EZH2 promotes migration and invasion of triple-negative breast cancer cells via regulating TIMP2-MMP-2/-9 pathway	否	无	Triple negative breast cancer (TNBC)	MDA-MB-468	E_01_0555	Cell extraction,western blot,Gene knockdown,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,quantitative RT-PCR,	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	EZH2		Cell extraction,western blot,Gene knockdown,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,quantitative RT-PCR,	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.			
29636998	chr17	78850169	78852169	TIMP2	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	human		High+Lowthroughput	EZH2 promotes migration and invasion of triple-negative breast cancer cells via regulating TIMP2-MMP-2/-9 pathway	否	无	Triple negative breast cancer (TNBC)	MDA-MB-468	E_01_0555	Cell extraction,western blot,Gene knockdown,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,quantitative RT-PCR,	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	TIMP2		Cell extraction,western blot,Gene knockdown,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,quantitative RT-PCR,	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.			
29636998	chr16	55386880	55388880	MMP2	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	human		High+Lowthroughput	EZH2 promotes migration and invasion of triple-negative breast cancer cells via regulating TIMP2-MMP-2/-9 pathway	否	无	Triple negative breast cancer (TNBC)	MDA-MB-468	E_01_0555	Cell extraction,western blot,Gene knockdown,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,quantitative RT-PCR,	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	MMP2		Cell extraction,western blot,Gene knockdown,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,quantitative RT-PCR,	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.			
29636998	chr20	46005981	46007981	MMP9	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	human		High+Lowthroughput	EZH2 promotes migration and invasion of triple-negative breast cancer cells via regulating TIMP2-MMP-2/-9 pathway	否	无	Triple negative breast cancer (TNBC)	MDA-MB-468	E_01_0555	Cell extraction,western blot,Gene knockdown,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,quantitative RT-PCR,	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.	MMP9		Cell extraction,western blot,Gene knockdown,Chromatin immunoprecipitation (ChIP) assay,RT-PCR,quantitative RT-PCR,	Enhancer of zeste homolog 2 (EZH2) is the catalytic core protein in the polycomb repressive complex 2 (PRC2), which catalyzes the trimethylation of histone H3 at lysine 27 (H3K27me3) and mediates gene silencing of the target genes that are involved in fundamental cellular processes, such as the cell fate decision, cell cycle regulation, senescence, cell differentiation, and cancer formation. A consistent association between TNBC metastasis and EZH2 has not been confirmed. The aim of this study was to investigate the role of EZH2 in the regulation of tissue inhibitor of metalloproteinase (TIMPs) and matrix metalloproteinases (MMPs) to promote metastasis of TNBC cells and to characterize the metastasis-associated genes regulated by EZH2 in TNBC cells. We found that high levels of EZH2 expression induce repression of TIMP2 transcription, leading to increased activity of MMP-2 and MMP-9 and thus to increased invasive activity of TNBC cells.			
29636889	chr12	2956797	2958797	TEAD4	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	human		High+Lowthroughput	Effect of TEAD4 on multilineage differentiation of muscle-derived stem cells	否	无	nothing		E_01_0556	Flow cytometry,immunohistochemical,histological staining,SDS-PAGE,Western blot,Quantitative RT-PCR,	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	Immunohistochemical staining	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	TEAD4		Flow cytometry,immunohistochemical,histological staining,SDS-PAGE,Western blot,Quantitative RT-PCR,	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.			
29636889	chr3	8731543	8733543	CAV3	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	human		High+Lowthroughput	Effect of TEAD4 on multilineage differentiation of muscle-derived stem cells	否	无	nothing		E_01_0556	Flow cytometry,immunohistochemical,histological staining,SDS-PAGE,Western blot,Quantitative RT-PCR,	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.		Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	Immunohistochemical staining	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.			Flow cytometry,immunohistochemical,histological staining,SDS-PAGE,Western blot,Quantitative RT-PCR,				CAV3
29636889	chr11	12671689	12673689	TEAD1	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	human		High+Lowthroughput	Effect of TEAD4 on multilineage differentiation of muscle-derived stem cells	否	无	nothing		E_01_0556	Flow cytometry,immunohistochemical,histological staining,SDS-PAGE,Western blot,Quantitative RT-PCR,	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	Immunohistochemical staining	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	TEAD1		Flow cytometry,immunohistochemical,histological staining,SDS-PAGE,Western blot,Quantitative RT-PCR,	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.			
29636889	chr19	49338067	49340067	TEAD2	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	human		High+Lowthroughput	Effect of TEAD4 on multilineage differentiation of muscle-derived stem cells	否	无	nothing		E_01_0556	Flow cytometry,immunohistochemical,histological staining,SDS-PAGE,Western blot,Quantitative RT-PCR,	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	Immunohistochemical staining	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	TEAD2		Flow cytometry,immunohistochemical,histological staining,SDS-PAGE,Western blot,Quantitative RT-PCR,	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.			
29636889	chr6	35470953	35472953	TEAD3	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	human		High+Lowthroughput	Effect of TEAD4 on multilineage differentiation of muscle-derived stem cells	否	无	nothing		E_01_0556	Flow cytometry,immunohistochemical,histological staining,SDS-PAGE,Western blot,Quantitative RT-PCR,	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	Immunohistochemical staining	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	TEAD3		Flow cytometry,immunohistochemical,histological staining,SDS-PAGE,Western blot,Quantitative RT-PCR,	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.			
29636889	chr4	2840932	2842932	ADD1	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	human		High+Lowthroughput	Effect of TEAD4 on multilineage differentiation of muscle-derived stem cells	否	无	nothing		E_01_0556	Flow cytometry,immunohistochemical,histological staining,SDS-PAGE,Western blot,Quantitative RT-PCR,	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.		Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.	Immunohistochemical staining	Finally, TEAD4-KD led to the failure of adipogenesis from bMDSCs. Together, our results support that TEAD4 is essential during adipogenic differentiation of bMDSCs. It has little effect on myogenesis of bMDSCs, and does not affect ostegenesis, neurogenesis, or pancreatic differentiation of bMDSCs. Our findings will be helpful for future study on the roles of the TEAD family during differentiation of MDSCs, and for controlling MDSC differentiation for stem cell applications.			Flow cytometry,immunohistochemical,histological staining,SDS-PAGE,Western blot,Quantitative RT-PCR,				ADD1
29636834	chr11	61796856	61798856	FADS1	We observed significant ASM between rs174537 and DNA methylation at key regulatory regions in the FADS region from leukocyte and CD4+ cells. DNA methylation from leukocytes also correlated with circulating omega-6 LC-PUFAs. These results support the use of peripheral whole blood samples, with leukocytes showing the most promise for future nutrigenomic studies evaluating epigenetic modifications affecting LC-PUFA biosynthesis in humans.	human		High+Lowthroughput	Allele-specific methylation in the FADS genomic region in DNA from human saliva, CD4+ cells, and total leukocytes	是	 rs174537	nothing	CD4+ cells	E_01_0557	PCR,GWAS,correlation analysis,	We observed significant ASM between rs174537 and DNA methylation at key regulatory regions in the FADS region from leukocyte and CD4+ cells. DNA methylation from leukocytes also correlated with circulating omega-6 LC-PUFAs. These results support the use of peripheral whole blood samples, with leukocytes showing the most promise for future nutrigenomic studies evaluating epigenetic modifications affecting LC-PUFA biosynthesis in humans.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We observed significant ASM between rs174537 and DNA methylation at key regulatory regions in the FADS region from leukocyte and CD4+ cells. DNA methylation from leukocytes also correlated with circulating omega-6 LC-PUFAs. These results support the use of peripheral whole blood samples, with leukocytes showing the most promise for future nutrigenomic studies evaluating epigenetic modifications affecting LC-PUFA biosynthesis in humans.		We observed significant ASM between rs174537 and DNA methylation at key regulatory regions in the FADS region from leukocyte and CD4+ cells. DNA methylation from leukocytes also correlated with circulating omega-6 LC-PUFAs. These results support the use of peripheral whole blood samples, with leukocytes showing the most promise for future nutrigenomic studies evaluating epigenetic modifications affecting LC-PUFA biosynthesis in humans.	Immunohistochemical staining	We observed significant ASM between rs174537 and DNA methylation at key regulatory regions in the FADS region from leukocyte and CD4+ cells. DNA methylation from leukocytes also correlated with circulating omega-6 LC-PUFAs. These results support the use of peripheral whole blood samples, with leukocytes showing the most promise for future nutrigenomic studies evaluating epigenetic modifications affecting LC-PUFA biosynthesis in humans.			PCR,GWAS,correlation analysis,				FADS1
29636834	chr11	61790368	61792368	FADS2	We observed significant ASM between rs174537 and DNA methylation at key regulatory regions in the FADS region from leukocyte and CD4+ cells. DNA methylation from leukocytes also correlated with circulating omega-6 LC-PUFAs. These results support the use of peripheral whole blood samples, with leukocytes showing the most promise for future nutrigenomic studies evaluating epigenetic modifications affecting LC-PUFA biosynthesis in humans.	human		High+Lowthroughput	Allele-specific methylation in the FADS genomic region in DNA from human saliva, CD4+ cells, and total leukocytes	是	 rs174537	nothing	CD4+ cells	E_01_0557	PCR,GWAS,correlation analysis,	We observed significant ASM between rs174537 and DNA methylation at key regulatory regions in the FADS region from leukocyte and CD4+ cells. DNA methylation from leukocytes also correlated with circulating omega-6 LC-PUFAs. These results support the use of peripheral whole blood samples, with leukocytes showing the most promise for future nutrigenomic studies evaluating epigenetic modifications affecting LC-PUFA biosynthesis in humans.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We observed significant ASM between rs174537 and DNA methylation at key regulatory regions in the FADS region from leukocyte and CD4+ cells. DNA methylation from leukocytes also correlated with circulating omega-6 LC-PUFAs. These results support the use of peripheral whole blood samples, with leukocytes showing the most promise for future nutrigenomic studies evaluating epigenetic modifications affecting LC-PUFA biosynthesis in humans.		We observed significant ASM between rs174537 and DNA methylation at key regulatory regions in the FADS region from leukocyte and CD4+ cells. DNA methylation from leukocytes also correlated with circulating omega-6 LC-PUFAs. These results support the use of peripheral whole blood samples, with leukocytes showing the most promise for future nutrigenomic studies evaluating epigenetic modifications affecting LC-PUFA biosynthesis in humans.	Immunohistochemical staining	We observed significant ASM between rs174537 and DNA methylation at key regulatory regions in the FADS region from leukocyte and CD4+ cells. DNA methylation from leukocytes also correlated with circulating omega-6 LC-PUFAs. These results support the use of peripheral whole blood samples, with leukocytes showing the most promise for future nutrigenomic studies evaluating epigenetic modifications affecting LC-PUFA biosynthesis in humans.			PCR,GWAS,correlation analysis,				FADS2
32396940	chr11	32173084	32175084	Nprl3	Functional analysis demonstrates that an erythroid-specific enhancer is located in intron 7 of lamprey nprl3, which corresponds to the NPRL3 intron 7 MCS-R1 enhancer of jawed vertebrates.	mouse		High+Lowthroughput	An evolutionarily ancient mechanism for regulation of hemoglobin expression in vertebrate red cells	否			Red blood cell (erythrocyte)	E_02_0342	ATAC-seq,Nanopore sequencing	Functional analysis demonstrates that an erythroid-specific enhancer is located in intron 7 of lamprey nprl3, which corresponds to the NPRL3 intron 7 MCS-R1 enhancer of jawed vertebrates.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Functional analysis demonstrates that an erythroid-specific enhancer is located in intron 7 of lamprey nprl3, which corresponds to the NPRL3 intron 7 MCS-R1 enhancer of jawed vertebrates.		Functional analysis demonstrates that an erythroid-specific enhancer is located in intron 7 of lamprey nprl3, which corresponds to the NPRL3 intron 7 MCS-R1 enhancer of jawed vertebrates.	Immunohistochemical staining	Functional analysis demonstrates that an erythroid-specific enhancer is located in intron 7 of lamprey nprl3, which corresponds to the NPRL3 intron 7 MCS-R1 enhancer of jawed vertebrates.			ATAC-seq,Nanopore sequencing				Nprl3
32386462	chrX	49247713	49249713	FOXP3	We show that the activity of the master transcription factor Forkhead-box protein 3 (FOXP3) attenuates p65 phosphorylation and nuclear translocation of the NF- B proteins p50, p65 and c-Rel following activation in human Treg.	human	lymphoid tissue	High+Lowthroughput	Attenuation of canonical NF-κB signaling maintains function and stability of human Treg	否		Immune tolerance	regulatory T cell	E_01_0558	Flow cytometry，RT-PCR，Western blotting	We show that the activity of the master transcription factor Forkhead-box protein 3 (FOXP3) attenuates p65 phosphorylation and nuclear translocation of the NF- B proteins p50, p65 and c-Rel following activation in human Treg.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We show that the activity of the master transcription factor Forkhead-box protein 3 (FOXP3) attenuates p65 phosphorylation and nuclear translocation of the NF- B proteins p50, p65 and c-Rel following activation in human Treg.	Immunohistochemical staining	We show that the activity of the master transcription factor Forkhead-box protein 3 (FOXP3) attenuates p65 phosphorylation and nuclear translocation of the NF- B proteins p50, p65 and c-Rel following activation in human Treg.	FOXP3		Flow cytometry，RT-PCR，Western blotting	We show that the activity of the master transcription factor Forkhead-box protein 3 (FOXP3) attenuates p65 phosphorylation and nuclear translocation of the NF- B proteins p50, p65 and c-Rel following activation in human Treg.			
32391884	chr9	127791794	127793794	FPGS	The intergenic SNP rs1382539 located in a regulatory element of DHFR was associated with increased levels of short-chain MTX polyglutamates (P = 1.1 10-8) due to suppression of enhancer activity, while rs35789560 in FPGS (p.R466C, P = 5.6 10-9) was associated with decreased levels of long-chain MTX polyglutamates through reduced catalytic activity.	human	blood	High+Lowthroughput	Effects of germline DHFR and FPGS variants on methotrexate metabolism and relapse of leukemia	是	rs1382539，rs35789560	Leukemia	leukocyte	E_01_0559	PCR	The intergenic SNP rs1382539 located in a regulatory element of DHFR was associated with increased levels of short-chain MTX polyglutamates (P = 1.1 10-8) due to suppression of enhancer activity, while rs35789560 in FPGS (p.R466C, P = 5.6 10-9) was associated with decreased levels of long-chain MTX polyglutamates through reduced catalytic activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The intergenic SNP rs1382539 located in a regulatory element of DHFR was associated with increased levels of short-chain MTX polyglutamates (P = 1.1 10-8) due to suppression of enhancer activity, while rs35789560 in FPGS (p.R466C, P = 5.6 10-9) was associated with decreased levels of long-chain MTX polyglutamates through reduced catalytic activity.		The intergenic SNP rs1382539 located in a regulatory element of DHFR was associated with increased levels of short-chain MTX polyglutamates (P = 1.1 10-8) due to suppression of enhancer activity, while rs35789560 in FPGS (p.R466C, P = 5.6 10-9) was associated with decreased levels of long-chain MTX polyglutamates through reduced catalytic activity.	Immunohistochemical staining	The intergenic SNP rs1382539 located in a regulatory element of DHFR was associated with increased levels of short-chain MTX polyglutamates (P = 1.1 10-8) due to suppression of enhancer activity, while rs35789560 in FPGS (p.R466C, P = 5.6 10-9) was associated with decreased levels of long-chain MTX polyglutamates through reduced catalytic activity.			PCR				FPGS
32393578	chr5	88714226	88716226	MEF2C	We found that this enhancement is mediated by the accumulation of phosphorylated p38 mitogen-activated protein (MAP) kinase in the nucleus, which drives the activation of the transcription factor myocyte enhancer factor 2C (MEF2C) and promotes the transcription of a subset of synaptic activity induced genes, including brain-derived neurotrophic factor (Bdnf) and activity-regulated cytoskeleton-associated protein (Arc).	human	Nervous tissue	High+Lowthroughput	The NMDA receptor subunit GluN3A regulates synaptic activity-induced and myocyte enhancer factor 2C (MEF2C)-dependent transcription	否				E_01_0560	quantitative real-time PCR, immunostaining, reporter gene assays, RNA sequencing	We found that this enhancement is mediated by the accumulation of phosphorylated p38 mitogen-activated protein (MAP) kinase in the nucleus, which drives the activation of the transcription factor myocyte enhancer factor 2C (MEF2C) and promotes the transcription of a subset of synaptic activity induced genes, including brain-derived neurotrophic factor (Bdnf) and activity-regulated cytoskeleton-associated protein (Arc).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found that this enhancement is mediated by the accumulation of phosphorylated p38 mitogen-activated protein (MAP) kinase in the nucleus, which drives the activation of the transcription factor myocyte enhancer factor 2C (MEF2C) and promotes the transcription of a subset of synaptic activity induced genes, including brain-derived neurotrophic factor (Bdnf) and activity-regulated cytoskeleton-associated protein (Arc).	Immunohistochemical staining	We found that this enhancement is mediated by the accumulation of phosphorylated p38 mitogen-activated protein (MAP) kinase in the nucleus, which drives the activation of the transcription factor myocyte enhancer factor 2C (MEF2C) and promotes the transcription of a subset of synaptic activity induced genes, including brain-derived neurotrophic factor (Bdnf) and activity-regulated cytoskeleton-associated protein (Arc).	MEF2C		quantitative real-time PCR, immunostaining, reporter gene assays, RNA sequencing	We found that this enhancement is mediated by the accumulation of phosphorylated p38 mitogen-activated protein (MAP) kinase in the nucleus, which drives the activation of the transcription factor myocyte enhancer factor 2C (MEF2C) and promotes the transcription of a subset of synaptic activity induced genes, including brain-derived neurotrophic factor (Bdnf) and activity-regulated cytoskeleton-associated protein (Arc).			
32394628	chr7	148804398	148806398	EZH2	Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of the polycomb repressive complex 2 (PRC2) along with embryonic ectoderm development (EED) and suppressor of zeste 12 (SUZ12), which implements transcriptional repression mainly by depositing tri-methylation marks at lysine 27 of histone H3 (H3K27me3).	human		High+Lowthroughput	Identification of catalytic and non-catalytic activity inhibitors against PRC2-EZH2 complex through multiple high-throughput screening campaigns	否		Breast cancer，prostate cancer	tumor cell	E_01_0561	high-throughput screening	Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of the polycomb repressive complex 2 (PRC2) along with embryonic ectoderm development (EED) and suppressor of zeste 12 (SUZ12), which implements transcriptional repression mainly by depositing tri-methylation marks at lysine 27 of histone H3 (H3K27me3).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of the polycomb repressive complex 2 (PRC2) along with embryonic ectoderm development (EED) and suppressor of zeste 12 (SUZ12), which implements transcriptional repression mainly by depositing tri-methylation marks at lysine 27 of histone H3 (H3K27me3).	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of the polycomb repressive complex 2 (PRC2) along with embryonic ectoderm development (EED) and suppressor of zeste 12 (SUZ12), which implements transcriptional repression mainly by depositing tri-methylation marks at lysine 27 of histone H3 (H3K27me3).	EZH2		high-throughput screening	Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of the polycomb repressive complex 2 (PRC2) along with embryonic ectoderm development (EED) and suppressor of zeste 12 (SUZ12), which implements transcriptional repression mainly by depositing tri-methylation marks at lysine 27 of histone H3 (H3K27me3).			
32397263	chr7	76300187	76302187	HSPB1	Furthermore, the resistant phenotype showed a downregulation of HSPB1, SLC15A2, FECH, SOD2 and an upregulation of HMBS and BIRC5 genes.	human	Epithelial tissues	High+Lowthroughput	Epigallocatechin Gallate Enhances MAL-PDT Cytotoxic Effect on PDT-Resistant Skin Cancer Squamous Cells	否		Skin Cancer	Human skin cell	E_01_0562	Flow cytometry，RT-qPCR，Western Blot	Furthermore, the resistant phenotype showed a downregulation of HSPB1, SLC15A2, FECH, SOD2 and an upregulation of HMBS and BIRC5 genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, the resistant phenotype showed a downregulation of HSPB1, SLC15A2, FECH, SOD2 and an upregulation of HMBS and BIRC5 genes.		Furthermore, the resistant phenotype showed a downregulation of HSPB1, SLC15A2, FECH, SOD2 and an upregulation of HMBS and BIRC5 genes.	Immunohistochemical staining	Furthermore, the resistant phenotype showed a downregulation of HSPB1, SLC15A2, FECH, SOD2 and an upregulation of HMBS and BIRC5 genes.			Flow cytometry，RT-qPCR，Western Blot				HSPB1
32398735	chr17	72118099	72120099	SOX9	Mechanistically, SOX9 may sensitize TNBC cells to THZ1, in a FOXC1-related manner, suggesting that SOX9 could be as a predictive factor of THZ1.	human		High+Lowthroughput	SOX9 interacts with FOXC1 to activate MYC and regulate CDK7 inhibitor sensitivity in triple-negative breast cancer	否		Triple-negative breast cancer	MDA-468 cell	E_01_0563	Immunohistochemistry，RNA isolation，quantitative RT-PCR，Western Blot，ChIP-Seq，ChIP-PCR，Co-immunoprecipitation assays	Mechanistically, SOX9 may sensitize TNBC cells to THZ1, in a FOXC1-related manner, suggesting that SOX9 could be as a predictive factor of THZ1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mechanistically, SOX9 may sensitize TNBC cells to THZ1, in a FOXC1-related manner, suggesting that SOX9 could be as a predictive factor of THZ1.	Immunohistochemical staining	Mechanistically, SOX9 may sensitize TNBC cells to THZ1, in a FOXC1-related manner, suggesting that SOX9 could be as a predictive factor of THZ1.	SOX9		Immunohistochemistry，RNA isolation，quantitative RT-PCR，Western Blot，ChIP-Seq，ChIP-PCR，Co-immunoprecipitation assays	Mechanistically, SOX9 may sensitize TNBC cells to THZ1, in a FOXC1-related manner, suggesting that SOX9 could be as a predictive factor of THZ1.			
32408898	chr20	34277918	34279918	AHCY	The amplification of the AHCY gene is paralleled by strong overexpression of AHCY at both the transcriptional and protein level, and persists upon culturing the resistant clone in a DZNep-free medium.	human		High+Lowthroughput	Acquired resistance to DZNep-mediated apoptosis is associated with copy number gains of AHCY in a B-cell lymphoma model	否		B-cell lymphoma model	Burkitt lymphoma cell	E_01_0564	Flow cytometry，Western blotting, RNA isolation，RT-PCR，Immunohistochemistry	The amplification of the AHCY gene is paralleled by strong overexpression of AHCY at both the transcriptional and protein level, and persists upon culturing the resistant clone in a DZNep-free medium.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The amplification of the AHCY gene is paralleled by strong overexpression of AHCY at both the transcriptional and protein level, and persists upon culturing the resistant clone in a DZNep-free medium.		The amplification of the AHCY gene is paralleled by strong overexpression of AHCY at both the transcriptional and protein level, and persists upon culturing the resistant clone in a DZNep-free medium.	Immunohistochemical staining	The amplification of the AHCY gene is paralleled by strong overexpression of AHCY at both the transcriptional and protein level, and persists upon culturing the resistant clone in a DZNep-free medium.			Flow cytometry，Western blotting, RNA isolation，RT-PCR，Immunohistochemistry				AHCY
32506582	chr8	42413974	42415974	SLC20A2	We identified a deletion of an enhancer of SLC20A2 expression, with carriers showing haploinsufficiency in similar ranges to loss-offunction alleles, and we observed reduced mRNA levels after deleting this element in a cellular model. We propose a 3-step strategy to identify and easily assess the effect of such events.	human		High+Lowthroughput	Haploinsufficiency of the Primary Familial Brain Calcification Gene SLC20A2 Mediated by Disruption of a Regulatory Element	否		Primary familial brain calci- fication	HEK293 cell	E_01_0565	RT-ddPCR	We identified a deletion of an enhancer of SLC20A2 expression, with carriers showing haploinsufficiency in similar ranges to loss-offunction alleles, and we observed reduced mRNA levels after deleting this element in a cellular model. We propose a 3-step strategy to identify and easily assess the effect of such events.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identified a deletion of an enhancer of SLC20A2 expression, with carriers showing haploinsufficiency in similar ranges to loss-offunction alleles, and we observed reduced mRNA levels after deleting this element in a cellular model. We propose a 3-step strategy to identify and easily assess the effect of such events.		We identified a deletion of an enhancer of SLC20A2 expression, with carriers showing haploinsufficiency in similar ranges to loss-offunction alleles, and we observed reduced mRNA levels after deleting this element in a cellular model. We propose a 3-step strategy to identify and easily assess the effect of such events.	Immunohistochemical staining	We identified a deletion of an enhancer of SLC20A2 expression, with carriers showing haploinsufficiency in similar ranges to loss-offunction alleles, and we observed reduced mRNA levels after deleting this element in a cellular model. We propose a 3-step strategy to identify and easily assess the effect of such events.			RT-ddPCR				SLC20A2
32506995	chr21	34785195	34787195	RUNX1	Finally, we evaluated the expression levels of LINC00160 and RUNX1 in various types of breast cancer and found that their expression positively correlated with the survival rate in ER+ breast cancer patients, implying that the estrogen-regulated LINC00160 and its neighboring RUNX1 might represent potential biomarkers for ER+ breast cancers.	human		High+Lowthroughput	Epigenomics-based identification of oestrogen-regulated long noncoding RNAs in ER+ breast cancer	否		Breast Cancer	MCF7 cell	E_01_0566	ChIP-seq，ATAC-seq，RNA isolation，quantitative RT-PCR	Finally, we evaluated the expression levels of LINC00160 and RUNX1 in various types of breast cancer and found that their expression positively correlated with the survival rate in ER+ breast cancer patients, implying that the estrogen-regulated LINC00160 and its neighboring RUNX1 might represent potential biomarkers for ER+ breast cancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Finally, we evaluated the expression levels of LINC00160 and RUNX1 in various types of breast cancer and found that their expression positively correlated with the survival rate in ER+ breast cancer patients, implying that the estrogen-regulated LINC00160 and its neighboring RUNX1 might represent potential biomarkers for ER+ breast cancers.	Immunohistochemical staining	Finally, we evaluated the expression levels of LINC00160 and RUNX1 in various types of breast cancer and found that their expression positively correlated with the survival rate in ER+ breast cancer patients, implying that the estrogen-regulated LINC00160 and its neighboring RUNX1 might represent potential biomarkers for ER+ breast cancers.	RUNX1		ChIP-seq，ATAC-seq，RNA isolation，quantitative RT-PCR	Finally, we evaluated the expression levels of LINC00160 and RUNX1 in various types of breast cancer and found that their expression positively correlated with the survival rate in ER+ breast cancer patients, implying that the estrogen-regulated LINC00160 and its neighboring RUNX1 might represent potential biomarkers for ER+ breast cancers.			
32509064	chr1	156461285	156463285	MEF2D	MEF2D-mediated effects on proliferation, migration, and invasion were explored in TSCC cells after transfection with MEF2D-siRNA.	human	connective tissue	High+Lowthroughput	Myocyte-specific enhancer factor 2D promotes tumorigenesis and progression in tongue squamous cell carcinoma	否		Tongue squamous cell carcinoma	TSCC cell	E_01_0567	RT-qPCR，Western blotting，IHC analysis	MEF2D-mediated effects on proliferation, migration, and invasion were explored in TSCC cells after transfection with MEF2D-siRNA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MEF2D-mediated effects on proliferation, migration, and invasion were explored in TSCC cells after transfection with MEF2D-siRNA.		MEF2D-mediated effects on proliferation, migration, and invasion were explored in TSCC cells after transfection with MEF2D-siRNA.	Immunohistochemical staining	MEF2D-mediated effects on proliferation, migration, and invasion were explored in TSCC cells after transfection with MEF2D-siRNA.			RT-qPCR，Western blotting，IHC analysis				MEF2D
32510323	chr16	67870486	67872486	EDC4	Importantly, we establish that EDC4 impairs MARF1 activity by preventing its LOTUS domains from binding target mRNAs.	human		High+Lowthroughput	A non-canonical role for the EDC4 decapping factor in regulating MARF1-mediated mRNA decay	否				E_01_0568	seCLIP-seq，siRNAs，RT-qPCR，Immunofluorescent staining，RNA immunoprecipitation assay	Importantly, we establish that EDC4 impairs MARF1 activity by preventing its LOTUS domains from binding target mRNAs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Importantly, we establish that EDC4 impairs MARF1 activity by preventing its LOTUS domains from binding target mRNAs.		Importantly, we establish that EDC4 impairs MARF1 activity by preventing its LOTUS domains from binding target mRNAs.	Immunohistochemical staining	Importantly, we establish that EDC4 impairs MARF1 activity by preventing its LOTUS domains from binding target mRNAs.			seCLIP-seq，siRNAs，RT-qPCR，Immunofluorescent staining，RNA immunoprecipitation assay				EDC4
32511315	chrX	15492185	15494185	ACE2	The ACE2 gene is expressed in SARS-CoV-2 target cells, including Type II Pneumocytes (Ziegler, 2020), and is activated by interferons.	human	connective tissue	High+Lowthroughput	Activation of the SARS-CoV-2 receptor Ace2 by cytokines through pan JAK-STAT enhancers	否		The novel coronavirus	mammary alveolar cell	E_01_0569	ChIP-seq，RNA-seq	The ACE2 gene is expressed in SARS-CoV-2 target cells, including Type II Pneumocytes (Ziegler, 2020), and is activated by interferons.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The ACE2 gene is expressed in SARS-CoV-2 target cells, including Type II Pneumocytes (Ziegler, 2020), and is activated by interferons.		The ACE2 gene is expressed in SARS-CoV-2 target cells, including Type II Pneumocytes (Ziegler, 2020), and is activated by interferons.	Immunohistochemical staining	The ACE2 gene is expressed in SARS-CoV-2 target cells, including Type II Pneumocytes (Ziegler, 2020), and is activated by interferons.			ChIP-seq，RNA-seq				ACE2
32521278	chr3	179145107	179147107	PIK3CA	Even for PIK3CA-mutated cancer, BDNF-AS overexpression is a predictive marker of endocrine resistance of HRpositive BC and indicates the application of mTOR inhibitor for reversing the resistance.	human		High+Lowthroughput	Enhancer-Driven lncRNA BDNF-AS Induces Endocrine Resistance and Malignant Progression of Breast Cancer through the RNH1/TRIM21/mTOR Cascade	否		Breast Cancer	MCF-7 cell	E_01_0570	siRNA /shRNA，Quantitative RT-PCR，ChIP-sequence，Western blot，Chromatin immunoprecipitation，RNA immunoprecipitation，Immunoprecipitation，Luciferase reporter assay	Even for PIK3CA-mutated cancer, BDNF-AS overexpression is a predictive marker of endocrine resistance of HRpositive BC and indicates the application of mTOR inhibitor for reversing the resistance.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Even for PIK3CA-mutated cancer, BDNF-AS overexpression is a predictive marker of endocrine resistance of HRpositive BC and indicates the application of mTOR inhibitor for reversing the resistance.		Even for PIK3CA-mutated cancer, BDNF-AS overexpression is a predictive marker of endocrine resistance of HRpositive BC and indicates the application of mTOR inhibitor for reversing the resistance.	Immunohistochemical staining	Even for PIK3CA-mutated cancer, BDNF-AS overexpression is a predictive marker of endocrine resistance of HRpositive BC and indicates the application of mTOR inhibitor for reversing the resistance.			siRNA /shRNA，Quantitative RT-PCR，ChIP-sequence，Western blot，Chromatin immunoprecipitation，RNA immunoprecipitation，Immunoprecipitation，Luciferase reporter assay				PIK3CA
32521813	chr10	112147455	112149455	GPAM	The mRNA of PLIN2 was induced by both ATL and GER at the highest concentrations.	human		High+Lowthroughput	The Hepatotoxicity of Alantolactone and Germacrone: Their Influence on Cholesterol and Lipid Metabolism in Differentiated HepaRG Cells	否		Metabolic dysregulation	HepaRG Cell	E_01_0571	Western Blotting	The mRNA of PLIN2 was induced by both ATL and GER at the highest concentrations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The mRNA of PLIN2 was induced by both ATL and GER at the highest concentrations.		The mRNA of PLIN2 was induced by both ATL and GER at the highest concentrations.	Immunohistochemical staining	The mRNA of PLIN2 was induced by both ATL and GER at the highest concentrations.			Western Blotting				GPAM
32320655	chr5	51380554	51382554	ISL1	Using a PageRank-based algorithm, we predict super-enhancer regulator ISL1 as a driver of this plasticity and validate this prediction by using CRISPR/dCas9-KRAB inhibition (CRISPRi) and CRISPR/dCas9-VP64 activation (CRISPRa) tools.	human		High+Lowthroughput	Super-Enhancer Redistribution as a Mechanism of Broad Gene Dysregulation in Repeatedly Drug-Treated Cancer Cells	否		Cancer	cancer cell	E_01_0572	GRO-seq, RNA-seq，RNA-seq，ChIP-seq，Western blotting，qRT_x005f_x0002_PCR，Immunofluorescent imaging，flow cytometry	Using a PageRank-based algorithm, we predict super-enhancer regulator ISL1 as a driver of this plasticity and validate this prediction by using CRISPR/dCas9-KRAB inhibition (CRISPRi) and CRISPR/dCas9-VP64 activation (CRISPRa) tools.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Using a PageRank-based algorithm, we predict super-enhancer regulator ISL1 as a driver of this plasticity and validate this prediction by using CRISPR/dCas9-KRAB inhibition (CRISPRi) and CRISPR/dCas9-VP64 activation (CRISPRa) tools.	Immunohistochemical staining	Using a PageRank-based algorithm, we predict super-enhancer regulator ISL1 as a driver of this plasticity and validate this prediction by using CRISPR/dCas9-KRAB inhibition (CRISPRi) and CRISPR/dCas9-VP64 activation (CRISPRa) tools.	ISL1		GRO-seq, RNA-seq，RNA-seq，ChIP-seq，Western blotting，qRT_x005f_x0002_PCR，Immunofluorescent imaging，flow cytometry	Using a PageRank-based algorithm, we predict super-enhancer regulator ISL1 as a driver of this plasticity and validate this prediction by using CRISPR/dCas9-KRAB inhibition (CRISPRi) and CRISPR/dCas9-VP64 activation (CRISPRa) tools.			
32321755	chr19	54613960	54615960	LILRB1	This region possesses multiple YY1 sites, and complexes of the promoter/enhancer combination were isolated using anti-YY1 in chromatin immunoprecipitation loop. CRISPR-mediated deletion of the 3-kb region lowers LILRB1 expression in human NKL cells.	human		High+Lowthroughput	LILRB1 Intron 1 Has a Polymorphic Regulatory Region That Enhances Transcription in NK Cells and Recruits YY1	是	rs1061679	Autoimmune diseases	NK cell	E_01_0573	quantitative PCR，ChIP	This region possesses multiple YY1 sites, and complexes of the promoter/enhancer combination were isolated using anti-YY1 in chromatin immunoprecipitation loop. CRISPR-mediated deletion of the 3-kb region lowers LILRB1 expression in human NKL cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This region possesses multiple YY1 sites, and complexes of the promoter/enhancer combination were isolated using anti-YY1 in chromatin immunoprecipitation loop. CRISPR-mediated deletion of the 3-kb region lowers LILRB1 expression in human NKL cells.		This region possesses multiple YY1 sites, and complexes of the promoter/enhancer combination were isolated using anti-YY1 in chromatin immunoprecipitation loop. CRISPR-mediated deletion of the 3-kb region lowers LILRB1 expression in human NKL cells.	Immunohistochemical staining	This region possesses multiple YY1 sites, and complexes of the promoter/enhancer combination were isolated using anti-YY1 in chromatin immunoprecipitation loop. CRISPR-mediated deletion of the 3-kb region lowers LILRB1 expression in human NKL cells.			quantitative PCR，ChIP				LILRB1
32321757	chr17	39755055	39757055	IKZF3	Pharmacological targeting of IKZF3 with the drug lenalidomide showed that IKZF3 is required for anti-CD3/CD28 mAb mediated induction of IL-10 but is dispensable for ex vivo IL-10 expression.	human	lymphoid tissue	High+Lowthroughput	IKZF3/Aiolos Is Associated with but Not Sufficient for the Expression of IL-10 by CD4(+) T Cells	否		Inflammatory	CD4 + T cell	E_01_0574	Flow cytometry，RNA isolation，Luciferase assay，quantitative PCR	Pharmacological targeting of IKZF3 with the drug lenalidomide showed that IKZF3 is required for anti-CD3/CD28 mAb mediated induction of IL-10 but is dispensable for ex vivo IL-10 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Pharmacological targeting of IKZF3 with the drug lenalidomide showed that IKZF3 is required for anti-CD3/CD28 mAb mediated induction of IL-10 but is dispensable for ex vivo IL-10 expression.	Immunohistochemical staining	Pharmacological targeting of IKZF3 with the drug lenalidomide showed that IKZF3 is required for anti-CD3/CD28 mAb mediated induction of IL-10 but is dispensable for ex vivo IL-10 expression.	IKZF3		Flow cytometry，RNA isolation，Luciferase assay，quantitative PCR	Pharmacological targeting of IKZF3 with the drug lenalidomide showed that IKZF3 is required for anti-CD3/CD28 mAb mediated induction of IL-10 but is dispensable for ex vivo IL-10 expression.			
32323737	chr17	42310954	42312954	STAT3	SETD7 knockdown activated the Janus kinase 2/signal transducer and activator of transcription 3 (STAT3) signaling pathway and enhanced lung cancer cell migration, whereas the STAT3-specific inhibitor Stattic abrogated the effect of SETD7 on cell migration. Taken together, these data indicated that SETD7 acts as a tumor suppressor, and the reduced expression of SETD7 may contribute to lung cancer progression.	human		High+Lowthroughput	Downregulation of SETD7 promotes migration and invasion of lung cancer cells via JAK2/STAT3 pathway	否		Lung cancer	Lung cancer cell	E_01_0575	siRNA，RT‑qPCR，Western blot	SETD7 knockdown activated the Janus kinase 2/signal transducer and activator of transcription 3 (STAT3) signaling pathway and enhanced lung cancer cell migration, whereas the STAT3-specific inhibitor Stattic abrogated the effect of SETD7 on cell migration. Taken together, these data indicated that SETD7 acts as a tumor suppressor, and the reduced expression of SETD7 may contribute to lung cancer progression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			SETD7 knockdown activated the Janus kinase 2/signal transducer and activator of transcription 3 (STAT3) signaling pathway and enhanced lung cancer cell migration, whereas the STAT3-specific inhibitor Stattic abrogated the effect of SETD7 on cell migration. Taken together, these data indicated that SETD7 acts as a tumor suppressor, and the reduced expression of SETD7 may contribute to lung cancer progression.	Immunohistochemical staining	SETD7 knockdown activated the Janus kinase 2/signal transducer and activator of transcription 3 (STAT3) signaling pathway and enhanced lung cancer cell migration, whereas the STAT3-specific inhibitor Stattic abrogated the effect of SETD7 on cell migration. Taken together, these data indicated that SETD7 acts as a tumor suppressor, and the reduced expression of SETD7 may contribute to lung cancer progression.	STAT3		siRNA，RT‑qPCR，Western blot	SETD7 knockdown activated the Janus kinase 2/signal transducer and activator of transcription 3 (STAT3) signaling pathway and enhanced lung cancer cell migration, whereas the STAT3-specific inhibitor Stattic abrogated the effect of SETD7 on cell migration. Taken together, these data indicated that SETD7 acts as a tumor suppressor, and the reduced expression of SETD7 may contribute to lung cancer progression.			
32326648	chr3	12285010	12287010	PPARG	While DPSCs differentiated readily along osteogenic and chondrogenic pathways, after 21 days in two different types of adipogenic induction media, DPSCs cultures did not contain lipid vacuoles and had low expression levels of the adipogenic genes proliferator-activated receptor gamma (PPARG), lipoprotein lipase (LPL) and CCAAT/enhancer-binding protein alpha (CEBPA).	human		High+Lowthroughput	The Expression Profile of Dental Pulp-Derived Stromal Cells Supports Their Limited Capacity to Differentiate into Adipogenic Cells	否		Adipogenesis		E_01_0576	Immunophenotypic Characterisation，RT-PCR，qRT-PCR，RNA Seq	While DPSCs differentiated readily along osteogenic and chondrogenic pathways, after 21 days in two different types of adipogenic induction media, DPSCs cultures did not contain lipid vacuoles and had low expression levels of the adipogenic genes proliferator-activated receptor gamma (PPARG), lipoprotein lipase (LPL) and CCAAT/enhancer-binding protein alpha (CEBPA).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			While DPSCs differentiated readily along osteogenic and chondrogenic pathways, after 21 days in two different types of adipogenic induction media, DPSCs cultures did not contain lipid vacuoles and had low expression levels of the adipogenic genes proliferator-activated receptor gamma (PPARG), lipoprotein lipase (LPL) and CCAAT/enhancer-binding protein alpha (CEBPA).	Immunohistochemical staining	While DPSCs differentiated readily along osteogenic and chondrogenic pathways, after 21 days in two different types of adipogenic induction media, DPSCs cultures did not contain lipid vacuoles and had low expression levels of the adipogenic genes proliferator-activated receptor gamma (PPARG), lipoprotein lipase (LPL) and CCAAT/enhancer-binding protein alpha (CEBPA).	PPARG		Immunophenotypic Characterisation，RT-PCR，qRT-PCR，RNA Seq	While DPSCs differentiated readily along osteogenic and chondrogenic pathways, after 21 days in two different types of adipogenic induction media, DPSCs cultures did not contain lipid vacuoles and had low expression levels of the adipogenic genes proliferator-activated receptor gamma (PPARG), lipoprotein lipase (LPL) and CCAAT/enhancer-binding protein alpha (CEBPA).			
32328192	chr19	15825511	15827511	UCA1	Moreover, overexpression of UCA1 promotes GC cell proliferation and inhibits cisplatin-induced apoptosis. Knockdown of UCA1 showed the opposite results. Besides, UCA1 exerted its function through interacting with EZH2 and regulates EZH2 expression, knockdown of EZH2 decreased cisplatin resistance of GC cells.	human		High+Lowthroughput	LncRNA UCA1 promotes cisplatin resistance in gastric cancer via recruiting EZH2 and activating PI3K/AKT pathway	否		Gastric cancer	GC cell	E_01_0577	qRT-PCR，CCK-8 Assay，Western blot，RNA immunoprecipitation，	Moreover, overexpression of UCA1 promotes GC cell proliferation and inhibits cisplatin-induced apoptosis. Knockdown of UCA1 showed the opposite results. Besides, UCA1 exerted its function through interacting with EZH2 and regulates EZH2 expression, knockdown of EZH2 decreased cisplatin resistance of GC cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, overexpression of UCA1 promotes GC cell proliferation and inhibits cisplatin-induced apoptosis. Knockdown of UCA1 showed the opposite results. Besides, UCA1 exerted its function through interacting with EZH2 and regulates EZH2 expression, knockdown of EZH2 decreased cisplatin resistance of GC cells.		Moreover, overexpression of UCA1 promotes GC cell proliferation and inhibits cisplatin-induced apoptosis. Knockdown of UCA1 showed the opposite results. Besides, UCA1 exerted its function through interacting with EZH2 and regulates EZH2 expression, knockdown of EZH2 decreased cisplatin resistance of GC cells.	Immunohistochemical staining	Moreover, overexpression of UCA1 promotes GC cell proliferation and inhibits cisplatin-induced apoptosis. Knockdown of UCA1 showed the opposite results. Besides, UCA1 exerted its function through interacting with EZH2 and regulates EZH2 expression, knockdown of EZH2 decreased cisplatin resistance of GC cells.			qRT-PCR，CCK-8 Assay，Western blot，RNA immunoprecipitation，				UCA1
32332020	chr20	44352418	44354418	HNF4A	Functionally, HNF4A promoted cancer proliferation and survival by transcriptional activation of many downstream targets, including HNF1A and factors of Interleukin signaling, in a lineage-specific manner.	human		High+Lowthroughput	Lineage-Specific Epigenomic and Genomic Activation of Oncogene HNF4A Promotes Gastrointestinal Adenocarcinomas	否		Gastrointestinal adenocarcinomas	Eso26 cell	E_01_0578	ELMER analyses，ChIP，Immunohistochemistry，4C-Seq	Functionally, HNF4A promoted cancer proliferation and survival by transcriptional activation of many downstream targets, including HNF1A and factors of Interleukin signaling, in a lineage-specific manner.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Functionally, HNF4A promoted cancer proliferation and survival by transcriptional activation of many downstream targets, including HNF1A and factors of Interleukin signaling, in a lineage-specific manner.	Immunohistochemical staining	Functionally, HNF4A promoted cancer proliferation and survival by transcriptional activation of many downstream targets, including HNF1A and factors of Interleukin signaling, in a lineage-specific manner.	HNF1A		ELMER analyses，ChIP，Immunohistochemistry，4C-Seq	Functionally, HNF4A promoted cancer proliferation and survival by transcriptional activation of many downstream targets, including HNF1A and factors of Interleukin signaling, in a lineage-specific manner.			
32333502	chr14	37586766	37588766	FOXA1	Enhancer activation was blocked at the chromatin level as evaluated by H3K27 acetylation (H3K27ac), H3K4 monomethylation (H3K4me1), and FOXA1, MED1 and BRD4 binding.	human		High+Lowthroughput	Darolutamide antagonizes androgen signaling by blocking enhancer and super-enhancer activation	否		Prostate cancer	VCaP cell	E_01_0579	RNA isolation，RNA-seq， ChIP seq，ChIP-seq，	Enhancer activation was blocked at the chromatin level as evaluated by H3K27 acetylation (H3K27ac), H3K4 monomethylation (H3K4me1), and FOXA1, MED1 and BRD4 binding.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer activation was blocked at the chromatin level as evaluated by H3K27 acetylation (H3K27ac), H3K4 monomethylation (H3K4me1), and FOXA1, MED1 and BRD4 binding.	Immunohistochemical staining	Enhancer activation was blocked at the chromatin level as evaluated by H3K27 acetylation (H3K27ac), H3K4 monomethylation (H3K4me1), and FOXA1, MED1 and BRD4 binding.	FOXA1		RNA isolation，RNA-seq， ChIP seq，ChIP-seq，	Enhancer activation was blocked at the chromatin level as evaluated by H3K27 acetylation (H3K27ac), H3K4 monomethylation (H3K4me1), and FOXA1, MED1 and BRD4 binding.			
32340270	chr1	161763935	161765935	ATF6	IR significantly increased reactive  oxygen species (ROS) production and the percentage of apoptotic cells without the up-regulation of Nrf2, of the related antioxidant response element (ARE) gene expression or of the pro-survival UPR activating transcription factor 6 (ATF6) gene, whereas it significantly increased the pro-apoptotic CCAAT-enhancer-binding protein homologous protein (CHOP).	human		High+Lowthroughput	Ezetimibe Prevents Ischemia/Reperfusion-Induced Oxidative Stress and Up-Regulates Nrf2/ARE and UPR Signaling Pathways	否		Ischemia	THP-1 cells	E_01_0580	Quantitative Real-Time PCR，Western Blot	IR significantly increased reactive  oxygen species (ROS) production and the percentage of apoptotic cells without the up-regulation of Nrf2, of the related antioxidant response element (ARE) gene expression or of the pro-survival UPR activating transcription factor 6 (ATF6) gene, whereas it significantly increased the pro-apoptotic CCAAT-enhancer-binding protein homologous protein (CHOP).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			IR significantly increased reactive  oxygen species (ROS) production and the percentage of apoptotic cells without the up-regulation of Nrf2, of the related antioxidant response element (ARE) gene expression or of the pro-survival UPR activating transcription factor 6 (ATF6) gene, whereas it significantly increased the pro-apoptotic CCAAT-enhancer-binding protein homologous protein (CHOP).	Immunohistochemical staining	IR significantly increased reactive  oxygen species (ROS) production and the percentage of apoptotic cells without the up-regulation of Nrf2, of the related antioxidant response element (ARE) gene expression or of the pro-survival UPR activating transcription factor 6 (ATF6) gene, whereas it significantly increased the pro-apoptotic CCAAT-enhancer-binding protein homologous protein (CHOP).	ATF6		Quantitative Real-Time PCR，Western Blot	IR significantly increased reactive  oxygen species (ROS) production and the percentage of apoptotic cells without the up-regulation of Nrf2, of the related antioxidant response element (ARE) gene expression or of the pro-survival UPR activating transcription factor 6 (ATF6) gene, whereas it significantly increased the pro-apoptotic CCAAT-enhancer-binding protein homologous protein (CHOP).			
32343676	chr14	37586949	37588949	FOXA1	These transcriptional hubs operate within the framework set by structural proteins CTCF and cohesins and are regulated by the cooperative action of master transcription factors, such as the androgen receptor (AR) and FOXA1.	human		High+Lowthroughput	The landscape of RNA polymerase II-associated chromatin interactions in prostate cancer	是	rs684232	Prostate cancer	prostate cell	E_01_0581	ChIA-PET，	These transcriptional hubs operate within the framework set by structural proteins CTCF and cohesins and are regulated by the cooperative action of master transcription factors, such as the androgen receptor (AR) and FOXA1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These transcriptional hubs operate within the framework set by structural proteins CTCF and cohesins and are regulated by the cooperative action of master transcription factors, such as the androgen receptor (AR) and FOXA1.	Immunohistochemical staining	These transcriptional hubs operate within the framework set by structural proteins CTCF and cohesins and are regulated by the cooperative action of master transcription factors, such as the androgen receptor (AR) and FOXA1.	FOXA1		ChIA-PET，	These transcriptional hubs operate within the framework set by structural proteins CTCF and cohesins and are regulated by the cooperative action of master transcription factors, such as the androgen receptor (AR) and FOXA1.			
32343676	chr20	22578355	22580355	FOXA2	These transcriptional hubs operate within the framework set by structural proteins CTCF and cohesins and are regulated by the cooperative action of master transcription factors, such as the androgen receptor (AR) and FOXA2.	human		High+Lowthroughput	The landscape of RNA polymerase II-associated chromatin interactions in prostate cancer	是	rs684232	Prostate cancer	PCa cell	E_01_0581	ChIA-PET，	These transcriptional hubs operate within the framework set by structural proteins CTCF and cohesins and are regulated by the cooperative action of master transcription factors, such as the androgen receptor (AR) and FOXA2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These transcriptional hubs operate within the framework set by structural proteins CTCF and cohesins and are regulated by the cooperative action of master transcription factors, such as the androgen receptor (AR) and FOXA2.	Immunohistochemical staining	These transcriptional hubs operate within the framework set by structural proteins CTCF and cohesins and are regulated by the cooperative action of master transcription factors, such as the androgen receptor (AR) and FOXA2.	FOXA2		ChIA-PET，	These transcriptional hubs operate within the framework set by structural proteins CTCF and cohesins and are regulated by the cooperative action of master transcription factors, such as the androgen receptor (AR) and FOXA2.			
32346422	chr19	15825536	15827536	UCA1	Finally, overexpression of MMP9 reversed the decreased proliferative and migratory abilities in ox-LDL-treated VSMCs overexpressing UCA1.	human	Musculature	High+Lowthroughput	Downregulated lncRNA UCA1 accelerates proliferation and migration of vascular smooth muscle cells by epigenetic regulation of MMP9	否			blood vessel smooth muscle cell	E_01_0582	qRT-PCR，Western blot，Immunofluorescence，ChIP，RNA immunoprecipitation，Western blotting	Finally, overexpression of MMP9 reversed the decreased proliferative and migratory abilities in ox-LDL-treated VSMCs overexpressing UCA1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Finally, overexpression of MMP9 reversed the decreased proliferative and migratory abilities in ox-LDL-treated VSMCs overexpressing UCA1.		Finally, overexpression of MMP9 reversed the decreased proliferative and migratory abilities in ox-LDL-treated VSMCs overexpressing UCA1.	Immunohistochemical staining	Finally, overexpression of MMP9 reversed the decreased proliferative and migratory abilities in ox-LDL-treated VSMCs overexpressing UCA1.			qRT-PCR，Western blot，Immunofluorescence，ChIP，RNA immunoprecipitation，Western blotting				UCA1
32348926	chr17	72118143	72120143	SOX9	Endocrine differentiation of hPPs was affected, as indicated by neurogenin-3 (NGN3) downregulation, owing to abnormal increases in SOX9 and hairy and enhancer of split-1(HES1) expression.	human		High+Lowthroughput	Effects of per- and poly-fluorinated alkyl substances on pancreatic and endocrine differentiation of human pluripotent stem cells	否			pancreatic A cell	E_01_0583	qRT-PCR，Western blot， Immunofluorescence	Endocrine differentiation of hPPs was affected, as indicated by neurogenin-3 (NGN3) downregulation, owing to abnormal increases in SOX9 and hairy and enhancer of split-1(HES1) expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Endocrine differentiation of hPPs was affected, as indicated by neurogenin-3 (NGN3) downregulation, owing to abnormal increases in SOX9 and hairy and enhancer of split-1(HES1) expression.	Immunohistochemical staining	Endocrine differentiation of hPPs was affected, as indicated by neurogenin-3 (NGN3) downregulation, owing to abnormal increases in SOX9 and hairy and enhancer of split-1(HES1) expression.	SOX9		qRT-PCR，Western blot， Immunofluorescence	Endocrine differentiation of hPPs was affected, as indicated by neurogenin-3 (NGN3) downregulation, owing to abnormal increases in SOX9 and hairy and enhancer of split-1(HES1) expression.			
32362325	chrX	49247655	49249655	FOXP3	Thus, naive Treg cell-specific CpG hypomethylation had a key role in controlling Treg cell-specific gene transcription and epigenetic modification.	human		High+Lowthroughput	Regulatory T Cell-Specific Epigenomic Region Variants Are a Key Determinant of Susceptibility to Common Autoimmune Diseases	是	rs231735，rs1024161，rs3087243	Autoimmune Diseases	T cell	E_01_0584	PBAT-seq, ChIP-seq, ATAC-seq,RNA-seq	Thus, naive Treg cell-specific CpG hypomethylation had a key role in controlling Treg cell-specific gene transcription and epigenetic modification.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, naive Treg cell-specific CpG hypomethylation had a key role in controlling Treg cell-specific gene transcription and epigenetic modification.	Immunohistochemical staining	Thus, naive Treg cell-specific CpG hypomethylation had a key role in controlling Treg cell-specific gene transcription and epigenetic modification.	FOXP3		PBAT-seq, ChIP-seq, ATAC-seq,RNA-seq	Thus, naive Treg cell-specific CpG hypomethylation had a key role in controlling Treg cell-specific gene transcription and epigenetic modification.			
32366581	chr1	167050287	167052287	GPA33	GPA33 identifies Treg cells in human blood that lack the ability to produce effector cytokines (IL-2, IFN-g, IL-17), regardless of differentiation stage.	human	lymphoid tissue	High+Lowthroughput	GPA33: A Marker to Identify Stable Human Regulatory T Cells	否			T cell	E_01_0585	， mRNA seq	GPA33 identifies Treg cells in human blood that lack the ability to produce effector cytokines (IL-2, IFN-g, IL-17), regardless of differentiation stage.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	GPA33 identifies Treg cells in human blood that lack the ability to produce effector cytokines (IL-2, IFN-g, IL-17), regardless of differentiation stage.		GPA33 identifies Treg cells in human blood that lack the ability to produce effector cytokines (IL-2, IFN-g, IL-17), regardless of differentiation stage.	Immunohistochemical staining	GPA33 identifies Treg cells in human blood that lack the ability to produce effector cytokines (IL-2, IFN-g, IL-17), regardless of differentiation stage.			， mRNA seq				GPA33
32368395	chr7	148804495	148806495	EZH2	We further demonstrated that CDK2 inhibitor is a more promising agent than EZH2 inhibitor in repressing TNBC and HGSOC due to a feedback increase in CDK2 activity by EZH2 inhibitor.	human		High+Lowthroughput	Inhibition of CDK2 reduces EZH2 phosphorylation and reactivates ERα expression in high-grade serous ovarian carcinoma	否		"High-grade 
serous ovarian carcinoma"	Triple-negative breast cancer cell	E_01_0586	，Immunoblotting analysis	We further demonstrated that CDK2 inhibitor is a more promising agent than EZH2 inhibitor in repressing TNBC and HGSOC due to a feedback increase in CDK2 activity by EZH2 inhibitor.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We further demonstrated that CDK2 inhibitor is a more promising agent than EZH2 inhibitor in repressing TNBC and HGSOC due to a feedback increase in CDK2 activity by EZH2 inhibitor.	Immunohistochemical staining	We further demonstrated that CDK2 inhibitor is a more promising agent than EZH2 inhibitor in repressing TNBC and HGSOC due to a feedback increase in CDK2 activity by EZH2 inhibitor.	EZH2		，Immunoblotting analysis	We further demonstrated that CDK2 inhibitor is a more promising agent than EZH2 inhibitor in repressing TNBC and HGSOC due to a feedback increase in CDK2 activity by EZH2 inhibitor.			
32376288	chr17	48721672	48723672	HOXB13	Consistent with this hypothesis, overexpression of HOXB13 in mesenchymal progenitor cells inhibited adipogenic, myogenic, and osteogenic differentiation.	human		High+Lowthroughput	HOXB13 controls cell state through super-enhancers	否		Malignant rhabdoid tumor	Rhabdomyoid tumor cell	E_01_0587	ChIP assay，qRT-PCR	Consistent with this hypothesis, overexpression of HOXB13 in mesenchymal progenitor cells inhibited adipogenic, myogenic, and osteogenic differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Consistent with this hypothesis, overexpression of HOXB13 in mesenchymal progenitor cells inhibited adipogenic, myogenic, and osteogenic differentiation.	Immunohistochemical staining	Consistent with this hypothesis, overexpression of HOXB13 in mesenchymal progenitor cells inhibited adipogenic, myogenic, and osteogenic differentiation.	HOXB13		ChIP assay，qRT-PCR	Consistent with this hypothesis, overexpression of HOXB13 in mesenchymal progenitor cells inhibited adipogenic, myogenic, and osteogenic differentiation.			
32376693	chr12	57456839	57458839	GLI1	Here, we provide evidence that GLI1 controls chromatin accessibility at distal regulatory regions by modulating the recruitment of SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily A, member 2 (SMARCA2) to these elements.	human		High+Lowthroughput	The transcription factor GLI1 cooperates with the chromatin remodeler SMARCA2 to regulate chromatin accessibility at distal DNA regulatory elements	否		Multiple malignancies	General Cell	E_01_0588	RNA-seq，ATAC-seq，RNA isolation，Immunoprecipations	Here, we provide evidence that GLI1 controls chromatin accessibility at distal regulatory regions by modulating the recruitment of SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily A, member 2 (SMARCA2) to these elements.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we provide evidence that GLI1 controls chromatin accessibility at distal regulatory regions by modulating the recruitment of SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily A, member 2 (SMARCA2) to these elements.	Immunohistochemical staining	Here, we provide evidence that GLI1 controls chromatin accessibility at distal regulatory regions by modulating the recruitment of SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily A, member 2 (SMARCA2) to these elements.	GLI1		RNA-seq，ATAC-seq，RNA isolation，Immunoprecipations	Here, we provide evidence that GLI1 controls chromatin accessibility at distal regulatory regions by modulating the recruitment of SWI/SNF-related, matrix-associated, actin-dependent regulator of chromatin, subfamily A, member 2 (SMARCA2) to these elements.			
32378752	chr1	8001410	8003410	ERRFI1	By binding to a component of the epigenetic modification complex enhancer of zeste homolog 2 (EZH2), ANRIL could maintain lysine residue 27 of histone 3 (H3K27me3) levels in the promoter of ERBB receptor feedback inhibitor 1 (ERRFI1), which is a tumor suppressor gene in CCA.	human		High+Lowthroughput	Long noncoding RNA ANRIL promotes the malignant progression of cholangiocarcinoma by epigenetically repressing ERRFI1 expression	否		Cholangiocarcinoma	CCA cell	E_01_0589	qRT-PCR，Flow cytometric，Chromatin immunoprecipitation assays，Western blot	By binding to a component of the epigenetic modification complex enhancer of zeste homolog 2 (EZH2), ANRIL could maintain lysine residue 27 of histone 3 (H3K27me3) levels in the promoter of ERBB receptor feedback inhibitor 1 (ERRFI1), which is a tumor suppressor gene in CCA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	By binding to a component of the epigenetic modification complex enhancer of zeste homolog 2 (EZH2), ANRIL could maintain lysine residue 27 of histone 3 (H3K27me3) levels in the promoter of ERBB receptor feedback inhibitor 1 (ERRFI1), which is a tumor suppressor gene in CCA.		By binding to a component of the epigenetic modification complex enhancer of zeste homolog 2 (EZH2), ANRIL could maintain lysine residue 27 of histone 3 (H3K27me3) levels in the promoter of ERBB receptor feedback inhibitor 1 (ERRFI1), which is a tumor suppressor gene in CCA.	Immunohistochemical staining	By binding to a component of the epigenetic modification complex enhancer of zeste homolog 2 (EZH2), ANRIL could maintain lysine residue 27 of histone 3 (H3K27me3) levels in the promoter of ERBB receptor feedback inhibitor 1 (ERRFI1), which is a tumor suppressor gene in CCA.			qRT-PCR，Flow cytometric，Chromatin immunoprecipitation assays，Western blot				ERRFI1
32384149	chr13	28000167	28002167	FLT3	Mutations in the FMS-like tyrosine kinase 3 (FLT3) gene in 13q12.2 are among the most common driver events in acute leukemia, leading to increased cell proliferation and survival through activation of the PI3K/AKT, RAS/MAPK and STAT5 signaling pathways.	human		High+Lowthroughput	13q12.2 deletions in acute lymphoblastic leukemia lead to upregulation of FLT3 through enhancer hijacking	有	无	Acute lymphoblastic leukemia	HEK293T	E_01_0590	RNA-seq	Mutations in the FMS-like tyrosine kinase 3 (FLT3) gene in 13q12.2 are among the most common driver events in acute leukemia, leading to increased cell proliferation and survival through activation of the PI3K/AKT, RAS/MAPK and STAT5 signaling pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mutations in the FMS-like tyrosine kinase 3 (FLT3) gene in 13q12.2 are among the most common driver events in acute leukemia, leading to increased cell proliferation and survival through activation of the PI3K/AKT, RAS/MAPK and STAT5 signaling pathways.	Immunohistochemical staining	Mutations in the FMS-like tyrosine kinase 3 (FLT3) gene in 13q12.2 are among the most common driver events in acute leukemia, leading to increased cell proliferation and survival through activation of the PI3K/AKT, RAS/MAPK and STAT5 signaling pathways.	FLT3		RNA-seq	Mutations in the FMS-like tyrosine kinase 3 (FLT3) gene in 13q12.2 are among the most common driver events in acute leukemia, leading to increased cell proliferation and survival through activation of the PI3K/AKT, RAS/MAPK and STAT5 signaling pathways.			
32409685	chr2	15937714	15939714	MYCN	We identified novel OCT4-binding sites in the MYC promoter/enhancer region that regulated MYC expression via phosphorylation by MAPKAPK2 (MK2). OCT4 phosphorylation at the S111 residue by MK2 was upstream of MYC transcriptional activation.	human	Nervous tissue	High+Lowthroughput	MYC transcription activation mediated by OCT4 as a mechanism of resistance to 13-cisRA-mediated differentiation in neuroblastoma	否		Neuroblastoma	neuroblastoma cell	E_01_0591	Immunoblotting，immunoprecipitation，RT-PCR，ChIP	We identified novel OCT4-binding sites in the MYC promoter/enhancer region that regulated MYC expression via phosphorylation by MAPKAPK2 (MK2). OCT4 phosphorylation at the S111 residue by MK2 was upstream of MYC transcriptional activation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We identified novel OCT4-binding sites in the MYC promoter/enhancer region that regulated MYC expression via phosphorylation by MAPKAPK2 (MK2). OCT4 phosphorylation at the S111 residue by MK2 was upstream of MYC transcriptional activation.	Immunohistochemical staining	We identified novel OCT4-binding sites in the MYC promoter/enhancer region that regulated MYC expression via phosphorylation by MAPKAPK2 (MK2). OCT4 phosphorylation at the S111 residue by MK2 was upstream of MYC transcriptional activation.	MYCN		Immunoblotting，immunoprecipitation，RT-PCR，ChIP	We identified novel OCT4-binding sites in the MYC promoter/enhancer region that regulated MYC expression via phosphorylation by MAPKAPK2 (MK2). OCT4 phosphorylation at the S111 residue by MK2 was upstream of MYC transcriptional activation.			
32427048	chr19	18371889	18373889	GDF15	Noncoding variation within a metformin-activated enhancer may increase GDF15 expression and help to predict GDF15 levels.	human		High+Lowthroughput	Noncoding SNPs associated with increased GDF15 levels located in a metformin-activated enhancer region upstream of GDF15	是	rs888663,rs62122429，rs4808791	Type 2 diabetes	HepG2 cell	E_01_0592	ChIP-seq	Noncoding variation within a metformin-activated enhancer may increase GDF15 expression and help to predict GDF15 levels.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Noncoding variation within a metformin-activated enhancer may increase GDF15 expression and help to predict GDF15 levels.	Immunohistochemical staining	Noncoding variation within a metformin-activated enhancer may increase GDF15 expression and help to predict GDF15 levels.	GDF15		ChIP-seq	Noncoding variation within a metformin-activated enhancer may increase GDF15 expression and help to predict GDF15 levels.			
32432037	chr9	81580658	81582658	TLE1	Our findings showed that TLE1 expression was common in PDAC cell lines.	human		High+Lowthroughput	Transducin-Like Enhancer of Split-1 Inhibits Malignant Behaviors in vitro and Predicts a Better Prognosis in Pancreatic Ductal Adenocarcinoma	否		Pancreatic Ductal Adenocarcinoma	 PDAC	E_01_0593	Western Blot，RNA Isolation，Real-Time Polymerase Chain Reaction，RNA Seq，Immunohistochemistry	Our findings showed that TLE1 expression was common in PDAC cell lines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our findings showed that TLE1 expression was common in PDAC cell lines.	Immunohistochemical staining	Our findings showed that TLE1 expression was common in PDAC cell lines.	TLE1		Western Blot，RNA Isolation，Real-Time Polymerase Chain Reaction，RNA Seq，Immunohistochemistry	Our findings showed that TLE1 expression was common in PDAC cell lines.			
32432675	chr1	8002032	8004032	ERRFI1	Taken together, our findings suggest that the progressive loss of the GC-dependent regulation and anti-tumorigenic function of ERRFI1 influences BCa progression and may contribute to the unfavorable effects of GC therapy in TNBC.	human	epithelial cells	High+Lowthroughput	Differential Glucocorticoid-Dependent Regulation and Function of the ERRFI1 Gene in Triple-Negative Breast Cancer	否		Triple-Negative Breast Cancer	MCF10A cell	E_01_0594	qPCR，ChIP-seq	Taken together, our findings suggest that the progressive loss of the GC-dependent regulation and anti-tumorigenic function of ERRFI1 influences BCa progression and may contribute to the unfavorable effects of GC therapy in TNBC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, our findings suggest that the progressive loss of the GC-dependent regulation and anti-tumorigenic function of ERRFI1 influences BCa progression and may contribute to the unfavorable effects of GC therapy in TNBC.		Taken together, our findings suggest that the progressive loss of the GC-dependent regulation and anti-tumorigenic function of ERRFI1 influences BCa progression and may contribute to the unfavorable effects of GC therapy in TNBC.	Immunohistochemical staining	Taken together, our findings suggest that the progressive loss of the GC-dependent regulation and anti-tumorigenic function of ERRFI1 influences BCa progression and may contribute to the unfavorable effects of GC therapy in TNBC.			qPCR，ChIP-seq				ERRFI1
32442411	chr4	176680985	176682985	VEGFC	Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.	human	Epithelial tissues	High+Lowthroughput	Systems Genetics in Human Endothelial Cells Identifies Non-coding Variants Modifying Enhancers, Expression, and Complex Disease Traits	是	rs12028528，rs7975658，rs6825977，rs17114036		aortic endothelial cell	E_01_0595	High-throughput Seq，eQTL Analysis，ChIP-seq，ATAC-seq，	Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.	Immunohistochemical staining	Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.	VEGFC		High-throughput Seq，eQTL Analysis，ChIP-seq，ATAC-seq，	Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.			
32442411	chr12	95073751	95075751	FGD6	Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.	human	Epithelial tissues	High+Lowthroughput	Systems Genetics in Human Endothelial Cells Identifies Non-coding Variants Modifying Enhancers, Expression, and Complex Disease Traits	是	rs12028528，rs7975658，rs6825977，rs17114036		aortic endothelial cell	E_01_0595	High-throughput Seq，eQTL Analysis，ChIP-seq，ATAC-seq，	Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.		Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.	Immunohistochemical staining	Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.			High-throughput Seq，eQTL Analysis，ChIP-seq，ATAC-seq，				FGD6
32442411	chr1	245151859	245153859	KIF26B	Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.	human	Epithelial tissues	High+Lowthroughput	Systems Genetics in Human Endothelial Cells Identifies Non-coding Variants Modifying Enhancers, Expression, and Complex Disease Traits	是	rs12028528，rs7975658，rs6825977，rs17114036		aortic endothelial cell	E_01_0595	High-throughput Seq，eQTL Analysis，ChIP-seq，ATAC-seq，	Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.		Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.	Immunohistochemical staining	Using CRISPR interference (CRISPRi), allele-specific reporter assays, and chromatin conformation capture, we validated candidate enhancer variants located up to 750 kb from their target genes, VEGFC, FGD6, and KIF26B.			High-throughput Seq，eQTL Analysis，ChIP-seq，ATAC-seq，				KIF26B
32453339	chr7	148804304	148806304	EZH2	We found that the enhancer of zeste homolog 2 (EZH2), which catalyzes the methylation at lysine 27 of histone H3, is a target of USP7 and is stabilized by USP7-mediated deubiquitination.	human	connective tissue	High+Lowthroughput	USP7 deubiquitinates and stabilizes EZH2 in prostate cancer cells	否		Prostate cancer	HEK293T	E_01_0596	Real-time RT-PCR，	We found that the enhancer of zeste homolog 2 (EZH2), which catalyzes the methylation at lysine 27 of histone H3, is a target of USP7 and is stabilized by USP7-mediated deubiquitination.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found that the enhancer of zeste homolog 2 (EZH2), which catalyzes the methylation at lysine 27 of histone H3, is a target of USP7 and is stabilized by USP7-mediated deubiquitination.	Immunohistochemical staining	We found that the enhancer of zeste homolog 2 (EZH2), which catalyzes the methylation at lysine 27 of histone H3, is a target of USP7 and is stabilized by USP7-mediated deubiquitination.	EZH2		Real-time RT-PCR，	We found that the enhancer of zeste homolog 2 (EZH2), which catalyzes the methylation at lysine 27 of histone H3, is a target of USP7 and is stabilized by USP7-mediated deubiquitination.			
32457600	chr22	42123282	42125282	CYP2D6	Results: Phasing predicted that the enhancer SNP can occur on numerous CYP2D6 haplotypes including CYP2D6*1, *2, *5, and *41 and suggested that linkage is incomplete, i.e., a portion of these alleles do not have the enhancer SNP.	human	connective tissue	High+Lowthroughput	"Long-Distance Phasing of a Tentative ""Enhancer"" Single-Nucleotide Polymorphism With CYP2D6 Star Allele Definitions"	是	rs5758550，rs16947		Liver Tissue Cell	E_01_0597	PCR	Results: Phasing predicted that the enhancer SNP can occur on numerous CYP2D6 haplotypes including CYP2D6*1, *2, *5, and *41 and suggested that linkage is incomplete, i.e., a portion of these alleles do not have the enhancer SNP.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Results: Phasing predicted that the enhancer SNP can occur on numerous CYP2D6 haplotypes including CYP2D6*1, *2, *5, and *41 and suggested that linkage is incomplete, i.e., a portion of these alleles do not have the enhancer SNP.		Results: Phasing predicted that the enhancer SNP can occur on numerous CYP2D6 haplotypes including CYP2D6*1, *2, *5, and *41 and suggested that linkage is incomplete, i.e., a portion of these alleles do not have the enhancer SNP.	Immunohistochemical staining	Results: Phasing predicted that the enhancer SNP can occur on numerous CYP2D6 haplotypes including CYP2D6*1, *2, *5, and *41 and suggested that linkage is incomplete, i.e., a portion of these alleles do not have the enhancer SNP.			PCR				CYP2D6
32461377	chr10	8042505	8044505	GATA3	Chromatin immunoprecipitation (ChIP) and RNA binding protein immunoprecipitation (RIP) demonstrated that lncRNA LOC645166 could increase the expression of GATA binding protein 3 (GATA3) via binding with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), leading to the activation of STAT3 and promoting chemoresistance in breast cancer.	human		High+Lowthroughput	Long noncoding RNA lnc-LOC645166 promotes adriamycin resistance via NF-κB/GATA3 axis in breast cancer	否		Breast cancer	MDA-MB-231 cell	E_01_0598	RT-qPCR,Flow cytometric analysis,Western blot,Chromatin immunoprecipitation assays	Chromatin immunoprecipitation (ChIP) and RNA binding protein immunoprecipitation (RIP) demonstrated that lncRNA LOC645166 could increase the expression of GATA binding protein 3 (GATA3) via binding with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), leading to the activation of STAT3 and promoting chemoresistance in breast cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Chromatin immunoprecipitation (ChIP) and RNA binding protein immunoprecipitation (RIP) demonstrated that lncRNA LOC645166 could increase the expression of GATA binding protein 3 (GATA3) via binding with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), leading to the activation of STAT3 and promoting chemoresistance in breast cancer.	Immunohistochemical staining	Chromatin immunoprecipitation (ChIP) and RNA binding protein immunoprecipitation (RIP) demonstrated that lncRNA LOC645166 could increase the expression of GATA binding protein 3 (GATA3) via binding with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), leading to the activation of STAT3 and promoting chemoresistance in breast cancer.	GATA3		RT-qPCR,Flow cytometric analysis,Western blot,Chromatin immunoprecipitation assays	Chromatin immunoprecipitation (ChIP) and RNA binding protein immunoprecipitation (RIP) demonstrated that lncRNA LOC645166 could increase the expression of GATA binding protein 3 (GATA3) via binding with nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), leading to the activation of STAT3 and promoting chemoresistance in breast cancer.			
32464274	chr5	177083579	177085579	FGFR4	These changes were associated with a significant reduction in FGFR4 transcript levels in treated cells. These decreases in H3K4me1 in the FGFR4 super enhancer were also associated with a 240-fold increase in KDM5B (JARID1B) mRNA levels.	human	Musculature	High+Lowthroughput	Molecular mechanisms of Guadecitabine induced FGFR4 down regulation in alveolar rhabdomyosarcomas	否		Alveolar rhabdomyosarcomas	RH30 cell	E_01_0599	Real-Time RT-PCR quantification,ChIP-seq,Immunoblotting,Immunocytochemistry	These changes were associated with a significant reduction in FGFR4 transcript levels in treated cells. These decreases in H3K4me1 in the FGFR4 super enhancer were also associated with a 240-fold increase in KDM5B (JARID1B) mRNA levels.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These changes were associated with a significant reduction in FGFR4 transcript levels in treated cells. These decreases in H3K4me1 in the FGFR4 super enhancer were also associated with a 240-fold increase in KDM5B (JARID1B) mRNA levels.		These changes were associated with a significant reduction in FGFR4 transcript levels in treated cells. These decreases in H3K4me1 in the FGFR4 super enhancer were also associated with a 240-fold increase in KDM5B (JARID1B) mRNA levels.	Immunohistochemical staining	These changes were associated with a significant reduction in FGFR4 transcript levels in treated cells. These decreases in H3K4me1 in the FGFR4 super enhancer were also associated with a 240-fold increase in KDM5B (JARID1B) mRNA levels.			Real-Time RT-PCR quantification,ChIP-seq,Immunoblotting,Immunocytochemistry				FGFR4
32467994	chr1	173856174	173858174	GAS5	The results showed that HG treatment   induced ER stress in ARPE 19 human adult retinal pigment epithelial cells by upregulating the expression levels of phosphorylated (p) protein kinase R like ER kinase, p eukaryotic initiation factor 2α, activating transcription factor 4 and CCAAT/enhancer-binding protein homologous protein.	human	Epithelial tissues	High+Lowthroughput	LncRNA GAS5 suppresses ER stress?induced apoptosis and inflammation by regulating SERCA2b in HG?treated retinal epithelial cell	否		Inflammation	ARPE 19 cell	E_01_0600	RT‑qPCR，Western blot，Flow cytometry	The results showed that HG treatment   induced ER stress in ARPE 19 human adult retinal pigment epithelial cells by upregulating the expression levels of phosphorylated (p) protein kinase R like ER kinase, p eukaryotic initiation factor 2α, activating transcription factor 4 and CCAAT/enhancer-binding protein homologous protein.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The results showed that HG treatment   induced ER stress in ARPE 19 human adult retinal pigment epithelial cells by upregulating the expression levels of phosphorylated (p) protein kinase R like ER kinase, p eukaryotic initiation factor 2α, activating transcription factor 4 and CCAAT/enhancer-binding protein homologous protein.	Immunohistochemical staining	The results showed that HG treatment   induced ER stress in ARPE 19 human adult retinal pigment epithelial cells by upregulating the expression levels of phosphorylated (p) protein kinase R like ER kinase, p eukaryotic initiation factor 2α, activating transcription factor 4 and CCAAT/enhancer-binding protein homologous protein.	GAS5		RT‑qPCR，Western blot，Flow cytometry	The results showed that HG treatment   induced ER stress in ARPE 19 human adult retinal pigment epithelial cells by upregulating the expression levels of phosphorylated (p) protein kinase R like ER kinase, p eukaryotic initiation factor 2α, activating transcription factor 4 and CCAAT/enhancer-binding protein homologous protein.			
32471508	chr1	181086111	181088111	IER5	PAF1 reduces CC radiosensitivity by inhibiting IER5 transcription, at least in part by regulating its enhancers.	human	Epithelial tissues	High+Lowthroughput	Novel role of PAF1 in attenuating radiosensitivity in cervical cancer by inhibiting IER5 transcription	否		Cervical cancer	Siha cell	E_01_0601	siRNAs，Western blotting，qRT-PCR，Immunohistochemistry，Immunofluorescence analysis，Flow cytometry，ChIP-qPCR	PAF1 reduces CC radiosensitivity by inhibiting IER5 transcription, at least in part by regulating its enhancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			PAF1 reduces CC radiosensitivity by inhibiting IER5 transcription, at least in part by regulating its enhancers.	Immunohistochemical staining	PAF1 reduces CC radiosensitivity by inhibiting IER5 transcription, at least in part by regulating its enhancers.	IER5		siRNAs，Western blotting，qRT-PCR，Immunohistochemistry，Immunofluorescence analysis，Flow cytometry，ChIP-qPCR	PAF1 reduces CC radiosensitivity by inhibiting IER5 transcription, at least in part by regulating its enhancers.			
32478125	chr1	207877984	207879984	CD34	Notably, similar editing improvement was observed when excess gRNA over Cas9 protein was used, providing a DNAfree alternative suitable for therapeutic applications.	human		High+Lowthroughput	Increasing CRISPR Efficiency and Measuring Its Specificity in HSPCs Using a Clinically Relevant System	否			hematopoietic stem and progenitor cell	E_01_0602	GUIDE-Seq，rhAmpSeq	Notably, similar editing improvement was observed when excess gRNA over Cas9 protein was used, providing a DNAfree alternative suitable for therapeutic applications.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Notably, similar editing improvement was observed when excess gRNA over Cas9 protein was used, providing a DNAfree alternative suitable for therapeutic applications.		Notably, similar editing improvement was observed when excess gRNA over Cas9 protein was used, providing a DNAfree alternative suitable for therapeutic applications.	Immunohistochemical staining	Notably, similar editing improvement was observed when excess gRNA over Cas9 protein was used, providing a DNAfree alternative suitable for therapeutic applications.			GUIDE-Seq，rhAmpSeq				CD34
32488243	chr1	247413679	247415679	NLRP3	Specific involvement of NLRP3 inflammasome activation in IL-1beta and IL-18 release after hormone withdrawal was investigated via application of the NLRP3 inflammasome inhibitor MCC950 at the time of hormone withdrawal.	human	connective tissue	High+Lowthroughput	Endometrial inflammasome activation accompanies menstruation and may have implications for systemic inflammatory events of the menstrual cycle	否		Endometrial inflammasome activation accompanies	endometrial stromal cell	E_01_0603	Immunohistochemistry，Fluorescent immunohistochemistry，Western immunoblotting	Specific involvement of NLRP3 inflammasome activation in IL-1beta and IL-18 release after hormone withdrawal was investigated via application of the NLRP3 inflammasome inhibitor MCC950 at the time of hormone withdrawal.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Specific involvement of NLRP3 inflammasome activation in IL-1beta and IL-18 release after hormone withdrawal was investigated via application of the NLRP3 inflammasome inhibitor MCC950 at the time of hormone withdrawal.		Specific involvement of NLRP3 inflammasome activation in IL-1beta and IL-18 release after hormone withdrawal was investigated via application of the NLRP3 inflammasome inhibitor MCC950 at the time of hormone withdrawal.	Immunohistochemical staining	Specific involvement of NLRP3 inflammasome activation in IL-1beta and IL-18 release after hormone withdrawal was investigated via application of the NLRP3 inflammasome inhibitor MCC950 at the time of hormone withdrawal.			Immunohistochemistry，Fluorescent immunohistochemistry，Western immunoblotting				NLRP3
32489294	chr9	136879139	136881139	TRAF2	TRAIP proteins are critical in programmed cell death, cell proliferation and differentiation, and embryonic development.	human		High+Lowthroughput	Molecular cloning, expression, overproduction and characterization of human TRAIP Leucine zipper protein	否		Apoptosis		E_01_0604	PCR	TRAIP proteins are critical in programmed cell death, cell proliferation and differentiation, and embryonic development.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TRAIP proteins are critical in programmed cell death, cell proliferation and differentiation, and embryonic development.	Immunohistochemical staining	TRAIP proteins are critical in programmed cell death, cell proliferation and differentiation, and embryonic development.	TRAF2		PCR	TRAIP proteins are critical in programmed cell death, cell proliferation and differentiation, and embryonic development.			
32499643	chr8	127733096	127735096	MYC	Furthermore, we show that CCAT1-5L a super-enhancer hub RNA interacts with the RNA-binding protein hnRNPK, as well as RNA derived from the MYC promoter and enhancer, to boost MYC transcription by modulating chromatin looping.	human		High+Lowthroughput	RIC-seq for global in situ profiling of RNA-RNA spatial interactions	否		Cancer	HeLa cell	E_01_0605	RIC-seq	Furthermore, we show that CCAT1-5L a super-enhancer hub RNA interacts with the RNA-binding protein hnRNPK, as well as RNA derived from the MYC promoter and enhancer, to boost MYC transcription by modulating chromatin looping.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Furthermore, we show that CCAT1-5L a super-enhancer hub RNA interacts with the RNA-binding protein hnRNPK, as well as RNA derived from the MYC promoter and enhancer, to boost MYC transcription by modulating chromatin looping.	Immunohistochemical staining	Furthermore, we show that CCAT1-5L a super-enhancer hub RNA interacts with the RNA-binding protein hnRNPK, as well as RNA derived from the MYC promoter and enhancer, to boost MYC transcription by modulating chromatin looping.	MYC		RIC-seq	Furthermore, we show that CCAT1-5L a super-enhancer hub RNA interacts with the RNA-binding protein hnRNPK, as well as RNA derived from the MYC promoter and enhancer, to boost MYC transcription by modulating chromatin looping.			
32505533	chr7	148804812	148806812	EZH2	Functional assays indicated that IL-6 secreted by vCAFs induced significant epigenetic alterations in ICC cells, particularly upregulating enhancer of zeste homolog 2 (EZH2) and thereby enhancing malignancy.	human	connective tissue	High+Lowthroughput	Single-cell transcriptomic architecture and intercellular crosstalk of human intrahepatic cholangiocarcinoma	否		Human intrahepatic cholangiocarcinoma	stromal cell	E_01_0606	scRNA-seq	Functional assays indicated that IL-6 secreted by vCAFs induced significant epigenetic alterations in ICC cells, particularly upregulating enhancer of zeste homolog 2 (EZH2) and thereby enhancing malignancy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Functional assays indicated that IL-6 secreted by vCAFs induced significant epigenetic alterations in ICC cells, particularly upregulating enhancer of zeste homolog 2 (EZH2) and thereby enhancing malignancy.	Immunohistochemical staining	Functional assays indicated that IL-6 secreted by vCAFs induced significant epigenetic alterations in ICC cells, particularly upregulating enhancer of zeste homolog 2 (EZH2) and thereby enhancing malignancy.	EZH2		scRNA-seq	Functional assays indicated that IL-6 secreted by vCAFs induced significant epigenetic alterations in ICC cells, particularly upregulating enhancer of zeste homolog 2 (EZH2) and thereby enhancing malignancy.			
32522577	chr3	97762164	97764164	ARL6	Reduced-expression of miR-143-3p enhanced the CdCl2-induced suppression of the osteogenesis of hBMSCs and inhibition of the Wnt/β-catenin pathway, effects that were reversed by down-regulated expression of ARL6.	human		High+Lowthroughput	MircoRNA-143-3p regulating ARL6 is involved in the cadmium-induced inhibition of osteogenic differentiation in human bone marrow mesenchymal stem cells	否				E_01_0607	QRT-PCR，RT-PCR，Western blots， Luciferase reporter assays	Reduced-expression of miR-143-3p enhanced the CdCl2-induced suppression of the osteogenesis of hBMSCs and inhibition of the Wnt/β-catenin pathway, effects that were reversed by down-regulated expression of ARL6.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Reduced-expression of miR-143-3p enhanced the CdCl2-induced suppression of the osteogenesis of hBMSCs and inhibition of the Wnt/β-catenin pathway, effects that were reversed by down-regulated expression of ARL6.		Reduced-expression of miR-143-3p enhanced the CdCl2-induced suppression of the osteogenesis of hBMSCs and inhibition of the Wnt/β-catenin pathway, effects that were reversed by down-regulated expression of ARL6.	Immunohistochemical staining	Reduced-expression of miR-143-3p enhanced the CdCl2-induced suppression of the osteogenesis of hBMSCs and inhibition of the Wnt/β-catenin pathway, effects that were reversed by down-regulated expression of ARL6.			QRT-PCR，RT-PCR，Western blots， Luciferase reporter assays				ARL6
32527767	chr13	23178617	23180617	SGCG	Concordantly, rs679482-A impairs native repressor activity and increases basal and DMRT2 mediated enhancer activity.	human		High+Lowthroughput	SGCG rs679482 Associates With Weight Loss Success in Response to an Intensively Supervised Outpatient Program	是	rs679482	Fat	C2C12 cell	E_01_0608	Genome-wide association analysis,ChIP	Concordantly, rs679482-A impairs native repressor activity and increases basal and DMRT2 mediated enhancer activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Concordantly, rs679482-A impairs native repressor activity and increases basal and DMRT2 mediated enhancer activity.		Concordantly, rs679482-A impairs native repressor activity and increases basal and DMRT2 mediated enhancer activity.	Immunohistochemical staining	Concordantly, rs679482-A impairs native repressor activity and increases basal and DMRT2 mediated enhancer activity.			Genome-wide association analysis,ChIP				SGCG
32533263	chr7	87500642	87502642	ABCB1	ased on these considerations, we hypothesize that ABCB1 could be a possible enhancer by confining azithromycin more extensively than expected when the trapping is solely dependent on the passive diffusion.	human		High+Lowthroughput	Intracellular ABCB1 as a Possible Mechanism to Explain the Synergistic Effect of Hydroxychloroquine-Azithromycin Combination in COVID-19 Therapy	否			Vero E6 cell	E_01_0609		ased on these considerations, we hypothesize that ABCB1 could be a possible enhancer by confining azithromycin more extensively than expected when the trapping is solely dependent on the passive diffusion.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			ased on these considerations, we hypothesize that ABCB1 could be a possible enhancer by confining azithromycin more extensively than expected when the trapping is solely dependent on the passive diffusion.	Immunohistochemical staining	ased on these considerations, we hypothesize that ABCB1 could be a possible enhancer by confining azithromycin more extensively than expected when the trapping is solely dependent on the passive diffusion.	ABCB1			ased on these considerations, we hypothesize that ABCB1 could be a possible enhancer by confining azithromycin more extensively than expected when the trapping is solely dependent on the passive diffusion.			
32537408	chr7	148804294	148806294	EZH2	"LncRNA UCA1 Antagonizes Arsenic-Induced Cell Cycle
Arrest through Destabilizing EZH2 and Facilitating NFATc2
Expression"	human	connective tissue	High+Lowthroughput	LncRNA UCA1 Antagonizes Arsenic-Induced Cell Cycle Arrest through Destabilizing EZH2 and Facilitating NFATc2 Expression	否		Urothelial cancer	hepatocyte	E_01_0610	qRT-PCR，Western blot，flow cytometry	"LncRNA UCA1 Antagonizes Arsenic-Induced Cell Cycle
Arrest through Destabilizing EZH2 and Facilitating NFATc2
Expression"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"LncRNA UCA1 Antagonizes Arsenic-Induced Cell Cycle
Arrest through Destabilizing EZH2 and Facilitating NFATc2
Expression"	Immunohistochemical staining	"LncRNA UCA1 Antagonizes Arsenic-Induced Cell Cycle
Arrest through Destabilizing EZH2 and Facilitating NFATc2
Expression"	EZH2		qRT-PCR，Western blot，flow cytometry	"LncRNA UCA1 Antagonizes Arsenic-Induced Cell Cycle
Arrest through Destabilizing EZH2 and Facilitating NFATc2
Expression"			
32548603	chr3	181708842	181710842	SOX2	In these regions, the C/EBP motif regulates HIOEC specific enhancer and regulates SOX2 and PITX2, thereby promoting wound healing of oral keratinocytes.	human	Epithelial tissues	High+Lowthroughput	Intrinsic Differences between the Open Chromatin Regions of Oral and Epidermal Keratinocytes	否				E_01_0611	ATAC-seq	In these regions, the C/EBP motif regulates HIOEC specific enhancer and regulates SOX2 and PITX2, thereby promoting wound healing of oral keratinocytes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In these regions, the C/EBP motif regulates HIOEC specific enhancer and regulates SOX2 and PITX2, thereby promoting wound healing of oral keratinocytes.	Immunohistochemical staining	In these regions, the C/EBP motif regulates HIOEC specific enhancer and regulates SOX2 and PITX2, thereby promoting wound healing of oral keratinocytes.	SOX2		ATAC-seq	In these regions, the C/EBP motif regulates HIOEC specific enhancer and regulates SOX2 and PITX2, thereby promoting wound healing of oral keratinocytes.			
32552749	chr4	73992599	73994599	CXCL5	Conditioned media of endometrial niche cells cocultured with eMSCs contained increased levels of C-X-C motif ligand 1 (CXCL1), CXCL5 and interleukin 6.	human	Epithelial tissues	High+Lowthroughput	Understanding the regulatory mechanisms of endometrial cells on activities of endometrial mesenchymal stem-like cells during menstruation	否		Menstruation	isolation procedure of endometrial cell	E_01_0612	Western blot,Flow cytometry,Qrt-PCR,WNT reporter assay,Immunofluorescence	Conditioned media of endometrial niche cells cocultured with eMSCs contained increased levels of C-X-C motif ligand 1 (CXCL1), CXCL5 and interleukin 6.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Conditioned media of endometrial niche cells cocultured with eMSCs contained increased levels of C-X-C motif ligand 1 (CXCL1), CXCL5 and interleukin 6.		Conditioned media of endometrial niche cells cocultured with eMSCs contained increased levels of C-X-C motif ligand 1 (CXCL1), CXCL5 and interleukin 6.	Immunohistochemical staining	Conditioned media of endometrial niche cells cocultured with eMSCs contained increased levels of C-X-C motif ligand 1 (CXCL1), CXCL5 and interleukin 6.			Western blot,Flow cytometry,Qrt-PCR,WNT reporter assay,Immunofluorescence				CXCL5
32555468	chr4	99273246	99275246	ADH1A	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.	human	Nervous tissue	High+Lowthroughput	Genetic variants associated with alcohol dependence co-ordinate regulation of ADH genes in gastrointestinal and adipose tissues	是	rs4699741-SCARB2,rs1229984, rs17028615,rs1789891, rs1789924, rs1826907,rs2066702		neuronal cell	E_01_0613	LD analysis	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.		Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.	Immunohistochemical staining	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.			LD analysis				ADH1A
32555468	chr4	99302297	99304297	ADH1B	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.	human	Nervous tissue	High+Lowthroughput	Genetic variants associated with alcohol dependence co-ordinate regulation of ADH genes in gastrointestinal and adipose tissues	是	rs4699741-SCARB2,rs1229984, rs17028615,rs1789891, rs1789924, rs1826907,rs2066702		neuronal cell	E_01_0613	LD analysis	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.		Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.	Immunohistochemical staining	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.			LD analysis				ADH1B
32555468	chr4	99334004	99336004	ADH1C	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.	human	Nervous tissue	High+Lowthroughput	Genetic variants associated with alcohol dependence co-ordinate regulation of ADH genes in gastrointestinal and adipose tissues	是	rs4699741-SCARB2,rs1229984, rs17028615,rs1789891, rs1789924, rs1826907,rs2066702		neuronal cell	E_01_0613	LD analysis	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.		Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.	Immunohistochemical staining	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.			LD analysis				ADH1C
32555468	chr4	99120847	99122847	ADH4	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.	human	Nervous tissue	High+Lowthroughput	Genetic variants associated with alcohol dependence co-ordinate regulation of ADH genes in gastrointestinal and adipose tissues	是	rs4699741-SCARB2,rs1229984, rs17028615,rs1789891, rs1789924, rs1826907,rs2066702		neuronal cell	E_01_0613	LD analysis	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.		Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.	Immunohistochemical staining	Identifed eQTLs produced a co-ordinated regulatory action between ADH genes, especially   between ADH1A and ADH1C within the subcutaneous adipose and gastrointestinal tissues.			LD analysis				ADH4
32566584	chr22	39516997	39518997	ATF4	Results: BC significantly inhibited AGE-induced cell death and apoptosis in H9c2 cells. BC had a suppressive effect on intracellular ROS production and antioxidative enzyme reduction. Moreover, BC decreased hyperactive endoplasmic reticulum (ER) stress and autophagy in H9c2 cells. Furthermore, BC exerted a cardioprotective effect in AGE-induced H9c2 cells via the activation of the PI3K/Akt/mTOR signaling pathway.	human	Musculature	High+Lowthroughput	Beta carotene protects H9c2 cardiomyocytes from advanced glycation end product-induced endoplasmic reticulum stress, apoptosis, and autophagy via the PI3K/Akt/mTOR signaling pathway	否		Diabetic cardiomyopathy	H2c9 cell	E_01_0614	flow cytometry，Western blotting，Enzyme-linked immunosorbent assay	Results: BC significantly inhibited AGE-induced cell death and apoptosis in H9c2 cells. BC had a suppressive effect on intracellular ROS production and antioxidative enzyme reduction. Moreover, BC decreased hyperactive endoplasmic reticulum (ER) stress and autophagy in H9c2 cells. Furthermore, BC exerted a cardioprotective effect in AGE-induced H9c2 cells via the activation of the PI3K/Akt/mTOR signaling pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Results: BC significantly inhibited AGE-induced cell death and apoptosis in H9c2 cells. BC had a suppressive effect on intracellular ROS production and antioxidative enzyme reduction. Moreover, BC decreased hyperactive endoplasmic reticulum (ER) stress and autophagy in H9c2 cells. Furthermore, BC exerted a cardioprotective effect in AGE-induced H9c2 cells via the activation of the PI3K/Akt/mTOR signaling pathway.	Immunohistochemical staining	Results: BC significantly inhibited AGE-induced cell death and apoptosis in H9c2 cells. BC had a suppressive effect on intracellular ROS production and antioxidative enzyme reduction. Moreover, BC decreased hyperactive endoplasmic reticulum (ER) stress and autophagy in H9c2 cells. Furthermore, BC exerted a cardioprotective effect in AGE-induced H9c2 cells via the activation of the PI3K/Akt/mTOR signaling pathway.	ATF4		flow cytometry，Western blotting，Enzyme-linked immunosorbent assay	Results: BC significantly inhibited AGE-induced cell death and apoptosis in H9c2 cells. BC had a suppressive effect on intracellular ROS production and antioxidative enzyme reduction. Moreover, BC decreased hyperactive endoplasmic reticulum (ER) stress and autophagy in H9c2 cells. Furthermore, BC exerted a cardioprotective effect in AGE-induced H9c2 cells via the activation of the PI3K/Akt/mTOR signaling pathway.			
32568442	chr6	32575193	32577193	HLA-DRB1	Polymorphisms predisposing to down-regulation of  HLA-DR facilitate the Th1-to-Th2 transition and promote HCC development, possibly via selecting the HCC-risk HBV mutations.	human	connective tissue	High+Lowthroughput	The genetic polymorphism down-regulating HLA-DRB1 enhancer activity facilitates HBV persistence, evolution and hepatocarcinogenesis in the Chinese Han population	是	rs3135395-T, rs3135338-C,rs477515-T	Cancer	HepG2 cell	E_01_0615	Statistical Analysis	Polymorphisms predisposing to down-regulation of  HLA-DR facilitate the Th1-to-Th2 transition and promote HCC development, possibly via selecting the HCC-risk HBV mutations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Polymorphisms predisposing to down-regulation of  HLA-DR facilitate the Th1-to-Th2 transition and promote HCC development, possibly via selecting the HCC-risk HBV mutations.		Polymorphisms predisposing to down-regulation of  HLA-DR facilitate the Th1-to-Th2 transition and promote HCC development, possibly via selecting the HCC-risk HBV mutations.	Immunohistochemical staining	Polymorphisms predisposing to down-regulation of  HLA-DR facilitate the Th1-to-Th2 transition and promote HCC development, possibly via selecting the HCC-risk HBV mutations.			Statistical Analysis				HLA-DRB1
32570918	chr7	16788652	16790652	AGR2	In conclusion, we revealed for the first time that ZEB1 regulates AGR2 at the transcriptional level, while AGR2 presence contributes to ZEB1 mRNA degradation.	human	connective tissue	High+Lowthroughput	ZEB1/miR-200c/AGR2: A New Regulatory Loop Modulating the Epithelial-Mesenchymal Transition in Lung Adenocarcinomas	否		Lung Adenocarcinomas	Lung cancer cell	E_01_0616	Western Blot,ChIP,Immunoprecipitation	In conclusion, we revealed for the first time that ZEB1 regulates AGR2 at the transcriptional level, while AGR2 presence contributes to ZEB1 mRNA degradation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, we revealed for the first time that ZEB1 regulates AGR2 at the transcriptional level, while AGR2 presence contributes to ZEB1 mRNA degradation.		In conclusion, we revealed for the first time that ZEB1 regulates AGR2 at the transcriptional level, while AGR2 presence contributes to ZEB1 mRNA degradation.	Immunohistochemical staining	In conclusion, we revealed for the first time that ZEB1 regulates AGR2 at the transcriptional level, while AGR2 presence contributes to ZEB1 mRNA degradation.			Western Blot,ChIP,Immunoprecipitation				AGR2
32579929	chr3	149366738	149368738	TM4SF1	These eRNAs help with the formation of a specific ERa-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses the transcription of target genes.	human		High+Lowthroughput	Enhancer RNAs Mediate Estrogen-Induced Decommissioning of Selective Enhancers by Recruiting ERα and Its Cofactor	否				E_01_0617	Real-time RT PCR,RNA tethering luciferase assay,3C assay,ChIP-qPCR ,ChIP-Seq,	These eRNAs help with the formation of a specific ERa-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses the transcription of target genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These eRNAs help with the formation of a specific ERa-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses the transcription of target genes.		These eRNAs help with the formation of a specific ERa-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses the transcription of target genes.	Immunohistochemical staining	These eRNAs help with the formation of a specific ERa-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses the transcription of target genes.			Real-time RT PCR,RNA tethering luciferase assay,3C assay,ChIP-qPCR ,ChIP-Seq,				TM4SF1
32579929	chr2	55863294	55865294	EFEMP1	These eRNAs help with the formation of a specific ERa-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses the transcription of target genes.	human		High+Lowthroughput	Enhancer RNAs Mediate Estrogen-Induced Decommissioning of Selective Enhancers by Recruiting ERα and Its Cofactor	否				E_01_0617	Real-time RT PCR,RNA tethering luciferase assay,3C assay,ChIP-qPCR ,ChIP-Seq,	These eRNAs help with the formation of a specific ERa-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses the transcription of target genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These eRNAs help with the formation of a specific ERa-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses the transcription of target genes.		These eRNAs help with the formation of a specific ERa-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses the transcription of target genes.	Immunohistochemical staining	These eRNAs help with the formation of a specific ERa-centered transcriptional complex and promote the association of the histone demethylase KDM2A, which dismisses RNA polymerase II from designated enhancers and suppresses the transcription of target genes.			Real-time RT PCR,RNA tethering luciferase assay,3C assay,ChIP-qPCR ,ChIP-Seq,				EFEMP1
32585424	chr1	161036785	161038785	USF1	All possible rearrangements include a head-to-head fusion between a completely duplicated PCSK9 and a chromosomal region, normally situated ~80 kb away, that includes HNF4 and USF1 binding sites that could promote transcription of the PCSK9 gene.	human		High+Lowthroughput	Molecular mechanism linking a novel PCSK9 copy number variant to severe hypercholesterolemia	否		Premature atherosclerosis		E_01_0618	Whole exome seq	All possible rearrangements include a head-to-head fusion between a completely duplicated PCSK9 and a chromosomal region, normally situated ~80 kb away, that includes HNF4 and USF1 binding sites that could promote transcription of the PCSK9 gene.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			All possible rearrangements include a head-to-head fusion between a completely duplicated PCSK9 and a chromosomal region, normally situated ~80 kb away, that includes HNF4 and USF1 binding sites that could promote transcription of the PCSK9 gene.	Immunohistochemical staining	All possible rearrangements include a head-to-head fusion between a completely duplicated PCSK9 and a chromosomal region, normally situated ~80 kb away, that includes HNF4 and USF1 binding sites that could promote transcription of the PCSK9 gene.	USF1		Whole exome seq	All possible rearrangements include a head-to-head fusion between a completely duplicated PCSK9 and a chromosomal region, normally situated ~80 kb away, that includes HNF4 and USF1 binding sites that could promote transcription of the PCSK9 gene.			
32585424	chr1	55036498	55038498	PCSK9	All possible rearrangements include a head-to-head fusion between a completely duplicated PCSK9 and a chromosomal region, normally situated ~80 kb away, that includes HNF4 and USF1 binding sites that could promote transcription of the PCSK9 gene.	human		High+Lowthroughput	Molecular mechanism linking a novel PCSK9 copy number variant to severe hypercholesterolemia	否		Premature atherosclerosis		E_01_0618	Whole exome seq	All possible rearrangements include a head-to-head fusion between a completely duplicated PCSK9 and a chromosomal region, normally situated ~80 kb away, that includes HNF4 and USF1 binding sites that could promote transcription of the PCSK9 gene.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	All possible rearrangements include a head-to-head fusion between a completely duplicated PCSK9 and a chromosomal region, normally situated ~80 kb away, that includes HNF4 and USF1 binding sites that could promote transcription of the PCSK9 gene.		All possible rearrangements include a head-to-head fusion between a completely duplicated PCSK9 and a chromosomal region, normally situated ~80 kb away, that includes HNF4 and USF1 binding sites that could promote transcription of the PCSK9 gene.	Immunohistochemical staining	All possible rearrangements include a head-to-head fusion between a completely duplicated PCSK9 and a chromosomal region, normally situated ~80 kb away, that includes HNF4 and USF1 binding sites that could promote transcription of the PCSK9 gene.			Whole exome seq				PCSK9
32586085	chr14	23627675	23629675	DHRS2	Conclusion: Our results revealed that DHRS2 is positively regulated by LEF1 in Jurkat cells, which indicates the capability of LEF1 as a tumor suppressor and, together with previous reports, suggests that LEF1 exhibits a regulatory role in T-ALL via not only its oncogenic targets but also tumor suppressor genes.	human		High+Lowthroughput	LEF1 Induces DHRS2 Gene Expression in Human Acute Leukemia Jurkat T-Cells	否		Human Acute	T cell	E_01_0619	siRNA Transfection,RNA Isolation,qRT-PCR,Western Blotting	Conclusion: Our results revealed that DHRS2 is positively regulated by LEF1 in Jurkat cells, which indicates the capability of LEF1 as a tumor suppressor and, together with previous reports, suggests that LEF1 exhibits a regulatory role in T-ALL via not only its oncogenic targets but also tumor suppressor genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Conclusion: Our results revealed that DHRS2 is positively regulated by LEF1 in Jurkat cells, which indicates the capability of LEF1 as a tumor suppressor and, together with previous reports, suggests that LEF1 exhibits a regulatory role in T-ALL via not only its oncogenic targets but also tumor suppressor genes.		Conclusion: Our results revealed that DHRS2 is positively regulated by LEF1 in Jurkat cells, which indicates the capability of LEF1 as a tumor suppressor and, together with previous reports, suggests that LEF1 exhibits a regulatory role in T-ALL via not only its oncogenic targets but also tumor suppressor genes.	Immunohistochemical staining	Conclusion: Our results revealed that DHRS2 is positively regulated by LEF1 in Jurkat cells, which indicates the capability of LEF1 as a tumor suppressor and, together with previous reports, suggests that LEF1 exhibits a regulatory role in T-ALL via not only its oncogenic targets but also tumor suppressor genes.			siRNA Transfection,RNA Isolation,qRT-PCR,Western Blotting				DHRS2
32586085	chr4	108045186	108047186	LEF1	Conclusion: Our results revealed that DHRS2 is positively regulated by LEF1 in Jurkat cells, which indicates the capability of LEF1 as a tumor suppressor and, together with previous reports, suggests that LEF1 exhibits a regulatory role in T-ALL via not only its oncogenic targets but also tumor suppressor genes.	human		High+Lowthroughput	LEF1 Induces DHRS2 Gene Expression in Human Acute Leukemia Jurkat T-Cells	否		Human Acute	T cell	E_01_0619	siRNA Transfection,RNA Isolation,qRT-PCR,Western Blotting	Conclusion: Our results revealed that DHRS2 is positively regulated by LEF1 in Jurkat cells, which indicates the capability of LEF1 as a tumor suppressor and, together with previous reports, suggests that LEF1 exhibits a regulatory role in T-ALL via not only its oncogenic targets but also tumor suppressor genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Conclusion: Our results revealed that DHRS2 is positively regulated by LEF1 in Jurkat cells, which indicates the capability of LEF1 as a tumor suppressor and, together with previous reports, suggests that LEF1 exhibits a regulatory role in T-ALL via not only its oncogenic targets but also tumor suppressor genes.	Immunohistochemical staining	Conclusion: Our results revealed that DHRS2 is positively regulated by LEF1 in Jurkat cells, which indicates the capability of LEF1 as a tumor suppressor and, together with previous reports, suggests that LEF1 exhibits a regulatory role in T-ALL via not only its oncogenic targets but also tumor suppressor genes.	LEF1		siRNA Transfection,RNA Isolation,qRT-PCR,Western Blotting	Conclusion: Our results revealed that DHRS2 is positively regulated by LEF1 in Jurkat cells, which indicates the capability of LEF1 as a tumor suppressor and, together with previous reports, suggests that LEF1 exhibits a regulatory role in T-ALL via not only its oncogenic targets but also tumor suppressor genes.			
32593213	chr7	16788696	16790696	AGR2	Our data showed that AGR2 upregulated both HIF-1α and HIF-2α expression in Caki-1 cells increasing the expression of HIF-activated genes (glucose transporter 1, phosphoglycerate kinase 1, vascular endothelial growth factor A, and transforming growth factor-alpha) under the hypoxic conditions.	human		High+Lowthroughput	Anterior gradient 2 promotes tumorigenesis through upregulation of CCAAT-enhancer binding protein beta and hypoxia-inducible factor-2α and subsequent secretion of interleukin-6, interleukin-8, and vascular endothelial growth factor in the Caki-1 clear cell renal cell carcinoma cell line	否		Renal cell carcinoma	Caki-1 cell	E_01_0620	Rtq-PCR,Western blot,Enzyme-linked immunosorbent assays,Statistical analysis	Our data showed that AGR2 upregulated both HIF-1α and HIF-2α expression in Caki-1 cells increasing the expression of HIF-activated genes (glucose transporter 1, phosphoglycerate kinase 1, vascular endothelial growth factor A, and transforming growth factor-alpha) under the hypoxic conditions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data showed that AGR2 upregulated both HIF-1α and HIF-2α expression in Caki-1 cells increasing the expression of HIF-activated genes (glucose transporter 1, phosphoglycerate kinase 1, vascular endothelial growth factor A, and transforming growth factor-alpha) under the hypoxic conditions.		Our data showed that AGR2 upregulated both HIF-1α and HIF-2α expression in Caki-1 cells increasing the expression of HIF-activated genes (glucose transporter 1, phosphoglycerate kinase 1, vascular endothelial growth factor A, and transforming growth factor-alpha) under the hypoxic conditions.	Immunohistochemical staining	Our data showed that AGR2 upregulated both HIF-1α and HIF-2α expression in Caki-1 cells increasing the expression of HIF-activated genes (glucose transporter 1, phosphoglycerate kinase 1, vascular endothelial growth factor A, and transforming growth factor-alpha) under the hypoxic conditions.			Rtq-PCR,Western blot,Enzyme-linked immunosorbent assays,Statistical analysis				AGR2
32600276	chr16	86507926	86509926	FOXF1	Array comparative genomic hybridization in patient one and patient two revealed copy-number variant (CNV) deletions, respectively, ~ 1.45 Mb in size involving FOXF1 and an ~ 0.7 Mb in size involving FOXF1 enhancer and leaving FOXF1 intact.	human	Epithelial tissues	High+Lowthroughput	Genotype-phenotype correlation in two Polish neonates with alveolar capillary dysplasia	否		Alveolar capillary dysplasia	epithelial cell	E_01_0621	Sanger seq,	Array comparative genomic hybridization in patient one and patient two revealed copy-number variant (CNV) deletions, respectively, ~ 1.45 Mb in size involving FOXF1 and an ~ 0.7 Mb in size involving FOXF1 enhancer and leaving FOXF1 intact.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Array comparative genomic hybridization in patient one and patient two revealed copy-number variant (CNV) deletions, respectively, ~ 1.45 Mb in size involving FOXF1 and an ~ 0.7 Mb in size involving FOXF1 enhancer and leaving FOXF1 intact.	Immunohistochemical staining	Array comparative genomic hybridization in patient one and patient two revealed copy-number variant (CNV) deletions, respectively, ~ 1.45 Mb in size involving FOXF1 and an ~ 0.7 Mb in size involving FOXF1 enhancer and leaving FOXF1 intact.	FOXF1		Sanger seq,	Array comparative genomic hybridization in patient one and patient two revealed copy-number variant (CNV) deletions, respectively, ~ 1.45 Mb in size involving FOXF1 and an ~ 0.7 Mb in size involving FOXF1 enhancer and leaving FOXF1 intact.			
32606728	chr7	148804477	148806477	EZH2	Treatment with diosgenin alone caused a dose-dependent decrease in the cell viability, and combined treatment with an EZH2 inhibitor plus GSK126 caused a further significant decrease.	human	Epithelial tissues	High+Lowthroughput	Diosgenin and GSK126 Produce Synergistic Effects on Epithelial-Mesenchymal Transition in Gastric Cancer Cells by Mediating EZH2 via the Rho/ROCK Signaling Pathway	否		Gastric cancer	MGC-803 cell	E_01_0622	RNA Extraction，Quantitative PCR，CCK-8 Assay，Flow Cytometry Analysis，Western Blot	Treatment with diosgenin alone caused a dose-dependent decrease in the cell viability, and combined treatment with an EZH2 inhibitor plus GSK126 caused a further significant decrease.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Treatment with diosgenin alone caused a dose-dependent decrease in the cell viability, and combined treatment with an EZH2 inhibitor plus GSK126 caused a further significant decrease.	Immunohistochemical staining	Treatment with diosgenin alone caused a dose-dependent decrease in the cell viability, and combined treatment with an EZH2 inhibitor plus GSK126 caused a further significant decrease.	EZH2		RNA Extraction，Quantitative PCR，CCK-8 Assay，Flow Cytometry Analysis，Western Blot	Treatment with diosgenin alone caused a dose-dependent decrease in the cell viability, and combined treatment with an EZH2 inhibitor plus GSK126 caused a further significant decrease.			
32618141	chr7	18084226	18086226	HDAC9	Genes of particular interest as novel candidate markers of the heart failure phenotype with reduced methylation were HDAC9, JARID2, and GREM1 and with increased methylation PDSS2.	human		High+Lowthroughput	DNA methylation patterns from peripheral blood separate coronary artery disease patients with and without heart failure	否		Ischaemic cardiomyopathy		E_01_0623		Genes of particular interest as novel candidate markers of the heart failure phenotype with reduced methylation were HDAC9, JARID2, and GREM1 and with increased methylation PDSS2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genes of particular interest as novel candidate markers of the heart failure phenotype with reduced methylation were HDAC9, JARID2, and GREM1 and with increased methylation PDSS2.		Genes of particular interest as novel candidate markers of the heart failure phenotype with reduced methylation were HDAC9, JARID2, and GREM1 and with increased methylation PDSS2.	Immunohistochemical staining	Genes of particular interest as novel candidate markers of the heart failure phenotype with reduced methylation were HDAC9, JARID2, and GREM1 and with increased methylation PDSS2.							HDAC9
32618141	chr6	107150118	107152118	PDSS2	Genes of particular interest as novel candidate markers of the heart failure phenotype with reduced methylation were HDAC9, JARID2, and GREM1 and with increased methylation PDSS2.	human		High+Lowthroughput	DNA methylation patterns from peripheral blood separate coronary artery disease patients with and without heart failure	否		Ischaemic cardiomyopathy		E_01_0623		Genes of particular interest as novel candidate markers of the heart failure phenotype with reduced methylation were HDAC9, JARID2, and GREM1 and with increased methylation PDSS2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genes of particular interest as novel candidate markers of the heart failure phenotype with reduced methylation were HDAC9, JARID2, and GREM1 and with increased methylation PDSS2.		Genes of particular interest as novel candidate markers of the heart failure phenotype with reduced methylation were HDAC9, JARID2, and GREM1 and with increased methylation PDSS2.	Immunohistochemical staining	Genes of particular interest as novel candidate markers of the heart failure phenotype with reduced methylation were HDAC9, JARID2, and GREM1 and with increased methylation PDSS2.							PDSS2
32626925	chr7	148804015	148806015	EZH2	In addition, enhancer of zeste homolog 2 (EZH2), a well-known oncogene, was proven to be a direct target of miR-144-3p, and its protein expression was negatively regulated by miR-144-3p. Moreover, EZH2 expression was increased, and inversely correlated with the miR-144-3p level in OSCC tissues.	human	Epithelial tissues	High+Lowthroughput	miR?144?3p inhibits tumor cell growth and invasion in oral squamous cell carcinoma through the?downregulation of the oncogenic gene, EZH2	否		Oral squamous cell carcinoma	HSC 2 cell	E_01_0624	RT‑qPCR,Cell transfection,Luciferase assay,Western blot	In addition, enhancer of zeste homolog 2 (EZH2), a well-known oncogene, was proven to be a direct target of miR-144-3p, and its protein expression was negatively regulated by miR-144-3p. Moreover, EZH2 expression was increased, and inversely correlated with the miR-144-3p level in OSCC tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, enhancer of zeste homolog 2 (EZH2), a well-known oncogene, was proven to be a direct target of miR-144-3p, and its protein expression was negatively regulated by miR-144-3p. Moreover, EZH2 expression was increased, and inversely correlated with the miR-144-3p level in OSCC tissues.	Immunohistochemical staining	In addition, enhancer of zeste homolog 2 (EZH2), a well-known oncogene, was proven to be a direct target of miR-144-3p, and its protein expression was negatively regulated by miR-144-3p. Moreover, EZH2 expression was increased, and inversely correlated with the miR-144-3p level in OSCC tissues.	EZH2		RT‑qPCR,Cell transfection,Luciferase assay,Western blot	In addition, enhancer of zeste homolog 2 (EZH2), a well-known oncogene, was proven to be a direct target of miR-144-3p, and its protein expression was negatively regulated by miR-144-3p. Moreover, EZH2 expression was increased, and inversely correlated with the miR-144-3p level in OSCC tissues.			
32617978	chr8	127732513	127734513	MYC	Overexpression of KDM4B promoted recruitment of AR to the c-Myc (MYC) gene enhancer and induced H3K9 demethylation, increasing AR-dependent transcription of c-Myc mRNA, which regulates the sensitivity to next generation AR-targeted therapy.	human,mouse	connective tissue	High+Lowthroughput	Targeting the KDM4B-AR-c-Myc axis promotes sensitivity to androgen receptor-targeted therapy in advanced prostate cancer	否		Prostate cancer	CWR22Rv1 cell	E_02_0343	RNA seq,ChIP assay,Immunohistochemistry,	Overexpression of KDM4B promoted recruitment of AR to the c-Myc (MYC) gene enhancer and induced H3K9 demethylation, increasing AR-dependent transcription of c-Myc mRNA, which regulates the sensitivity to next generation AR-targeted therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Overexpression of KDM4B promoted recruitment of AR to the c-Myc (MYC) gene enhancer and induced H3K9 demethylation, increasing AR-dependent transcription of c-Myc mRNA, which regulates the sensitivity to next generation AR-targeted therapy.		Overexpression of KDM4B promoted recruitment of AR to the c-Myc (MYC) gene enhancer and induced H3K9 demethylation, increasing AR-dependent transcription of c-Myc mRNA, which regulates the sensitivity to next generation AR-targeted therapy.	Immunohistochemical staining	Overexpression of KDM4B promoted recruitment of AR to the c-Myc (MYC) gene enhancer and induced H3K9 demethylation, increasing AR-dependent transcription of c-Myc mRNA, which regulates the sensitivity to next generation AR-targeted therapy.			RNA seq,ChIP assay,Immunohistochemistry,				MYC
32617979	chr8	127732819	127734819	MYC	Overexpression of KDM4B promoted recruitment of AR to the c-Myc (MYC) gene enhancer and induced H3K10 demethylation, increasing AR-dependent transcription of c-Myc mRNA, which regulates the sensitivity to next generation AR-targeted therapy.	human,mouse	connective tissue	High+Lowthroughput	Targeting the KDM5B-AR-c-Myc axis promotes sensitivity to androgen receptor-targeted therapy in advanced prostate cancer	否		Prostate cancer	LNCaP	E_02_0344	RNA seq,ChIP assay,Immunohistochemistry,	Overexpression of KDM4B promoted recruitment of AR to the c-Myc (MYC) gene enhancer and induced H3K10 demethylation, increasing AR-dependent transcription of c-Myc mRNA, which regulates the sensitivity to next generation AR-targeted therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Overexpression of KDM4B promoted recruitment of AR to the c-Myc (MYC) gene enhancer and induced H3K10 demethylation, increasing AR-dependent transcription of c-Myc mRNA, which regulates the sensitivity to next generation AR-targeted therapy.		Overexpression of KDM4B promoted recruitment of AR to the c-Myc (MYC) gene enhancer and induced H3K10 demethylation, increasing AR-dependent transcription of c-Myc mRNA, which regulates the sensitivity to next generation AR-targeted therapy.	Immunohistochemical staining	Overexpression of KDM4B promoted recruitment of AR to the c-Myc (MYC) gene enhancer and induced H3K10 demethylation, increasing AR-dependent transcription of c-Myc mRNA, which regulates the sensitivity to next generation AR-targeted therapy.			RNA seq,ChIP assay,Immunohistochemistry,				MYC
32392346	chr21	34784729	34786729	RUNX1	The intermediate stage most proximal to HE, which we term pre-HE, is characterized by increased accessibility of chromatin enriched for SOX, FOX, GATA, and SMAD motifs.	human,mouse		High+Lowthroughput	Developmental trajectory of prehematopoietic stem cell formation from endothelium	否			IAC cell	E_02_0345	scRNA-Seq，scATAC-Seq	The intermediate stage most proximal to HE, which we term pre-HE, is characterized by increased accessibility of chromatin enriched for SOX, FOX, GATA, and SMAD motifs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The intermediate stage most proximal to HE, which we term pre-HE, is characterized by increased accessibility of chromatin enriched for SOX, FOX, GATA, and SMAD motifs.		The intermediate stage most proximal to HE, which we term pre-HE, is characterized by increased accessibility of chromatin enriched for SOX, FOX, GATA, and SMAD motifs.	Immunohistochemical staining	The intermediate stage most proximal to HE, which we term pre-HE, is characterized by increased accessibility of chromatin enriched for SOX, FOX, GATA, and SMAD motifs.			scRNA-Seq，scATAC-Seq				RUNX1
32375045	chr4	56904890	56906890	REST	we reveal the transcriptional repressor RE-1 silencing transcription factor (REST) as a barrier for b cell gene expression in the reprogramming of pancreatic exocrine cells.	human,mouse		High+Lowthroughput	REST Inhibits Direct Reprogramming of Pancreatic Exocrine to Endocrine Cells by Preventing PDX1-Mediated Activation of Endocrine Genes	否		Diabetes	endocrine cell	E_02_0346	quantitative real-time PCR，Immunofluorescence，Flow cytometry，RNA-Seq，immunoprecipitation	we reveal the transcriptional repressor RE-1 silencing transcription factor (REST) as a barrier for b cell gene expression in the reprogramming of pancreatic exocrine cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	we reveal the transcriptional repressor RE-1 silencing transcription factor (REST) as a barrier for b cell gene expression in the reprogramming of pancreatic exocrine cells.		we reveal the transcriptional repressor RE-1 silencing transcription factor (REST) as a barrier for b cell gene expression in the reprogramming of pancreatic exocrine cells.	Immunohistochemical staining	we reveal the transcriptional repressor RE-1 silencing transcription factor (REST) as a barrier for b cell gene expression in the reprogramming of pancreatic exocrine cells.			quantitative real-time PCR，Immunofluorescence，Flow cytometry，RNA-Seq，immunoprecipitation				REST
32433819	chr19	17822384	17824384	JAK3	Moreover, using gainand loss-of-function approaches, we demonstrate that downstream molecules of Wnt3a signaling, including Dvl3 and β-catenin, are responsible for the negative regulatory role of Wnt3a.	human,mouse		High+Lowthroughput	JAK3 restrains inflammatory responses and protects against periodontal disease through Wnt3a signaling	否		Periodontal disease	THP-1 cells	E_02_0347	Western blot,siRNA，Immunoprecipitation，RT-PCR	Moreover, using gainand loss-of-function approaches, we demonstrate that downstream molecules of Wnt3a signaling, including Dvl3 and β-catenin, are responsible for the negative regulatory role of Wnt3a.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, using gainand loss-of-function approaches, we demonstrate that downstream molecules of Wnt3a signaling, including Dvl3 and β-catenin, are responsible for the negative regulatory role of Wnt3a.		Moreover, using gainand loss-of-function approaches, we demonstrate that downstream molecules of Wnt3a signaling, including Dvl3 and β-catenin, are responsible for the negative regulatory role of Wnt3a.	Immunohistochemical staining	Moreover, using gainand loss-of-function approaches, we demonstrate that downstream molecules of Wnt3a signaling, including Dvl3 and β-catenin, are responsible for the negative regulatory role of Wnt3a.			Western blot,siRNA，Immunoprecipitation，RT-PCR				JAK3
32461639	chrX	7437073	7439073	Foxp3	IsoDCA-producing consortia increased the number of colonic RORγt-expressing Treg cells in a CNS1-dependent manner, suggesting enhanced extrathymic diferentiation.	human,mouse	lymphoid tissue	High+Lowthroughput	Bacterial metabolism of bile acids promotes generation of peripheral regulatory T cells	否			T cell	E_02_0348	RNA-seq，Luciferase assays	IsoDCA-producing consortia increased the number of colonic RORγt-expressing Treg cells in a CNS1-dependent manner, suggesting enhanced extrathymic diferentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	IsoDCA-producing consortia increased the number of colonic RORγt-expressing Treg cells in a CNS1-dependent manner, suggesting enhanced extrathymic diferentiation.		IsoDCA-producing consortia increased the number of colonic RORγt-expressing Treg cells in a CNS1-dependent manner, suggesting enhanced extrathymic diferentiation.	Immunohistochemical staining	IsoDCA-producing consortia increased the number of colonic RORγt-expressing Treg cells in a CNS1-dependent manner, suggesting enhanced extrathymic diferentiation.			RNA-seq，Luciferase assays				Foxp3
32474518	chr7	148804991	148806991	EZH2	LMP1 upregulated the expression of EZH2, which increased the stability of aTregs in vitro.	human,mouse		High+Lowthroughput	Targeting EZH2 depletes LMP1-induced activated regulatory T cells enhancing antitumor immunity in nasopharyngeal carcinoma	否		Nasopharyngeal carcinoma	nasopharyngeal carcinoma cell	E_02_0349	Flow cytometry，Immunohistochemical and immunofluorescent analysis	LMP1 upregulated the expression of EZH2, which increased the stability of aTregs in vitro.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	LMP1 upregulated the expression of EZH2, which increased the stability of aTregs in vitro.		LMP1 upregulated the expression of EZH2, which increased the stability of aTregs in vitro.	Immunohistochemical staining	LMP1 upregulated the expression of EZH2, which increased the stability of aTregs in vitro.			Flow cytometry，Immunohistochemical and immunofluorescent analysis				EZH2
32502841	chr7	55015920	55017920	EGFR	Our results indicated regorafenib reduced EGF-induced EGFR and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activity.	human,mouse		High+Lowthroughput	Regorafenib suppresses epidermal growth factor receptor signaling-modulated progression of colorectal cancer	否		Colorectal cancer	CT26 cell	E_02_0350	Western blotting， Immunohistochemistry	Our results indicated regorafenib reduced EGF-induced EGFR and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results indicated regorafenib reduced EGF-induced EGFR and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activity.		Our results indicated regorafenib reduced EGF-induced EGFR and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activity.	Immunohistochemical staining	Our results indicated regorafenib reduced EGF-induced EGFR and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activity.			Western blotting， Immunohistochemistry				EGFR
32555380	chr11	44561492	44563492	CD82	Our results illustrate that, by hijacking Lef1 and CD82, vIRF1 upregulates CDCP1 to promote angiogenesis and cell invasion.	human,mouse	Epithelial tissues	High+Lowthroughput	An oncogenic viral interferon regulatory factor upregulates CUB domain-containing protein 1 to promote angiogenesis by hijacking transcription factor lymphoid enhancer-binding factor 1 and metastasis suppressor CD82	否		Kaposi s sarcoma	HUVECs	E_02_0351	Immunohistochemistry (IHC) staining，RT-qPCR，western blotting，Luciferase reporter assay，Immunofluorescence assay (IFA)，DNA ChIP assay	Our results illustrate that, by hijacking Lef1 and CD82, vIRF1 upregulates CDCP1 to promote angiogenesis and cell invasion.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results illustrate that, by hijacking Lef1 and CD82, vIRF1 upregulates CDCP1 to promote angiogenesis and cell invasion.		Our results illustrate that, by hijacking Lef1 and CD82, vIRF1 upregulates CDCP1 to promote angiogenesis and cell invasion.	Immunohistochemical staining	Our results illustrate that, by hijacking Lef1 and CD82, vIRF1 upregulates CDCP1 to promote angiogenesis and cell invasion.			Immunohistochemistry (IHC) staining，RT-qPCR，western blotting，Luciferase reporter assay，Immunofluorescence assay (IFA)，DNA ChIP assay				CD82
32380038	chr14	60641121	60643121	SIX1	Therefore, we identified FBWX7 as an important regulator of cardiac hypertrophy via modulating the EZH2-SIX1 axis.	human,mouse	Epithelial tissues	High+Lowthroughput	FBXW7 promotes pathological cardiac hypertrophy by targeting EZH2-SIX1 signaling	否		Cardiac hypertrophy	endothelial cell	E_02_0352	qRT-PCR，Western blot	Therefore, we identified FBWX7 as an important regulator of cardiac hypertrophy via modulating the EZH2-SIX1 axis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, we identified FBWX7 as an important regulator of cardiac hypertrophy via modulating the EZH2-SIX1 axis.		Therefore, we identified FBWX7 as an important regulator of cardiac hypertrophy via modulating the EZH2-SIX1 axis.	Immunohistochemical staining	Therefore, we identified FBWX7 as an important regulator of cardiac hypertrophy via modulating the EZH2-SIX1 axis.			qRT-PCR，Western blot				SIX1
32407713	chr1	156460830	156462830	MEF2D	Functional analysis demonstrated that MEF2D upregulation significantly rescued the decreased viability of OGD/R-injured neurons and suppressed OGD/R-induced apoptosis and reactive oxygen species (ROS) production.	human,mouse	Nervous tissue	High+Lowthroughput	MEF2D upregulation protects neurons from oxygen-glucose deprivation/re-oxygenation-induced injury by enhancing Nrf2 activation	否		Cerebral ischemia	HT22 neuronal cell	E_02_0353	siRNA，RT-qPCR，Western blot，Luciferase reporter assay	Functional analysis demonstrated that MEF2D upregulation significantly rescued the decreased viability of OGD/R-injured neurons and suppressed OGD/R-induced apoptosis and reactive oxygen species (ROS) production.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Functional analysis demonstrated that MEF2D upregulation significantly rescued the decreased viability of OGD/R-injured neurons and suppressed OGD/R-induced apoptosis and reactive oxygen species (ROS) production.		Functional analysis demonstrated that MEF2D upregulation significantly rescued the decreased viability of OGD/R-injured neurons and suppressed OGD/R-induced apoptosis and reactive oxygen species (ROS) production.	Immunohistochemical staining	Functional analysis demonstrated that MEF2D upregulation significantly rescued the decreased viability of OGD/R-injured neurons and suppressed OGD/R-induced apoptosis and reactive oxygen species (ROS) production.			siRNA，RT-qPCR，Western blot，Luciferase reporter assay				MEF2D
32324256	chr6	45325492	45327492	RUNX2	RUNX2 and EGR1 co repressed Htra1 and increased the expression levels of other osteoblast marker genes, such as osterix, osteocalcin, and osteoprotegerin at the messenger RNA and protein level.	human,mouse		High+Lowthroughput	RUNX2 co-operates with EGR1 to regulate osteogenic differentiation through Htra1 enhancers	否		Osteogenic differentiation	preosteoblast	E_02_0354	ChIP and Re‐ChIP assays，RNA extraction，quantitative reverse transcription PCR，RNA extraction，quantitative reverse transcription PCR	RUNX2 and EGR1 co repressed Htra1 and increased the expression levels of other osteoblast marker genes, such as osterix, osteocalcin, and osteoprotegerin at the messenger RNA and protein level.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RUNX2 and EGR1 co repressed Htra1 and increased the expression levels of other osteoblast marker genes, such as osterix, osteocalcin, and osteoprotegerin at the messenger RNA and protein level.		RUNX2 and EGR1 co repressed Htra1 and increased the expression levels of other osteoblast marker genes, such as osterix, osteocalcin, and osteoprotegerin at the messenger RNA and protein level.	Immunohistochemical staining	RUNX2 and EGR1 co repressed Htra1 and increased the expression levels of other osteoblast marker genes, such as osterix, osteocalcin, and osteoprotegerin at the messenger RNA and protein level.			ChIP and Re‐ChIP assays，RNA extraction，quantitative reverse transcription PCR，RNA extraction，quantitative reverse transcription PCR				RUNX2
32324256	chr5	138463046	138465046	EGR1	RUNX2 and EGR1 co repressed Htra1 and increased the expression levels of other osteoblast marker genes, such as osterix, osteocalcin, and osteoprotegerin at the messenger RNA and protein level.	human,mouse		High+Lowthroughput	RUNX2 co-operates with EGR1 to regulate osteogenic differentiation through Htra1 enhancers	否		Osteogenic differentiation	preosteoblast	E_02_0354	ChIP and Re‐ChIP assays，RNA extraction，quantitative reverse transcription PCR，RNA extraction，quantitative reverse transcription PCR	RUNX2 and EGR1 co repressed Htra1 and increased the expression levels of other osteoblast marker genes, such as osterix, osteocalcin, and osteoprotegerin at the messenger RNA and protein level.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RUNX2 and EGR1 co repressed Htra1 and increased the expression levels of other osteoblast marker genes, such as osterix, osteocalcin, and osteoprotegerin at the messenger RNA and protein level.		RUNX2 and EGR1 co repressed Htra1 and increased the expression levels of other osteoblast marker genes, such as osterix, osteocalcin, and osteoprotegerin at the messenger RNA and protein level.	Immunohistochemical staining	RUNX2 and EGR1 co repressed Htra1 and increased the expression levels of other osteoblast marker genes, such as osterix, osteocalcin, and osteoprotegerin at the messenger RNA and protein level.			ChIP and Re‐ChIP assays，RNA extraction，quantitative reverse transcription PCR，RNA extraction，quantitative reverse transcription PCR				EGR1
32378708	chr11	27651837	27653837	BDNF	Of the neurotrophins, the literature describing the expression and function of brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, neurotrophin receptor kinase-2 (NTRK2), has been expanding rapidly.	human,mouse	Nervous tissue	High+Lowthroughput	Brain-derived neurotrophic factor (BDNF) expression and function in the mammalian reproductive Tract	否		Endometriosis	hippocampal neuron	E_02_0355	RT-PCR	Of the neurotrophins, the literature describing the expression and function of brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, neurotrophin receptor kinase-2 (NTRK2), has been expanding rapidly.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Of the neurotrophins, the literature describing the expression and function of brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, neurotrophin receptor kinase-2 (NTRK2), has been expanding rapidly.		Of the neurotrophins, the literature describing the expression and function of brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, neurotrophin receptor kinase-2 (NTRK2), has been expanding rapidly.	Immunohistochemical staining	Of the neurotrophins, the literature describing the expression and function of brain-derived neurotrophic factor (BDNF) and its high-affinity receptor, neurotrophin receptor kinase-2 (NTRK2), has been expanding rapidly.			RT-PCR				BDNF
32450132	chr17	27054366	27056366	Nkx2-5	We have now found evidence for another aspect of cardiac transcription factor cooperativity between Nkx2-5 and the cardiac enriched MADS domain transcription factor Srf.	human,mouse		High+Lowthroughput	Second heart field-specific expression of Nkx2-5 requires promoter proximal interaction with Srf	否			precursor cell	E_02_0356	ChIP	We have now found evidence for another aspect of cardiac transcription factor cooperativity between Nkx2-5 and the cardiac enriched MADS domain transcription factor Srf.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We have now found evidence for another aspect of cardiac transcription factor cooperativity between Nkx2-5 and the cardiac enriched MADS domain transcription factor Srf.		We have now found evidence for another aspect of cardiac transcription factor cooperativity between Nkx2-5 and the cardiac enriched MADS domain transcription factor Srf.	Immunohistochemical staining	We have now found evidence for another aspect of cardiac transcription factor cooperativity between Nkx2-5 and the cardiac enriched MADS domain transcription factor Srf.			ChIP				Nkx2-5
32432967	chr10	94935572	94937572	CYP2C9	There was no significant effect of rutin on the modulation of intestinal transit, CYP2C9 inhibition, and CYP2C9/CYP2C11 expression to boost the oral exposure of diclofenac. 5.	human,mouse		High+Lowthroughput	Effect of rutin on pharmacokinetic modulation of diclofenac in rats	否		Inflammatory		E_02_0357	qRT PCR	There was no significant effect of rutin on the modulation of intestinal transit, CYP2C9 inhibition, and CYP2C9/CYP2C11 expression to boost the oral exposure of diclofenac. 5.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	There was no significant effect of rutin on the modulation of intestinal transit, CYP2C9 inhibition, and CYP2C9/CYP2C11 expression to boost the oral exposure of diclofenac. 5.		There was no significant effect of rutin on the modulation of intestinal transit, CYP2C9 inhibition, and CYP2C9/CYP2C11 expression to boost the oral exposure of diclofenac. 5.	Immunohistochemical staining	There was no significant effect of rutin on the modulation of intestinal transit, CYP2C9 inhibition, and CYP2C9/CYP2C11 expression to boost the oral exposure of diclofenac. 5.			qRT PCR				CYP2C9
32544883	chr5	51380949	51382949	ISL1	Modulated expression of neurotrophic factors in sciatic nerves in rats with DM developed by intraperitoneal injection of 0.45% streptozotocin, suggesting that ISL1 could delay DM progression and promote neural regeneration and repair after sciatic nerve damage.	human,mouse	connective tissue	High+Lowthroughput	microRNA-9 and -29a regulate the progression of diabetic peripheral neuropathy via ISL1-mediated sonic hedgehog signaling pathway	否		Diabetic Peripheral	Embryonic kidney cells	E_02_0358	Dual luciferase reporter gene assay，RT-qPCR，Western blot，Immunohistochemistry	Modulated expression of neurotrophic factors in sciatic nerves in rats with DM developed by intraperitoneal injection of 0.45% streptozotocin, suggesting that ISL1 could delay DM progression and promote neural regeneration and repair after sciatic nerve damage.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Modulated expression of neurotrophic factors in sciatic nerves in rats with DM developed by intraperitoneal injection of 0.45% streptozotocin, suggesting that ISL1 could delay DM progression and promote neural regeneration and repair after sciatic nerve damage.		Modulated expression of neurotrophic factors in sciatic nerves in rats with DM developed by intraperitoneal injection of 0.45% streptozotocin, suggesting that ISL1 could delay DM progression and promote neural regeneration and repair after sciatic nerve damage.	Immunohistochemical staining	Modulated expression of neurotrophic factors in sciatic nerves in rats with DM developed by intraperitoneal injection of 0.45% streptozotocin, suggesting that ISL1 could delay DM progression and promote neural regeneration and repair after sciatic nerve damage.			Dual luciferase reporter gene assay，RT-qPCR，Western blot，Immunohistochemistry				ISL1
32229665	chr18	69473339	69475339	Tcf4	Results: Chamomile extract modulated the Wnt pathway in colonic tissues, where it significantly downregulated Wnt5a, β-catenin, T cell factor (Tcf4), lymphoid enhancer factor 1 (Lef1), c-Myc and Cyclin D1 expression levels, while it upregulated adenomatous polyposis coli (APC) and glycogen synthase kinase (GSK3β) expression levels. This extract significantly reduced COX-2 levels and iNOS activities.	mouse		High+Lowthroughput	Protective effect of Matricaria chamomilla extract against 1,2-dimethylhydrazine-induced colorectal cancer in mice	否		Colorectal cancer	goblet cell	E_02_0359	Molecular assays，RT-PCR	Results: Chamomile extract modulated the Wnt pathway in colonic tissues, where it significantly downregulated Wnt5a, β-catenin, T cell factor (Tcf4), lymphoid enhancer factor 1 (Lef1), c-Myc and Cyclin D1 expression levels, while it upregulated adenomatous polyposis coli (APC) and glycogen synthase kinase (GSK3β) expression levels. This extract significantly reduced COX-2 levels and iNOS activities.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Results: Chamomile extract modulated the Wnt pathway in colonic tissues, where it significantly downregulated Wnt5a, β-catenin, T cell factor (Tcf4), lymphoid enhancer factor 1 (Lef1), c-Myc and Cyclin D1 expression levels, while it upregulated adenomatous polyposis coli (APC) and glycogen synthase kinase (GSK3β) expression levels. This extract significantly reduced COX-2 levels and iNOS activities.		Results: Chamomile extract modulated the Wnt pathway in colonic tissues, where it significantly downregulated Wnt5a, β-catenin, T cell factor (Tcf4), lymphoid enhancer factor 1 (Lef1), c-Myc and Cyclin D1 expression levels, while it upregulated adenomatous polyposis coli (APC) and glycogen synthase kinase (GSK3β) expression levels. This extract significantly reduced COX-2 levels and iNOS activities.	Immunohistochemical staining	Results: Chamomile extract modulated the Wnt pathway in colonic tissues, where it significantly downregulated Wnt5a, β-catenin, T cell factor (Tcf4), lymphoid enhancer factor 1 (Lef1), c-Myc and Cyclin D1 expression levels, while it upregulated adenomatous polyposis coli (APC) and glycogen synthase kinase (GSK3β) expression levels. This extract significantly reduced COX-2 levels and iNOS activities.			Molecular assays，RT-PCR				Tcf4
32241803	chr10	23189894	23191894	PTF1A	We demonstrate a requirement for positive transcriptional autoregulatory feedback to attain the level of the neuronal specification factor PTF1A necessary for generating correctly balanced neuronal circuits.	mouse	Nervous tissue	High+Lowthroughput	Positive autofeedback regulation of Ptf1a transcription generates the levels of PTF1A required to generate itch circuit neurons	否			Astrocyte	E_02_0360	Tissue preparation, immunohistochemistry, in situ hybridization,RT-qPCR，RNA-seq	We demonstrate a requirement for positive transcriptional autoregulatory feedback to attain the level of the neuronal specification factor PTF1A necessary for generating correctly balanced neuronal circuits.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We demonstrate a requirement for positive transcriptional autoregulatory feedback to attain the level of the neuronal specification factor PTF1A necessary for generating correctly balanced neuronal circuits.		We demonstrate a requirement for positive transcriptional autoregulatory feedback to attain the level of the neuronal specification factor PTF1A necessary for generating correctly balanced neuronal circuits.	Immunohistochemical staining	We demonstrate a requirement for positive transcriptional autoregulatory feedback to attain the level of the neuronal specification factor PTF1A necessary for generating correctly balanced neuronal circuits.			Tissue preparation, immunohistochemistry, in situ hybridization,RT-qPCR，RNA-seq				PTF1A
32303558	chr3	180986412	180988412	SOX2-OT	SOX2-OT has been shown to repress the expression of SOX2, which plays roles in development, in maintaining pluripotent stem cell populations, and in neural differentiation in the cortex especially impacting GABAergic neurons (Ferri et al. 2004; Cavallaro et al.  2008; Zhang and Cui 2014; Shahryari et al. 2015; Knauss et al.	mouse		High+Lowthroughput	Leveraging mouse chromatin data for heritability enrichment informs common disease architecture and reveals cortical layer contributions to schizophrenia	是	rs1805203，rs1805645	Schizophrenia		E_02_0361	ATAC-seq	SOX2-OT has been shown to repress the expression of SOX2, which plays roles in development, in maintaining pluripotent stem cell populations, and in neural differentiation in the cortex especially impacting GABAergic neurons (Ferri et al. 2004; Cavallaro et al.  2008; Zhang and Cui 2014; Shahryari et al. 2015; Knauss et al.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SOX2-OT has been shown to repress the expression of SOX2, which plays roles in development, in maintaining pluripotent stem cell populations, and in neural differentiation in the cortex especially impacting GABAergic neurons (Ferri et al. 2004; Cavallaro et al.  2008; Zhang and Cui 2014; Shahryari et al. 2015; Knauss et al.		SOX2-OT has been shown to repress the expression of SOX2, which plays roles in development, in maintaining pluripotent stem cell populations, and in neural differentiation in the cortex especially impacting GABAergic neurons (Ferri et al. 2004; Cavallaro et al.  2008; Zhang and Cui 2014; Shahryari et al. 2015; Knauss et al.	Immunohistochemical staining	SOX2-OT has been shown to repress the expression of SOX2, which plays roles in development, in maintaining pluripotent stem cell populations, and in neural differentiation in the cortex especially impacting GABAergic neurons (Ferri et al. 2004; Cavallaro et al.  2008; Zhang and Cui 2014; Shahryari et al. 2015; Knauss et al.			ATAC-seq				SOX2-OT
32310225	chr12	3474448	3476448	Asxl2	Asxl2ΔLysM mice resisted HFD-induced adipose tissue macrophage infiltration and inflammatory cytokine gene expression.	mouse	bone marrow	High+Lowthroughput	Myeloid-specific Asxl2 deletion limits diet-induced obesity by regulating energy expenditure	否		Obesity	bone marrow cell	E_02_0362	RNA extraction，siRNA，flow cytometry，Immunohistochemical staining，Western blot，RNA-seqqPCR	Asxl2ΔLysM mice resisted HFD-induced adipose tissue macrophage infiltration and inflammatory cytokine gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Asxl2ΔLysM mice resisted HFD-induced adipose tissue macrophage infiltration and inflammatory cytokine gene expression.		Asxl2ΔLysM mice resisted HFD-induced adipose tissue macrophage infiltration and inflammatory cytokine gene expression.	Immunohistochemical staining	Asxl2ΔLysM mice resisted HFD-induced adipose tissue macrophage infiltration and inflammatory cytokine gene expression.			RNA extraction，siRNA，flow cytometry，Immunohistochemical staining，Western blot，RNA-seqqPCR				Asxl2
32370249	chr7	148804496	148806496	EZH2	H3K27 trimethylation (H3K27me3) by EZH2 is a key mechanism responsible for gene repression.	mouse	lymphoid tissue	High+Lowthroughput	The Role of the Histone Methyltransferase EZH2 in Liver Inflammation and Fibrosis in STAM NASH Mice	否		Liver Inflammation and Fibrosis	B cell	E_02_0363	Real-Time Polymerase Chain Reaction	H3K27 trimethylation (H3K27me3) by EZH2 is a key mechanism responsible for gene repression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	H3K27 trimethylation (H3K27me3) by EZH2 is a key mechanism responsible for gene repression.		H3K27 trimethylation (H3K27me3) by EZH2 is a key mechanism responsible for gene repression.	Immunohistochemical staining	H3K27 trimethylation (H3K27me3) by EZH2 is a key mechanism responsible for gene repression.			Real-Time Polymerase Chain Reaction				EZH2
32442533	chr10	68557663	68559663	TET1	We show that the combined presence of 5-methylcytosine (5mC) and 5hmC correlates with transcriptional activity of associated genes.	mouse	Nervous tissue	High+Lowthroughput	TET1 and 5-Hydroxymethylation Preserve the Stem Cell State of Mouse Trophoblast	否			stem cell	E_02_0364	meDIP-qPCR	We show that the combined presence of 5-methylcytosine (5mC) and 5hmC correlates with transcriptional activity of associated genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We show that the combined presence of 5-methylcytosine (5mC) and 5hmC correlates with transcriptional activity of associated genes.		We show that the combined presence of 5-methylcytosine (5mC) and 5hmC correlates with transcriptional activity of associated genes.	Immunohistochemical staining	We show that the combined presence of 5-methylcytosine (5mC) and 5hmC correlates with transcriptional activity of associated genes.			meDIP-qPCR				TET1
32443487	chr7	34815535	34817535	Cebpa	Adipogenesis is induced by the increased expression of adipogenesis-inducing genes such as Cebpa, Fabp4, Pparg and Srebp1.	mouse	Nervous tissue	High+Lowthroughput	Antiadipogenic Effects of Mixtures of Cornus officinalis and Ribes fasciculatum Extracts on 3T3-L1 Preadipocytes and High-Fat Diet-Induced Mice	否		Obesity	3T3-L1 cell	E_02_0365	Quantitative Reverse-Transcription Polymerase Chain Reaction	Adipogenesis is induced by the increased expression of adipogenesis-inducing genes such as Cebpa, Fabp4, Pparg and Srebp1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Adipogenesis is induced by the increased expression of adipogenesis-inducing genes such as Cebpa, Fabp4, Pparg and Srebp1.		Adipogenesis is induced by the increased expression of adipogenesis-inducing genes such as Cebpa, Fabp4, Pparg and Srebp1.	Immunohistochemical staining	Adipogenesis is induced by the increased expression of adipogenesis-inducing genes such as Cebpa, Fabp4, Pparg and Srebp1.			Quantitative Reverse-Transcription Polymerase Chain Reaction				Cebpa
32443487	chr3	10266134	10268134	Fabp4	Adipogenesis is induced by the increased expression of adipogenesis-inducing genes such as Cebpa, Fabp4, Pparg and Srebp1.	mouse	Nervous tissue	High+Lowthroughput	Antiadipogenic Effects of Mixtures of Cornus officinalis and Ribes fasciculatum Extracts on 3T3-L1 Preadipocytes and High-Fat Diet-Induced Mice	否		Obesity	3T3-L1 cell	E_02_0365	Quantitative Reverse-Transcription Polymerase Chain Reaction	Adipogenesis is induced by the increased expression of adipogenesis-inducing genes such as Cebpa, Fabp4, Pparg and Srebp1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Adipogenesis is induced by the increased expression of adipogenesis-inducing genes such as Cebpa, Fabp4, Pparg and Srebp1.		Adipogenesis is induced by the increased expression of adipogenesis-inducing genes such as Cebpa, Fabp4, Pparg and Srebp1.	Immunohistochemical staining	Adipogenesis is induced by the increased expression of adipogenesis-inducing genes such as Cebpa, Fabp4, Pparg and Srebp1.			Quantitative Reverse-Transcription Polymerase Chain Reaction				Fabp4
32447612	chr17	42310817	42312817	STAT3	To gain an understanding of the efects of alcohol on IL-6 signal transduction, we studied activation/expression of IL-6 signal transduction partners STAT3 (Signal Transducer and Activator of Transcription), CCAAT-enhancer binding protein (C/EBP) beta, and p42/p44 mitogen-activated protein   kinase (MAPK) at the protein level. Cerebella of transgenic mice that express elevated levels of astrocyte produced IL-6 in the CNS were studied.	mouse	Nervous tissue	High+Lowthroughput	Alcohol alters IL-6 Signal Transduction in the CNS of Transgenic Mice with Increased Astrocyte Expression of IL-6	否		CNS disorders	Astrocyte	E_02_0366	PCR	To gain an understanding of the efects of alcohol on IL-6 signal transduction, we studied activation/expression of IL-6 signal transduction partners STAT3 (Signal Transducer and Activator of Transcription), CCAAT-enhancer binding protein (C/EBP) beta, and p42/p44 mitogen-activated protein   kinase (MAPK) at the protein level. Cerebella of transgenic mice that express elevated levels of astrocyte produced IL-6 in the CNS were studied.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To gain an understanding of the efects of alcohol on IL-6 signal transduction, we studied activation/expression of IL-6 signal transduction partners STAT3 (Signal Transducer and Activator of Transcription), CCAAT-enhancer binding protein (C/EBP) beta, and p42/p44 mitogen-activated protein   kinase (MAPK) at the protein level. Cerebella of transgenic mice that express elevated levels of astrocyte produced IL-6 in the CNS were studied.		To gain an understanding of the efects of alcohol on IL-6 signal transduction, we studied activation/expression of IL-6 signal transduction partners STAT3 (Signal Transducer and Activator of Transcription), CCAAT-enhancer binding protein (C/EBP) beta, and p42/p44 mitogen-activated protein   kinase (MAPK) at the protein level. Cerebella of transgenic mice that express elevated levels of astrocyte produced IL-6 in the CNS were studied.	Immunohistochemical staining	To gain an understanding of the efects of alcohol on IL-6 signal transduction, we studied activation/expression of IL-6 signal transduction partners STAT3 (Signal Transducer and Activator of Transcription), CCAAT-enhancer binding protein (C/EBP) beta, and p42/p44 mitogen-activated protein   kinase (MAPK) at the protein level. Cerebella of transgenic mice that express elevated levels of astrocyte produced IL-6 in the CNS were studied.			PCR				STAT3
32499679	chr13	83649540	83651540	Mef2c	We proved that Mef2c (Myocyte-specific enhancer factor 2C), a member of the MEF2 subfamily, is the target gene of lncRNA-11496.	mouse	Nervous tissue	High+Lowthroughput	Downregulation of lncRNA-11496 in the Brain Contributes to Microglia Apoptosis via Regulation of Mef2c in Chronic T. gondii Infection Mice	否		Toxoplasma gondii	microglial cell	E_02_0367	qRT-PCR,Western Blot,Immunohistochemistry andImmunofluorescence Assays	We proved that Mef2c (Myocyte-specific enhancer factor 2C), a member of the MEF2 subfamily, is the target gene of lncRNA-11496.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We proved that Mef2c (Myocyte-specific enhancer factor 2C), a member of the MEF2 subfamily, is the target gene of lncRNA-11496.		We proved that Mef2c (Myocyte-specific enhancer factor 2C), a member of the MEF2 subfamily, is the target gene of lncRNA-11496.	Immunohistochemical staining	We proved that Mef2c (Myocyte-specific enhancer factor 2C), a member of the MEF2 subfamily, is the target gene of lncRNA-11496.			qRT-PCR,Western Blot,Immunohistochemistry andImmunofluorescence Assays				Mef2c
32554463	chr3	8725839	8727839	Hey1	Unlike Ezh2 loss-of-function, dual inactivation of Ezh1 and Ezh2 triggered overexpression of the transcriptional repressor Hesrelated family BHLH transcription factor with YRPW motif 1 (Hey1), downregulation of Six2, and unscheduled activation of Wnt4-driven differentiation, resulting in early termination of nephrogenesis and severe renal dysgenesis.	mouse	connective tissue	High+Lowthroughput	The polycomb proteins EZH1 and EZH2 co-regulate chromatin accessibility and nephron progenitor cell lifespan in mice	否		Nasopharynx cancer	nephron progenitor cell	E_02_0368	immunohistochemistry，Section in situ hybridization，ATAC-seq，RNA-seq，	Unlike Ezh2 loss-of-function, dual inactivation of Ezh1 and Ezh2 triggered overexpression of the transcriptional repressor Hesrelated family BHLH transcription factor with YRPW motif 1 (Hey1), downregulation of Six2, and unscheduled activation of Wnt4-driven differentiation, resulting in early termination of nephrogenesis and severe renal dysgenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Unlike Ezh2 loss-of-function, dual inactivation of Ezh1 and Ezh2 triggered overexpression of the transcriptional repressor Hesrelated family BHLH transcription factor with YRPW motif 1 (Hey1), downregulation of Six2, and unscheduled activation of Wnt4-driven differentiation, resulting in early termination of nephrogenesis and severe renal dysgenesis.		Unlike Ezh2 loss-of-function, dual inactivation of Ezh1 and Ezh2 triggered overexpression of the transcriptional repressor Hesrelated family BHLH transcription factor with YRPW motif 1 (Hey1), downregulation of Six2, and unscheduled activation of Wnt4-driven differentiation, resulting in early termination of nephrogenesis and severe renal dysgenesis.	Immunohistochemical staining	Unlike Ezh2 loss-of-function, dual inactivation of Ezh1 and Ezh2 triggered overexpression of the transcriptional repressor Hesrelated family BHLH transcription factor with YRPW motif 1 (Hey1), downregulation of Six2, and unscheduled activation of Wnt4-driven differentiation, resulting in early termination of nephrogenesis and severe renal dysgenesis.			immunohistochemistry，Section in situ hybridization，ATAC-seq，RNA-seq，				Hey1
32561533	chr7	55016526	55018526	EGFR	Endocan facilitated EGFR signaling via direct 12 binding and enhancing of the EGF-EGFR interaction and supported the growth of 13 tumors driven by mutated EGFR.	mouse		High+Lowthroughput	Circulating Proteoglycan Endocan Mediates EGFR-Driven Progression of Non-Small Cell Lung Cancer	否		Lung cancer	NCI-H1975	E_02_0369	qPCR，Immunoprecipitation，Western blotting， immunohistochemical，Flow cytometry	Endocan facilitated EGFR signaling via direct 12 binding and enhancing of the EGF-EGFR interaction and supported the growth of 13 tumors driven by mutated EGFR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Endocan facilitated EGFR signaling via direct 12 binding and enhancing of the EGF-EGFR interaction and supported the growth of 13 tumors driven by mutated EGFR.		Endocan facilitated EGFR signaling via direct 12 binding and enhancing of the EGF-EGFR interaction and supported the growth of 13 tumors driven by mutated EGFR.	Immunohistochemical staining	Endocan facilitated EGFR signaling via direct 12 binding and enhancing of the EGF-EGFR interaction and supported the growth of 13 tumors driven by mutated EGFR.			qPCR，Immunoprecipitation，Western blotting， immunohistochemical，Flow cytometry				EGFR
32615080	chr12	102393416	102395416	IGF1	Azithromycin disturbed hepatocyte differentiation, maturation and metabolic function via upregulating GR-C/EBPα signal and reducing the   expression and secretion levels of IGF1 in HepG2 cells.	mouse		High+Lowthroughput	GR-C/EBPα-IGF1 axis mediated azithromycin-induced liver developmental toxicity in fetal mice	否		Perinatal mycoplasma infection	HepG2 cell	E_02_0370	Immunostaining，RT-qPCR，Western blotting	Azithromycin disturbed hepatocyte differentiation, maturation and metabolic function via upregulating GR-C/EBPα signal and reducing the   expression and secretion levels of IGF1 in HepG2 cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Azithromycin disturbed hepatocyte differentiation, maturation and metabolic function via upregulating GR-C/EBPα signal and reducing the   expression and secretion levels of IGF1 in HepG2 cells.		Azithromycin disturbed hepatocyte differentiation, maturation and metabolic function via upregulating GR-C/EBPα signal and reducing the   expression and secretion levels of IGF1 in HepG2 cells.	Immunohistochemical staining	Azithromycin disturbed hepatocyte differentiation, maturation and metabolic function via upregulating GR-C/EBPα signal and reducing the   expression and secretion levels of IGF1 in HepG2 cells.			Immunostaining，RT-qPCR，Western blotting				IGF1
32622945	chr5	36149227	36151227	SKP2	Using Estradiol-inducible K562-C/EBPα-ER cells as yet another model of granulocytic differentiation, we further confirmed that SKP2 overexpression indeed inhibits granulocytic differentiation by mitigating C/EBPα stability.	mouse		High+Lowthroughput	E3 ligase SCF(SKP2) ubiquitinates and degrades tumor suppressor C/EBPα in acute myeloid leukemia	否		Acute Myeloid Leukemia	HL-60	E_02_0371	Western blot，Co-immunoprecipitation，Immunophenotyping analysis，flow cytometer，Quantitative real-time PCR	Using Estradiol-inducible K562-C/EBPα-ER cells as yet another model of granulocytic differentiation, we further confirmed that SKP2 overexpression indeed inhibits granulocytic differentiation by mitigating C/EBPα stability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Using Estradiol-inducible K562-C/EBPα-ER cells as yet another model of granulocytic differentiation, we further confirmed that SKP2 overexpression indeed inhibits granulocytic differentiation by mitigating C/EBPα stability.		Using Estradiol-inducible K562-C/EBPα-ER cells as yet another model of granulocytic differentiation, we further confirmed that SKP2 overexpression indeed inhibits granulocytic differentiation by mitigating C/EBPα stability.	Immunohistochemical staining	Using Estradiol-inducible K562-C/EBPα-ER cells as yet another model of granulocytic differentiation, we further confirmed that SKP2 overexpression indeed inhibits granulocytic differentiation by mitigating C/EBPα stability.			Western blot，Co-immunoprecipitation，Immunophenotyping analysis，flow cytometer，Quantitative real-time PCR				SKP2
32622946	chr5	36149144	36151144	SKP2	Using Estradiol-inducible K562-C/EBPα-ER cells as yet another model of granulocytic differentiation, we further confirmed that SKP2 overexpression indeed inhibits granulocytic differentiation by mitigating C/EBPα stability.	mouse		High+Lowthroughput	E3 ligase SCF(SKP3) ubiquitinates and degrades tumor suppressor C/EBPα in acute myeloid leukemia	否		Acute Myeloid Leukemia	U937	E_02_0372	Western blot，Co-immunoprecipitation，Immunophenotyping analysis，flow cytometer，Quantitative real-time PCR	Using Estradiol-inducible K562-C/EBPα-ER cells as yet another model of granulocytic differentiation, we further confirmed that SKP2 overexpression indeed inhibits granulocytic differentiation by mitigating C/EBPα stability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Using Estradiol-inducible K562-C/EBPα-ER cells as yet another model of granulocytic differentiation, we further confirmed that SKP2 overexpression indeed inhibits granulocytic differentiation by mitigating C/EBPα stability.		Using Estradiol-inducible K562-C/EBPα-ER cells as yet another model of granulocytic differentiation, we further confirmed that SKP2 overexpression indeed inhibits granulocytic differentiation by mitigating C/EBPα stability.	Immunohistochemical staining	Using Estradiol-inducible K562-C/EBPα-ER cells as yet another model of granulocytic differentiation, we further confirmed that SKP2 overexpression indeed inhibits granulocytic differentiation by mitigating C/EBPα stability.			Western blot，Co-immunoprecipitation，Immunophenotyping analysis，flow cytometer，Quantitative real-time PCR				SKP2
32298702	chr7	148804089	148806089	EZH2	In addition, a significant increase in the pro-inflammatory cytokine (IL-1β and TNF-α) levels was observed in rats after GSK 126 treatment, and IL-1β administration increased seizure severity, suggesting that the inflammatory response was involved in the regulation of seizure development by EZH2.	mouse	Nervous tissue	High+Lowthroughput	Inhibition of EZH2 attenuates inhibitory synaptic transmission via the pro-inflammatory pathway in rats	否		Febrile seizures		E_02_0373	Enzyme-linked immunosorbent assay，Western blot，qRT-PCR	In addition, a significant increase in the pro-inflammatory cytokine (IL-1β and TNF-α) levels was observed in rats after GSK 126 treatment, and IL-1β administration increased seizure severity, suggesting that the inflammatory response was involved in the regulation of seizure development by EZH2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, a significant increase in the pro-inflammatory cytokine (IL-1β and TNF-α) levels was observed in rats after GSK 126 treatment, and IL-1β administration increased seizure severity, suggesting that the inflammatory response was involved in the regulation of seizure development by EZH2.		In addition, a significant increase in the pro-inflammatory cytokine (IL-1β and TNF-α) levels was observed in rats after GSK 126 treatment, and IL-1β administration increased seizure severity, suggesting that the inflammatory response was involved in the regulation of seizure development by EZH2.	Immunohistochemical staining	In addition, a significant increase in the pro-inflammatory cytokine (IL-1β and TNF-α) levels was observed in rats after GSK 126 treatment, and IL-1β administration increased seizure severity, suggesting that the inflammatory response was involved in the regulation of seizure development by EZH2.			Enzyme-linked immunosorbent assay，Western blot，qRT-PCR				EZH2
32302712	chr11	6414970	6416970	Purb	On the one hand, Lnc19959.2 up-regulate ApoA4 expression via ubiquitinated transcription inhibitor factor Purb; on the other hand, lnc19959.2-hnRNPA2B1 complex acts on Cpt1a, Tm7sf2 and Gpam in some ways to reduce the efficiency of RNA polymerase II occupy on the target gene promoter.	mouse		High+Lowthroughput	The novel long noncoding RNA Lnc19959.2 modulates triglyceride metabolism-associated genes through the interaction with Purb and hnRNPA2B1	否		Hypertriglyceridemia	Brl-3a	E_02_0374	RNA extraction and Transcriptome sequencing，Quantitative real-time PCR，RACE，RNA immunoprecipitation，Chromatin immunoprecipitation	On the one hand, Lnc19959.2 up-regulate ApoA4 expression via ubiquitinated transcription inhibitor factor Purb; on the other hand, lnc19959.2-hnRNPA2B1 complex acts on Cpt1a, Tm7sf2 and Gpam in some ways to reduce the efficiency of RNA polymerase II occupy on the target gene promoter.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	On the one hand, Lnc19959.2 up-regulate ApoA4 expression via ubiquitinated transcription inhibitor factor Purb; on the other hand, lnc19959.2-hnRNPA2B1 complex acts on Cpt1a, Tm7sf2 and Gpam in some ways to reduce the efficiency of RNA polymerase II occupy on the target gene promoter.		On the one hand, Lnc19959.2 up-regulate ApoA4 expression via ubiquitinated transcription inhibitor factor Purb; on the other hand, lnc19959.2-hnRNPA2B1 complex acts on Cpt1a, Tm7sf2 and Gpam in some ways to reduce the efficiency of RNA polymerase II occupy on the target gene promoter.	Immunohistochemical staining	On the one hand, Lnc19959.2 up-regulate ApoA4 expression via ubiquitinated transcription inhibitor factor Purb; on the other hand, lnc19959.2-hnRNPA2B1 complex acts on Cpt1a, Tm7sf2 and Gpam in some ways to reduce the efficiency of RNA polymerase II occupy on the target gene promoter.			RNA extraction and Transcriptome sequencing，Quantitative real-time PCR，RACE，RNA immunoprecipitation，Chromatin immunoprecipitation				Purb
32337955	chr1	247412880	247414880	NLRP3	Treatment with melodinhenine B attenuated the altered expression of NF-κB, IL-1β, NLRP3, ZO-1, and occluding proteins in the brain tissue of I/R-induced neuronal injury rats.	mouse	Nervous tissue	High+Lowthroughput	Melodinhenine B attenuates NLRP3 expression in a cerebral ischemia/reperfusion-induced neuronal injury rat model	否		Neuronal injury		E_02_0375	Western blotting，Immunohistochemical analysis	Treatment with melodinhenine B attenuated the altered expression of NF-κB, IL-1β, NLRP3, ZO-1, and occluding proteins in the brain tissue of I/R-induced neuronal injury rats.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Treatment with melodinhenine B attenuated the altered expression of NF-κB, IL-1β, NLRP3, ZO-1, and occluding proteins in the brain tissue of I/R-induced neuronal injury rats.		Treatment with melodinhenine B attenuated the altered expression of NF-κB, IL-1β, NLRP3, ZO-1, and occluding proteins in the brain tissue of I/R-induced neuronal injury rats.	Immunohistochemical staining	Treatment with melodinhenine B attenuated the altered expression of NF-κB, IL-1β, NLRP3, ZO-1, and occluding proteins in the brain tissue of I/R-induced neuronal injury rats.			Western blotting，Immunohistochemical analysis				NLRP3
32346844	chr7	148804686	148806686	EZH2	We found that EZH2 levels were markedly upregulated during BPA-induced neuropathic pain in vivo and in vitro, stimulating pro-inflammatory cytokines (IL- 1b, TNF-a, and IL-6) secretion in vivo.	mouse	lymphoid tissue	High+Lowthroughput	Increased EZH2 Levels in Anterior Cingulate Cortex Microglia Aggravate Neuropathic Pain by Inhibiting Autophagy Following Brachial Plexus Avulsion in Rats	否		Brachial Plexus Avulsion	immune cell	E_02_0376	Western Blot，q-RT PCR，Immunofluorescence Analysis	We found that EZH2 levels were markedly upregulated during BPA-induced neuropathic pain in vivo and in vitro, stimulating pro-inflammatory cytokines (IL- 1b, TNF-a, and IL-6) secretion in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found that EZH2 levels were markedly upregulated during BPA-induced neuropathic pain in vivo and in vitro, stimulating pro-inflammatory cytokines (IL- 1b, TNF-a, and IL-6) secretion in vivo.		We found that EZH2 levels were markedly upregulated during BPA-induced neuropathic pain in vivo and in vitro, stimulating pro-inflammatory cytokines (IL- 1b, TNF-a, and IL-6) secretion in vivo.	Immunohistochemical staining	We found that EZH2 levels were markedly upregulated during BPA-induced neuropathic pain in vivo and in vitro, stimulating pro-inflammatory cytokines (IL- 1b, TNF-a, and IL-6) secretion in vivo.			Western Blot，q-RT PCR，Immunofluorescence Analysis				EZH2
32355753	chr1	10447362	10449362	CORT	These data demonstrate that CORT can attenuate ISO-induced acute myocardial injury in rats likely by reducing lipid peroxidation, and inhibiting endoplasmic reticulum stress and autophagy.	mouse	Nervous tissue	High+Lowthroughput	Cardioprotection of cortistatin against isoproterenol-induced myocardial injury in rats	否		Myocardial injury	dendritic cell	E_02_0377	Western blotting	These data demonstrate that CORT can attenuate ISO-induced acute myocardial injury in rats likely by reducing lipid peroxidation, and inhibiting endoplasmic reticulum stress and autophagy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These data demonstrate that CORT can attenuate ISO-induced acute myocardial injury in rats likely by reducing lipid peroxidation, and inhibiting endoplasmic reticulum stress and autophagy.		These data demonstrate that CORT can attenuate ISO-induced acute myocardial injury in rats likely by reducing lipid peroxidation, and inhibiting endoplasmic reticulum stress and autophagy.	Immunohistochemical staining	These data demonstrate that CORT can attenuate ISO-induced acute myocardial injury in rats likely by reducing lipid peroxidation, and inhibiting endoplasmic reticulum stress and autophagy.			Western blotting				CORT
32363643	chr2	202203540	202205540	SUMO1	A significant increase in small ubiquitin-like modifier 1 (SUMO1) and sumoylated C/ EBPα protein levels were observed in BPD rats, and the levels of the sumoylated C/EBPα were associated with the pulmonary surfactant proteins (SPs).	mouse	Epithelial tissues	High+Lowthroughput	Sumoylation of CCAAT-enhancer-binding protein α inhibits lung differentiation in Bronchopulmonary Dysplasia model rats	否		Bronchopulmonary dysplasia	epithelial cell	E_02_0378	RT-PCR, Western blot，Co_x005f_x0002_immunoprecipitation	A significant increase in small ubiquitin-like modifier 1 (SUMO1) and sumoylated C/ EBPα protein levels were observed in BPD rats, and the levels of the sumoylated C/EBPα were associated with the pulmonary surfactant proteins (SPs).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A significant increase in small ubiquitin-like modifier 1 (SUMO1) and sumoylated C/ EBPα protein levels were observed in BPD rats, and the levels of the sumoylated C/EBPα were associated with the pulmonary surfactant proteins (SPs).		A significant increase in small ubiquitin-like modifier 1 (SUMO1) and sumoylated C/ EBPα protein levels were observed in BPD rats, and the levels of the sumoylated C/EBPα were associated with the pulmonary surfactant proteins (SPs).	Immunohistochemical staining	A significant increase in small ubiquitin-like modifier 1 (SUMO1) and sumoylated C/ EBPα protein levels were observed in BPD rats, and the levels of the sumoylated C/EBPα were associated with the pulmonary surfactant proteins (SPs).			RT-PCR, Western blot，Co_x005f_x0002_immunoprecipitation				SUMO1
32602773	chr10	67881781	67883781	SIRT1	Similarly, we observed an increased SIRT1 activity in the liver of AIA rats compared to healthy controls which decreased under high doses of GCs.	mouse		High+Lowthroughput	Characterizing the dynamic and functional DNA methylation landscape in the developing human cortex	否		Inflammation，endorsing inflammation, articular destruction	peripheral blood mononuclear cell	E_02_0379	RT-PCR	Similarly, we observed an increased SIRT1 activity in the liver of AIA rats compared to healthy controls which decreased under high doses of GCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Similarly, we observed an increased SIRT1 activity in the liver of AIA rats compared to healthy controls which decreased under high doses of GCs.		Similarly, we observed an increased SIRT1 activity in the liver of AIA rats compared to healthy controls which decreased under high doses of GCs.	Immunohistochemical staining	Similarly, we observed an increased SIRT1 activity in the liver of AIA rats compared to healthy controls which decreased under high doses of GCs.			RT-PCR				SIRT1
32344637	chr4	153681236	153683236	TLR2	These mechanisms included B-cell maturation, antibody-mediated opsonization of mycobacteria, Fc-receptor (FcR)-mediated phagocytosis, macrophage response, interference with the α-Gal antagonistic effect of the toll-like receptor 2 (TLR2)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB)-mediated immune response, and upregulation of pro-inflammatory cytokines.	mouse		High+Lowthroughput	Vaccination with Alpha-Gal Protects Against Mycobacterial Infection in the Zebrafish Model of Tuberculosis	否		Tuberculosis	B cell	E_02_0380	Flow Cytometry	These mechanisms included B-cell maturation, antibody-mediated opsonization of mycobacteria, Fc-receptor (FcR)-mediated phagocytosis, macrophage response, interference with the α-Gal antagonistic effect of the toll-like receptor 2 (TLR2)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB)-mediated immune response, and upregulation of pro-inflammatory cytokines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These mechanisms included B-cell maturation, antibody-mediated opsonization of mycobacteria, Fc-receptor (FcR)-mediated phagocytosis, macrophage response, interference with the α-Gal antagonistic effect of the toll-like receptor 2 (TLR2)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB)-mediated immune response, and upregulation of pro-inflammatory cytokines.		These mechanisms included B-cell maturation, antibody-mediated opsonization of mycobacteria, Fc-receptor (FcR)-mediated phagocytosis, macrophage response, interference with the α-Gal antagonistic effect of the toll-like receptor 2 (TLR2)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB)-mediated immune response, and upregulation of pro-inflammatory cytokines.	Immunohistochemical staining	These mechanisms included B-cell maturation, antibody-mediated opsonization of mycobacteria, Fc-receptor (FcR)-mediated phagocytosis, macrophage response, interference with the α-Gal antagonistic effect of the toll-like receptor 2 (TLR2)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB)-mediated immune response, and upregulation of pro-inflammatory cytokines.			Flow Cytometry				TLR2
30463291	chr8	144312388	144314388	DGAT1	The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.	mouse	white adipose tissue	High+Lowthroughput	Ishige okamurae Extract Suppresses Obesity and Hepatic Steatosis in High Fat Diet-Induced Obese Mice	否	无	Hepatic steatosis, obesity		E_02_0381	 Cell Viability Assay,Western Blot Analysis,Oil Red O Staining	The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.		The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.	Immunohistochemical staining	The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.			 Cell Viability Assay,Western Blot Analysis,Oil Red O Staining				DGAT1
30463291	chr10	88950780	88952780	FAS	The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.	mouse	white adipose tissue	High+Lowthroughput	Ishige okamurae Extract Suppresses Obesity and Hepatic Steatosis in High Fat Diet-Induced Obese Mice	否	无	Hepatic steatosis, obesity		E_02_0381	 Cell Viability Assay,Western Blot Analysis,Oil Red O Staining	The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.		The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.	Immunohistochemical staining	The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.			 Cell Viability Assay,Western Blot Analysis,Oil Red O Staining				FAS
30463291	chr1	53194024	53196024	CPT2	The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.	mouse		High+Lowthroughput	Ishige okamurae Extract Suppresses Obesity and Hepatic Steatosis in High Fat Diet-Induced Obese Mice	否	无	Hepatic steatosis, obesity	3T3-L1 preadipocytes	E_02_0381	 Cell Viability Assay,Western Blot Analysis,Oil Red O Staining	The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.		The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.	Immunohistochemical staining	The obesity suppression was associated with reductions in expression of adipogenic proteins, such as C/EBPα and PPARγ, increases in expression of lipolytic enzymes, such as adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), in WAT of HFD-fed mice. In addition, IOE-treated mice had lower hepatic TG content, associated with lower protein expression of lipogenic genes, such as diglyceride acyltransferase 1 (DGAT1), sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS). IOE treatment also reduced serum free fatty acid concentration, probably through the upregulation of β-oxidation genes, suggested by increases in AMPKα and CPT1 expression in WAT and liver.			 Cell Viability Assay,Western Blot Analysis,Oil Red O Staining				CPT2
30462329	chr5	143486631	143488631	Rac1	Co-treatment with Fasudil prevented axonal degeneration by mitigating neurite extension/retraction incoordination caused by methylmercury-induced suppression of Rac1 in vitro and in subacute methylmercury-intoxicated rats.	mouses		High+Lowthroughput	Fasudil, a Rho-Associated Coiled Coil-Forming Protein Kinase Inhibitor, Recovers Methylmercury-Induced Axonal Degeneration by Changing Microglial Phenotype in Rats	否	无	Chronic Methyl-mercury Poisoning 	microglial cell	E_02_0382	ROCK activity assay,Western blot	Co-treatment with Fasudil prevented axonal degeneration by mitigating neurite extension/retraction incoordination caused by methylmercury-induced suppression of Rac1 in vitro and in subacute methylmercury-intoxicated rats.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Co-treatment with Fasudil prevented axonal degeneration by mitigating neurite extension/retraction incoordination caused by methylmercury-induced suppression of Rac1 in vitro and in subacute methylmercury-intoxicated rats.		Co-treatment with Fasudil prevented axonal degeneration by mitigating neurite extension/retraction incoordination caused by methylmercury-induced suppression of Rac1 in vitro and in subacute methylmercury-intoxicated rats.	Immunohistochemical staining	Co-treatment with Fasudil prevented axonal degeneration by mitigating neurite extension/retraction incoordination caused by methylmercury-induced suppression of Rac1 in vitro and in subacute methylmercury-intoxicated rats.			ROCK activity assay,Western blot				Rac1
30459414	chr1	156460934	156462934	MEF2D	We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 	human		High+Lowthroughput	A rare regulatory variant in the MEF2D gene affects gene regulation and splicing and is associated with a SLE sub-phenotype in Swedish cohorts	是	rs200395694,rs867059436, rs576275580	Systemic lupus erythematosus	T, B, NK cell	E_01_0625	Gene array capture，Seq,Gene array capture	We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 		We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 	Immunohistochemical staining	We identified a rare regulatory variant rs200395694:G > T located in intron 4 of the MEF2D gene encoding the myocyte-specific enhancer factor 2D transcription factor and associated with SLE in Swedish cohorts (504 SLE patients and 839 healthy controls, p = 0.014, CI = 1.1 10). 			Gene array capture，Seq,Gene array capture				MEF2D
30456456	chr8	144311977	144313977	DGAT1	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	mouse		High+Lowthroughput	Butyric acid induces spontaneous adipocytic differentiation of porcine bone marrow-derived mesenchymal stem cells	否	无	nothing	mesenchymal stem cell	E_02_0383	Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.		Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Immunohistochemical staining	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.			Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 				DGAT1
30456456	chr10	88950750	88952750	FAS	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	mouse		High+Lowthroughput	Butyric acid induces spontaneous adipocytic differentiation of porcine bone marrow-derived mesenchymal stem cells	否	无	nothing	mesenchymal stem cell	E_02_0383	Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.		Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Immunohistochemical staining	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.			Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 				FAS
30456456	chr1	53194354	53196354	CPT2	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	mouse		High+Lowthroughput	Butyric acid induces spontaneous adipocytic differentiation of porcine bone marrow-derived mesenchymal stem cells	否	无	nothing	mesenchymal stem cell	E_02_0383	Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.		Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.	Immunohistochemical staining	Treatment with BA modulated the expression of adipocytic differentiation markers: peroxisome proliferator-activated receptor γ and CCAAT/enhancer binding protein α were significantly increased by both BA-2.5 and BA-5 throughout the study, while lipoprotein lipase and fatty acid-binding protein 4 were increased by BA-5 at day 3, and decreased by both BA-5 and BA- 2.5 later throughout the study.			Proliferation study,Differentiation study,Differentiation study,Cytochemical staining 				CPT2
30456215	chr11	65495184	65497184	MALAT1	MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 	human		High+Lowthroughput	Transcriptional Profiling of Hypoxia-Regulated Non-coding RNAs in Human Primary Endothelial Cells	否	无	Human atherosclerotic lesions	 Primary endothelial cell	E_01_0626	GRO-Seq and RNA-Seq,	MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 	Immunohistochemical staining	MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 	MALAT1		GRO-Seq and RNA-Seq,	MALAT1, HYMAI, LOC730101, KIAA1656, and LOC339803 were found differentially expressed in human atherosclerotic lesions, compared to normal vascular tissue, and may thus serve as potential biomarkers for lesion hypoxia. 			
30455249	chr8	101489305	101491305	GRHL2	pS118-ER occupied a subset of ER binding sites which were associated with the active enhancer mark, acetylated H3K27. Unlike ER, pS118-ER sites were enriched in GRHL2 DNA binding motifs, and estrogen treatment increased GRHL2 recruitment to sites occupied by pS118-ER. 	human		High+Lowthroughput	The Phosphorylated Estrogen Receptor α (ER) Cistrome Identifies a Subset of Active Enhancers Enriched for Direct ER-DNA Binding and the Transcription Factor GRHL2	否	无	nothing	MCF-7 cell	E_01_0627	Western Blot，Transfection，Chromatin Immunoprecipitation，Specificity and Affinity for Proteins (SNAP) Array,ChIP-seq	pS118-ER occupied a subset of ER binding sites which were associated with the active enhancer mark, acetylated H3K27. Unlike ER, pS118-ER sites were enriched in GRHL2 DNA binding motifs, and estrogen treatment increased GRHL2 recruitment to sites occupied by pS118-ER. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			pS118-ER occupied a subset of ER binding sites which were associated with the active enhancer mark, acetylated H3K27. Unlike ER, pS118-ER sites were enriched in GRHL2 DNA binding motifs, and estrogen treatment increased GRHL2 recruitment to sites occupied by pS118-ER. 	Immunohistochemical staining	pS118-ER occupied a subset of ER binding sites which were associated with the active enhancer mark, acetylated H3K27. Unlike ER, pS118-ER sites were enriched in GRHL2 DNA binding motifs, and estrogen treatment increased GRHL2 recruitment to sites occupied by pS118-ER. 	GRHL2		Western Blot，Transfection，Chromatin Immunoprecipitation，Specificity and Affinity for Proteins (SNAP) Array,ChIP-seq	pS118-ER occupied a subset of ER binding sites which were associated with the active enhancer mark, acetylated H3K27. Unlike ER, pS118-ER sites were enriched in GRHL2 DNA binding motifs, and estrogen treatment increased GRHL2 recruitment to sites occupied by pS118-ER. 			
30453884	chr15	78562655	78564655	CHRNA5	rs4887074 is associated with CHRNB4 expression, and along with two regulatory variants of CHRNA3 and CHRNA5, modulates the effect of rs16969968 on nicotine dependence risk.  	human	peripheral tissues	High+Lowthroughput	Combined genetic influence of the nicotinic receptor gene cluster CHRNA5/A3/B4 on nicotine dependence	是	rs16969968, rs880395, rs1948, rs4887074	Nicotine dependence and other smoking related disorders		E_01_0628	Logistic regression，Multivariate regression	rs4887074 is associated with CHRNB4 expression, and along with two regulatory variants of CHRNA3 and CHRNA5, modulates the effect of rs16969968 on nicotine dependence risk.  	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	rs4887074 is associated with CHRNB4 expression, and along with two regulatory variants of CHRNA3 and CHRNA5, modulates the effect of rs16969968 on nicotine dependence risk.  		rs4887074 is associated with CHRNB4 expression, and along with two regulatory variants of CHRNA3 and CHRNA5, modulates the effect of rs16969968 on nicotine dependence risk.  	Immunohistochemical staining	rs4887074 is associated with CHRNB4 expression, and along with two regulatory variants of CHRNA3 and CHRNA5, modulates the effect of rs16969968 on nicotine dependence risk.  			Logistic regression，Multivariate regression				CHRNA5
30453072	chr1	78074974	78076974	Pax3	We discovered that myoblast determining factor (MyoD) binding elements play a key role and participate in the transcriptional regulation of MYHM2528 1 expression in zebrafish embryos. We further discovered that paired box protein (Pax3) are required for promoting MYHM2528 1 expression and myocyte enhancer factor- 2 (MEF2) binding sites participate in the transcriptional regulation of MYHM2528 1 expression in slow/fast skeletal muscles. Our study also confirmed that the nuclear factor of activated T-cell (NFAT) binding sites take part in the transcriptional regulation of MYHM2528 1 expression in slow and fast muscles fiber in relation to indeterminate muscle growth. 	mouse		High+Lowthroughput	Multiple transcription factors mediating the expressional regulation of myosin heavy chain gene involved in the indeterminate muscle growth of fish	否	无		epithelial cell	E_02_0384	Immunohistochemical analysis，Real-time PCR	We discovered that myoblast determining factor (MyoD) binding elements play a key role and participate in the transcriptional regulation of MYHM2528 1 expression in zebrafish embryos. We further discovered that paired box protein (Pax3) are required for promoting MYHM2528 1 expression and myocyte enhancer factor- 2 (MEF2) binding sites participate in the transcriptional regulation of MYHM2528 1 expression in slow/fast skeletal muscles. Our study also confirmed that the nuclear factor of activated T-cell (NFAT) binding sites take part in the transcriptional regulation of MYHM2528 1 expression in slow and fast muscles fiber in relation to indeterminate muscle growth. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We discovered that myoblast determining factor (MyoD) binding elements play a key role and participate in the transcriptional regulation of MYHM2528 1 expression in zebrafish embryos. We further discovered that paired box protein (Pax3) are required for promoting MYHM2528 1 expression and myocyte enhancer factor- 2 (MEF2) binding sites participate in the transcriptional regulation of MYHM2528 1 expression in slow/fast skeletal muscles. Our study also confirmed that the nuclear factor of activated T-cell (NFAT) binding sites take part in the transcriptional regulation of MYHM2528 1 expression in slow and fast muscles fiber in relation to indeterminate muscle growth. 		We discovered that myoblast determining factor (MyoD) binding elements play a key role and participate in the transcriptional regulation of MYHM2528 1 expression in zebrafish embryos. We further discovered that paired box protein (Pax3) are required for promoting MYHM2528 1 expression and myocyte enhancer factor- 2 (MEF2) binding sites participate in the transcriptional regulation of MYHM2528 1 expression in slow/fast skeletal muscles. Our study also confirmed that the nuclear factor of activated T-cell (NFAT) binding sites take part in the transcriptional regulation of MYHM2528 1 expression in slow and fast muscles fiber in relation to indeterminate muscle growth. 	Immunohistochemical staining	We discovered that myoblast determining factor (MyoD) binding elements play a key role and participate in the transcriptional regulation of MYHM2528 1 expression in zebrafish embryos. We further discovered that paired box protein (Pax3) are required for promoting MYHM2528 1 expression and myocyte enhancer factor- 2 (MEF2) binding sites participate in the transcriptional regulation of MYHM2528 1 expression in slow/fast skeletal muscles. Our study also confirmed that the nuclear factor of activated T-cell (NFAT) binding sites take part in the transcriptional regulation of MYHM2528 1 expression in slow and fast muscles fiber in relation to indeterminate muscle growth. 			Immunohistochemical analysis，Real-time PCR				Pax3
30452487	chr7	148804413	148806413	EZH2	Enhancer of Zeste Homolog 2 (EZH2), a histone-lysine N-methyltransferase and a component of the Polycomb Repressive Complex 2, has been shown to play a role in GvHD pathology. 	mouse		High+Lowthroughput	Selective targeting of histone modification fails to prevent graft versus host disease after hematopoietic cell transplantation	否	无	Graft versus host disease	T cell	E_02_0385	Flow cytometric analysis，In vitro T cell activation	Enhancer of Zeste Homolog 2 (EZH2), a histone-lysine N-methyltransferase and a component of the Polycomb Repressive Complex 2, has been shown to play a role in GvHD pathology. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of Zeste Homolog 2 (EZH2), a histone-lysine N-methyltransferase and a component of the Polycomb Repressive Complex 2, has been shown to play a role in GvHD pathology. 		Enhancer of Zeste Homolog 2 (EZH2), a histone-lysine N-methyltransferase and a component of the Polycomb Repressive Complex 2, has been shown to play a role in GvHD pathology. 	Immunohistochemical staining	Enhancer of Zeste Homolog 2 (EZH2), a histone-lysine N-methyltransferase and a component of the Polycomb Repressive Complex 2, has been shown to play a role in GvHD pathology. 			Flow cytometric analysis，In vitro T cell activation				EZH2
30451839	chr2	60447405	60449405	BCL11A	At a therapeutically relevant site within the BCL11A erythroid enhancer, Cas9-Cas9 nucleases produced precise deletions that comprised up to 97% of all sequence alterations. Thus Cas9-Cas9 chimeras represent an important tool that could be particularly valuable for therapeutic genome editing applications where a precise cleavage position and defined sequence end products are desirable. 	human		High+Lowthroughput	Orthogonal Cas9-Cas9 chimeras provide a versatile platform for genome editing	否	无	nothing	Embryonic kidney cells	E_01_0629	transfection/electroporation,GFP-reporter assay,Immunofluorescence,Western blot,deep sequencing,GUIDE-seq off-target analysis	At a therapeutically relevant site within the BCL11A erythroid enhancer, Cas9-Cas9 nucleases produced precise deletions that comprised up to 97% of all sequence alterations. Thus Cas9-Cas9 chimeras represent an important tool that could be particularly valuable for therapeutic genome editing applications where a precise cleavage position and defined sequence end products are desirable. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	At a therapeutically relevant site within the BCL11A erythroid enhancer, Cas9-Cas9 nucleases produced precise deletions that comprised up to 97% of all sequence alterations. Thus Cas9-Cas9 chimeras represent an important tool that could be particularly valuable for therapeutic genome editing applications where a precise cleavage position and defined sequence end products are desirable. 		At a therapeutically relevant site within the BCL11A erythroid enhancer, Cas9-Cas9 nucleases produced precise deletions that comprised up to 97% of all sequence alterations. Thus Cas9-Cas9 chimeras represent an important tool that could be particularly valuable for therapeutic genome editing applications where a precise cleavage position and defined sequence end products are desirable. 	Immunohistochemical staining	At a therapeutically relevant site within the BCL11A erythroid enhancer, Cas9-Cas9 nucleases produced precise deletions that comprised up to 97% of all sequence alterations. Thus Cas9-Cas9 chimeras represent an important tool that could be particularly valuable for therapeutic genome editing applications where a precise cleavage position and defined sequence end products are desirable. 			transfection/electroporation,GFP-reporter assay,Immunofluorescence,Western blot,deep sequencing,GUIDE-seq off-target analysis				BCL11A
30450701	chr1	26174578	26176578	CNKSR1	CNKSR1 gene defect can cause syndromic autosomal recessiveintellectual disability	human		High+Lowthroughput	CNKSR1 gene defect can cause syndromic autosomal recessive intellectual disability	是	rs10916983，rs849961	Syndromic autosomal recessive intellectual disability	Lymphoblast	E_01_0630	Protein extraction，Western blot analysis，Quantitative RT–PCR analysis of RNAi knockdown，Immunostaining	CNKSR1 gene defect can cause syndromic autosomal recessiveintellectual disability	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CNKSR1 gene defect can cause syndromic autosomal recessiveintellectual disability		CNKSR1 gene defect can cause syndromic autosomal recessiveintellectual disability	Immunohistochemical staining	CNKSR1 gene defect can cause syndromic autosomal recessiveintellectual disability			Protein extraction，Western blot analysis，Quantitative RT–PCR analysis of RNAi knockdown，Immunostaining				CNKSR1
30448425	chr17	42310893	42312893	STAT3	HSP90 inhibitor ganetespib blocks pro-inflammatory responses in heat shock treated N9 cells via a signalling mechanism involving HSP90β and STAT3. 	human		High+Lowthroughput	Inhibition of HSP90β by ganetespib blocks the microglial signalling of evoked pro-inflammatory responses to heat shock	否	无	Heat shock	microglial cell	E_01_0631	Cell viability assay,ELISA,Flow Cytometry,Quantitative real-time polymerase chain reaction,Western blot,siRNA transfection,Immunofluorescence	HSP90 inhibitor ganetespib blocks pro-inflammatory responses in heat shock treated N9 cells via a signalling mechanism involving HSP90β and STAT3. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			HSP90 inhibitor ganetespib blocks pro-inflammatory responses in heat shock treated N9 cells via a signalling mechanism involving HSP90β and STAT3. 	Immunohistochemical staining	HSP90 inhibitor ganetespib blocks pro-inflammatory responses in heat shock treated N9 cells via a signalling mechanism involving HSP90β and STAT3. 	STAT3		Cell viability assay,ELISA,Flow Cytometry,Quantitative real-time polymerase chain reaction,Western blot,siRNA transfection,Immunofluorescence	HSP90 inhibitor ganetespib blocks pro-inflammatory responses in heat shock treated N9 cells via a signalling mechanism involving HSP90β and STAT3. 			
30446688	chr4	190171332	190173332	DUX4	Anti-myogenic properties of DUX4 in human myogenic progenitor cells, and provide an example of enhancer disruption in the downregulation of MYF5. 	human		High+Lowthroughput	Low level DUX4 expression disrupts myogenesis through deregulation of myogenic gene expression	否	无	Facioscapulohumeral muscular dystrophy	myoblast cell	E_01_0632	Annexin V/7-AAD staining,Luciferase assay,RT-qPCR,immunostaining,western blots	Anti-myogenic properties of DUX4 in human myogenic progenitor cells, and provide an example of enhancer disruption in the downregulation of MYF5. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Anti-myogenic properties of DUX4 in human myogenic progenitor cells, and provide an example of enhancer disruption in the downregulation of MYF5. 	Immunohistochemical staining	Anti-myogenic properties of DUX4 in human myogenic progenitor cells, and provide an example of enhancer disruption in the downregulation of MYF5. 	DUX4L1		Annexin V/7-AAD staining,Luciferase assay,RT-qPCR,immunostaining,western blots	Anti-myogenic properties of DUX4 in human myogenic progenitor cells, and provide an example of enhancer disruption in the downregulation of MYF5. 			
30446688	chr12	80714223	80716223	MYF5	Anti-myogenic properties of DUX4 in human myogenic progenitor cells, and provide an example of enhancer disruption in the downregulation of MYF5. 	human		High+Lowthroughput	Low level DUX4 expression disrupts myogenesis through deregulation of myogenic gene expression	否	无	Facioscapulohumeral muscular dystrophy	myoblast cell	E_01_0632	Annexin V/7-AAD staining,Luciferase assay,RT-qPCR,immunostaining,western blots	Anti-myogenic properties of DUX4 in human myogenic progenitor cells, and provide an example of enhancer disruption in the downregulation of MYF5. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Anti-myogenic properties of DUX4 in human myogenic progenitor cells, and provide an example of enhancer disruption in the downregulation of MYF5. 	Immunohistochemical staining	Anti-myogenic properties of DUX4 in human myogenic progenitor cells, and provide an example of enhancer disruption in the downregulation of MYF5. 	MYF5		Annexin V/7-AAD staining,Luciferase assay,RT-qPCR,immunostaining,western blots	Anti-myogenic properties of DUX4 in human myogenic progenitor cells, and provide an example of enhancer disruption in the downregulation of MYF5. 			
30446587	chr4	108044811	108046811	LEF1	Niclosamide blocks the transcription of DCLK1-B by interrupting the binding of LEF1 to DCLK1-B promoter. DCLK1-B depletion impairs cancer stemness resulting in reduced survival potential and increased apoptosis, thus sensitizing CRC to chemoradiation. 	human		High+Lowthroughput	Inhibition of LEF1-Mediated DCLK1 by Niclosamide Attenuates Colorectal Cancer Stemness	否	无	colorectal cancer 		E_01_0633	Luciferase reporter assay, Western blot,immunofluorescence analysis,histopathological analysis ,short tandem repeat profiling analysis, cell proliferation assay, MTT assay,FACS analysis	Niclosamide blocks the transcription of DCLK1-B by interrupting the binding of LEF1 to DCLK1-B promoter. DCLK1-B depletion impairs cancer stemness resulting in reduced survival potential and increased apoptosis, thus sensitizing CRC to chemoradiation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Niclosamide blocks the transcription of DCLK1-B by interrupting the binding of LEF1 to DCLK1-B promoter. DCLK1-B depletion impairs cancer stemness resulting in reduced survival potential and increased apoptosis, thus sensitizing CRC to chemoradiation. 	Immunohistochemical staining	Niclosamide blocks the transcription of DCLK1-B by interrupting the binding of LEF1 to DCLK1-B promoter. DCLK1-B depletion impairs cancer stemness resulting in reduced survival potential and increased apoptosis, thus sensitizing CRC to chemoradiation. 	LEF1		Luciferase reporter assay, Western blot,immunofluorescence analysis,histopathological analysis ,short tandem repeat profiling analysis, cell proliferation assay, MTT assay,FACS analysis	Niclosamide blocks the transcription of DCLK1-B by interrupting the binding of LEF1 to DCLK1-B promoter. DCLK1-B depletion impairs cancer stemness resulting in reduced survival potential and increased apoptosis, thus sensitizing CRC to chemoradiation. 			
30446251	chrX	49247427	49249427	FOXP3	The expanded human Tregs had demethylated FOXP3 and CTLA4 signatures and were immunosuppressive. These results describe a next-generation immunotherapy using a long-lived and Treg-selective IL-2 that activates and expands functional Tregs in vivo. 	mouse		High+Lowthroughput	A long-lived IL-2 mutein that selectively activates and expands regulatory T cells as a therapy for autoimmune disease	否	无	Autoimmune diseases	T cell	E_02_0386	Surface plasmon resonance,DNA demethylation of FOXP3 and CTLA4,	The expanded human Tregs had demethylated FOXP3 and CTLA4 signatures and were immunosuppressive. These results describe a next-generation immunotherapy using a long-lived and Treg-selective IL-2 that activates and expands functional Tregs in vivo. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expanded human Tregs had demethylated FOXP3 and CTLA4 signatures and were immunosuppressive. These results describe a next-generation immunotherapy using a long-lived and Treg-selective IL-2 that activates and expands functional Tregs in vivo. 		The expanded human Tregs had demethylated FOXP3 and CTLA4 signatures and were immunosuppressive. These results describe a next-generation immunotherapy using a long-lived and Treg-selective IL-2 that activates and expands functional Tregs in vivo. 	Immunohistochemical staining	The expanded human Tregs had demethylated FOXP3 and CTLA4 signatures and were immunosuppressive. These results describe a next-generation immunotherapy using a long-lived and Treg-selective IL-2 that activates and expands functional Tregs in vivo. 			Surface plasmon resonance,DNA demethylation of FOXP3 and CTLA4,				FOXP3
30445632	chr9	2618555	2620555	VLDLR	An enhancer of VLDLR expression and suggest that altered binding of one or more factors bound to rs3780181 alleles decreases enhancer activity and reduces at least VLDLR expression, leading to increased TC and LDL-C. 	human,mouse		High+Lowthroughput	Enhancer deletion and allelic effects define a regulatory molecular mechanism at the VLDLR cholesterol GWAS locus	是	rs3780181	Cardiovascular disease		E_02_0387	Transcriptional reporter and EMSAs， DNA affinity pull-down assay，dual-luciferase reporter assay，DNA-affinity capture assay， tandem mass spectrometry analysis	An enhancer of VLDLR expression and suggest that altered binding of one or more factors bound to rs3780181 alleles decreases enhancer activity and reduces at least VLDLR expression, leading to increased TC and LDL-C. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	An enhancer of VLDLR expression and suggest that altered binding of one or more factors bound to rs3780181 alleles decreases enhancer activity and reduces at least VLDLR expression, leading to increased TC and LDL-C. 		An enhancer of VLDLR expression and suggest that altered binding of one or more factors bound to rs3780181 alleles decreases enhancer activity and reduces at least VLDLR expression, leading to increased TC and LDL-C. 	Immunohistochemical staining	An enhancer of VLDLR expression and suggest that altered binding of one or more factors bound to rs3780181 alleles decreases enhancer activity and reduces at least VLDLR expression, leading to increased TC and LDL-C. 			Transcriptional reporter and EMSAs， DNA affinity pull-down assay，dual-luciferase reporter assay，DNA-affinity capture assay， tandem mass spectrometry analysis				VLDLR
30445463	chr5	88714221	88716221	MEF2C	Mutations in myocyte enhancer factor 2C (MEF2C), an important transcription factor in neurodevelopment, are associated with a Rett-like syndrome. Structural variants (SVs) upstream of MEF2C, that do not disrupt the gene itself, have also been found in patients with a similar phenotype, suggesting that disruption of MEF2C regulatory elements can also cause a Rett-like phenotype.	human		High+Lowthroughput	A neuronal enhancer network upstream of MEF2C is compromised in patients with Rett-like characteristics	否	无	Neurodevelopmental disorders (e.g., Rett like syndrome)	Radial glial cell	E_02_0388	4Cseq,ATAC-se,RNA isolation, cDNA synthesis,quantitative PCR,4C peak conservation,4C peak ZipperPlot analyses,Luciferase enhancer assays,ATAC-seq	Mutations in myocyte enhancer factor 2C (MEF2C), an important transcription factor in neurodevelopment, are associated with a Rett-like syndrome. Structural variants (SVs) upstream of MEF2C, that do not disrupt the gene itself, have also been found in patients with a similar phenotype, suggesting that disruption of MEF2C regulatory elements can also cause a Rett-like phenotype.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mutations in myocyte enhancer factor 2C (MEF2C), an important transcription factor in neurodevelopment, are associated with a Rett-like syndrome. Structural variants (SVs) upstream of MEF2C, that do not disrupt the gene itself, have also been found in patients with a similar phenotype, suggesting that disruption of MEF2C regulatory elements can also cause a Rett-like phenotype.		Mutations in myocyte enhancer factor 2C (MEF2C), an important transcription factor in neurodevelopment, are associated with a Rett-like syndrome. Structural variants (SVs) upstream of MEF2C, that do not disrupt the gene itself, have also been found in patients with a similar phenotype, suggesting that disruption of MEF2C regulatory elements can also cause a Rett-like phenotype.	Immunohistochemical staining	Mutations in myocyte enhancer factor 2C (MEF2C), an important transcription factor in neurodevelopment, are associated with a Rett-like syndrome. Structural variants (SVs) upstream of MEF2C, that do not disrupt the gene itself, have also been found in patients with a similar phenotype, suggesting that disruption of MEF2C regulatory elements can also cause a Rett-like phenotype.			4Cseq,ATAC-se,RNA isolation, cDNA synthesis,quantitative PCR,4C peak conservation,4C peak ZipperPlot analyses,Luciferase enhancer assays,ATAC-seq				MEF2C
30442871	chr12	120299714	120301714	SIRT4	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	mouse		High+Lowthroughput	Study of expression analysis of SIRT4 and the coordinate regulation of bovine adipocyte differentiation by SIRT4 and its transcription factors	否	无	nothing	bovine adipocytes	E_02_0389	qPCR,Immunofluorescence assays,Cell isolation, culture, and transfection,Site-directed mutagenesis,Knock down,EMSAs	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 		E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	Immunohistochemical staining	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 			qPCR,Immunofluorescence assays,Cell isolation, culture, and transfection,Site-directed mutagenesis,Knock down,EMSAs				SIRT4
30442871	chr20	33672666	33674666	E2F1	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	mouse		High+Lowthroughput	Study of expression analysis of SIRT4 and the coordinate regulation of bovine adipocyte differentiation by SIRT4 and its transcription factors	否	无	nothing	bovine adipocytes	E_02_0389	qPCR,Immunofluorescence assays,Cell isolation, culture, and transfection,Site-directed mutagenesis,Knock down,EMSAs	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 		E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	Immunohistochemical staining	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 			qPCR,Immunofluorescence assays,Cell isolation, culture, and transfection,Site-directed mutagenesis,Knock down,EMSAs				E2F1
30442871	chr7	27138639	27140639	HOXA5	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	mouse		High+Lowthroughput	Study of expression analysis of SIRT4 and the coordinate regulation of bovine adipocyte differentiation by SIRT4 and its transcription factors	否	无	nothing	bovine adipocytes	E_02_0389	qPCR,Immunofluorescence assays,Cell isolation, culture, and transfection,Site-directed mutagenesis,Knock down,EMSAs	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 		E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	Immunohistochemical staining	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 			qPCR,Immunofluorescence assays,Cell isolation, culture, and transfection,Site-directed mutagenesis,Knock down,EMSAs				HOXA5
30442871	chr6	389024	391024	IRF4	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	mouse		High+Lowthroughput	Study of expression analysis of SIRT4 and the coordinate regulation of bovine adipocyte differentiation by SIRT4 and its transcription factors	否	无	nothing	bovine adipocytes	E_02_0389	qPCR,Immunofluorescence assays,Cell isolation, culture, and transfection,Site-directed mutagenesis,Knock down,EMSAs	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 		E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	Immunohistochemical staining	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 			qPCR,Immunofluorescence assays,Cell isolation, culture, and transfection,Site-directed mutagenesis,Knock down,EMSAs				IRF4
30442871	chr2	207527251	207529251	CREB1	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	mouse		High+Lowthroughput	Study of expression analysis of SIRT4 and the coordinate regulation of bovine adipocyte differentiation by SIRT4 and its transcription factors	否	无	nothing	bovine adipocytes	E_02_0389	qPCR,Immunofluorescence assays,Cell isolation, culture, and transfection,Site-directed mutagenesis,Knock down,EMSAs	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 		E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 	Immunohistochemical staining	E2F1, CEBPβ, and HOXA5 transcriptionally activate SIRT4 expression, whereas, IRF4, PAX4, and CREB1 transcriptionally repress SIRT4 expression. We further verified that SIRT4 knockdown could affect the ability of these transcription factors to regulate the differentiation of bovine adipocytes. 			qPCR,Immunofluorescence assays,Cell isolation, culture, and transfection,Site-directed mutagenesis,Knock down,EMSAs				CREB1
30430607	chr19	33297457	33299457	CEBPA	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	human		High+Lowthroughput	Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is linked to poor prognosis in PTEN deleted and TMPRSS2:ERG fusion type prostate cancers	否	无	prostatic cancer	tumor cell	E_01_0634	Immunohistochemistry,	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	Immunohistochemical staining	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	CEBPA		Immunohistochemistry,	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."			
30430607	chr21	38377315	38379315	ERG	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	human		High+Lowthroughput	Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is linked to poor prognosis in PTEN deleted and TMPRSS2:ERG fusion type prostate cancers	否	无	prostatic cancer	tumor cell	E_01_0634	Immunohistochemistry,	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	Immunohistochemical staining	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	ERG		Immunohistochemistry,	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."			
30430607	chr21	41461274	41463274	TMPRSS2	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	human		High+Lowthroughput	Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is linked to poor prognosis in PTEN deleted and TMPRSS2:ERG fusion type prostate cancers	否	无	prostatic cancer	tumor cell	E_01_0634	Immunohistochemistry,	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	Immunohistochemical staining	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	TMPRSS2		Immunohistochemistry,	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."			
30430607	chr10	87859710	87861710	PTEN	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	human		High+Lowthroughput	Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is linked to poor prognosis in PTEN deleted and TMPRSS2:ERG fusion type prostate cancers	否	无	prostatic cancer	tumor cell	E_01_0634	Immunohistochemistry,	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	Immunohistochemical staining	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."	PTEN		Immunohistochemistry,	"Loss of CCAAT-enhancer-binding protein alpha (CEBPA) is
linked to poor prognosis in PTEN deleted and TMPRSS2:ERG
fusion type prostate cancers."			
30428538	chr11	75397365	75399365	RPS3	The EHEC NleH1 effector inhibits the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway by reducing the nuclear translocation of the ribosomal protein S3 (RPS3). NleH1 prevents RPS3 phosphorylation by the IκB kinase-β (IKKβ). IKKβ is a central kinase in the NF-κB pathway, yet NleH1 only restricts the phosphorylation of a subset of the IKKβ substrates. We hypothesized that a protein cofactor might dictate this inhibitory specificity.	human		High+Lowthroughput	Hsp90 Interacts with the Bacterial Effector NleH1	否	无	nothing	B cell	E_01_0635	Protein purification,Cell culture and transfection,Co-immunoprecipitation assay,Mass Spectrometry,RNA interference and transfection,	The EHEC NleH1 effector inhibits the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway by reducing the nuclear translocation of the ribosomal protein S3 (RPS3). NleH1 prevents RPS3 phosphorylation by the IκB kinase-β (IKKβ). IKKβ is a central kinase in the NF-κB pathway, yet NleH1 only restricts the phosphorylation of a subset of the IKKβ substrates. We hypothesized that a protein cofactor might dictate this inhibitory specificity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The EHEC NleH1 effector inhibits the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway by reducing the nuclear translocation of the ribosomal protein S3 (RPS3). NleH1 prevents RPS3 phosphorylation by the IκB kinase-β (IKKβ). IKKβ is a central kinase in the NF-κB pathway, yet NleH1 only restricts the phosphorylation of a subset of the IKKβ substrates. We hypothesized that a protein cofactor might dictate this inhibitory specificity.		The EHEC NleH1 effector inhibits the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway by reducing the nuclear translocation of the ribosomal protein S3 (RPS3). NleH1 prevents RPS3 phosphorylation by the IκB kinase-β (IKKβ). IKKβ is a central kinase in the NF-κB pathway, yet NleH1 only restricts the phosphorylation of a subset of the IKKβ substrates. We hypothesized that a protein cofactor might dictate this inhibitory specificity.	Immunohistochemical staining	The EHEC NleH1 effector inhibits the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway by reducing the nuclear translocation of the ribosomal protein S3 (RPS3). NleH1 prevents RPS3 phosphorylation by the IκB kinase-β (IKKβ). IKKβ is a central kinase in the NF-κB pathway, yet NleH1 only restricts the phosphorylation of a subset of the IKKβ substrates. We hypothesized that a protein cofactor might dictate this inhibitory specificity.			Protein purification,Cell culture and transfection,Co-immunoprecipitation assay,Mass Spectrometry,RNA interference and transfection,				RPS3
30429326	chr19	16321911	16323911	KLF2	H3K27ac/H3K4me2 ChIP with whole-genome sequencing (ChIP-seq), and CRISPR interference in human aortic endothelial cells (HAECs),CAD/IS-protective allele at rs17114036 creates a binding site for transcription factor Krüppel-like factor 2 (KLF2), which increases the enhancer activity under unidirectional flow. 	human		High+Lowthroughput	Genetic variant at coronary artery disease and ischemic stroke locus 1p32.2 regulates endothelial responses to hemodynamics，ChIP-PCR，luciferase assays 	是	无	Coronary artery disease and ischemic stroke	aortic endothelial cell	E_01_0636	ATAC-Seq，Genome-wide association studies (GWAS)，ChIP-seq，	H3K27ac/H3K4me2 ChIP with whole-genome sequencing (ChIP-seq), and CRISPR interference in human aortic endothelial cells (HAECs),CAD/IS-protective allele at rs17114036 creates a binding site for transcription factor Krüppel-like factor 2 (KLF2), which increases the enhancer activity under unidirectional flow. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			H3K27ac/H3K4me2 ChIP with whole-genome sequencing (ChIP-seq), and CRISPR interference in human aortic endothelial cells (HAECs),CAD/IS-protective allele at rs17114036 creates a binding site for transcription factor Krüppel-like factor 2 (KLF2), which increases the enhancer activity under unidirectional flow. 	Immunohistochemical staining	H3K27ac/H3K4me2 ChIP with whole-genome sequencing (ChIP-seq), and CRISPR interference in human aortic endothelial cells (HAECs),CAD/IS-protective allele at rs17114036 creates a binding site for transcription factor Krüppel-like factor 2 (KLF2), which increases the enhancer activity under unidirectional flow. 	KLF2		ATAC-Seq，Genome-wide association studies (GWAS)，ChIP-seq，	H3K27ac/H3K4me2 ChIP with whole-genome sequencing (ChIP-seq), and CRISPR interference in human aortic endothelial cells (HAECs),CAD/IS-protective allele at rs17114036 creates a binding site for transcription factor Krüppel-like factor 2 (KLF2), which increases the enhancer activity under unidirectional flow. 			
30428345	chr3	189628920	189630920	TP63	The transcription factor TP63 (DNp63) is sufficient to install and sustain the enhancer landscape and transcriptional signature of the squamous lineage in human PDA cells. We also demonstrate that TP63-driven enhancer reprogramming promotes aggressive tumor phenotypes, including enhanced cell motility and invasion, and an accelerated growth of primary PDA tumors and metastases in vivo.	human		High+Lowthroughput	TP63-Mediated Enhancer Reprogramming Drives the Squamous Subtype of Pancreatic Ductal Adenocarcinoma	是	无	Squamous subtype		E_01_0637	Plasmid Construction，Lentiviral Production and Infection，In Vitro Phenotypic Assays，CRISPR-Based Targeting，shRNA targeting in BxPC3 cells and hF3 organoids，In Vivo Transplantation Experiments，Histology and Immunohistochemistry，Cell Lysate Preparation for Western Blot Analysis，RNA Extraction and RT-PCR，RNA-seq Library Construction，ChIP and ChIP-Seq Library Construction，RNA-Seq Data Analysis，ChIP-Seq Analysis	The transcription factor TP63 (DNp63) is sufficient to install and sustain the enhancer landscape and transcriptional signature of the squamous lineage in human PDA cells. We also demonstrate that TP63-driven enhancer reprogramming promotes aggressive tumor phenotypes, including enhanced cell motility and invasion, and an accelerated growth of primary PDA tumors and metastases in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The transcription factor TP63 (DNp63) is sufficient to install and sustain the enhancer landscape and transcriptional signature of the squamous lineage in human PDA cells. We also demonstrate that TP63-driven enhancer reprogramming promotes aggressive tumor phenotypes, including enhanced cell motility and invasion, and an accelerated growth of primary PDA tumors and metastases in vivo.	Immunohistochemical staining	The transcription factor TP63 (DNp63) is sufficient to install and sustain the enhancer landscape and transcriptional signature of the squamous lineage in human PDA cells. We also demonstrate that TP63-driven enhancer reprogramming promotes aggressive tumor phenotypes, including enhanced cell motility and invasion, and an accelerated growth of primary PDA tumors and metastases in vivo.	TP63		Plasmid Construction，Lentiviral Production and Infection，In Vitro Phenotypic Assays，CRISPR-Based Targeting，shRNA targeting in BxPC3 cells and hF3 organoids，In Vivo Transplantation Experiments，Histology and Immunohistochemistry，Cell Lysate Preparation for Western Blot Analysis，RNA Extraction and RT-PCR，RNA-seq Library Construction，ChIP and ChIP-Seq Library Construction，RNA-Seq Data Analysis，ChIP-Seq Analysis	The transcription factor TP63 (DNp63) is sufficient to install and sustain the enhancer landscape and transcriptional signature of the squamous lineage in human PDA cells. We also demonstrate that TP63-driven enhancer reprogramming promotes aggressive tumor phenotypes, including enhanced cell motility and invasion, and an accelerated growth of primary PDA tumors and metastases in vivo.			
30427204	chr10	42055300	42057300	Foxo3	Foxo3 promotes cell proliferation and inhibits myotube differentiation in chicken myoblast cells. Therefore, the regulation of Foxo3 could be applied to improve muscle differentiation in commercial poultry.	mouse		High+Lowthroughput	Forkhead box O3 promotes cell proliferation and inhibits myotube differentiation in chicken myoblast cells	否	无	nothing		E_02_0390	qRT-PCR，Western blot，Cell imaging，knockdown vector transfection	Foxo3 promotes cell proliferation and inhibits myotube differentiation in chicken myoblast cells. Therefore, the regulation of Foxo3 could be applied to improve muscle differentiation in commercial poultry.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Foxo3 promotes cell proliferation and inhibits myotube differentiation in chicken myoblast cells. Therefore, the regulation of Foxo3 could be applied to improve muscle differentiation in commercial poultry.		Foxo3 promotes cell proliferation and inhibits myotube differentiation in chicken myoblast cells. Therefore, the regulation of Foxo3 could be applied to improve muscle differentiation in commercial poultry.	Immunohistochemical staining	Foxo3 promotes cell proliferation and inhibits myotube differentiation in chicken myoblast cells. Therefore, the regulation of Foxo3 could be applied to improve muscle differentiation in commercial poultry.			qRT-PCR，Western blot，Cell imaging，knockdown vector transfection				Foxo3
30422892	chr10	102741141	102743141	WBP1L	The intronic SNP rs176185, which may influence promoter histone, enhancer histone, DNase and regulatory motifs and showed ciseQTL effect on WBP1L, was associated with hypertension in the Chinese Han population (P = 0.0119). 	human		High+Lowthroughput	Detection of Putative Functional Single Nucleotide Polymorphisms in Blood Pressure Loci and Validation of Association Between Single Nucleotide Polymorphism in WBP1L and Hypertension in the Chinese Han Population	否	rs176185	Hypertension, coronary artery disease, or ischemic stroke	leukocyte	E_01_0638	DNA Extraction，SNP Genotyping	The intronic SNP rs176185, which may influence promoter histone, enhancer histone, DNase and regulatory motifs and showed ciseQTL effect on WBP1L, was associated with hypertension in the Chinese Han population (P = 0.0119). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The intronic SNP rs176185, which may influence promoter histone, enhancer histone, DNase and regulatory motifs and showed ciseQTL effect on WBP1L, was associated with hypertension in the Chinese Han population (P = 0.0119). 		The intronic SNP rs176185, which may influence promoter histone, enhancer histone, DNase and regulatory motifs and showed ciseQTL effect on WBP1L, was associated with hypertension in the Chinese Han population (P = 0.0119). 	Immunohistochemical staining	The intronic SNP rs176185, which may influence promoter histone, enhancer histone, DNase and regulatory motifs and showed ciseQTL effect on WBP1L, was associated with hypertension in the Chinese Han population (P = 0.0119). 			DNA Extraction，SNP Genotyping				WBP1L
30419347	chr15	61854218	61856218	Myc	Myc plays a key role in aggressive proliferation-related phenotypes exhibited by breast cancer cells expressing ERα mutations. 	human		High+Lowthroughput	Estrogen-independent Myc overexpression confers endocrine therapy resistance on breast cancer cells expressing ERαY537S and ERαD538G mutations	否	无	Metastatic breast cancer	T47D and MCF7 cells	E_01_0639	3 qRT-PCR,Western blot,siRNA knockdowns, Chromatin immunoprecipitation (ChIP),Lentivirus infection,Cell invasion assay,RNAseq	Myc plays a key role in aggressive proliferation-related phenotypes exhibited by breast cancer cells expressing ERα mutations. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Myc plays a key role in aggressive proliferation-related phenotypes exhibited by breast cancer cells expressing ERα mutations. 		Myc plays a key role in aggressive proliferation-related phenotypes exhibited by breast cancer cells expressing ERα mutations. 	Immunohistochemical staining	Myc plays a key role in aggressive proliferation-related phenotypes exhibited by breast cancer cells expressing ERα mutations. 			3 qRT-PCR,Western blot,siRNA knockdowns, Chromatin immunoprecipitation (ChIP),Lentivirus infection,Cell invasion assay,RNAseq				Myc
30417100	chr4	105143331	105145331	TET2	TET2 is frequently mutated or dysregulated in multiple human cancers, and loss of TET2 is associated with changes in DNA methylation patterns. 	human		High+Lowthroughput	TET2 coactivates gene expression through demethylation of enhancers	否	无	cancer	MCF7 cell	E_01_0640	RNA-seq analysis,ChIP-seq analysis, Western blot	TET2 is frequently mutated or dysregulated in multiple human cancers, and loss of TET2 is associated with changes in DNA methylation patterns. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	TET2 is frequently mutated or dysregulated in multiple human cancers, and loss of TET2 is associated with changes in DNA methylation patterns. 		TET2 is frequently mutated or dysregulated in multiple human cancers, and loss of TET2 is associated with changes in DNA methylation patterns. 	Immunohistochemical staining	TET2 is frequently mutated or dysregulated in multiple human cancers, and loss of TET2 is associated with changes in DNA methylation patterns. 			RNA-seq analysis,ChIP-seq analysis, Western blot				TET2
30416963	chr6	34233962	34235962	HMGA1	Entire DNA sequence upstream the transcription start sites is probably involved in vanadate-induced inhibition, the short sequence downstream of position 464 and is sufficient for inhibition. Potential targets of vanadate are the transcription factors FoxO1 and HMGA1, two downstream targets of the insulin signaling pathway which have been shown to mediate the inhibitory effect of insulin on IR gene expression. 	mouses		High+Lowthroughput	Vanadate inhibits transcription of the rat insulin receptor gene via a proximal sequence of the 5'flanking region	否	无	liver cancer	Cancer cell	E_02_0391	Cloning，Extraction，Sequence analysis，	Entire DNA sequence upstream the transcription start sites is probably involved in vanadate-induced inhibition, the short sequence downstream of position 464 and is sufficient for inhibition. Potential targets of vanadate are the transcription factors FoxO1 and HMGA1, two downstream targets of the insulin signaling pathway which have been shown to mediate the inhibitory effect of insulin on IR gene expression. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Entire DNA sequence upstream the transcription start sites is probably involved in vanadate-induced inhibition, the short sequence downstream of position 464 and is sufficient for inhibition. Potential targets of vanadate are the transcription factors FoxO1 and HMGA1, two downstream targets of the insulin signaling pathway which have been shown to mediate the inhibitory effect of insulin on IR gene expression. 		Entire DNA sequence upstream the transcription start sites is probably involved in vanadate-induced inhibition, the short sequence downstream of position 464 and is sufficient for inhibition. Potential targets of vanadate are the transcription factors FoxO1 and HMGA1, two downstream targets of the insulin signaling pathway which have been shown to mediate the inhibitory effect of insulin on IR gene expression. 	Immunohistochemical staining	Entire DNA sequence upstream the transcription start sites is probably involved in vanadate-induced inhibition, the short sequence downstream of position 464 and is sufficient for inhibition. Potential targets of vanadate are the transcription factors FoxO1 and HMGA1, two downstream targets of the insulin signaling pathway which have been shown to mediate the inhibitory effect of insulin on IR gene expression. 			Cloning，Extraction，Sequence analysis，				HMGA1
30416088	chr17	85795937	85796217	Gm29418	Over-expression of Gm29418 led to an increase in Six2 mRNA expression levels in a mouse MM cell line. In conclusion, we identified a lncRNA, Gm29418, in nephron progenitor cells that has an enhancer-like function on a key regulatory gene, Six2 	mouse		Low+High throughput	Comprehensive analysis of chromatin signature and transcriptome uncovers functional lncRNAs expressed in nephron progenitor cells	否	--	--	nephron progenitor cell	E_02_0392	ChIP-seq	We conducted comprehensive analyses of the chromatin signature and transcriptome by RNA_x0002_seq and ChIP-seq.We found seventeen lncRNAs that were expressed specifically in MM cells with an active chromatin signature, while remaining silenced in a bivalent chromatin state in non-MM cells.Out of these MM specific lncRNAs, we identified a lncRNA, Gm29418, in a distal enhancer region of Six2,a key regulatory gene of MM cells.	Enhancer	--	ChIP-seq,RNA-seq,qRT-PCR	We conducted comprehensive analyses of the chromatin signature and transcriptome by RNA_x0002_seq and ChIP-seq.We found seventeen lncRNAs that were expressed specifically in MM cells with an active chromatin signature, while remaining silenced in a bivalent chromatin state in non-MM cells.Out of these MM specific lncRNAs, we identified a lncRNA, Gm29418, in a distal enhancer region of Six2,a key regulatory gene of MM cells.	Six2	--	--	--	--	--	--	--	--	--	Six2
30414142	chr13	40553554	40555554	FOXO1	We will discuss classical and emerging technologies by which one can understand the role of binding of specific transcription factors in regulation of transcription of FOXO genes. 	mouse		High+Lowthroughput	Identification of Transcription Factor-Binding Sites in the Mouse FOXO1 Promoter	否	无			E_02_0393		We will discuss classical and emerging technologies by which one can understand the role of binding of specific transcription factors in regulation of transcription of FOXO genes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We will discuss classical and emerging technologies by which one can understand the role of binding of specific transcription factors in regulation of transcription of FOXO genes. 		We will discuss classical and emerging technologies by which one can understand the role of binding of specific transcription factors in regulation of transcription of FOXO genes. 	Immunohistochemical staining	We will discuss classical and emerging technologies by which one can understand the role of binding of specific transcription factors in regulation of transcription of FOXO genes. 							FOXO1
30411085	chr4	108044928	108046928	LEF1	LEF1 plays a pivotal role in HCC progression through transcriptional regulation of Oct4 and EMT regulators. LEF1 plays a pivotal role in HCC progression through transcriptional regulation of Oct4 and EMT regulators. 	human		High+Lowthroughput	Lymphoid Enhancer Factor 1 Contributes to Hepatocellular Carcinoma Progression Through Transcriptional Regulation of Epithelial-Mesenchymal Transition Regulators and Stemness Genes	否	无	Hepatocellular carcinoma	HCC cell lines	E_01_0641	ChIP-seq,IHC staining,western blot,colony formation assay, and invasion assay,Luc assay,cloning of gene promoter regions,site-directed mutagenesis,transient transfections	LEF1 plays a pivotal role in HCC progression through transcriptional regulation of Oct4 and EMT regulators. LEF1 plays a pivotal role in HCC progression through transcriptional regulation of Oct4 and EMT regulators. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			LEF1 plays a pivotal role in HCC progression through transcriptional regulation of Oct4 and EMT regulators. LEF1 plays a pivotal role in HCC progression through transcriptional regulation of Oct4 and EMT regulators. 	Immunohistochemical staining	LEF1 plays a pivotal role in HCC progression through transcriptional regulation of Oct4 and EMT regulators. LEF1 plays a pivotal role in HCC progression through transcriptional regulation of Oct4 and EMT regulators. 	LEF1		ChIP-seq,IHC staining,western blot,colony formation assay, and invasion assay,Luc assay,cloning of gene promoter regions,site-directed mutagenesis,transient transfections	LEF1 plays a pivotal role in HCC progression through transcriptional regulation of Oct4 and EMT regulators. LEF1 plays a pivotal role in HCC progression through transcriptional regulation of Oct4 and EMT regulators. 			
30407878	chr12	55739984	55741984	GDF11	"GDF11 antagonizes TNF-a–induced inflammation
and protects against the development of
inflammatory arthritis in mice"	mouse		High+Lowthroughput	GDF11 antagonizes TNF-α-induced inflammation and protects against the development of inflammatory arthritis in mice	否	无	Inflammatory arthritis in mice		E_02_0394		"GDF11 antagonizes TNF-a–induced inflammation
and protects against the development of
inflammatory arthritis in mice"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"GDF11 antagonizes TNF-a–induced inflammation
and protects against the development of
inflammatory arthritis in mice"		"GDF11 antagonizes TNF-a–induced inflammation
and protects against the development of
inflammatory arthritis in mice"	Immunohistochemical staining	"GDF11 antagonizes TNF-a–induced inflammation
and protects against the development of
inflammatory arthritis in mice"							GDF11
31097419	chr6	31572783	31574783	TNF	Our genome-wide analysis has identified the escape of genes from transcriptional repression in FLS as a novel mechanism potentially contributing to the chronic unremitting synovitis observed in RA. Our finding that TNF induces sustained chromatin activation in regulatory elements of the genes that escape repression in RA FLS suggests that altering or targeting chromatin states in FLS (eg, with inhibitors of BET proteins) is an attractive therapeutic strateg	human		High+Lowthroughput	"TNF-induced inflammatory genes escape repression
in fibroblast-like synoviocytes: transcriptomic and epigenomic analysis"	否	无	inflammation	macrophage	E_01_0642	chiP-seq ，aTac-seq ，RNAseq ，RT-qPCR ，bioinformatics analysis ， statistical analysis	Our genome-wide analysis has identified the escape of genes from transcriptional repression in FLS as a novel mechanism potentially contributing to the chronic unremitting synovitis observed in RA. Our finding that TNF induces sustained chromatin activation in regulatory elements of the genes that escape repression in RA FLS suggests that altering or targeting chromatin states in FLS (eg, with inhibitors of BET proteins) is an attractive therapeutic strateg	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our genome-wide analysis has identified the escape of genes from transcriptional repression in FLS as a novel mechanism potentially contributing to the chronic unremitting synovitis observed in RA. Our finding that TNF induces sustained chromatin activation in regulatory elements of the genes that escape repression in RA FLS suggests that altering or targeting chromatin states in FLS (eg, with inhibitors of BET proteins) is an attractive therapeutic strateg	Immunohistochemical staining	Our genome-wide analysis has identified the escape of genes from transcriptional repression in FLS as a novel mechanism potentially contributing to the chronic unremitting synovitis observed in RA. Our finding that TNF induces sustained chromatin activation in regulatory elements of the genes that escape repression in RA FLS suggests that altering or targeting chromatin states in FLS (eg, with inhibitors of BET proteins) is an attractive therapeutic strateg	TNF		chiP-seq ，aTac-seq ，RNAseq ，RT-qPCR ，bioinformatics analysis ， statistical analysis	Our genome-wide analysis has identified the escape of genes from transcriptional repression in FLS as a novel mechanism potentially contributing to the chronic unremitting synovitis observed in RA. Our finding that TNF induces sustained chromatin activation in regulatory elements of the genes that escape repression in RA FLS suggests that altering or targeting chromatin states in FLS (eg, with inhibitors of BET proteins) is an attractive therapeutic strateg			
31026067	chr11	1992169	1994169	H19	Cytidine cytidine adenosine adenosine thymidine (CCAAT) enhancer binding protein α (CEBP α) and peroxisome proliferator activated receptor γ are two important lipogenic and adipogenic transcription factors and markers in adipogenic differentiation.The long noncoding RNA (lncRNA) H19 is related to multiple cellular differentiation, including adipogenic differentiation.miR 30a inhibition promoted the mRNA expression and the protein levels of C8orf4 and adipogenic differentiation	human		High+Lowthroughput	"PIK3CD induces cell growth and invasion by activating
AKT/GSK-3β/β-catenin signaling in colorectal cancer"	否	无	Obesity related disorders	mesenchymal stem cell	E_01_0643	Cell transfection ，Immunoblotting ，Real‐time PCR ，RIP ，Luciferase reporter assay 	Cytidine cytidine adenosine adenosine thymidine (CCAAT) enhancer binding protein α (CEBP α) and peroxisome proliferator activated receptor γ are two important lipogenic and adipogenic transcription factors and markers in adipogenic differentiation.The long noncoding RNA (lncRNA) H19 is related to multiple cellular differentiation, including adipogenic differentiation.miR 30a inhibition promoted the mRNA expression and the protein levels of C8orf4 and adipogenic differentiation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cytidine cytidine adenosine adenosine thymidine (CCAAT) enhancer binding protein α (CEBP α) and peroxisome proliferator activated receptor γ are two important lipogenic and adipogenic transcription factors and markers in adipogenic differentiation.The long noncoding RNA (lncRNA) H19 is related to multiple cellular differentiation, including adipogenic differentiation.miR 30a inhibition promoted the mRNA expression and the protein levels of C8orf4 and adipogenic differentiation		Cytidine cytidine adenosine adenosine thymidine (CCAAT) enhancer binding protein α (CEBP α) and peroxisome proliferator activated receptor γ are two important lipogenic and adipogenic transcription factors and markers in adipogenic differentiation.The long noncoding RNA (lncRNA) H19 is related to multiple cellular differentiation, including adipogenic differentiation.miR 30a inhibition promoted the mRNA expression and the protein levels of C8orf4 and adipogenic differentiation	Immunohistochemical staining	Cytidine cytidine adenosine adenosine thymidine (CCAAT) enhancer binding protein α (CEBP α) and peroxisome proliferator activated receptor γ are two important lipogenic and adipogenic transcription factors and markers in adipogenic differentiation.The long noncoding RNA (lncRNA) H19 is related to multiple cellular differentiation, including adipogenic differentiation.miR 30a inhibition promoted the mRNA expression and the protein levels of C8orf4 and adipogenic differentiation			Cell transfection ，Immunoblotting ，Real‐time PCR ，RIP ，Luciferase reporter assay 				H19
30865855	chr14	21495515	21497515	METTL3	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	human		High+Lowthroughput	"METTL3 inhibits BMSC adipogenic differentiation by
targeting the JAK1/STAT5/C/EBPb pathway via an m6A-YTHDF2–dependent manner"	否	无	Obesity	Bone marrow stem cell	E_01_0644	flow cytometry ，Real-time quantitative PCR ， staining ，Protein extraction ，Western blot ，Cell transfection ，Immunofluorescence assay ，Quantitative analysis ，Chromatin immunoprecipitation assay ，Luciferase reporter assay	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 		The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 	Immunohistochemical staining	The deletion of m6A writer protein methyltransferaselike (METTL)3 in porcine BMSCs (pBMSCs) could promote adipogenesis and janus kinase (JAK)1 protein expressionvia anm6 A-dependent way. Knockdown ofMETTL3 decreasedmRNAm6 A levels of JAK1, leading to enhanced YTH m6 A RNA binding protein 2 (YTHDF2)-dependent JAK1 mRNA stability. We further demonstrated that JAK1 activated signal transducer and activator of transcription (STAT) 5 through regulation of its phosphorylation to bind to the promoter of CCAAT/enhancer binding protein (C/EBP) b, which could ultimately lead to a modulated adipogenic process. 			flow cytometry ，Real-time quantitative PCR ， staining ，Protein extraction ，Western blot ，Cell transfection ，Immunofluorescence assay ，Quantitative analysis ，Chromatin immunoprecipitation assay ，Luciferase reporter assay				METTL3
30826407	chr2	226728494	226730494	IRS1	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	human		High+Lowthroughput	A PDE3A Promoter Polymorphism Regulates cAMP-Induced Transcriptional Activity in Failing Human Myocardium	否	无	Type 2 diabetes mellitus	HeLa cell	E_01_0645	Nuclear magnetic resonance (NMR) spectroscopy analysis ，RNA extraction and real-time PCR ，Western blot analysis ，Histopathological analysis ,Analysis of glycated hemoglobin and β-cell function	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 		Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 	Immunohistochemical staining	Phosphatidylinositol-3-kinase (PI3K), 74 insulin receptor substrate 1 (IRS1), and glucose transporter 4 (GLUT4) play crucial roles in 75 glucose metabolism and insulin resistance.  The mechanism begins with the stimulation of 76 insulin receptor intrinsic kinase activity to activate PI3K signaling. Then, PI3K inhibits the 77 c-Jun N-terminal kinase 1 (JNK1) activity in succession. Moreover, GLUT4, which is 78 regulated by insulin, is able to reduce glucose levels through participating in the IRS/PI3K 79 signaling pathway (Chen et al., 2018). 			Nuclear magnetic resonance (NMR) spectroscopy analysis ，RNA extraction and real-time PCR ，Western blot analysis ，Histopathological analysis ,Analysis of glycated hemoglobin and β-cell function				IRS1
30402268	chr1	247413739	247415739	NLRP3	Functional experiments in the HA20 patients immune cells uncovered a novel caspase-8-dependent mechanism of NLRP3 inflammasome hyperresponsiveness that mediated the excessive secretion of interleukin-1β and interleukin-18. 	human		High+Lowthroughput	Haploinsufficiency of A20 impairs protein-protein interactome and leads into caspase-8-dependent enhancement of NLRP3 inflammasome activation	否	无	Inflammatory and autoimmune diseases		E_01_0646	Luciferase assay,Affinity purification and mass spectrometry,Culture and stimulation of peripheral blood mononuclear cells (PBMCs),Quantitative real-time PCR	Functional experiments in the HA20 patients immune cells uncovered a novel caspase-8-dependent mechanism of NLRP3 inflammasome hyperresponsiveness that mediated the excessive secretion of interleukin-1β and interleukin-18. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Functional experiments in the HA20 patients immune cells uncovered a novel caspase-8-dependent mechanism of NLRP3 inflammasome hyperresponsiveness that mediated the excessive secretion of interleukin-1β and interleukin-18. 		Functional experiments in the HA20 patients immune cells uncovered a novel caspase-8-dependent mechanism of NLRP3 inflammasome hyperresponsiveness that mediated the excessive secretion of interleukin-1β and interleukin-18. 	Immunohistochemical staining	Functional experiments in the HA20 patients immune cells uncovered a novel caspase-8-dependent mechanism of NLRP3 inflammasome hyperresponsiveness that mediated the excessive secretion of interleukin-1β and interleukin-18. 			Luciferase assay,Affinity purification and mass spectrometry,Culture and stimulation of peripheral blood mononuclear cells (PBMCs),Quantitative real-time PCR				NLRP3
30396177	chr5	138462782	138464782	EGR1	Our data suggests that EGR1 prevents HNSCC metastasis through downregulation of MMP9 and MDM2. EGR1 might be a potential candidate to attenuate HNSCC metastasis.	mouse		High+Lowthroughput	Early Growth Response 1-Dependent Downregulation of Matrix Metalloproteinase 9 and Mouse Double Minute 2 Attenuates Head and Neck Squamous Cell Carcinoma Metastasis	否	无	Head and neck squamous cell carcinoma	Head and Neck Squamous Cell	E_02_0395	TCGA RNAseq,Immunohistochemical analysis, overexpression vector transfection,Quantitative real-time PCR (qPCR),Western blot,Matrigel invasion assay,Promoter–luciferase assay,Chromatin immunoprecipitation (ChIP) analysis	Our data suggests that EGR1 prevents HNSCC metastasis through downregulation of MMP9 and MDM2. EGR1 might be a potential candidate to attenuate HNSCC metastasis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data suggests that EGR1 prevents HNSCC metastasis through downregulation of MMP9 and MDM2. EGR1 might be a potential candidate to attenuate HNSCC metastasis.		Our data suggests that EGR1 prevents HNSCC metastasis through downregulation of MMP9 and MDM2. EGR1 might be a potential candidate to attenuate HNSCC metastasis.	Immunohistochemical staining	Our data suggests that EGR1 prevents HNSCC metastasis through downregulation of MMP9 and MDM2. EGR1 might be a potential candidate to attenuate HNSCC metastasis.			TCGA RNAseq,Immunohistochemical analysis, overexpression vector transfection,Quantitative real-time PCR (qPCR),Western blot,Matrigel invasion assay,Promoter–luciferase assay,Chromatin immunoprecipitation (ChIP) analysis				EGR1
30387181	chr12	2854445	2856445	FOXM1	Downregulation of miR 134 attenuated DADS induced antitumor capacity. Further bioinformatics prediction analysis revealed that the 3 untranslated region (3 UTR) of Forkhead Box M1 (FOXM1) harbored miR 134 binding sites, and overexpression of miR 134 repressed the luciferase activity of the reporting vector containing FOXM1 3 UTR.	human		High+Lowthroughput	Diallyl disulfide suppresses FOXM1-mediated proliferation and invasion in osteosarcoma by upregulating miR-134	否	无	Osteosarcoma	U2OS and MG-63	E_01_0647	cell transfection,Quantitative real‐time polymerase Dual‐luciferase reporter assay,Western blo,chain reaction,Cell viability assay,Cell colony formation assay,Cell invasion assay	Downregulation of miR 134 attenuated DADS induced antitumor capacity. Further bioinformatics prediction analysis revealed that the 3 untranslated region (3 UTR) of Forkhead Box M1 (FOXM1) harbored miR 134 binding sites, and overexpression of miR 134 repressed the luciferase activity of the reporting vector containing FOXM1 3 UTR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Downregulation of miR 134 attenuated DADS induced antitumor capacity. Further bioinformatics prediction analysis revealed that the 3 untranslated region (3 UTR) of Forkhead Box M1 (FOXM1) harbored miR 134 binding sites, and overexpression of miR 134 repressed the luciferase activity of the reporting vector containing FOXM1 3 UTR.	Immunohistochemical staining	Downregulation of miR 134 attenuated DADS induced antitumor capacity. Further bioinformatics prediction analysis revealed that the 3 untranslated region (3 UTR) of Forkhead Box M1 (FOXM1) harbored miR 134 binding sites, and overexpression of miR 134 repressed the luciferase activity of the reporting vector containing FOXM1 3 UTR.	FOXM1		cell transfection,Quantitative real‐time polymerase Dual‐luciferase reporter assay,Western blo,chain reaction,Cell viability assay,Cell colony formation assay,Cell invasion assay	Downregulation of miR 134 attenuated DADS induced antitumor capacity. Further bioinformatics prediction analysis revealed that the 3 untranslated region (3 UTR) of Forkhead Box M1 (FOXM1) harbored miR 134 binding sites, and overexpression of miR 134 repressed the luciferase activity of the reporting vector containing FOXM1 3 UTR.			
30383452	chr16	69562149	69564149	NFAT5	Whereas originally described as a hypertonicity-responsive transcription factor, these findings identify NFAT5 as a novel molecular determinant of biomechanically induced phenotype changes of VSMCs and wall stress-induced arterial remodeling processes.	mouse		High+Lowthroughput	Genetic ablation of NFAT5/TonEBP in smooth muscle cells impairs flow- and pressure-induced arterial remodeling in mice	否	无	nothing		E_02_0396	Viral transduction,Immunofluorescence analyses,Western blot,	Whereas originally described as a hypertonicity-responsive transcription factor, these findings identify NFAT5 as a novel molecular determinant of biomechanically induced phenotype changes of VSMCs and wall stress-induced arterial remodeling processes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Whereas originally described as a hypertonicity-responsive transcription factor, these findings identify NFAT5 as a novel molecular determinant of biomechanically induced phenotype changes of VSMCs and wall stress-induced arterial remodeling processes.		Whereas originally described as a hypertonicity-responsive transcription factor, these findings identify NFAT5 as a novel molecular determinant of biomechanically induced phenotype changes of VSMCs and wall stress-induced arterial remodeling processes.	Immunohistochemical staining	Whereas originally described as a hypertonicity-responsive transcription factor, these findings identify NFAT5 as a novel molecular determinant of biomechanically induced phenotype changes of VSMCs and wall stress-induced arterial remodeling processes.			Viral transduction,Immunofluorescence analyses,Western blot,				NFAT5
30383449	chr19	10651482	10653482	ILF3	Together these data suggest that in endothelial cells, the RNA stability protein, ILF3, plays a novel and central role in angiogenesis.	human		High+Lowthroughput	RNA stability protein ILF3 mediates cytokine-induced angiogenesis	否	无	Cardiac ischemia, neurodegeneration, respiratory distress, tissue hypoxia		E_01_0648	Immunohistochemistry and immunocytochemistry，Small interfering RNA knockdown，Western blot，Migration assay，Proliferation assay，Apoptosis assay，Quantitative RT-PCR，RNA immunoprecipitation	Together these data suggest that in endothelial cells, the RNA stability protein, ILF3, plays a novel and central role in angiogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Together these data suggest that in endothelial cells, the RNA stability protein, ILF3, plays a novel and central role in angiogenesis.	Immunohistochemical staining	Together these data suggest that in endothelial cells, the RNA stability protein, ILF3, plays a novel and central role in angiogenesis.	ILF3		Immunohistochemistry and immunocytochemistry，Small interfering RNA knockdown，Western blot，Migration assay，Proliferation assay，Apoptosis assay，Quantitative RT-PCR，RNA immunoprecipitation	Together these data suggest that in endothelial cells, the RNA stability protein, ILF3, plays a novel and central role in angiogenesis.			
30380057	chr2	19447848	19449848	Ptf1a	Taken together, these data demonstrate substantial transcriptome changes in the Sd mouse, and indicate that the effect of the ERV insertion on Ptf1a expression may be mediated by increased chromatin accessibility at a conserved Ptf1a enhancer. 	mouse		High+Lowthroughput	Genome-wide chromatin accessibility and transcriptome profiling show minimal epigenome changes and coordinated transcriptional dysregulation of hedgehog signaling in Danforth's short tail mice	否	无	nothing	acinar cell	E_02_0397	mRNA-seq,ATAC-seq,GO enrichment,ChIP-seq,X-gal staining, Immunofluorescence	Taken together, these data demonstrate substantial transcriptome changes in the Sd mouse, and indicate that the effect of the ERV insertion on Ptf1a expression may be mediated by increased chromatin accessibility at a conserved Ptf1a enhancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, these data demonstrate substantial transcriptome changes in the Sd mouse, and indicate that the effect of the ERV insertion on Ptf1a expression may be mediated by increased chromatin accessibility at a conserved Ptf1a enhancer. 		Taken together, these data demonstrate substantial transcriptome changes in the Sd mouse, and indicate that the effect of the ERV insertion on Ptf1a expression may be mediated by increased chromatin accessibility at a conserved Ptf1a enhancer. 	Immunohistochemical staining	Taken together, these data demonstrate substantial transcriptome changes in the Sd mouse, and indicate that the effect of the ERV insertion on Ptf1a expression may be mediated by increased chromatin accessibility at a conserved Ptf1a enhancer. 			mRNA-seq,ATAC-seq,GO enrichment,ChIP-seq,X-gal staining, Immunofluorescence				Ptf1a
30376989	chr1	29144924	29146924	SRSF4	Here we demonstrate that increased SRSF4 expression stimulates exon 6 inclusion, and that reduced SRSF4 expression promotes exon 6 exclusion. 	human		High+Lowthroughput	Binding of SRSF4 to a novel enhancer modulates splicing of exon 6 of Fas pre-mRNA	否	无	nothing	HCT116 cell	E_01_0649	Viral infection，RT-PCR，Immunoblotting，RNA binding assay，Electrophoretic Mobility Shift Assay (EMSA)	Here we demonstrate that increased SRSF4 expression stimulates exon 6 inclusion, and that reduced SRSF4 expression promotes exon 6 exclusion. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we demonstrate that increased SRSF4 expression stimulates exon 6 inclusion, and that reduced SRSF4 expression promotes exon 6 exclusion. 		Here we demonstrate that increased SRSF4 expression stimulates exon 6 inclusion, and that reduced SRSF4 expression promotes exon 6 exclusion. 	Immunohistochemical staining	Here we demonstrate that increased SRSF4 expression stimulates exon 6 inclusion, and that reduced SRSF4 expression promotes exon 6 exclusion. 			Viral infection，RT-PCR，Immunoblotting，RNA binding assay，Electrophoretic Mobility Shift Assay (EMSA)				SRSF4
30376817	chr5	88713851	88715851	MEF2C	MEF2C mutations are associated with a broad clinical spectrum, ranged from classical RTT to non-syndromic ID. Through our study, it can be inferred that there is correlation between the phenotype and MEF2C-genotype, the mutation site. Overall, the MEF2C gene mutational analysis should be performed in ID cohort, especially in patients with features overlapped with RTT 	human		High+Lowthroughput	Novel MEF2C point mutations in Chinese patients with Rett (-like) syndrome or non-syndromic intellectual disability: insights into genotype-phenotype correlation	否	无	Rett (− like) syndrome or nonsyndromic intellectual disability in China		E_01_0650	Seq	MEF2C mutations are associated with a broad clinical spectrum, ranged from classical RTT to non-syndromic ID. Through our study, it can be inferred that there is correlation between the phenotype and MEF2C-genotype, the mutation site. Overall, the MEF2C gene mutational analysis should be performed in ID cohort, especially in patients with features overlapped with RTT 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MEF2C mutations are associated with a broad clinical spectrum, ranged from classical RTT to non-syndromic ID. Through our study, it can be inferred that there is correlation between the phenotype and MEF2C-genotype, the mutation site. Overall, the MEF2C gene mutational analysis should be performed in ID cohort, especially in patients with features overlapped with RTT 	Immunohistochemical staining	MEF2C mutations are associated with a broad clinical spectrum, ranged from classical RTT to non-syndromic ID. Through our study, it can be inferred that there is correlation between the phenotype and MEF2C-genotype, the mutation site. Overall, the MEF2C gene mutational analysis should be performed in ID cohort, especially in patients with features overlapped with RTT 	MEF2C		Seq	MEF2C mutations are associated with a broad clinical spectrum, ranged from classical RTT to non-syndromic ID. Through our study, it can be inferred that there is correlation between the phenotype and MEF2C-genotype, the mutation site. Overall, the MEF2C gene mutational analysis should be performed in ID cohort, especially in patients with features overlapped with RTT 			
30372441	chr7	19018038	19020038	TWIST1	Accordingly, haploinsufficiency of TWIST1 can cause limb and craniofacial malformations as part of Saethre-Chotzen syndrome. 	human		High+Lowthroughput	Unraveling the transcriptional regulation of TWIST1 in limb development	否	无	Saethri - chotzen syndrome	HEK293T	E_01_0651	ChIP-seq，ChIP-qPCR，4c-seq，Whole-mount in situ hybridization	Accordingly, haploinsufficiency of TWIST1 can cause limb and craniofacial malformations as part of Saethre-Chotzen syndrome. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Accordingly, haploinsufficiency of TWIST1 can cause limb and craniofacial malformations as part of Saethre-Chotzen syndrome. 	Immunohistochemical staining	Accordingly, haploinsufficiency of TWIST1 can cause limb and craniofacial malformations as part of Saethre-Chotzen syndrome. 	TWIST1		ChIP-seq，ChIP-qPCR，4c-seq，Whole-mount in situ hybridization	Accordingly, haploinsufficiency of TWIST1 can cause limb and craniofacial malformations as part of Saethre-Chotzen syndrome. 			
30368870	chr7	148804504	148806504	EZH2	These findings indicated that ANCR upregulates EZH2 expression and physically binds to EZH2 in LF MSCs to suppress chondrogenic differentiation and calcification. Therefore, downregulated ANCR contributes to increasing of chondrocyte like cells and calcium deposition in CLF. ANCR may serve as a therapeutic target for CLF. 	human		High+Lowthroughput	Downregulation of antidifferentiation noncoding RNA promotes chondrogenic differentiation and calcification of ligamentum flavum-derived mesenchymal stem cells	否	无	Calcification of the ligamentum flavum (CLF)	mesenchymal stem cell	E_01_0652		These findings indicated that ANCR upregulates EZH2 expression and physically binds to EZH2 in LF MSCs to suppress chondrogenic differentiation and calcification. Therefore, downregulated ANCR contributes to increasing of chondrocyte like cells and calcium deposition in CLF. ANCR may serve as a therapeutic target for CLF. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These findings indicated that ANCR upregulates EZH2 expression and physically binds to EZH2 in LF MSCs to suppress chondrogenic differentiation and calcification. Therefore, downregulated ANCR contributes to increasing of chondrocyte like cells and calcium deposition in CLF. ANCR may serve as a therapeutic target for CLF. 	Immunohistochemical staining	These findings indicated that ANCR upregulates EZH2 expression and physically binds to EZH2 in LF MSCs to suppress chondrogenic differentiation and calcification. Therefore, downregulated ANCR contributes to increasing of chondrocyte like cells and calcium deposition in CLF. ANCR may serve as a therapeutic target for CLF. 	EZH2			These findings indicated that ANCR upregulates EZH2 expression and physically binds to EZH2 in LF MSCs to suppress chondrogenic differentiation and calcification. Therefore, downregulated ANCR contributes to increasing of chondrocyte like cells and calcium deposition in CLF. ANCR may serve as a therapeutic target for CLF. 			
30366903	chr3	133743131	133745131	TF	Depletion of the intestinal TF CDX2 before this cis element transition stabilizes foregut enhancers, reinforces ectopic transcriptional programs, and hence imposes foregut identities on the midgut. Later in development, as the window of chromatin plasticity elapses, CDX2 depletion weakens intestinal, without strengthening foregut, enhancers. 	human		High+Lowthroughput	Enhancer, transcriptional, and cell fate plasticity precedes intestinal determination during endoderm development	否	无	nothing	embryonic cell 	E_01_0653	RNA-seq, ATAC-seq, ChIP-seq	Depletion of the intestinal TF CDX2 before this cis element transition stabilizes foregut enhancers, reinforces ectopic transcriptional programs, and hence imposes foregut identities on the midgut. Later in development, as the window of chromatin plasticity elapses, CDX2 depletion weakens intestinal, without strengthening foregut, enhancers. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Depletion of the intestinal TF CDX2 before this cis element transition stabilizes foregut enhancers, reinforces ectopic transcriptional programs, and hence imposes foregut identities on the midgut. Later in development, as the window of chromatin plasticity elapses, CDX2 depletion weakens intestinal, without strengthening foregut, enhancers. 		Depletion of the intestinal TF CDX2 before this cis element transition stabilizes foregut enhancers, reinforces ectopic transcriptional programs, and hence imposes foregut identities on the midgut. Later in development, as the window of chromatin plasticity elapses, CDX2 depletion weakens intestinal, without strengthening foregut, enhancers. 	Immunohistochemical staining	Depletion of the intestinal TF CDX2 before this cis element transition stabilizes foregut enhancers, reinforces ectopic transcriptional programs, and hence imposes foregut identities on the midgut. Later in development, as the window of chromatin plasticity elapses, CDX2 depletion weakens intestinal, without strengthening foregut, enhancers. 			RNA-seq, ATAC-seq, ChIP-seq				TF
30366903	chr13	27958369	27960369	CDX2	Depletion of the intestinal TF CDX2 before this cis element transition stabilizes foregut enhancers, reinforces ectopic transcriptional programs, and hence imposes foregut identities on the midgut. Later in development, as the window of chromatin plasticity elapses, CDX2 depletion weakens intestinal, without strengthening foregut, enhancers. 	human		High+Lowthroughput	Enhancer, transcriptional, and cell fate plasticity precedes intestinal determination during endoderm development	否	无	nothing	embryonic cell 	E_01_0653	RNA-seq, ATAC-seq, ChIP-seq	Depletion of the intestinal TF CDX2 before this cis element transition stabilizes foregut enhancers, reinforces ectopic transcriptional programs, and hence imposes foregut identities on the midgut. Later in development, as the window of chromatin plasticity elapses, CDX2 depletion weakens intestinal, without strengthening foregut, enhancers. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Depletion of the intestinal TF CDX2 before this cis element transition stabilizes foregut enhancers, reinforces ectopic transcriptional programs, and hence imposes foregut identities on the midgut. Later in development, as the window of chromatin plasticity elapses, CDX2 depletion weakens intestinal, without strengthening foregut, enhancers. 	Immunohistochemical staining	Depletion of the intestinal TF CDX2 before this cis element transition stabilizes foregut enhancers, reinforces ectopic transcriptional programs, and hence imposes foregut identities on the midgut. Later in development, as the window of chromatin plasticity elapses, CDX2 depletion weakens intestinal, without strengthening foregut, enhancers. 	CDX2		RNA-seq, ATAC-seq, ChIP-seq	Depletion of the intestinal TF CDX2 before this cis element transition stabilizes foregut enhancers, reinforces ectopic transcriptional programs, and hence imposes foregut identities on the midgut. Later in development, as the window of chromatin plasticity elapses, CDX2 depletion weakens intestinal, without strengthening foregut, enhancers. 			
30365933	chr9	21138792	21140792	Keap1	Thus, the , -unsaturated carbonyl is necessary for the interaction of compounds, such as shogaol, with Keap1, and these findings may be useful for screening novel ICH therapeutic agents that increase HO-1 expression. 	human		High+Lowthroughput	Shogaol but not gingerol has a neuroprotective effect on hemorrhagic brain injury: Contribution of the α, β-unsaturated carbonyl to heme oxygenase-1 expression	否	无	Hemorrhagic brain injury	microglial cell	E_01_0654	LDH release assay, Luciferase assay,Quantitative real-time RT-PCR,Western blot, Immunohistochemical staining,	Thus, the , -unsaturated carbonyl is necessary for the interaction of compounds, such as shogaol, with Keap1, and these findings may be useful for screening novel ICH therapeutic agents that increase HO-1 expression. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, the , -unsaturated carbonyl is necessary for the interaction of compounds, such as shogaol, with Keap1, and these findings may be useful for screening novel ICH therapeutic agents that increase HO-1 expression. 		Thus, the , -unsaturated carbonyl is necessary for the interaction of compounds, such as shogaol, with Keap1, and these findings may be useful for screening novel ICH therapeutic agents that increase HO-1 expression. 	Immunohistochemical staining	Thus, the , -unsaturated carbonyl is necessary for the interaction of compounds, such as shogaol, with Keap1, and these findings may be useful for screening novel ICH therapeutic agents that increase HO-1 expression. 			LDH release assay, Luciferase assay,Quantitative real-time RT-PCR,Western blot, Immunohistochemical staining,				Keap1
30365070	chr6	125744351	125746351	HEY2	In conclusion, the results demonstrated that miR-98 reduced the production of Aβ and improved oxidative stress and mitochondrial dysfunction through activation of the Notch signaling pathway by binding to HEY2 in AD mice. 	mouse	"hippocampal 
tissues"	High+Lowthroughput	MicroRNA-98 reduces amyloid β-protein production and improves oxidative stress and mitochondrial dysfunction through the Notch signaling pathway via HEY2 in Alzheimer's disease mice	否	无	Alzheimer disease	Hippocampal neuron	E_02_0398	Hematoxylin and eosin (H&E) staining,Immunohistochemistry,TUNEL staining,RT‑qPCR,Western blot,	In conclusion, the results demonstrated that miR-98 reduced the production of Aβ and improved oxidative stress and mitochondrial dysfunction through activation of the Notch signaling pathway by binding to HEY2 in AD mice. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, the results demonstrated that miR-98 reduced the production of Aβ and improved oxidative stress and mitochondrial dysfunction through activation of the Notch signaling pathway by binding to HEY2 in AD mice. 		In conclusion, the results demonstrated that miR-98 reduced the production of Aβ and improved oxidative stress and mitochondrial dysfunction through activation of the Notch signaling pathway by binding to HEY2 in AD mice. 	Immunohistochemical staining	In conclusion, the results demonstrated that miR-98 reduced the production of Aβ and improved oxidative stress and mitochondrial dysfunction through activation of the Notch signaling pathway by binding to HEY2 in AD mice. 			Hematoxylin and eosin (H&E) staining,Immunohistochemistry,TUNEL staining,RT‑qPCR,Western blot,				HEY2
30361341	chr8	127732519	127734519	MYC	Genome-wide correlation of gene expression and chromatin accessibility predicts tens of thousands of putative interactions between distal regulatory elements and gene promoters, including key oncogenes and targets in cancer immunotherapy, such as MYC, SRC, BCL2, and PDL1.	human		High+Lowthroughput	The chromatin accessibility landscape of primary human cancers	否	无	Primary human cancers	cancer cell	E_01_0655	ATAC-seq,HiChIP, immune infiltration analysis	Genome-wide correlation of gene expression and chromatin accessibility predicts tens of thousands of putative interactions between distal regulatory elements and gene promoters, including key oncogenes and targets in cancer immunotherapy, such as MYC, SRC, BCL2, and PDL1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Genome-wide correlation of gene expression and chromatin accessibility predicts tens of thousands of putative interactions between distal regulatory elements and gene promoters, including key oncogenes and targets in cancer immunotherapy, such as MYC, SRC, BCL2, and PDL1.	Immunohistochemical staining	Genome-wide correlation of gene expression and chromatin accessibility predicts tens of thousands of putative interactions between distal regulatory elements and gene promoters, including key oncogenes and targets in cancer immunotherapy, such as MYC, SRC, BCL2, and PDL1.	MYC		ATAC-seq,HiChIP, immune infiltration analysis	Genome-wide correlation of gene expression and chromatin accessibility predicts tens of thousands of putative interactions between distal regulatory elements and gene promoters, including key oncogenes and targets in cancer immunotherapy, such as MYC, SRC, BCL2, and PDL1.			
30361093	chr14	81469015	81471015	SEL1L	Taken together with these results, it is suggested that HRD1 and its stabilizer (SEL1L) are key molecules for elucidating the pathogenesis and treatment of PD. 	human		High+Lowthroughput	Ubiquitin ligase HMG-CoA reductase degradation 1 (HRD1) prevents cell death in a cellular model of Parkinson's disease	否	无	Parkinson's disease	SH-SY5Y human neuroblastoma cells	E_01_0656	MTT assay,RNA interference,RNA isolation,quantitative real-time PCR,. Western blot	Taken together with these results, it is suggested that HRD1 and its stabilizer (SEL1L) are key molecules for elucidating the pathogenesis and treatment of PD. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together with these results, it is suggested that HRD1 and its stabilizer (SEL1L) are key molecules for elucidating the pathogenesis and treatment of PD. 		Taken together with these results, it is suggested that HRD1 and its stabilizer (SEL1L) are key molecules for elucidating the pathogenesis and treatment of PD. 	Immunohistochemical staining	Taken together with these results, it is suggested that HRD1 and its stabilizer (SEL1L) are key molecules for elucidating the pathogenesis and treatment of PD. 			MTT assay,RNA interference,RNA isolation,quantitative real-time PCR,. Western blot				SEL1L
30359362	chr14	100235907	100237907	YY1	Our data therefore reveal a key role for CTCF-YY1 dependent looping in the HPV life cycle and identify a regulatory mechanism that could be disrupted in HPV carcinogenesis. 	human		High+Lowthroughput	Disruption of CTCF-YY1-dependent looping of the human papillomavirus genome activates differentiation-induced viral oncogene transcription	否	无	Human papillomas		E_01_0657	ChIP,Chromatin immunoprecipitation,Western blot,RNA-Seq,FAIRE,qRT-PCR,3C	Our data therefore reveal a key role for CTCF-YY1 dependent looping in the HPV life cycle and identify a regulatory mechanism that could be disrupted in HPV carcinogenesis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our data therefore reveal a key role for CTCF-YY1 dependent looping in the HPV life cycle and identify a regulatory mechanism that could be disrupted in HPV carcinogenesis. 	Immunohistochemical staining	Our data therefore reveal a key role for CTCF-YY1 dependent looping in the HPV life cycle and identify a regulatory mechanism that could be disrupted in HPV carcinogenesis. 	YY1		ChIP,Chromatin immunoprecipitation,Western blot,RNA-Seq,FAIRE,qRT-PCR,3C	Our data therefore reveal a key role for CTCF-YY1 dependent looping in the HPV life cycle and identify a regulatory mechanism that could be disrupted in HPV carcinogenesis. 			
30359362	chr16	67560015	67562015	CTCF	Our data therefore reveal a key role for CTCF-YY1 dependent looping in the HPV life cycle and identify a regulatory mechanism that could be disrupted in HPV carcinogenesis. 	human		High+Lowthroughput	Disruption of CTCF-YY1-dependent looping of the human papillomavirus genome activates differentiation-induced viral oncogene transcription	否	无	Human papillomas		E_01_0657	ChIP,Chromatin immunoprecipitation,Western blot,RNA-Seq,FAIRE,qRT-PCR,3C	Our data therefore reveal a key role for CTCF-YY1 dependent looping in the HPV life cycle and identify a regulatory mechanism that could be disrupted in HPV carcinogenesis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our data therefore reveal a key role for CTCF-YY1 dependent looping in the HPV life cycle and identify a regulatory mechanism that could be disrupted in HPV carcinogenesis. 	Immunohistochemical staining	Our data therefore reveal a key role for CTCF-YY1 dependent looping in the HPV life cycle and identify a regulatory mechanism that could be disrupted in HPV carcinogenesis. 	CTCF		ChIP,Chromatin immunoprecipitation,Western blot,RNA-Seq,FAIRE,qRT-PCR,3C	Our data therefore reveal a key role for CTCF-YY1 dependent looping in the HPV life cycle and identify a regulatory mechanism that could be disrupted in HPV carcinogenesis. 			
30358439	chrX	72326686	72328686	HDAC8	These data suggest that HDAC8 contributes to pulmonary fibrosis and that there is a therapeutic potential for HDAC8 inhibitors to treat IPF as well as other fibrotic lung diseases 	human	lung tissue	High+Lowthroughput	HDAC8 inhibition ameliorates pulmonary fibrosis	否	无	Idiopathic pulmonary fibrosis (IPF)	normal human lung fibroblasts 	E_01_0658	RNA interference，Immunoblots，Immunoprecipitation，Immunofluorescent staining，Type I collagen gel contraction assay ，qRT-PCR，ChIP-qPCR	These data suggest that HDAC8 contributes to pulmonary fibrosis and that there is a therapeutic potential for HDAC8 inhibitors to treat IPF as well as other fibrotic lung diseases 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These data suggest that HDAC8 contributes to pulmonary fibrosis and that there is a therapeutic potential for HDAC8 inhibitors to treat IPF as well as other fibrotic lung diseases 		These data suggest that HDAC8 contributes to pulmonary fibrosis and that there is a therapeutic potential for HDAC8 inhibitors to treat IPF as well as other fibrotic lung diseases 	Immunohistochemical staining	These data suggest that HDAC8 contributes to pulmonary fibrosis and that there is a therapeutic potential for HDAC8 inhibitors to treat IPF as well as other fibrotic lung diseases 			RNA interference，Immunoblots，Immunoprecipitation，Immunofluorescent staining，Type I collagen gel contraction assay ，qRT-PCR，ChIP-qPCR				HDAC8
30357366	chr1	6783119	6785119	CAMTA1	Our data reveal that TDP-43 can function as an mRNA-specific translational enhancer. Moreover, since CAMTA1 and DENND4A are linked to neurodegeneration, they suggest that this function could contribute to disease. 	human		High+Lowthroughput	TDP-43 enhances translation of specific mRNAs linked to neurodegenerative disease	否	无	Amyotrophic lateral sclerosis and frontotemporal dementia	Motor neuron like cells	E_01_0659	TRAP immunoprecipitations,RNA extraction, qRT-PCR,Crosslink immunoprecipitation (CLIP),Immunostaining,Reporter transfection, dual luciferase assays, knockdown	Our data reveal that TDP-43 can function as an mRNA-specific translational enhancer. Moreover, since CAMTA1 and DENND4A are linked to neurodegeneration, they suggest that this function could contribute to disease. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data reveal that TDP-43 can function as an mRNA-specific translational enhancer. Moreover, since CAMTA1 and DENND4A are linked to neurodegeneration, they suggest that this function could contribute to disease. 		Our data reveal that TDP-43 can function as an mRNA-specific translational enhancer. Moreover, since CAMTA1 and DENND4A are linked to neurodegeneration, they suggest that this function could contribute to disease. 	Immunohistochemical staining	Our data reveal that TDP-43 can function as an mRNA-specific translational enhancer. Moreover, since CAMTA1 and DENND4A are linked to neurodegeneration, they suggest that this function could contribute to disease. 			TRAP immunoprecipitations,RNA extraction, qRT-PCR,Crosslink immunoprecipitation (CLIP),Immunostaining,Reporter transfection, dual luciferase assays, knockdown				CAMTA1
30357366	chr15	65655039	65657039	DENND4A	Our data reveal that TDP-43 can function as an mRNA-specific translational enhancer. Moreover, since CAMTA1 and DENND4A are linked to neurodegeneration, they suggest that this function could contribute to disease. 	human		High+Lowthroughput	TDP-43 enhances translation of specific mRNAs linked to neurodegenerative disease	否	无	Amyotrophic lateral sclerosis and frontotemporal dementia	Motor neuron like cells	E_01_0659	TRAP immunoprecipitations,RNA extraction, qRT-PCR,Crosslink immunoprecipitation (CLIP),Immunostaining,Reporter transfection, dual luciferase assays, knockdown	Our data reveal that TDP-43 can function as an mRNA-specific translational enhancer. Moreover, since CAMTA1 and DENND4A are linked to neurodegeneration, they suggest that this function could contribute to disease. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data reveal that TDP-43 can function as an mRNA-specific translational enhancer. Moreover, since CAMTA1 and DENND4A are linked to neurodegeneration, they suggest that this function could contribute to disease. 		Our data reveal that TDP-43 can function as an mRNA-specific translational enhancer. Moreover, since CAMTA1 and DENND4A are linked to neurodegeneration, they suggest that this function could contribute to disease. 	Immunohistochemical staining	Our data reveal that TDP-43 can function as an mRNA-specific translational enhancer. Moreover, since CAMTA1 and DENND4A are linked to neurodegeneration, they suggest that this function could contribute to disease. 			TRAP immunoprecipitations,RNA extraction, qRT-PCR,Crosslink immunoprecipitation (CLIP),Immunostaining,Reporter transfection, dual luciferase assays, knockdown				DENND4A
30356873	chr11	27652426	27654426	BDNF	These results together suggest that DSS and CUS can induce the comorbidities of chronic pain and depression-like behavior. The pathology of this comorbidity involves loss of microglia within the mPFC with subsequent activation of NF-κB-p65 and down-regulation of BDNF/p-CREB signaling 	human		High+Lowthroughput	Loss of Microglia and Impaired Brain-Neurotrophic Factor Signaling Pathway in a Comorbid Model of Chronic Pain and Depression	否	无	Major depressive disorder (MDD) and chronic pain	microglial cell	E_01_0660	Quantitative RT-PCR,Open Field Test (OFT),Tail Suspension Test (TST),Forced Swimming Test (FST),Immunohistochemistry,Western Blot,Visceromotor Response (VMR)	These results together suggest that DSS and CUS can induce the comorbidities of chronic pain and depression-like behavior. The pathology of this comorbidity involves loss of microglia within the mPFC with subsequent activation of NF-κB-p65 and down-regulation of BDNF/p-CREB signaling 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These results together suggest that DSS and CUS can induce the comorbidities of chronic pain and depression-like behavior. The pathology of this comorbidity involves loss of microglia within the mPFC with subsequent activation of NF-κB-p65 and down-regulation of BDNF/p-CREB signaling 	Immunohistochemical staining	These results together suggest that DSS and CUS can induce the comorbidities of chronic pain and depression-like behavior. The pathology of this comorbidity involves loss of microglia within the mPFC with subsequent activation of NF-κB-p65 and down-regulation of BDNF/p-CREB signaling 	BDNF		Quantitative RT-PCR,Open Field Test (OFT),Tail Suspension Test (TST),Forced Swimming Test (FST),Immunohistochemistry,Western Blot,Visceromotor Response (VMR)	These results together suggest that DSS and CUS can induce the comorbidities of chronic pain and depression-like behavior. The pathology of this comorbidity involves loss of microglia within the mPFC with subsequent activation of NF-κB-p65 and down-regulation of BDNF/p-CREB signaling 			
30354296	chr8	58487490	58489490	CYP7A1	Two interacting regulatory SNPs modulate CYP7A1 expression and are associated with risk of coronary artery disease and diabetes mellitus.	human		High+Lowthroughput	Interactions Between Regulatory Variants in CYP7A1 (Cholesterol 7α-Hydroxylase) Promoter and Enhancer Regions Regulate CYP7A1 Expression	是	rs3808607, rs9297994,rs2081687, rs983812, rs8192870, rs9297994	Coronary artery disease and diabetes	Hepatocellular carcinoma cells	E_01_0661	4C assay,chromatin immunoprecipitation qPCR assay,eporter gene assays ,CRISPR -mediated genome editing	Two interacting regulatory SNPs modulate CYP7A1 expression and are associated with risk of coronary artery disease and diabetes mellitus.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Two interacting regulatory SNPs modulate CYP7A1 expression and are associated with risk of coronary artery disease and diabetes mellitus.		Two interacting regulatory SNPs modulate CYP7A1 expression and are associated with risk of coronary artery disease and diabetes mellitus.	Immunohistochemical staining	Two interacting regulatory SNPs modulate CYP7A1 expression and are associated with risk of coronary artery disease and diabetes mellitus.			4C assay,chromatin immunoprecipitation qPCR assay,eporter gene assays ,CRISPR -mediated genome editing				CYP7A1
30354239	chr11	108113833	108115833	ACAT1	Elimination of ACAT1 in bone marrow-derived cells aggravates cutaneous xanthoma and atherosclerosis. The development of cutaneous xanthoma is induced mainly via the NLRP3 inflammasome activation.	mouse,human		High+Lowthroughput	Inflammasome Activation Aggravates Cutaneous Xanthomatosis and Atherosclerosis in ACAT1 (Acyl-CoA Cholesterol Acyltransferase 1) Deficiency in Bone Marrow	否	无	Cutaneous xanthomatosis and atherosclerosis	Mouse peritoneal macrophages	E_02_0399	Quantitative Real-Time Polymerase Chain Reaction,ELISA	Elimination of ACAT1 in bone marrow-derived cells aggravates cutaneous xanthoma and atherosclerosis. The development of cutaneous xanthoma is induced mainly via the NLRP3 inflammasome activation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Elimination of ACAT1 in bone marrow-derived cells aggravates cutaneous xanthoma and atherosclerosis. The development of cutaneous xanthoma is induced mainly via the NLRP3 inflammasome activation.		Elimination of ACAT1 in bone marrow-derived cells aggravates cutaneous xanthoma and atherosclerosis. The development of cutaneous xanthoma is induced mainly via the NLRP3 inflammasome activation.	Immunohistochemical staining	Elimination of ACAT1 in bone marrow-derived cells aggravates cutaneous xanthoma and atherosclerosis. The development of cutaneous xanthoma is induced mainly via the NLRP3 inflammasome activation.			Quantitative Real-Time Polymerase Chain Reaction,ELISA				ACAT1
30354239	chr1	247413913	247415913	NLRP3	Elimination of ACAT1 in bone marrow-derived cells aggravates cutaneous xanthoma and atherosclerosis. The development of cutaneous xanthoma is induced mainly via the NLRP3 inflammasome activation.	mouse,human		High+Lowthroughput	Inflammasome Activation Aggravates Cutaneous Xanthomatosis and Atherosclerosis in ACAT1 (Acyl-CoA Cholesterol Acyltransferase 1) Deficiency in Bone Marrow	否	无	Cutaneous xanthomatosis and atherosclerosis	Mouse peritoneal macrophages	E_02_0399	Quantitative Real-Time Polymerase Chain Reaction,ELISA	Elimination of ACAT1 in bone marrow-derived cells aggravates cutaneous xanthoma and atherosclerosis. The development of cutaneous xanthoma is induced mainly via the NLRP3 inflammasome activation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Elimination of ACAT1 in bone marrow-derived cells aggravates cutaneous xanthoma and atherosclerosis. The development of cutaneous xanthoma is induced mainly via the NLRP3 inflammasome activation.		Elimination of ACAT1 in bone marrow-derived cells aggravates cutaneous xanthoma and atherosclerosis. The development of cutaneous xanthoma is induced mainly via the NLRP3 inflammasome activation.	Immunohistochemical staining	Elimination of ACAT1 in bone marrow-derived cells aggravates cutaneous xanthoma and atherosclerosis. The development of cutaneous xanthoma is induced mainly via the NLRP3 inflammasome activation.			Quantitative Real-Time Polymerase Chain Reaction,ELISA				NLRP3
30352365	chr8	24381876	24383876	ADAMDEC1	We demonstrated that binding of the enhancer RNAs produced from the upstream enhancer were critically important and that p300 bound to both the RNA from the enhancer and the DNA at the enhancer. P300 binding to the enhancer was dependent on NFκB. These data define the critical pathways regulating the expression of ADAMDEC1 and extend our knowledge of the roles of enhancer RNAs and mechanistically links p300 and enhancer RNAs. 	human		High+Lowthroughput	Enhancer RNA and NFκB-dependent P300 regulation of ADAMDEC1	否	无	Systemic lupus erythematosus	Primary monocytes	E_01_0662	Luciferase reporter assay, ChIP assays,RNA immunoprecipitation assays	We demonstrated that binding of the enhancer RNAs produced from the upstream enhancer were critically important and that p300 bound to both the RNA from the enhancer and the DNA at the enhancer. P300 binding to the enhancer was dependent on NFκB. These data define the critical pathways regulating the expression of ADAMDEC1 and extend our knowledge of the roles of enhancer RNAs and mechanistically links p300 and enhancer RNAs. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We demonstrated that binding of the enhancer RNAs produced from the upstream enhancer were critically important and that p300 bound to both the RNA from the enhancer and the DNA at the enhancer. P300 binding to the enhancer was dependent on NFκB. These data define the critical pathways regulating the expression of ADAMDEC1 and extend our knowledge of the roles of enhancer RNAs and mechanistically links p300 and enhancer RNAs. 		We demonstrated that binding of the enhancer RNAs produced from the upstream enhancer were critically important and that p300 bound to both the RNA from the enhancer and the DNA at the enhancer. P300 binding to the enhancer was dependent on NFκB. These data define the critical pathways regulating the expression of ADAMDEC1 and extend our knowledge of the roles of enhancer RNAs and mechanistically links p300 and enhancer RNAs. 	Immunohistochemical staining	We demonstrated that binding of the enhancer RNAs produced from the upstream enhancer were critically important and that p300 bound to both the RNA from the enhancer and the DNA at the enhancer. P300 binding to the enhancer was dependent on NFκB. These data define the critical pathways regulating the expression of ADAMDEC1 and extend our knowledge of the roles of enhancer RNAs and mechanistically links p300 and enhancer RNAs. 			Luciferase reporter assay, ChIP assays,RNA immunoprecipitation assays				ADAMDEC1
30349541	chrX	7437025	7439025	Foxp3	CCAAT/enhancer-binding protein (C/EBP) functions as a safeguard that enhances Treg cell generation by dampening the inhibitory effect of IFN-c and IL-4 on Foxp3 expression. These results establish C/EBP as a new molecular target for enhancing the formation and stability of Treg cells in inflammatory environments. 	mouse		High+Lowthroughput	Regulation of Lymphatic GM-CSF Expression by the E3 Ubiquitin Ligase Cbl-b	否	无	inflammation	regulatory T cell	E_02_0400	Retroviral transduction,Intracellular staining,Quantitative real-time PCR,Chromatin immunoprecipitation assays,Bisulfite sequencing,Electrophoretic mobility shift assay	CCAAT/enhancer-binding protein (C/EBP) functions as a safeguard that enhances Treg cell generation by dampening the inhibitory effect of IFN-c and IL-4 on Foxp3 expression. These results establish C/EBP as a new molecular target for enhancing the formation and stability of Treg cells in inflammatory environments. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CCAAT/enhancer-binding protein (C/EBP) functions as a safeguard that enhances Treg cell generation by dampening the inhibitory effect of IFN-c and IL-4 on Foxp3 expression. These results establish C/EBP as a new molecular target for enhancing the formation and stability of Treg cells in inflammatory environments. 		CCAAT/enhancer-binding protein (C/EBP) functions as a safeguard that enhances Treg cell generation by dampening the inhibitory effect of IFN-c and IL-4 on Foxp3 expression. These results establish C/EBP as a new molecular target for enhancing the formation and stability of Treg cells in inflammatory environments. 	Immunohistochemical staining	CCAAT/enhancer-binding protein (C/EBP) functions as a safeguard that enhances Treg cell generation by dampening the inhibitory effect of IFN-c and IL-4 on Foxp3 expression. These results establish C/EBP as a new molecular target for enhancing the formation and stability of Treg cells in inflammatory environments. 			Retroviral transduction,Intracellular staining,Quantitative real-time PCR,Chromatin immunoprecipitation assays,Bisulfite sequencing,Electrophoretic mobility shift assay				Foxp3
30349303	chr5	34653615	34655615	RAI14	RAI14 knockdown inhibited proliferation, migration and invasion and promoted apoptosis by downregulating the Akt pathway in gastric cancer cells, and RAB31 might be a downstream target gene of RAI14, providing a novel sight into the molecular mechanism of RAI14 and a potential target for gastric cancer treatment.	human		High+Lowthroughput	Knockdown of RAI14 suppresses the progression of gastric cancer	否	无	gastric cancer	gastric cancer cell	E_01_0663	"Western blot,Cell proliferation and colony formation 
assay,Cell migration assay,Cell apoptosis assay,RT-qPCR"	RAI14 knockdown inhibited proliferation, migration and invasion and promoted apoptosis by downregulating the Akt pathway in gastric cancer cells, and RAB31 might be a downstream target gene of RAI14, providing a novel sight into the molecular mechanism of RAI14 and a potential target for gastric cancer treatment.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RAI14 knockdown inhibited proliferation, migration and invasion and promoted apoptosis by downregulating the Akt pathway in gastric cancer cells, and RAB31 might be a downstream target gene of RAI14, providing a novel sight into the molecular mechanism of RAI14 and a potential target for gastric cancer treatment.		RAI14 knockdown inhibited proliferation, migration and invasion and promoted apoptosis by downregulating the Akt pathway in gastric cancer cells, and RAB31 might be a downstream target gene of RAI14, providing a novel sight into the molecular mechanism of RAI14 and a potential target for gastric cancer treatment.	Immunohistochemical staining	RAI14 knockdown inhibited proliferation, migration and invasion and promoted apoptosis by downregulating the Akt pathway in gastric cancer cells, and RAB31 might be a downstream target gene of RAI14, providing a novel sight into the molecular mechanism of RAI14 and a potential target for gastric cancer treatment.			"Western blot,Cell proliferation and colony formation 
assay,Cell migration assay,Cell apoptosis assay,RT-qPCR"				RAI14
30349303	chr18	9705684	9707684	RAB31	RAI14 knockdown inhibited proliferation, migration and invasion and promoted apoptosis by downregulating the Akt pathway in gastric cancer cells, and RAB31 might be a downstream target gene of RAI14, providing a novel sight into the molecular mechanism of RAI14 and a potential target for gastric cancer treatment.	human		High+Lowthroughput	Knockdown of RAI14 suppresses the progression of gastric cancer	否	无	gastric cancer	gastric cancer cell	E_01_0663	"Western blot,Cell proliferation and colony formation 
assay,Cell migration assay,Cell apoptosis assay,RT-qPCR"	RAI14 knockdown inhibited proliferation, migration and invasion and promoted apoptosis by downregulating the Akt pathway in gastric cancer cells, and RAB31 might be a downstream target gene of RAI14, providing a novel sight into the molecular mechanism of RAI14 and a potential target for gastric cancer treatment.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RAI14 knockdown inhibited proliferation, migration and invasion and promoted apoptosis by downregulating the Akt pathway in gastric cancer cells, and RAB31 might be a downstream target gene of RAI14, providing a novel sight into the molecular mechanism of RAI14 and a potential target for gastric cancer treatment.		RAI14 knockdown inhibited proliferation, migration and invasion and promoted apoptosis by downregulating the Akt pathway in gastric cancer cells, and RAB31 might be a downstream target gene of RAI14, providing a novel sight into the molecular mechanism of RAI14 and a potential target for gastric cancer treatment.	Immunohistochemical staining	RAI14 knockdown inhibited proliferation, migration and invasion and promoted apoptosis by downregulating the Akt pathway in gastric cancer cells, and RAB31 might be a downstream target gene of RAI14, providing a novel sight into the molecular mechanism of RAI14 and a potential target for gastric cancer treatment.			"Western blot,Cell proliferation and colony formation 
assay,Cell migration assay,Cell apoptosis assay,RT-qPCR"				RAB31
30349097	chr12	64449530	64451530	TBK1	Collectively, these data reveal an evolutionarily conserved and critical role of TBK1/IKKε suppression in expanding functional β-cell mass.	mouse		High+Lowthroughput	Inhibition of TBK1/IKKε Promotes Regeneration of Pancreatic β-cells	否	无	diabetes	Beta cell	E_02_0401	Immunohistochemistry, glucose-stimulated insulin secretion (GSIS) assay	Collectively, these data reveal an evolutionarily conserved and critical role of TBK1/IKKε suppression in expanding functional β-cell mass.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Collectively, these data reveal an evolutionarily conserved and critical role of TBK1/IKKε suppression in expanding functional β-cell mass.		Collectively, these data reveal an evolutionarily conserved and critical role of TBK1/IKKε suppression in expanding functional β-cell mass.	Immunohistochemical staining	Collectively, these data reveal an evolutionarily conserved and critical role of TBK1/IKKε suppression in expanding functional β-cell mass.			Immunohistochemistry, glucose-stimulated insulin secretion (GSIS) assay				TBK1
30346835	chr3	13546059	13548059	FBLN2	Some key hypomethylation sites in enhancer regions and key hypermethylation sites in CGIs for regulating key genes are, respectively, found, such as oncogenes ESR1 and ERBB2 and tumor suppressor genes FBLN2, CEBPA, and FAT4. This suggests that the recognizing methylation status of these genes will be useful for the diagnosis of breast cancer.	human		High+Lowthroughput	Relationship Between DNA Methylation in Key Region and the Differential Expressions of Genes in Human Breast Tumor Tissue	否	无	Breast neoplasms	breast cancer cell	E_01_0664	DNA Methylation	Some key hypomethylation sites in enhancer regions and key hypermethylation sites in CGIs for regulating key genes are, respectively, found, such as oncogenes ESR1 and ERBB2 and tumor suppressor genes FBLN2, CEBPA, and FAT4. This suggests that the recognizing methylation status of these genes will be useful for the diagnosis of breast cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Some key hypomethylation sites in enhancer regions and key hypermethylation sites in CGIs for regulating key genes are, respectively, found, such as oncogenes ESR1 and ERBB2 and tumor suppressor genes FBLN2, CEBPA, and FAT4. This suggests that the recognizing methylation status of these genes will be useful for the diagnosis of breast cancer.		Some key hypomethylation sites in enhancer regions and key hypermethylation sites in CGIs for regulating key genes are, respectively, found, such as oncogenes ESR1 and ERBB2 and tumor suppressor genes FBLN2, CEBPA, and FAT4. This suggests that the recognizing methylation status of these genes will be useful for the diagnosis of breast cancer.	Immunohistochemical staining	Some key hypomethylation sites in enhancer regions and key hypermethylation sites in CGIs for regulating key genes are, respectively, found, such as oncogenes ESR1 and ERBB2 and tumor suppressor genes FBLN2, CEBPA, and FAT4. This suggests that the recognizing methylation status of these genes will be useful for the diagnosis of breast cancer.			DNA Methylation				FBLN2
30346835	chr4	125312022	125314022	FAT4	Some key hypomethylation sites in enhancer regions and key hypermethylation sites in CGIs for regulating key genes are, respectively, found, such as oncogenes ESR1 and ERBB2 and tumor suppressor genes FBLN2, CEBPA, and FAT4. This suggests that the recognizing methylation status of these genes will be useful for the diagnosis of breast cancer.	human		High+Lowthroughput	Relationship Between DNA Methylation in Key Region and the Differential Expressions of Genes in Human Breast Tumor Tissue	否	无	Breast neoplasms	breast cancer cell	E_01_0664	DNA Methylation	Some key hypomethylation sites in enhancer regions and key hypermethylation sites in CGIs for regulating key genes are, respectively, found, such as oncogenes ESR1 and ERBB2 and tumor suppressor genes FBLN2, CEBPA, and FAT4. This suggests that the recognizing methylation status of these genes will be useful for the diagnosis of breast cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Some key hypomethylation sites in enhancer regions and key hypermethylation sites in CGIs for regulating key genes are, respectively, found, such as oncogenes ESR1 and ERBB2 and tumor suppressor genes FBLN2, CEBPA, and FAT4. This suggests that the recognizing methylation status of these genes will be useful for the diagnosis of breast cancer.		Some key hypomethylation sites in enhancer regions and key hypermethylation sites in CGIs for regulating key genes are, respectively, found, such as oncogenes ESR1 and ERBB2 and tumor suppressor genes FBLN2, CEBPA, and FAT4. This suggests that the recognizing methylation status of these genes will be useful for the diagnosis of breast cancer.	Immunohistochemical staining	Some key hypomethylation sites in enhancer regions and key hypermethylation sites in CGIs for regulating key genes are, respectively, found, such as oncogenes ESR1 and ERBB2 and tumor suppressor genes FBLN2, CEBPA, and FAT4. This suggests that the recognizing methylation status of these genes will be useful for the diagnosis of breast cancer.			DNA Methylation				FAT4
30344724	chr22	39516937	39518937	ATF4	It was indicated that Rg3 exerted pro-apoptotic activity against the gallbladder cancer cell line GBC-SD through the ER stress-mediated signaling pathway. This was demonstrated by increased expression of phosphorylation of eukaryotic translation-initiation factor 2α (eIF2α), activating transcription factor 4 (ATF4), CCAAT/enhancer-binding protein homologous protein and lipocalin 2.	human		High+Lowthroughput	Antitumor effect of ginsenoside Rg3 on gallbladder cancer by inducing endoplasmic reticulum stress-mediated apoptosis in vitro and in vivo	否	无	Gallbladder cancer	Gallbladder cancer cell	E_01_0665	flow cytometry, western blot analysis, ELISA and reverse transcription-quantitative polymerase chain reaction (RT-qPCR),siRNA sequences synthesis,	It was indicated that Rg3 exerted pro-apoptotic activity against the gallbladder cancer cell line GBC-SD through the ER stress-mediated signaling pathway. This was demonstrated by increased expression of phosphorylation of eukaryotic translation-initiation factor 2α (eIF2α), activating transcription factor 4 (ATF4), CCAAT/enhancer-binding protein homologous protein and lipocalin 2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			It was indicated that Rg3 exerted pro-apoptotic activity against the gallbladder cancer cell line GBC-SD through the ER stress-mediated signaling pathway. This was demonstrated by increased expression of phosphorylation of eukaryotic translation-initiation factor 2α (eIF2α), activating transcription factor 4 (ATF4), CCAAT/enhancer-binding protein homologous protein and lipocalin 2.	Immunohistochemical staining	It was indicated that Rg3 exerted pro-apoptotic activity against the gallbladder cancer cell line GBC-SD through the ER stress-mediated signaling pathway. This was demonstrated by increased expression of phosphorylation of eukaryotic translation-initiation factor 2α (eIF2α), activating transcription factor 4 (ATF4), CCAAT/enhancer-binding protein homologous protein and lipocalin 2.	ATF4		flow cytometry, western blot analysis, ELISA and reverse transcription-quantitative polymerase chain reaction (RT-qPCR),siRNA sequences synthesis,	It was indicated that Rg3 exerted pro-apoptotic activity against the gallbladder cancer cell line GBC-SD through the ER stress-mediated signaling pathway. This was demonstrated by increased expression of phosphorylation of eukaryotic translation-initiation factor 2α (eIF2α), activating transcription factor 4 (ATF4), CCAAT/enhancer-binding protein homologous protein and lipocalin 2.			
30344723	chr7	148804250	148806250	EZH2	Furthermore, Enhancer of zeste homolog 2 (EZH2) was demonstrated to be a direct target of miR 214 in CC. An MTT assay demonstrated that upregulating miR 214 expression or knocking down the expression of EZH2 impaired the proliferation of a CC cell line. 	human		High+Lowthroughput	microRNA-214 suppresses the growth of cervical cancer cells by targeting EZH2	否	无	cervical carcinoma	cervical cancer cells	E_01_0666	Transient transfection,RT‑qPCR,Western blot,Cell proliferation assay,luciferase reporter assay	Furthermore, Enhancer of zeste homolog 2 (EZH2) was demonstrated to be a direct target of miR 214 in CC. An MTT assay demonstrated that upregulating miR 214 expression or knocking down the expression of EZH2 impaired the proliferation of a CC cell line. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Furthermore, Enhancer of zeste homolog 2 (EZH2) was demonstrated to be a direct target of miR 214 in CC. An MTT assay demonstrated that upregulating miR 214 expression or knocking down the expression of EZH2 impaired the proliferation of a CC cell line. 	Immunohistochemical staining	Furthermore, Enhancer of zeste homolog 2 (EZH2) was demonstrated to be a direct target of miR 214 in CC. An MTT assay demonstrated that upregulating miR 214 expression or knocking down the expression of EZH2 impaired the proliferation of a CC cell line. 	EZH2		Transient transfection,RT‑qPCR,Western blot,Cell proliferation assay,luciferase reporter assay	Furthermore, Enhancer of zeste homolog 2 (EZH2) was demonstrated to be a direct target of miR 214 in CC. An MTT assay demonstrated that upregulating miR 214 expression or knocking down the expression of EZH2 impaired the proliferation of a CC cell line. 			
30343006	chr7	148804374	148806374	EZH2	EZH2-expressing lung adenocarcinomas were shown to express the PD-L1 protein more frequentlym than were nonexpressing lesions. This study provides the first evidence of a possible association between the EZH2 and PD-L1 expression in patients with resected lung adenocarcinoma.	human		High+Lowthroughput	A Positive Correlation Between the EZH2 and PD-L1 Expression in Resected Lung Adenocarcinomas	否	无	Lung adenocarcinoma	promote tumor cell	E_01_0667	Immunohistochemical Analyses	EZH2-expressing lung adenocarcinomas were shown to express the PD-L1 protein more frequentlym than were nonexpressing lesions. This study provides the first evidence of a possible association between the EZH2 and PD-L1 expression in patients with resected lung adenocarcinoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2-expressing lung adenocarcinomas were shown to express the PD-L1 protein more frequentlym than were nonexpressing lesions. This study provides the first evidence of a possible association between the EZH2 and PD-L1 expression in patients with resected lung adenocarcinoma.	Immunohistochemical staining	EZH2-expressing lung adenocarcinomas were shown to express the PD-L1 protein more frequentlym than were nonexpressing lesions. This study provides the first evidence of a possible association between the EZH2 and PD-L1 expression in patients with resected lung adenocarcinoma.	EZH2		Immunohistochemical Analyses	EZH2-expressing lung adenocarcinomas were shown to express the PD-L1 protein more frequentlym than were nonexpressing lesions. This study provides the first evidence of a possible association between the EZH2 and PD-L1 expression in patients with resected lung adenocarcinoma.			
30342896	chr8	22685034	22687034	EGR3	Through weighted gene co-expression analysis, EGR3 was found to be related to the keratinocyte differentiation-related module as an important part of the skin-specific genetic network. 	human		High+Lowthroughput	EGR3 Is a Late Epidermal Differentiation Regulator that Establishes the Skin-Specific Gene Network	否	无	nothing	Human primary epidermal keratinocytes	E_01_0668	Quantitative real-time reverse transcriptaseePCR，Immunohistochemistry	Through weighted gene co-expression analysis, EGR3 was found to be related to the keratinocyte differentiation-related module as an important part of the skin-specific genetic network. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Through weighted gene co-expression analysis, EGR3 was found to be related to the keratinocyte differentiation-related module as an important part of the skin-specific genetic network. 		Through weighted gene co-expression analysis, EGR3 was found to be related to the keratinocyte differentiation-related module as an important part of the skin-specific genetic network. 	Immunohistochemical staining	Through weighted gene co-expression analysis, EGR3 was found to be related to the keratinocyte differentiation-related module as an important part of the skin-specific genetic network. 			Quantitative real-time reverse transcriptaseePCR，Immunohistochemistry				EGR3
30341286	chr7	148804560	148806560	EZH2	Thus, these results suggest that targeting EZH2 protects against AKI through a mechanism associated with the preservation of adhesion/junctions, reduction of matrix metalloproteinases and attenuation of the Raf-1/ERK1/2 pathway. 	human		High+Lowthroughput	Targeting enhancer of zeste homolog 2 protects against acute kidney injury	否	无	Acute kidney injury	Proximal tubular epithelial  cells	E_01_0669	Transfection of siRNA into cells，Immunoblot analyses，Histochemical and immunofluorescence staining	Thus, these results suggest that targeting EZH2 protects against AKI through a mechanism associated with the preservation of adhesion/junctions, reduction of matrix metalloproteinases and attenuation of the Raf-1/ERK1/2 pathway. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus, these results suggest that targeting EZH2 protects against AKI through a mechanism associated with the preservation of adhesion/junctions, reduction of matrix metalloproteinases and attenuation of the Raf-1/ERK1/2 pathway. 	Immunohistochemical staining	Thus, these results suggest that targeting EZH2 protects against AKI through a mechanism associated with the preservation of adhesion/junctions, reduction of matrix metalloproteinases and attenuation of the Raf-1/ERK1/2 pathway. 	EZH2		Transfection of siRNA into cells，Immunoblot analyses，Histochemical and immunofluorescence staining	Thus, these results suggest that targeting EZH2 protects against AKI through a mechanism associated with the preservation of adhesion/junctions, reduction of matrix metalloproteinases and attenuation of the Raf-1/ERK1/2 pathway. 			
30337687	chrX	152895420	152897420	ZNF185		human		High+Lowthroughput	ZNF185 is a p63 target gene critical for epidermal differentiation and squamous cell carcinoma development	否	无	Epidermal differentiation and squamous cell carcinoma		E_01_0670	Poorly differentiated, including head and neck, cervical and oesophageal, squamous cell carcinomas display loss of ZNF185 expression. Together, these studies reinforce that p63 is a crucial gene for maintaining epithelial tissue integrity and support the deregulation of the cell-cell adhesion programme,which plays a critical role in carcinoma development. 		Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq				Immunohistochemical staining				Poorly differentiated, including head and neck, cervical and oesophageal, squamous cell carcinomas display loss of ZNF185 expression. Together, these studies reinforce that p63 is a crucial gene for maintaining epithelial tissue integrity and support the deregulation of the cell-cell adhesion programme,which plays a critical role in carcinoma development. 				ZNF185
30335887	chr15	73991784	73993784	PML	Collectively, this study uncovers a novel mechanism of PML/RARα mediated transcriptional activation and enriches our knowledge of the onco fusion protein mediated transcription activation.	human		High+Lowthroughput	PML/RARa blocks the differentiation and promotes the proliferation of acute promyelocytic leukemia through activating MYB expression by transcriptional and epigenetic regulation mechanisms	否	无	Acute promyelocytic leukemia		E_01_0671	"Chromatin immunoprecipitation‐
sequencing data analysis,Luciferase reporter gene assay,Retrovirus transfection,Reverse transcription‐quantitative
real‐time PCR,ChIP‐quantitative PCR"	Collectively, this study uncovers a novel mechanism of PML/RARα mediated transcriptional activation and enriches our knowledge of the onco fusion protein mediated transcription activation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Collectively, this study uncovers a novel mechanism of PML/RARα mediated transcriptional activation and enriches our knowledge of the onco fusion protein mediated transcription activation.	Immunohistochemical staining	Collectively, this study uncovers a novel mechanism of PML/RARα mediated transcriptional activation and enriches our knowledge of the onco fusion protein mediated transcription activation.	PML		"Chromatin immunoprecipitation‐
sequencing data analysis,Luciferase reporter gene assay,Retrovirus transfection,Reverse transcription‐quantitative
real‐time PCR,ChIP‐quantitative PCR"	Collectively, this study uncovers a novel mechanism of PML/RARα mediated transcriptional activation and enriches our knowledge of the onco fusion protein mediated transcription activation.			
30333752	chr22	29600833	29602833	NF2	Schwannomas are common, highly morbid, and medically untreatable tumors that can arise in patients with germline as well as somatic mutations in NF2. These mutations most commonly result in the loss of function of the NF2 encoded protein, Merlin.	mouse		High+Lowthroughput	Trans-Chalcone Attenuates Pain and Inflammation in Experimental Acute Gout Arthritis in Mice	否	无	Gouty arthritis	inflammatory cell	E_02_0402	Fluorescence assay,RT-qPCR,	Schwannomas are common, highly morbid, and medically untreatable tumors that can arise in patients with germline as well as somatic mutations in NF2. These mutations most commonly result in the loss of function of the NF2 encoded protein, Merlin.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Schwannomas are common, highly morbid, and medically untreatable tumors that can arise in patients with germline as well as somatic mutations in NF2. These mutations most commonly result in the loss of function of the NF2 encoded protein, Merlin.		Schwannomas are common, highly morbid, and medically untreatable tumors that can arise in patients with germline as well as somatic mutations in NF2. These mutations most commonly result in the loss of function of the NF2 encoded protein, Merlin.	Immunohistochemical staining	Schwannomas are common, highly morbid, and medically untreatable tumors that can arise in patients with germline as well as somatic mutations in NF2. These mutations most commonly result in the loss of function of the NF2 encoded protein, Merlin.			Fluorescence assay,RT-qPCR,				NF2
30327653	chr19	6884691	6886691	ADGRE1	ADGRE1 mRNA was expressed by macrophages in each species, with inter-species variation both in expression level and response to lipopolysaccharide (LPS) stimulation.	mouse		High+Lowthroughput	ADGRE1 (EMR1, F4/80) Is a Rapidly-Evolving Gene Expressed in Mammalian Monocyte-Macrophages	否	无	nothing	Macrophage	E_02_0403	ELISA，Flow Cytometry，Immunohistochemistry，RNA-Seq	ADGRE1 mRNA was expressed by macrophages in each species, with inter-species variation both in expression level and response to lipopolysaccharide (LPS) stimulation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ADGRE1 mRNA was expressed by macrophages in each species, with inter-species variation both in expression level and response to lipopolysaccharide (LPS) stimulation.		ADGRE1 mRNA was expressed by macrophages in each species, with inter-species variation both in expression level and response to lipopolysaccharide (LPS) stimulation.	Immunohistochemical staining	ADGRE1 mRNA was expressed by macrophages in each species, with inter-species variation both in expression level and response to lipopolysaccharide (LPS) stimulation.			ELISA，Flow Cytometry，Immunohistochemistry，RNA-Seq				ADGRE1
30327417	chr16	10440279	10442279	NFAT5	Our results uncover an NFAT5-regulated mechanism that maintains CIITA and MHCII expression in macrophages and thus modulates their T lymphocyte priming capacity 	mouse		Low throughput	Macrophage-specific MHCII expression is regulated by a remote Ciita enhancer controlled by NFAT5	否	--	--	macrophage	E_02_0404	qChIP	"We then analyzed peak A and Ciita promoter I by qChIP in NFAT5-deficient or control macrophages for different histone modifications that are enriched in gene enhancers (H3K4me1)
or promoters (H3K4me3) and a modification that marks transcribed regions and active enhancers.We observed that peak A region had a slightly higher content in H3K4me1 compared with Ciita promoter I, and this was NFAT5 independent."	Enhancer	--	ChIP-seq	ChIP-seq analysis of wild-type and NFAT5-deficient BMDMs showing the position of NFAT5-binding site peak A 47 kb upstream of the Ciita locus.	C2ta,EG669998,Gm9475,Mhc2ta	--	--	--	Nfat5	AI225870,B130038B15Rik,CAG-8,CAG80,NFATL1,OREBP,TonEBP,mKIAA0827,nfatz	qChIP	We therefore asked whether NFAT5 bound these regulatory regions. Quantitative chromatin immunoprecipitation (qChIP) with a combination of two polyclonal antibodies to NFAT5 detected its specific binding to promoter I of Ciita and the promoter of H2-Ab both in untreated macrophages as well as in macrophages treated with IFNγ.This result indicated that NFAT5 is a relevant factor to control Ciita expression in macrophages through its myeloid promoter I. Altogether,our analysis of primary myeloid and lymphoid APCs uncovered a selective requirement of NFAT5 in macrophages for expressing CIITA and MHCII.	--	--	Ciita
30325409	chr8	47734236	47736236	CEBPD	Thus although our results support the notion that CEBPD acts as a tumor suppressor in HCC, its action does not involve impairing compartment expansion per se but more likely acts through improving anti-cancer immunity. 	human		High+Lowthroughput	Action and clinical significance of CCAAT/enhancer-binding protein delta in hepatocellular carcinoma	否	无	Hepatocellular carcinoma	Huh7 , HepG2 cells	E_01_0672	Lentiviral-shRNA packaging and infectionWestern blot，Quantitative Real-time PCR(qRT-PCR)，Cell proliferation and Colony formation assa，y	Thus although our results support the notion that CEBPD acts as a tumor suppressor in HCC, its action does not involve impairing compartment expansion per se but more likely acts through improving anti-cancer immunity. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Thus although our results support the notion that CEBPD acts as a tumor suppressor in HCC, its action does not involve impairing compartment expansion per se but more likely acts through improving anti-cancer immunity. 	Immunohistochemical staining	Thus although our results support the notion that CEBPD acts as a tumor suppressor in HCC, its action does not involve impairing compartment expansion per se but more likely acts through improving anti-cancer immunity. 	CEBPD		Lentiviral-shRNA packaging and infectionWestern blot，Quantitative Real-time PCR(qRT-PCR)，Cell proliferation and Colony formation assa，y	Thus although our results support the notion that CEBPD acts as a tumor suppressor in HCC, its action does not involve impairing compartment expansion per se but more likely acts through improving anti-cancer immunity. 			
30325084	chr13	118803388	118805388	Fgf10	Fgf10 is expressed in various tissues and organs, such as the limb bud, heart, inner ear and head mesenchyme. Previous studies identified Fgf10 enhancers for the inner ear and heart. 	mouse		High+Lowthroughput	Characterization of cis-regulatory elements for Fgf10 expression in the chick embryo	否	无	nothing	Chick LPM cells	E_02_0405	Luciferase reporter assay，Quantitative RT-PCR，RT-PCR	Fgf10 is expressed in various tissues and organs, such as the limb bud, heart, inner ear and head mesenchyme. Previous studies identified Fgf10 enhancers for the inner ear and heart. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Fgf10 is expressed in various tissues and organs, such as the limb bud, heart, inner ear and head mesenchyme. Previous studies identified Fgf10 enhancers for the inner ear and heart. 		Fgf10 is expressed in various tissues and organs, such as the limb bud, heart, inner ear and head mesenchyme. Previous studies identified Fgf10 enhancers for the inner ear and heart. 	Immunohistochemical staining	Fgf10 is expressed in various tissues and organs, such as the limb bud, heart, inner ear and head mesenchyme. Previous studies identified Fgf10 enhancers for the inner ear and heart. 			Luciferase reporter assay，Quantitative RT-PCR，RT-PCR				Fgf10
30324804	chr6	106042833	106044833	ATG5	Monitoring expression of ATG5, a key link between autophagy and apoptosis, we established that this correction correlates with reduction of enhanced autophagy activation, a typical feature of thalassemic polychromatophilic normoblasts.	human		High+Lowthroughput	A Novel BaEVRless-Pseudotyped γ-Globin Lentiviral Vector Drives High and Stable Fetal Hemoglobin Expression and Improves Thalassemic Erythropoiesis In Vitro	否	无	β- Thalassemia major	CD34 + cells	E_01_0673	quantitative real-time PCR，Flow cytometry and apoptosis assay，cell isolation and transduction	Monitoring expression of ATG5, a key link between autophagy and apoptosis, we established that this correction correlates with reduction of enhanced autophagy activation, a typical feature of thalassemic polychromatophilic normoblasts.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Monitoring expression of ATG5, a key link between autophagy and apoptosis, we established that this correction correlates with reduction of enhanced autophagy activation, a typical feature of thalassemic polychromatophilic normoblasts.		Monitoring expression of ATG5, a key link between autophagy and apoptosis, we established that this correction correlates with reduction of enhanced autophagy activation, a typical feature of thalassemic polychromatophilic normoblasts.	Immunohistochemical staining	Monitoring expression of ATG5, a key link between autophagy and apoptosis, we established that this correction correlates with reduction of enhanced autophagy activation, a typical feature of thalassemic polychromatophilic normoblasts.			quantitative real-time PCR，Flow cytometry and apoptosis assay，cell isolation and transduction				ATG5
30321476	chr9	134314290	134316290	RXRA	We therefore used an existing randomised trial to test the hypothesis that maternal gestational vitamin D supplementation would lead to reduced perinatal RXRA locus DNA methylation. 	human	Umbilical cord (fetal) tissue	High+Lowthroughput	Gestational Vitamin D Supplementation Leads to Reduced Perinatal RXRA DNA Methylation: Results From the MAVIDOS Trial	否	无	Maternal vitamin D osteoporosis		E_01_0674	DNA methylation analysis,Quantitative DNA methylation analysis,RXRA methylation analysis,chemiluminescent assay,chemiluminescent assay,pyrosequencing	We therefore used an existing randomised trial to test the hypothesis that maternal gestational vitamin D supplementation would lead to reduced perinatal RXRA locus DNA methylation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We therefore used an existing randomised trial to test the hypothesis that maternal gestational vitamin D supplementation would lead to reduced perinatal RXRA locus DNA methylation. 	Immunohistochemical staining	We therefore used an existing randomised trial to test the hypothesis that maternal gestational vitamin D supplementation would lead to reduced perinatal RXRA locus DNA methylation. 	RXRA		DNA methylation analysis,Quantitative DNA methylation analysis,RXRA methylation analysis,chemiluminescent assay,chemiluminescent assay,pyrosequencing	We therefore used an existing randomised trial to test the hypothesis that maternal gestational vitamin D supplementation would lead to reduced perinatal RXRA locus DNA methylation. 			
30321325	chr16	30759122	30761122	RNF40	Our findings suggest that RNF40 plays a central role in the maintenance of tumorigenic features and inflammatory signaling by promoting nuclear NF-κB activity.	mouse		High+Lowthroughput	Loss of RNF40 Decreases NF-κB Activity in Colorectal Cancer Cells and Reduces Colitis Burden in Mice	否	无	colorectal cancer 	Human colorectal carcinoma cell	E_02_0406	siRNA transfection,Cell fractionation,Western blotting,Immunofluorescence,H&E staining and immunohistochemistry (IHC),qRT-PCR	Our findings suggest that RNF40 plays a central role in the maintenance of tumorigenic features and inflammatory signaling by promoting nuclear NF-κB activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our findings suggest that RNF40 plays a central role in the maintenance of tumorigenic features and inflammatory signaling by promoting nuclear NF-κB activity.		Our findings suggest that RNF40 plays a central role in the maintenance of tumorigenic features and inflammatory signaling by promoting nuclear NF-κB activity.	Immunohistochemical staining	Our findings suggest that RNF40 plays a central role in the maintenance of tumorigenic features and inflammatory signaling by promoting nuclear NF-κB activity.			siRNA transfection,Cell fractionation,Western blotting,Immunofluorescence,H&E staining and immunohistochemistry (IHC),qRT-PCR				RNF40
30321177	chr10	43074329	43076329	RET	The p.Cys630 = variant created new exonic splicing enhancer motifs that enhanced SRp55 recruitment to the mutant allele, leading to more efficient maturation of its pre-mRNA and an increased abundance of mature mRNA encoding a constitutively active RET receptor.	human	Neoplastic tissues	High+Lowthroughput	A synonymous RET substitution enhances the oncogenic effect of an in-cis missense mutation by increasing constitutive splicing efficiency	否	无	Medullary thyroid carcinoma (MTC)	HeLa cell	E_01_0675	Sanger sequencing,Next-generation sequencing (NGS),Real-time PCR,RNA immunoprecipitation (RIP)	The p.Cys630 = variant created new exonic splicing enhancer motifs that enhanced SRp55 recruitment to the mutant allele, leading to more efficient maturation of its pre-mRNA and an increased abundance of mature mRNA encoding a constitutively active RET receptor.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The p.Cys630 = variant created new exonic splicing enhancer motifs that enhanced SRp55 recruitment to the mutant allele, leading to more efficient maturation of its pre-mRNA and an increased abundance of mature mRNA encoding a constitutively active RET receptor.		The p.Cys630 = variant created new exonic splicing enhancer motifs that enhanced SRp55 recruitment to the mutant allele, leading to more efficient maturation of its pre-mRNA and an increased abundance of mature mRNA encoding a constitutively active RET receptor.	Immunohistochemical staining	The p.Cys630 = variant created new exonic splicing enhancer motifs that enhanced SRp55 recruitment to the mutant allele, leading to more efficient maturation of its pre-mRNA and an increased abundance of mature mRNA encoding a constitutively active RET receptor.			Sanger sequencing,Next-generation sequencing (NGS),Real-time PCR,RNA immunoprecipitation (RIP)				RET
30319691	chr8	56158399	56160399	PLAG1	Three of the five SNPs were located in promoter or enhancer regions, and transcription factor (TF) binding affinity calculations showed dramatic changes (| Log2FC| > 2) of three TFs (PLAG1, RREB1, and ZBTB33) for two motifs containing SNPs rs2075650 and rs157580. In addition, our GWAS showed that both rs2075650 and rs157580 were significantly associated with the poliovirus receptorrelated 2 (PVRL2) gene (FDR < 0.25), which is involved in spreading of herpes simplex virus (HSV). 	human		High+Lowthroughput	Genome-Wide Association and Mechanistic Studies Indicate That Immune Response Contributes to Alzheimer's Disease Development	是	rs2075650，rs157580	Alzheimer disease	brain-resident immune cell	E_01_0676	quantitative trait loci (eQTL)analysis，immunoassay	Three of the five SNPs were located in promoter or enhancer regions, and transcription factor (TF) binding affinity calculations showed dramatic changes (| Log2FC| > 2) of three TFs (PLAG1, RREB1, and ZBTB33) for two motifs containing SNPs rs2075650 and rs157580. In addition, our GWAS showed that both rs2075650 and rs157580 were significantly associated with the poliovirus receptorrelated 2 (PVRL2) gene (FDR < 0.25), which is involved in spreading of herpes simplex virus (HSV). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Three of the five SNPs were located in promoter or enhancer regions, and transcription factor (TF) binding affinity calculations showed dramatic changes (| Log2FC| > 2) of three TFs (PLAG1, RREB1, and ZBTB33) for two motifs containing SNPs rs2075650 and rs157580. In addition, our GWAS showed that both rs2075650 and rs157580 were significantly associated with the poliovirus receptorrelated 2 (PVRL2) gene (FDR < 0.25), which is involved in spreading of herpes simplex virus (HSV). 		Three of the five SNPs were located in promoter or enhancer regions, and transcription factor (TF) binding affinity calculations showed dramatic changes (| Log2FC| > 2) of three TFs (PLAG1, RREB1, and ZBTB33) for two motifs containing SNPs rs2075650 and rs157580. In addition, our GWAS showed that both rs2075650 and rs157580 were significantly associated with the poliovirus receptorrelated 2 (PVRL2) gene (FDR < 0.25), which is involved in spreading of herpes simplex virus (HSV). 	Immunohistochemical staining	Three of the five SNPs were located in promoter or enhancer regions, and transcription factor (TF) binding affinity calculations showed dramatic changes (| Log2FC| > 2) of three TFs (PLAG1, RREB1, and ZBTB33) for two motifs containing SNPs rs2075650 and rs157580. In addition, our GWAS showed that both rs2075650 and rs157580 were significantly associated with the poliovirus receptorrelated 2 (PVRL2) gene (FDR < 0.25), which is involved in spreading of herpes simplex virus (HSV). 			quantitative trait loci (eQTL)analysis，immunoassay				PLAG1
30314898	chr1	202807906	202809906	PCAT6	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer	human	normal lung tissues	High+Lowthroughput	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer	否	无	Non small cell carcinoma	NSCLC cell	E_01_0677	RNA isolation and quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR)，MTT assay，Flow cytometric analysis，Transwell assay，Western blot analysis，RNA-binding protein immunoprecipitation (RIP) assay，Chromatin immunoprecipitation (ChIP) assays	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer		Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer	Immunohistochemical staining	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer			RNA isolation and quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR)，MTT assay，Flow cytometric analysis，Transwell assay，Western blot analysis，RNA-binding protein immunoprecipitation (RIP) assay，Chromatin immunoprecipitation (ChIP) assays				PCAT6
30314898	chr7	148804660	148806660	EZH2	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer	human	normal lung tissues	High+Lowthroughput	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer	否	无	Non small cell carcinoma	NSCLC cell	E_01_0677	RNA isolation and quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR)，MTT assay，Flow cytometric analysis，Transwell assay，Western blot analysis，RNA-binding protein immunoprecipitation (RIP) assay，Chromatin immunoprecipitation (ChIP) assays	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer	Immunohistochemical staining	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer	EZH2		RNA isolation and quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR)，MTT assay，Flow cytometric analysis，Transwell assay，Western blot analysis，RNA-binding protein immunoprecipitation (RIP) assay，Chromatin immunoprecipitation (ChIP) assays	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer			
30314898	chr13	20970731	20972731	LATS2	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer	human	normal lung tissues	High+Lowthroughput	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer	否	无	Non small cell carcinoma	NSCLC cell	E_01_0677	RNA isolation and quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR)，MTT assay，Flow cytometric analysis，Transwell assay，Western blot analysis，RNA-binding protein immunoprecipitation (RIP) assay，Chromatin immunoprecipitation (ChIP) assays	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer		Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer	Immunohistochemical staining	Long noncoding RNA PCAT6 functions as an oncogene by binding to EZH2 and suppressing LATS2 in non-small-cell lung cancer			RNA isolation and quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR)，MTT assay，Flow cytometric analysis，Transwell assay，Western blot analysis，RNA-binding protein immunoprecipitation (RIP) assay，Chromatin immunoprecipitation (ChIP) assays				LATS2
30310321	chr10	129464370	129466370	MGMT	An enhancer variant of MGMT rs10764901 affects the regulatory activity of enhancer by altering the binding affinity of transcription factors and is associated with glioma susceptibility.	human		High+Lowthroughput	An intronic genetic variation of MGMT affects enhancer activity and is associated with glioma susceptibility	是	rs10764901	Gliomas	U251 cell	E_01_0678	Dual-Luciferase Reporter Assay，electrophoretic mobility shift assays (EMSA)，PCR，Seq	An enhancer variant of MGMT rs10764901 affects the regulatory activity of enhancer by altering the binding affinity of transcription factors and is associated with glioma susceptibility.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	An enhancer variant of MGMT rs10764901 affects the regulatory activity of enhancer by altering the binding affinity of transcription factors and is associated with glioma susceptibility.		An enhancer variant of MGMT rs10764901 affects the regulatory activity of enhancer by altering the binding affinity of transcription factors and is associated with glioma susceptibility.	Immunohistochemical staining	An enhancer variant of MGMT rs10764901 affects the regulatory activity of enhancer by altering the binding affinity of transcription factors and is associated with glioma susceptibility.			Dual-Luciferase Reporter Assay，electrophoretic mobility shift assays (EMSA)，PCR，Seq				MGMT
30307955	chr1	145989806	145991806	TXNIP	As indicated by our results, tranilast alleviated cGVHD-elicited inflammation and fibrosis by suppressing the expression and/or activation of TXNIP and NF-κB and preventing EMT.	mouse		High+Lowthroughput	Therapeutic potential of tranilast for the treatment of chronic graft-versus-host disease in mice	否	无	Chronic graft versus host disease	hematopoietic stem cell	E_02_0407	Histological analysis and immunohistochemistry,Immunoblotting analysis,Enzyme linked immunosorbent assay (ELISA)	As indicated by our results, tranilast alleviated cGVHD-elicited inflammation and fibrosis by suppressing the expression and/or activation of TXNIP and NF-κB and preventing EMT.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	As indicated by our results, tranilast alleviated cGVHD-elicited inflammation and fibrosis by suppressing the expression and/or activation of TXNIP and NF-κB and preventing EMT.		As indicated by our results, tranilast alleviated cGVHD-elicited inflammation and fibrosis by suppressing the expression and/or activation of TXNIP and NF-κB and preventing EMT.	Immunohistochemical staining	As indicated by our results, tranilast alleviated cGVHD-elicited inflammation and fibrosis by suppressing the expression and/or activation of TXNIP and NF-κB and preventing EMT.			Histological analysis and immunohistochemistry,Immunoblotting analysis,Enzyme linked immunosorbent assay (ELISA)				TXNIP
30307772	chr8	144288777	144290777	HSF1	We show here that theTNF-agene, apleiotropicNkBS inducer, is a direct target of heat shock factor 1 (HSF1). HumanHSF1 drives this process by assembling a multiprotein activation complex at a heat shock element (HSE) located at the 39-UTR of the TNF-a gene (HSE5).	human		High+Lowthroughput	HSF1 mediated TNF-α production during proteotoxic stress response pioneers proinflammatory signal in human cells	否	无	Cellular upregulation of the proteotoxic stress response	HEK293cell, HCT116cell,PC3cell,HT1080 cell	E_01_0679	Chromatin immunoprecipitation,Chromatin conformation capture assay,Semi-quantitative RT-PCR and quantitative RT-PCR,EMSA,MTT cytotoxicity assay,RNA transfection, Immunoprecipitation,Immunoblot	We show here that theTNF-agene, apleiotropicNkBS inducer, is a direct target of heat shock factor 1 (HSF1). HumanHSF1 drives this process by assembling a multiprotein activation complex at a heat shock element (HSE) located at the 39-UTR of the TNF-a gene (HSE5).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We show here that theTNF-agene, apleiotropicNkBS inducer, is a direct target of heat shock factor 1 (HSF1). HumanHSF1 drives this process by assembling a multiprotein activation complex at a heat shock element (HSE) located at the 39-UTR of the TNF-a gene (HSE5).	Immunohistochemical staining	We show here that theTNF-agene, apleiotropicNkBS inducer, is a direct target of heat shock factor 1 (HSF1). HumanHSF1 drives this process by assembling a multiprotein activation complex at a heat shock element (HSE) located at the 39-UTR of the TNF-a gene (HSE5).	HSF1		Chromatin immunoprecipitation,Chromatin conformation capture assay,Semi-quantitative RT-PCR and quantitative RT-PCR,EMSA,MTT cytotoxicity assay,RNA transfection, Immunoprecipitation,Immunoblot	We show here that theTNF-agene, apleiotropicNkBS inducer, is a direct target of heat shock factor 1 (HSF1). HumanHSF1 drives this process by assembling a multiprotein activation complex at a heat shock element (HSE) located at the 39-UTR of the TNF-a gene (HSE5).			
30301799	chr3	128476289	128478289	GATA2	By inducing the generation and function of hematopoietic stem and progenitor cells, the master regulator of hematopoiesis GATA- 2 controls the production of all blood cell types. Heterozygous GATA2 mutations cause immunodeficiency, myelodysplastic syndrome, and acute myeloid leukemia.	human		High+Lowthroughput	Human leukemia mutations corrupt but do not abrogate GATA-2 function	否	无	Human leukemia mutations		E_01_0680	Quantitative Real-Time RT-PCR，Quantitative ChIP，Immunofluorescence，Colony Forming Unit Assay，Flow Cytometry	By inducing the generation and function of hematopoietic stem and progenitor cells, the master regulator of hematopoiesis GATA- 2 controls the production of all blood cell types. Heterozygous GATA2 mutations cause immunodeficiency, myelodysplastic syndrome, and acute myeloid leukemia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			By inducing the generation and function of hematopoietic stem and progenitor cells, the master regulator of hematopoiesis GATA- 2 controls the production of all blood cell types. Heterozygous GATA2 mutations cause immunodeficiency, myelodysplastic syndrome, and acute myeloid leukemia.	Immunohistochemical staining	By inducing the generation and function of hematopoietic stem and progenitor cells, the master regulator of hematopoiesis GATA- 2 controls the production of all blood cell types. Heterozygous GATA2 mutations cause immunodeficiency, myelodysplastic syndrome, and acute myeloid leukemia.	GATA2		Quantitative Real-Time RT-PCR，Quantitative ChIP，Immunofluorescence，Colony Forming Unit Assay，Flow Cytometry	By inducing the generation and function of hematopoietic stem and progenitor cells, the master regulator of hematopoiesis GATA- 2 controls the production of all blood cell types. Heterozygous GATA2 mutations cause immunodeficiency, myelodysplastic syndrome, and acute myeloid leukemia.			
30301396	chr9	81581030	81583030	TLE1	Therefore, when evaluating spindle cell tumors in which the differential may include both a melanoma and synovial sarcoma, TLE1 expression should be interpreted with caution and in conjunction with an immunohistochemical panel. 	human		High+Lowthroughput	Expression of TLE1 in Malignant Melanoma With Spindle Cell Morphology: A Potential Diagnostic Pitfall	否	无	Malignant melanoma		E_01_0681	Immunohistochemical studies	Therefore, when evaluating spindle cell tumors in which the differential may include both a melanoma and synovial sarcoma, TLE1 expression should be interpreted with caution and in conjunction with an immunohistochemical panel. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Therefore, when evaluating spindle cell tumors in which the differential may include both a melanoma and synovial sarcoma, TLE1 expression should be interpreted with caution and in conjunction with an immunohistochemical panel. 	Immunohistochemical staining	Therefore, when evaluating spindle cell tumors in which the differential may include both a melanoma and synovial sarcoma, TLE1 expression should be interpreted with caution and in conjunction with an immunohistochemical panel. 	TLE1		Immunohistochemical studies	Therefore, when evaluating spindle cell tumors in which the differential may include both a melanoma and synovial sarcoma, TLE1 expression should be interpreted with caution and in conjunction with an immunohistochemical panel. 			
30297428	chr6	100382241	100384241	SIM1	The risk locus resides on the same topologically associating domain as SIM1 and interacts with the SIM1 promoter, and the rs17185536- T risk allele showed differential enhancer activity. 	human		High+Lowthroughput	Genetic variation in the SIM1 locus is associated with erectile dysfunction	是	rs17185536	erectile dysfunction 	HEK 293T	E_01_0682	GWAS Analysis，Luciferase Assays	The risk locus resides on the same topologically associating domain as SIM1 and interacts with the SIM1 promoter, and the rs17185536- T risk allele showed differential enhancer activity. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The risk locus resides on the same topologically associating domain as SIM1 and interacts with the SIM1 promoter, and the rs17185536- T risk allele showed differential enhancer activity. 	Immunohistochemical staining	The risk locus resides on the same topologically associating domain as SIM1 and interacts with the SIM1 promoter, and the rs17185536- T risk allele showed differential enhancer activity. 	SIM1		GWAS Analysis，Luciferase Assays	The risk locus resides on the same topologically associating domain as SIM1 and interacts with the SIM1 promoter, and the rs17185536- T risk allele showed differential enhancer activity. 			
30296588	chr7	117284315	117286315	CFTR	These data suggest that CFTR regulatory elements may harbor novel CF disease causing variants that warrant further investigation, both for genetic screening protocols and functional assays. 	human		High+Lowthroughput	Screening for Regulatory Variants in 460 kb Encompassing the CFTR Locus in Cystic Fibrosis Patients	否	无	Cystic fibrosis	Caco228 cell，16HBE14o-29 cell	E_01_0683	Transient Luciferase Assays， transient assays，Dual-Luciferase Reporter Assay，Bioinformatic Variant Analysis	These data suggest that CFTR regulatory elements may harbor novel CF disease causing variants that warrant further investigation, both for genetic screening protocols and functional assays. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These data suggest that CFTR regulatory elements may harbor novel CF disease causing variants that warrant further investigation, both for genetic screening protocols and functional assays. 	Immunohistochemical staining	These data suggest that CFTR regulatory elements may harbor novel CF disease causing variants that warrant further investigation, both for genetic screening protocols and functional assays. 	CFTR		Transient Luciferase Assays， transient assays，Dual-Luciferase Reporter Assay，Bioinformatic Variant Analysis	These data suggest that CFTR regulatory elements may harbor novel CF disease causing variants that warrant further investigation, both for genetic screening protocols and functional assays. 			
30295986	chr2	9838078	9840078	Gata3	"These studies identify a novel distal enhancer of Gata3 with high activity in lens and indicate that BMP and FGF signaling can up_x005f_x0002_regulate expression of Gata3 in differentiating lens fiber cells through the identified Gata3 
enhancer and promoter elements."	mouse		Low throughput	Identification of Novel Gata3 Distal Enhancers Active in Mouse Embryonic Lens	否	--	--		E_02_0408	Luciferase Reporter Assay,qPCR	We next employed a transient transfection assay to test putative Gata3 Enhancers in Gata3-expressing 293T cells using a heterologous TATA promoter that drives Luciferasegene expression. Here we describe the identification of a novel bipartite Gata3 lens-specific Enhancer located ~18 kb upstream from its transcriptional start site. We also found that a 5 kb Gata3 promoter possesses low activity in the lens.	Enhancer	--	Luciferase Reporter Assay,qPCR	"Here we describe the identification of a novel bipartite Gata3 lens-specific enhancer located
18 kb upstream from its transcriptional start site. We also found that a 5-kb Gata3 promoter possesses low activity in the lens. The bipartite enhancer contains arrays of AP-1, Ets-, and Smad1/5-binding sites as well as binding sites for lensassociated DNA-binding factors."	Gata-3,jal	--	--	--	--	--	--	--	--	--	Gata3
30293785	chr20	47206342	47208342	ZMYND8	ZMYND8 controls Igh diversification in mature B lymphocytes by regulating the activity of the 30 Igh super-enhancer. 	human		High+Lowthroughput	The Chromatin Reader ZMYND8 Regulates Igh Enhancers to Promote Immunoglobulin Class Switch Recombination	否	无	nothing	CH12 cell	E_01_0684	Retroviral Infection,Immunoisolation of RIF1FH Complexes,Mass Spectrometric Analysis,CRISPR-Cas9 Gene Targeting,Cell Lysates and CoIP Assay,Flow Cytometry,Quantitative PCR,Immunofluorescence,Clonogenic Assay,Metaphase Analysis,End Resection Assay,CRISPR-Cas9-Induced CSR Assay,MutPE-Seq,ChIP-Seq,RNA-Seq,GRO-Seq,Switch Junction Analysis,SHM Analysis	ZMYND8 controls Igh diversification in mature B lymphocytes by regulating the activity of the 30 Igh super-enhancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ZMYND8 controls Igh diversification in mature B lymphocytes by regulating the activity of the 30 Igh super-enhancer. 		ZMYND8 controls Igh diversification in mature B lymphocytes by regulating the activity of the 30 Igh super-enhancer. 	Immunohistochemical staining	ZMYND8 controls Igh diversification in mature B lymphocytes by regulating the activity of the 30 Igh super-enhancer. 			Retroviral Infection,Immunoisolation of RIF1FH Complexes,Mass Spectrometric Analysis,CRISPR-Cas9 Gene Targeting,Cell Lysates and CoIP Assay,Flow Cytometry,Quantitative PCR,Immunofluorescence,Clonogenic Assay,Metaphase Analysis,End Resection Assay,CRISPR-Cas9-Induced CSR Assay,MutPE-Seq,ChIP-Seq,RNA-Seq,GRO-Seq,Switch Junction Analysis,SHM Analysis				ZMYND8
30286132	chr17	39725638	39727638	MIEN1	Knocking out MIEN1 in these breast cancer cells will allow future studies to determine the exact role MIEN1 plays in breast tumor metastasis, which might lead to production of novel therapeutics to treat this and other caners	human		High+Lowthroughput	CRISPR deletion of MIEN1 in breast cancer cells	否	无	mammary cancer	breast cancer cell	E_01_0685	Transfection and CRISPR genome editing，Sequencing，Western blot	Knocking out MIEN1 in these breast cancer cells will allow future studies to determine the exact role MIEN1 plays in breast tumor metastasis, which might lead to production of novel therapeutics to treat this and other caners	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Knocking out MIEN1 in these breast cancer cells will allow future studies to determine the exact role MIEN1 plays in breast tumor metastasis, which might lead to production of novel therapeutics to treat this and other caners		Knocking out MIEN1 in these breast cancer cells will allow future studies to determine the exact role MIEN1 plays in breast tumor metastasis, which might lead to production of novel therapeutics to treat this and other caners	Immunohistochemical staining	Knocking out MIEN1 in these breast cancer cells will allow future studies to determine the exact role MIEN1 plays in breast tumor metastasis, which might lead to production of novel therapeutics to treat this and other caners			Transfection and CRISPR genome editing，Sequencing，Western blot				MIEN1
30285846	chr22	19327664	19329664	HIRA	Together, our results provide novel insights into the mechanism by which the HIRA complex specificallyrecognizes and deposits H3.3 at promoters and enhancers of developmental genes, which plays a critical role in neural differentiation of mES cells.	mouse		High+Lowthroughput	UBN1/2 of HIRA complex is responsible for recognition and deposition of H3.3 at cis-regulatory elements of genes in mouse ES cells	否	无	nothing	ES cell	E_02_0409	Co-immunoprecipitation，GST pull-down assays，Immunofluorescence，ChIP-qPCR，ChIP-seq，RNA preparation, RT-qPCR and poly(A) RNA-seq	Together, our results provide novel insights into the mechanism by which the HIRA complex specificallyrecognizes and deposits H3.3 at promoters and enhancers of developmental genes, which plays a critical role in neural differentiation of mES cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Together, our results provide novel insights into the mechanism by which the HIRA complex specificallyrecognizes and deposits H3.3 at promoters and enhancers of developmental genes, which plays a critical role in neural differentiation of mES cells.		Together, our results provide novel insights into the mechanism by which the HIRA complex specificallyrecognizes and deposits H3.3 at promoters and enhancers of developmental genes, which plays a critical role in neural differentiation of mES cells.	Immunohistochemical staining	Together, our results provide novel insights into the mechanism by which the HIRA complex specificallyrecognizes and deposits H3.3 at promoters and enhancers of developmental genes, which plays a critical role in neural differentiation of mES cells.			Co-immunoprecipitation，GST pull-down assays，Immunofluorescence，ChIP-qPCR，ChIP-seq，RNA preparation, RT-qPCR and poly(A) RNA-seq				HIRA
30285829	chr16	50739227	50741227	CYLD	Via its regulation of NF-κB activation, CYLD may be involved in the pathogenesis of synovial inflammation in RA as well as in the pro-inflammatory effects and hyperproliferation of RA-FLSs. CYLD may therefore provide a potential target for the treatment of RA.	human	Synovial tissues	High+Lowthroughput	CYLD suppression enhances the pro-inflammatory effects and hyperproliferation of rheumatoid arthritis fibroblast-like synoviocytes by enhancing NF-κB activation	否	无	Rheumatoid arthritis	synovial cell	E_01_0686	Immunohistochemistry (IHC),Immunofluorescence (IF) staining,RT-PCR,Western blot,ELISA,Cell proliferation assay,y flow cytometry 	Via its regulation of NF-κB activation, CYLD may be involved in the pathogenesis of synovial inflammation in RA as well as in the pro-inflammatory effects and hyperproliferation of RA-FLSs. CYLD may therefore provide a potential target for the treatment of RA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Via its regulation of NF-κB activation, CYLD may be involved in the pathogenesis of synovial inflammation in RA as well as in the pro-inflammatory effects and hyperproliferation of RA-FLSs. CYLD may therefore provide a potential target for the treatment of RA.		Via its regulation of NF-κB activation, CYLD may be involved in the pathogenesis of synovial inflammation in RA as well as in the pro-inflammatory effects and hyperproliferation of RA-FLSs. CYLD may therefore provide a potential target for the treatment of RA.	Immunohistochemical staining	Via its regulation of NF-κB activation, CYLD may be involved in the pathogenesis of synovial inflammation in RA as well as in the pro-inflammatory effects and hyperproliferation of RA-FLSs. CYLD may therefore provide a potential target for the treatment of RA.			Immunohistochemistry (IHC),Immunofluorescence (IF) staining,RT-PCR,Western blot,ELISA,Cell proliferation assay,y flow cytometry 				CYLD
30284014	chr7	129609040	129611040	NRF1	Furthermore, in line with the epigenome in DIO mice, palmitate treatment caused increase in H3K27ac and induction of β-oxidation genes; these responses were blunted when NRF1, GABPA or MEF2A were suppressed. 	mouse		High+Lowthroughput	Genome-wide profiling of histone H3K27 acetylation featured fatty acid signalling in pancreatic beta cells in diet-induced obesity in mice	否	无	Obesity and type 2 diabetes	Beta cell	E_02_0410	RNA-Seq，ChIP-Seq，qPCR，TSS	Furthermore, in line with the epigenome in DIO mice, palmitate treatment caused increase in H3K27ac and induction of β-oxidation genes; these responses were blunted when NRF1, GABPA or MEF2A were suppressed. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, in line with the epigenome in DIO mice, palmitate treatment caused increase in H3K27ac and induction of β-oxidation genes; these responses were blunted when NRF1, GABPA or MEF2A were suppressed. 		Furthermore, in line with the epigenome in DIO mice, palmitate treatment caused increase in H3K27ac and induction of β-oxidation genes; these responses were blunted when NRF1, GABPA or MEF2A were suppressed. 	Immunohistochemical staining	Furthermore, in line with the epigenome in DIO mice, palmitate treatment caused increase in H3K27ac and induction of β-oxidation genes; these responses were blunted when NRF1, GABPA or MEF2A were suppressed. 			RNA-Seq，ChIP-Seq，qPCR，TSS				NRF1
30283453	chr21	44283260	44285260	AIRE	Our findings indicate that the mature mTEC chromatin landscape is laid down early in mTEC differentiation, and that AIRE is not required for large-scale re-patterning of chromatin in mTEC.	mouse		High+Lowthroughput	Comprehensively Profiling the Chromatin Architecture of Tissue Restricted Antigen Expression in Thymic Epithelial Cells Over Development	否	无	nothing	epithelial cell of thymus	E_02_0411	ChIP,Histone ChIP-Seq Analysis,ATAC-Seq,RNA-Seq	Our findings indicate that the mature mTEC chromatin landscape is laid down early in mTEC differentiation, and that AIRE is not required for large-scale re-patterning of chromatin in mTEC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our findings indicate that the mature mTEC chromatin landscape is laid down early in mTEC differentiation, and that AIRE is not required for large-scale re-patterning of chromatin in mTEC.		Our findings indicate that the mature mTEC chromatin landscape is laid down early in mTEC differentiation, and that AIRE is not required for large-scale re-patterning of chromatin in mTEC.	Immunohistochemical staining	Our findings indicate that the mature mTEC chromatin landscape is laid down early in mTEC differentiation, and that AIRE is not required for large-scale re-patterning of chromatin in mTEC.			ChIP,Histone ChIP-Seq Analysis,ATAC-Seq,RNA-Seq				AIRE
30283292	chr1	161763468	161765468	ATF6	Melatonin could protect against neuronal apoptosis via suppression of ATF6/CHOP arm of ER-stress-response pathway.	human		High+Lowthroughput	Melatonin Protects Against Neuronal Apoptosis via Suppression of the ATF6/CHOP Pathway in a Rat Model of Intracerebral Hemorrhage	否	无	cerebral hemorrhage	neuronal cell	E_01_0687	Evans Blue (EB) Staining，Immunofluorescence，Western Blot，Small Interfering RNA and Intracerebroventricular Injection，RT-PCR	Melatonin could protect against neuronal apoptosis via suppression of ATF6/CHOP arm of ER-stress-response pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Melatonin could protect against neuronal apoptosis via suppression of ATF6/CHOP arm of ER-stress-response pathway.	Immunohistochemical staining	Melatonin could protect against neuronal apoptosis via suppression of ATF6/CHOP arm of ER-stress-response pathway.	ATF6		Evans Blue (EB) Staining，Immunofluorescence，Western Blot，Small Interfering RNA and Intracerebroventricular Injection，RT-PCR	Melatonin could protect against neuronal apoptosis via suppression of ATF6/CHOP arm of ER-stress-response pathway.			
30276662	chr13	83649606	83651606	Mef2c	Thus, our results reveal the specific expression and functionalrelevance of Mef2c in developing Purkinje cells and offer insight to how disruption of the expression of Mef2c in a GABAergic neuronal subtype may lead to pathogenesis of cerebellar-associated disorders.	human		High+Lowthroughput	Myocyte Enhancer Factor 2c Regulates Dendritic Complexity and Connectivity of Cerebellar Purkinje Cells	否	无	 	Purkinje cell	E_01_0688	situ hybridization analysis，immunohistochemical analysis	Thus, our results reveal the specific expression and functionalrelevance of Mef2c in developing Purkinje cells and offer insight to how disruption of the expression of Mef2c in a GABAergic neuronal subtype may lead to pathogenesis of cerebellar-associated disorders.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, our results reveal the specific expression and functionalrelevance of Mef2c in developing Purkinje cells and offer insight to how disruption of the expression of Mef2c in a GABAergic neuronal subtype may lead to pathogenesis of cerebellar-associated disorders.		Thus, our results reveal the specific expression and functionalrelevance of Mef2c in developing Purkinje cells and offer insight to how disruption of the expression of Mef2c in a GABAergic neuronal subtype may lead to pathogenesis of cerebellar-associated disorders.	Immunohistochemical staining	Thus, our results reveal the specific expression and functionalrelevance of Mef2c in developing Purkinje cells and offer insight to how disruption of the expression of Mef2c in a GABAergic neuronal subtype may lead to pathogenesis of cerebellar-associated disorders.			situ hybridization analysis，immunohistochemical analysis				Mef2c
30274972	chr4	105143201	105145201	TET2	Hence TET2 plays a critical role in the GC reaction and its loss of function results in lymphomagenesis through failure to activate genes linked to GC exit signals.	mouse		High+Lowthroughput	TET2 Deficiency Causes Germinal Center Hyperplasia, Impairs Plasma Cell Differentiation, and Promotes B-cell Lymphomagenesis	否	无	B cell lymphoma	B cell	E_02_0412	ELISA and ELISPOT,Flow cytometry analysis,Histology and immunohistochemistry,Genomic DNA and RNA extraction,DNA seq,quantification of methylation,ChIP,Quantitative real-time PCR,hMeDIP-seq,RNA-seq	Hence TET2 plays a critical role in the GC reaction and its loss of function results in lymphomagenesis through failure to activate genes linked to GC exit signals.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hence TET2 plays a critical role in the GC reaction and its loss of function results in lymphomagenesis through failure to activate genes linked to GC exit signals.		Hence TET2 plays a critical role in the GC reaction and its loss of function results in lymphomagenesis through failure to activate genes linked to GC exit signals.	Immunohistochemical staining	Hence TET2 plays a critical role in the GC reaction and its loss of function results in lymphomagenesis through failure to activate genes linked to GC exit signals.			ELISA and ELISPOT,Flow cytometry analysis,Histology and immunohistochemistry,Genomic DNA and RNA extraction,DNA seq,quantification of methylation,ChIP,Quantitative real-time PCR,hMeDIP-seq,RNA-seq				TET2
30274685	chr7	148804548	148806548	EZH2	MiR-137 suppressed migration and invasion by targeting EZH2-STAT3 signaling pathway in HCC cells in vitro and in vivo, suggesting miR-137-EZH2-STAT3 may be a potential therapeutic target for treatment of human hepatocellular carcinoma	human		High+Lowthroughput	MiR-137 suppresses migration and invasion by targeting EZH2-STAT3 signaling in human hepatocellular carcinoma	否	无	Human hepatocellular carcinoma	hepatocellular carcinoma cell	E_01_0689	Cell transfection，qPCR，Wound-healing assay，Transwell assay，Dual-luciferase reporter assay， Western blotting analysis	MiR-137 suppressed migration and invasion by targeting EZH2-STAT3 signaling pathway in HCC cells in vitro and in vivo, suggesting miR-137-EZH2-STAT3 may be a potential therapeutic target for treatment of human hepatocellular carcinoma	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MiR-137 suppressed migration and invasion by targeting EZH2-STAT3 signaling pathway in HCC cells in vitro and in vivo, suggesting miR-137-EZH2-STAT3 may be a potential therapeutic target for treatment of human hepatocellular carcinoma	Immunohistochemical staining	MiR-137 suppressed migration and invasion by targeting EZH2-STAT3 signaling pathway in HCC cells in vitro and in vivo, suggesting miR-137-EZH2-STAT3 may be a potential therapeutic target for treatment of human hepatocellular carcinoma	EZH2		Cell transfection，qPCR，Wound-healing assay，Transwell assay，Dual-luciferase reporter assay， Western blotting analysis	MiR-137 suppressed migration and invasion by targeting EZH2-STAT3 signaling pathway in HCC cells in vitro and in vivo, suggesting miR-137-EZH2-STAT3 may be a potential therapeutic target for treatment of human hepatocellular carcinoma			
30274685	chr17	42310752	42312752	STAT3	MiR-137 suppressed migration and invasion by targeting EZH2-STAT3 signaling pathway in HCC cells in vitro and in vivo, suggesting miR-137-EZH2-STAT3 may be a potential therapeutic target for treatment of human hepatocellular carcinoma	human		High+Lowthroughput	MiR-137 suppresses migration and invasion by targeting EZH2-STAT3 signaling in human hepatocellular carcinoma	否	无	Human hepatocellular carcinoma	hepatocellular carcinoma cell	E_01_0689	Cell transfection，qPCR，Wound-healing assay，Transwell assay，Dual-luciferase reporter assay， Western blotting analysis	MiR-137 suppressed migration and invasion by targeting EZH2-STAT3 signaling pathway in HCC cells in vitro and in vivo, suggesting miR-137-EZH2-STAT3 may be a potential therapeutic target for treatment of human hepatocellular carcinoma	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MiR-137 suppressed migration and invasion by targeting EZH2-STAT3 signaling pathway in HCC cells in vitro and in vivo, suggesting miR-137-EZH2-STAT3 may be a potential therapeutic target for treatment of human hepatocellular carcinoma	Immunohistochemical staining	MiR-137 suppressed migration and invasion by targeting EZH2-STAT3 signaling pathway in HCC cells in vitro and in vivo, suggesting miR-137-EZH2-STAT3 may be a potential therapeutic target for treatment of human hepatocellular carcinoma	STAT3		Cell transfection，qPCR，Wound-healing assay，Transwell assay，Dual-luciferase reporter assay， Western blotting analysis	MiR-137 suppressed migration and invasion by targeting EZH2-STAT3 signaling pathway in HCC cells in vitro and in vivo, suggesting miR-137-EZH2-STAT3 may be a potential therapeutic target for treatment of human hepatocellular carcinoma			
30270123	chr7	27159901	27161901	HOXA9	Therapeutic targeting of HOXA9-dependent enhancer reorganization can be an effective therapeutic strategy in acute leukemia with HOXA9 overexpression. 	human		High+Lowthroughput	HOXA9 Reprograms the Enhancer Landscape to Promote Leukemogenesis	否	无	leukemia	progenitor cell	E_01_0690	Flow Cytometry,Cell Proliferation and Colony Formation Assays,Immunoprecipitation,4C-seq Analysis,ChIP, ChIP-Seq and Bioinformatics Analyses,Real-time PCR and RNA-seq Analyses,Global Analysis on the Enhancer Landscape	Therapeutic targeting of HOXA9-dependent enhancer reorganization can be an effective therapeutic strategy in acute leukemia with HOXA9 overexpression. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Therapeutic targeting of HOXA9-dependent enhancer reorganization can be an effective therapeutic strategy in acute leukemia with HOXA9 overexpression. 	Immunohistochemical staining	Therapeutic targeting of HOXA9-dependent enhancer reorganization can be an effective therapeutic strategy in acute leukemia with HOXA9 overexpression. 	HOXA9		Flow Cytometry,Cell Proliferation and Colony Formation Assays,Immunoprecipitation,4C-seq Analysis,ChIP, ChIP-Seq and Bioinformatics Analyses,Real-time PCR and RNA-seq Analyses,Global Analysis on the Enhancer Landscape	Therapeutic targeting of HOXA9-dependent enhancer reorganization can be an effective therapeutic strategy in acute leukemia with HOXA9 overexpression. 			
30266822	chr20	32355424	32357424	ASXL1	Thus, in addition to promoting myeloid malignancies, ASXL1 controls epigenetic reprogramming of osteoclasts to regulate bone resorption and mass. 	human		High+Lowthroughput	ASXL1 impairs osteoclast formation by epigenetic regulation of NFATc1	否	无	Myeloid malignancies	osteoclast	E_01_0691	Histone extraction, histone western blot，Lentivirus infection，ChIP assay，ChIP-seq	Thus, in addition to promoting myeloid malignancies, ASXL1 controls epigenetic reprogramming of osteoclasts to regulate bone resorption and mass. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, in addition to promoting myeloid malignancies, ASXL1 controls epigenetic reprogramming of osteoclasts to regulate bone resorption and mass. 		Thus, in addition to promoting myeloid malignancies, ASXL1 controls epigenetic reprogramming of osteoclasts to regulate bone resorption and mass. 	Immunohistochemical staining	Thus, in addition to promoting myeloid malignancies, ASXL1 controls epigenetic reprogramming of osteoclasts to regulate bone resorption and mass. 			Histone extraction, histone western blot，Lentivirus infection，ChIP assay，ChIP-seq				ASXL1
30262664	chr14	100891966	100893966	MEG8	"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."	human		High+Lowthroughput	MEG8 long noncoding RNA contributes to epigenetic progression of the epithelial-mesenchymal transition of lung and pancreatic cancer cells	否	无	Lung and pancreatic cancer	A549 cell，  LC-2/ad cell，Panc1 cell	E_01_0692	"Quantitative PCR，Cell migration assay，Chromatin immunoprecipitation (ChIP) assays，RNA immunoprecipitation (RIP)，Chromatin isolation by RNA purification (ChIRP) 
assays"	"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."		"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."	Immunohistochemical staining	"Our findings indicate that MEG8 lncRNA significantly contributes to epigenetic EMT induction and increase our understanding of the lncRNA-mediated regulatory mechanisms 
involved in malignant progression of cancer."			"Quantitative PCR，Cell migration assay，Chromatin immunoprecipitation (ChIP) assays，RNA immunoprecipitation (RIP)，Chromatin isolation by RNA purification (ChIRP) 
assays"				MEG8
30259241	chr12	55740136	55742136	GDF11	Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 	human		High+Lowthroughput	GDF11 Antagonizes Psoriasis-like Skin Inflammation via Suppression of NF-κB Signaling Pathway	否	无	Psoriasiform skin inflammation	Mouse leukemic monocyte macrophages	E_01_0693	miRNA transfection，Real-Time PCR,Western Blot,Immunofluorescence,ELISA Assays	Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 	Immunohistochemical staining	Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 	GDF11		miRNA transfection，Real-Time PCR,Western Blot,Immunofluorescence,ELISA Assays	Additionally, the activation of nuclear NF-κB (nuclear factor κ-light-chainenhancer of activated B cells) signaling pathway was repressed by GDF11 treatment. Collectively, GDF11 may represent a promising molecular target for the prevention and treatment of psoriasis-like skin inflammation. 			
30257372	chr8	127077104	127079104	PRNCR1	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	human		High+Lowthroughput	LncRNA PRNCR1 interacts with HEY2 to abolish miR-448-mediated growth inhibition in non-small cell lung cancer	否	无	Non small cell lung cancer	A549 cell, SK-MES-1 cell, Calu-3 cell，H1299 cell，NHBE cell	E_01_0694	Cell transfection,RNA isolation,qRT-PCR analysi, Cell proliferation assays, Transwell assays,Luciferase reporter analysis,RIP assay, Western blot assay	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 		Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	Immunohistochemical staining	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 			Cell transfection,RNA isolation,qRT-PCR analysi, Cell proliferation assays, Transwell assays,Luciferase reporter analysis,RIP assay, Western blot assay				PRNCR1
30257372	chr6	125744682	125746682	HEY2	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	human		High+Lowthroughput	LncRNA PRNCR1 interacts with HEY2 to abolish miR-448-mediated growth inhibition in non-small cell lung cancer	否	无	Non small cell lung cancer	A549 cell, SK-MES-1 cell, Calu-3 cell，H1299 cell，NHBE cell	E_01_0694	Cell transfection,RNA isolation,qRT-PCR analysi, Cell proliferation assays, Transwell assays,Luciferase reporter analysis,RIP assay, Western blot assay	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	Immunohistochemical staining	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 	HEY2		Cell transfection,RNA isolation,qRT-PCR analysi, Cell proliferation assays, Transwell assays,Luciferase reporter analysis,RIP assay, Western blot assay	Taken all together, we confirmed that lncRNA PRNCR1 upregulates HEY2 to promote tumor progression in NSCLC by competitively binding miR-448. 			
30257211	chr16	67559479	67561479	CTCF	The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x005f_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.	mouse		High+Lowthroughput	Stochastic Gene Choice during Cellular Differentiation	否	无	nothing	embryonic stem cell	E_02_0413	Single-Cell qRT-PCR,Chromatin Immunoprecipitation,Bisulfite Sequencing	The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x005f_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x005f_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.		The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x005f_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.	Immunohistochemical staining	The expression frequencycorrelates highly with CTCF binding to the promoters and follows dynamically the changes in the binding during the differentiation. These findings aid in un_x005f_x0002_derstanding the interplay between cellular differenti_x0002_ation and stochastic gene choice.			Single-Cell qRT-PCR,Chromatin Immunoprecipitation,Bisulfite Sequencing				CTCF
30256540	chr16	55386943	55388943	MMP2	These results suggested that exosomal lnc-MMP2-2 might regulate the migration and invasion of lung cancer cells into the vasculature by promoting MMP2 expression, suggesting this lncRNA as a novel therapeutic target and predictive marker of tumor metastasis in lung cancer	human		High+Lowthroughput	TGF-β-mediated exosomal lnc-MMP2-2 regulates migration and invasion of lung cancer cells to the vasculature by promoting MMP2 expression	否	无	lung cancer		E_01_0695	"qRT-PCR,Immunofluorescence,Western blot,Wound healing assay,Transwell assays,Luciferase assay,Immunohistochemistry and in situ 
hybridization"	These results suggested that exosomal lnc-MMP2-2 might regulate the migration and invasion of lung cancer cells into the vasculature by promoting MMP2 expression, suggesting this lncRNA as a novel therapeutic target and predictive marker of tumor metastasis in lung cancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These results suggested that exosomal lnc-MMP2-2 might regulate the migration and invasion of lung cancer cells into the vasculature by promoting MMP2 expression, suggesting this lncRNA as a novel therapeutic target and predictive marker of tumor metastasis in lung cancer	Immunohistochemical staining	These results suggested that exosomal lnc-MMP2-2 might regulate the migration and invasion of lung cancer cells into the vasculature by promoting MMP2 expression, suggesting this lncRNA as a novel therapeutic target and predictive marker of tumor metastasis in lung cancer	MMP2		"qRT-PCR,Immunofluorescence,Western blot,Wound healing assay,Transwell assays,Luciferase assay,Immunohistochemistry and in situ 
hybridization"	These results suggested that exosomal lnc-MMP2-2 might regulate the migration and invasion of lung cancer cells into the vasculature by promoting MMP2 expression, suggesting this lncRNA as a novel therapeutic target and predictive marker of tumor metastasis in lung cancer			
30252132	chr4	74442566	74444566	AREG	Expression of the epidermal growth factor ligands amphiregulin (AREG) and epiregulin (EREG) is positively correlated with a response to EGFR-targeted therapies in colorectal cancer. 	human		High+Lowthroughput	Epigenetic regulation of Amphiregulin and Epiregulin in colorectal cancer	否	无	colorectal cancer 	SW480 cell，RKO cell，HCT116 cell，Caco2 cell	E_01_0696	RNA isolation and Real-time PCR analysis,Methylation analysis,Luciferase reporter analysis,immunohistochemistry	Expression of the epidermal growth factor ligands amphiregulin (AREG) and epiregulin (EREG) is positively correlated with a response to EGFR-targeted therapies in colorectal cancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Expression of the epidermal growth factor ligands amphiregulin (AREG) and epiregulin (EREG) is positively correlated with a response to EGFR-targeted therapies in colorectal cancer. 		Expression of the epidermal growth factor ligands amphiregulin (AREG) and epiregulin (EREG) is positively correlated with a response to EGFR-targeted therapies in colorectal cancer. 	Immunohistochemical staining	Expression of the epidermal growth factor ligands amphiregulin (AREG) and epiregulin (EREG) is positively correlated with a response to EGFR-targeted therapies in colorectal cancer. 			RNA isolation and Real-time PCR analysis,Methylation analysis,Luciferase reporter analysis,immunohistochemistry				AREG
30252132	chr4	74362391	74364391	EREG	Expression of the epidermal growth factor ligands amphiregulin (AREG) and epiregulin (EREG) is positively correlated with a response to EGFR-targeted therapies in colorectal cancer. 	human		High+Lowthroughput	Epigenetic regulation of Amphiregulin and Epiregulin in colorectal cancer	否	无	colorectal cancer 	SW480 cell，RKO cell，HCT116 cell，Caco2 cell	E_01_0696	RNA isolation and Real-time PCR analysis,Methylation analysis,Luciferase reporter analysis,immunohistochemistry	Expression of the epidermal growth factor ligands amphiregulin (AREG) and epiregulin (EREG) is positively correlated with a response to EGFR-targeted therapies in colorectal cancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Expression of the epidermal growth factor ligands amphiregulin (AREG) and epiregulin (EREG) is positively correlated with a response to EGFR-targeted therapies in colorectal cancer. 		Expression of the epidermal growth factor ligands amphiregulin (AREG) and epiregulin (EREG) is positively correlated with a response to EGFR-targeted therapies in colorectal cancer. 	Immunohistochemical staining	Expression of the epidermal growth factor ligands amphiregulin (AREG) and epiregulin (EREG) is positively correlated with a response to EGFR-targeted therapies in colorectal cancer. 			RNA isolation and Real-time PCR analysis,Methylation analysis,Luciferase reporter analysis,immunohistochemistry				EREG
30250574	chr16	69704597	69706597	NQO1	STE unregulated phosphorylated p53, NF κB p65, Nrf2, HO 1, and NQO1 expression levels in the hOMF cells. The present study demonstrated that STE appears to promote oral disease. 	human		High+Lowthroughput	Smokeless tobacco extract inhibits proliferation and promotes apoptosis in oral mucous fibroblasts	否	无	Diabetes, inflammation, cancer	fibroblast	E_01_0697	RT‑qPCR,Western blot,Cell viability assay,Immunofluorescence assay,Flow cytometric analysis	STE unregulated phosphorylated p53, NF κB p65, Nrf2, HO 1, and NQO1 expression levels in the hOMF cells. The present study demonstrated that STE appears to promote oral disease. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	STE unregulated phosphorylated p53, NF κB p65, Nrf2, HO 1, and NQO1 expression levels in the hOMF cells. The present study demonstrated that STE appears to promote oral disease. 		STE unregulated phosphorylated p53, NF κB p65, Nrf2, HO 1, and NQO1 expression levels in the hOMF cells. The present study demonstrated that STE appears to promote oral disease. 	Immunohistochemical staining	STE unregulated phosphorylated p53, NF κB p65, Nrf2, HO 1, and NQO1 expression levels in the hOMF cells. The present study demonstrated that STE appears to promote oral disease. 			RT‑qPCR,Western blot,Cell viability assay,Immunofluorescence assay,Flow cytometric analysis				NQO1
30245624	chr1	231623939	231625939	DISC1	Overall, our experiments demonstrated implication of DISC1 × D2R protein-protein interactions into mechanisms of cognitive and synaptic plasticity, which help to further understand molecular-cellular mechanisms of APD of the next generation.	mouse		High+Lowthroughput	Uncoupling DISC1 × D2R Protein-Protein Interactions Facilitates Latent Inhibition in Disc1-L100P Animal Model of Schizophrenia and Enhances Synaptic Plasticity via D2 Receptors	否	无	Schizophrenia		E_02_0414		Overall, our experiments demonstrated implication of DISC1 × D2R protein-protein interactions into mechanisms of cognitive and synaptic plasticity, which help to further understand molecular-cellular mechanisms of APD of the next generation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Overall, our experiments demonstrated implication of DISC1 × D2R protein-protein interactions into mechanisms of cognitive and synaptic plasticity, which help to further understand molecular-cellular mechanisms of APD of the next generation.		Overall, our experiments demonstrated implication of DISC1 × D2R protein-protein interactions into mechanisms of cognitive and synaptic plasticity, which help to further understand molecular-cellular mechanisms of APD of the next generation.	Immunohistochemical staining	Overall, our experiments demonstrated implication of DISC1 × D2R protein-protein interactions into mechanisms of cognitive and synaptic plasticity, which help to further understand molecular-cellular mechanisms of APD of the next generation.							DISC1
30245028	chr3	128476533	128478533	GATA2	The rs2523393 A allele creates a GATA2 binding site in a progesterone-responsive distal enhancer that loops to the HLA-F promoter.	human		High+Lowthroughput	An Ancient Fecundability-Associated Polymorphism Creates a GATA2 Binding Site in a Distal Enhancer of HLA-F	是	rs2523393	nothing	endometrial stromal cell	E_01_0698	ChIP-Seq,Luciferase Assays, Hi-C	The rs2523393 A allele creates a GATA2 binding site in a progesterone-responsive distal enhancer that loops to the HLA-F promoter.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The rs2523393 A allele creates a GATA2 binding site in a progesterone-responsive distal enhancer that loops to the HLA-F promoter.	Immunohistochemical staining	The rs2523393 A allele creates a GATA2 binding site in a progesterone-responsive distal enhancer that loops to the HLA-F promoter.	GATA2		ChIP-Seq,Luciferase Assays, Hi-C	The rs2523393 A allele creates a GATA2 binding site in a progesterone-responsive distal enhancer that loops to the HLA-F promoter.			
30232013	chr1	107054092	107056092	PRMT6	Our work suggests that PRMT6 via H3R2me2a interferes with the deposition of adjacent histone marks and modulates the activity of important differentiation-associated genes by opposing transcriptional effects. 	mouse		High+Lowthroughput	Genomic Location of PRMT6-Dependent H3R2 Methylation Is Linked to the Transcriptional Outcome of Associated Genes	否	无	nothing	NT2/D1 cell,U2OS cell,HeLa cell,HEK293T cell	E_02_0415	Flow Cytometry，RNA Isolation, RT-qPCR,  RNA-Seq，ChIP-qPCR， ChIP-Seq	Our work suggests that PRMT6 via H3R2me2a interferes with the deposition of adjacent histone marks and modulates the activity of important differentiation-associated genes by opposing transcriptional effects. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our work suggests that PRMT6 via H3R2me2a interferes with the deposition of adjacent histone marks and modulates the activity of important differentiation-associated genes by opposing transcriptional effects. 		Our work suggests that PRMT6 via H3R2me2a interferes with the deposition of adjacent histone marks and modulates the activity of important differentiation-associated genes by opposing transcriptional effects. 	Immunohistochemical staining	Our work suggests that PRMT6 via H3R2me2a interferes with the deposition of adjacent histone marks and modulates the activity of important differentiation-associated genes by opposing transcriptional effects. 			Flow Cytometry，RNA Isolation, RT-qPCR,  RNA-Seq，ChIP-qPCR， ChIP-Seq				PRMT6
30228822	chr17	42697888	42699888	EZH1	In the present study, our group discovered that a histone methyltransferase enhancer of zeste1 (EZH1) was drastically downregulated in Thp1 cells stimulated by TCP, indicating that EZH1 may participate in the macrophage phenotype shifting. 	human		High+Lowthroughput	EZH1 Is Associated with TCP-Induced Bone Regeneration through Macrophage Polarization	否	无	nothing	THP-1 cell	E_01_0699	Hematoxylin-Eosin Staining,Alizarin Red Staining and Alkaline Phosphatase Staining,Western Blotting,Protein Extraction,Reverse Transcription and Quantitative PCR	In the present study, our group discovered that a histone methyltransferase enhancer of zeste1 (EZH1) was drastically downregulated in Thp1 cells stimulated by TCP, indicating that EZH1 may participate in the macrophage phenotype shifting. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, our group discovered that a histone methyltransferase enhancer of zeste1 (EZH1) was drastically downregulated in Thp1 cells stimulated by TCP, indicating that EZH1 may participate in the macrophage phenotype shifting. 		In the present study, our group discovered that a histone methyltransferase enhancer of zeste1 (EZH1) was drastically downregulated in Thp1 cells stimulated by TCP, indicating that EZH1 may participate in the macrophage phenotype shifting. 	Immunohistochemical staining	In the present study, our group discovered that a histone methyltransferase enhancer of zeste1 (EZH1) was drastically downregulated in Thp1 cells stimulated by TCP, indicating that EZH1 may participate in the macrophage phenotype shifting. 			Hematoxylin-Eosin Staining,Alizarin Red Staining and Alkaline Phosphatase Staining,Western Blotting,Protein Extraction,Reverse Transcription and Quantitative PCR				EZH1
30226578	chr9	134132591	134134591	WDR5	These results further understanding of a potential post-translational modification of WDR5, and imply that the methylation of lysines on HMT complex components is crucial for regulating human carcinogenesis. 	human		High+Lowthroughput	Lysines 207 and 325 methylation of WDR5 catalyzed by SETD6 promotes breast cancer cell proliferation and migration	否	无	mammary cancer	breast cancer cell	E_01_0700	In vitro methylation assay and mass spectrometry analysis,Immunoprecipitation,Western blotting,Colony formation assay,Wound healing and cell migration assay	These results further understanding of a potential post-translational modification of WDR5, and imply that the methylation of lysines on HMT complex components is crucial for regulating human carcinogenesis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results further understanding of a potential post-translational modification of WDR5, and imply that the methylation of lysines on HMT complex components is crucial for regulating human carcinogenesis. 		These results further understanding of a potential post-translational modification of WDR5, and imply that the methylation of lysines on HMT complex components is crucial for regulating human carcinogenesis. 	Immunohistochemical staining	These results further understanding of a potential post-translational modification of WDR5, and imply that the methylation of lysines on HMT complex components is crucial for regulating human carcinogenesis. 			In vitro methylation assay and mass spectrometry analysis,Immunoprecipitation,Western blotting,Colony formation assay,Wound healing and cell migration assay				WDR5
30219228	chr4	15601897	15603897	FBXL5	Our researches suggest that miR-1306e3p is a tumor enhancer in regulating of HCC metastasis, and miR-1306e3p may be clinically utilized as a factor for the clinical diagnosis and prognosis of HCC.	human	primary HCC tissues 	High+Lowthroughput	miR-1306-3p targets FBXL5 to promote metastasis of hepatocellular carcinoma through suppressing snail degradation	否	无	Hepatocellular carcinoma		E_01_0701	Lentivirus infection,Transient transfection,RNA isolation, reverse transcription,  QPCR,Transwell and boyden assays,Wound healing assay,Western blot, Luciferase reporter assay, Chromatin immunoprecipitation assay,In situ hybridization (ISH),Immunohistochemistry (IHC)	Our researches suggest that miR-1306e3p is a tumor enhancer in regulating of HCC metastasis, and miR-1306e3p may be clinically utilized as a factor for the clinical diagnosis and prognosis of HCC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our researches suggest that miR-1306e3p is a tumor enhancer in regulating of HCC metastasis, and miR-1306e3p may be clinically utilized as a factor for the clinical diagnosis and prognosis of HCC.		Our researches suggest that miR-1306e3p is a tumor enhancer in regulating of HCC metastasis, and miR-1306e3p may be clinically utilized as a factor for the clinical diagnosis and prognosis of HCC.	Immunohistochemical staining	Our researches suggest that miR-1306e3p is a tumor enhancer in regulating of HCC metastasis, and miR-1306e3p may be clinically utilized as a factor for the clinical diagnosis and prognosis of HCC.			Lentivirus infection,Transient transfection,RNA isolation, reverse transcription,  QPCR,Transwell and boyden assays,Wound healing assay,Western blot, Luciferase reporter assay, Chromatin immunoprecipitation assay,In situ hybridization (ISH),Immunohistochemistry (IHC)				FBXL5
29436621	chr18	55219776	55221776	TCF4	This implied that a high expression of TCF4 isoforms may lead to Wnt/β-catenin signal activation and potentially promote malignant glioma development. 	human		High+Lowthroughput	Expression and functional analysis of TCF4 isoforms in human glioma cells	否	无	Human gliomas	U251cell,A172cell,U-87MGcell	E_01_0702	RT‑PCR, cell transfection,MTT assay,Flow cytometry,Wound healing assay	This implied that a high expression of TCF4 isoforms may lead to Wnt/β-catenin signal activation and potentially promote malignant glioma development. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			This implied that a high expression of TCF4 isoforms may lead to Wnt/β-catenin signal activation and potentially promote malignant glioma development. 	Immunohistochemical staining	This implied that a high expression of TCF4 isoforms may lead to Wnt/β-catenin signal activation and potentially promote malignant glioma development. 	TCF4		RT‑PCR, cell transfection,MTT assay,Flow cytometry,Wound healing assay	This implied that a high expression of TCF4 isoforms may lead to Wnt/β-catenin signal activation and potentially promote malignant glioma development. 			
29435295	chr7	148804639	148806639	EZH2	None of these cases exhibited any correlation with age, sex, smoking, stage or treatment, whereas IHC staining was able to identify candidate responders to anti-PD-L1/PD-1 immunotherapy, Rova-T therapy, or EZH2 inhibitor therapy.	human		High+Lowthroughput	Identification of candidate responders for anti-PD-L1/PD-1 immunotherapy, Rova-T therapy, or EZH2 inhibitory therapy in small-cell lung cancer	否	无	small cell lung cancer	SCLC  cell	E_01_0703	Immunohistochemical (IHC) staining	None of these cases exhibited any correlation with age, sex, smoking, stage or treatment, whereas IHC staining was able to identify candidate responders to anti-PD-L1/PD-1 immunotherapy, Rova-T therapy, or EZH2 inhibitor therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			None of these cases exhibited any correlation with age, sex, smoking, stage or treatment, whereas IHC staining was able to identify candidate responders to anti-PD-L1/PD-1 immunotherapy, Rova-T therapy, or EZH2 inhibitor therapy.	Immunohistochemical staining	None of these cases exhibited any correlation with age, sex, smoking, stage or treatment, whereas IHC staining was able to identify candidate responders to anti-PD-L1/PD-1 immunotherapy, Rova-T therapy, or EZH2 inhibitor therapy.	EZH2		Immunohistochemical (IHC) staining	None of these cases exhibited any correlation with age, sex, smoking, stage or treatment, whereas IHC staining was able to identify candidate responders to anti-PD-L1/PD-1 immunotherapy, Rova-T therapy, or EZH2 inhibitor therapy.			
29435081	chr8	127397745	127399745	CCAT2	Thus, CCAT2 might play a critical role in EOC progression and serve as a valuable target for the treatment of ovarian cancer. 	human		High+Lowthroughput	Long non-coding RNA CCAT2 promotes epithelial-mesenchymal transition involving Wnt/β-catenin pathway in epithelial ovarian carcinoma cells	否	无	oophoroma	Epithelial ovarian cancer cell	E_01_0704	Total RNA extraction,RT‑qPCR,Small interfering RNAs (siRNAs) and transfection,Monolayer wound healing assay,Transwell invasion assay,Western blot,TOP‑FLASH luciferase assay	Thus, CCAT2 might play a critical role in EOC progression and serve as a valuable target for the treatment of ovarian cancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Thus, CCAT2 might play a critical role in EOC progression and serve as a valuable target for the treatment of ovarian cancer. 		Thus, CCAT2 might play a critical role in EOC progression and serve as a valuable target for the treatment of ovarian cancer. 	Immunohistochemical staining	Thus, CCAT2 might play a critical role in EOC progression and serve as a valuable target for the treatment of ovarian cancer. 			Total RNA extraction,RT‑qPCR,Small interfering RNAs (siRNAs) and transfection,Monolayer wound healing assay,Transwell invasion assay,Western blot,TOP‑FLASH luciferase assay				CCAT2
29435063	chr7	148803958	148805958	EZH2	The results of the study revealed that p16 was negatively regulated by EZH2 in ovarian cancer, and that p16 and EZH2 are important in the tumorigenesis of ovarian cancer. EZH2 and p16 represent potential biomarkers for the diagnosis of ovarian cancer and as targets for ovarian cancer gene therapy	human		High+Lowthroughput	Inhibition of enhancer of zeste homolog 2 increases the expression of p16 and suppresses the proliferation and migration of ovarian carcinoma cells in vitro and in vivo	否	无	oophoroma	A2780cell,SKOV3cell	E_01_0705	Lentivirus construction and transduction，RNA extraction，RT‑qPCR,Protein isolation,western blot analysis,Cell proliferation assay,Cell migration assay	The results of the study revealed that p16 was negatively regulated by EZH2 in ovarian cancer, and that p16 and EZH2 are important in the tumorigenesis of ovarian cancer. EZH2 and p16 represent potential biomarkers for the diagnosis of ovarian cancer and as targets for ovarian cancer gene therapy	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The results of the study revealed that p16 was negatively regulated by EZH2 in ovarian cancer, and that p16 and EZH2 are important in the tumorigenesis of ovarian cancer. EZH2 and p16 represent potential biomarkers for the diagnosis of ovarian cancer and as targets for ovarian cancer gene therapy	Immunohistochemical staining	The results of the study revealed that p16 was negatively regulated by EZH2 in ovarian cancer, and that p16 and EZH2 are important in the tumorigenesis of ovarian cancer. EZH2 and p16 represent potential biomarkers for the diagnosis of ovarian cancer and as targets for ovarian cancer gene therapy	EZH2		Lentivirus construction and transduction，RNA extraction，RT‑qPCR,Protein isolation,western blot analysis,Cell proliferation assay,Cell migration assay	The results of the study revealed that p16 was negatively regulated by EZH2 in ovarian cancer, and that p16 and EZH2 are important in the tumorigenesis of ovarian cancer. EZH2 and p16 represent potential biomarkers for the diagnosis of ovarian cancer and as targets for ovarian cancer gene therapy			
29435024	chr7	148804550	148806550	EZH2	The data presented in the present study is the first to indicate that EZH2 is upregulated in CRC and may serve as a predictor of poor outcome for patients with CRC. 	human		High+Lowthroughput	Expression of EZH2 is associated with poor outcome in colorectal cancer	否	无	colorectal cancer 	HCEC cell	E_01_0706	RNA interference,Cell proliferation assay,RT‑qPCR,Western blot,Immunohistochemical analysis	The data presented in the present study is the first to indicate that EZH2 is upregulated in CRC and may serve as a predictor of poor outcome for patients with CRC. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The data presented in the present study is the first to indicate that EZH2 is upregulated in CRC and may serve as a predictor of poor outcome for patients with CRC. 	Immunohistochemical staining	The data presented in the present study is the first to indicate that EZH2 is upregulated in CRC and may serve as a predictor of poor outcome for patients with CRC. 	EZH2		RNA interference,Cell proliferation assay,RT‑qPCR,Western blot,Immunohistochemical analysis	The data presented in the present study is the first to indicate that EZH2 is upregulated in CRC and may serve as a predictor of poor outcome for patients with CRC. 			
29432919	chr11	102107729	102109729	YAP1	Our results revealed the essential role of YAP1 and the YAP1-TEADs complex in regulating osteoclastogenesis and related gene expression. 	human		High+Lowthroughput	YAP1 is essential for osteoclastogenesis through a TEADs-dependent mechanism	否	无	nothing	Bone marrow-derived macrophages	E_01_0707	Quantitative real-time PCR,Co-immunoprecipitation, Western blotting, Electrophoretic mobility shift assay	Our results revealed the essential role of YAP1 and the YAP1-TEADs complex in regulating osteoclastogenesis and related gene expression. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our results revealed the essential role of YAP1 and the YAP1-TEADs complex in regulating osteoclastogenesis and related gene expression. 	Immunohistochemical staining	Our results revealed the essential role of YAP1 and the YAP1-TEADs complex in regulating osteoclastogenesis and related gene expression. 	YAP1		Quantitative real-time PCR,Co-immunoprecipitation, Western blotting, Electrophoretic mobility shift assay	Our results revealed the essential role of YAP1 and the YAP1-TEADs complex in regulating osteoclastogenesis and related gene expression. 			
29425687	chr17	42310341	42312341	STAT3	These dual functions of ASCJ9 to suppress PCa proliferation and invasion (via altering STAT3 sumoylation) may help us to develop a better anti-AR compound that may overcome the current antiandrogens unwanted side of increasing the metastasis to better suppress the castration-resistant PCa progression. 	human		High+Lowthroughput	ASC-J9(?) suppresses prostate cancer cell invasion via altering the sumoylation-phosphorylation of STAT3	否	无	prostatic cancer	prostate cancer cell	E_01_0708	Cell Invasion Assay,3D invasion assay,Quantitative PCR,Western Blot,Transient transfection,Lentiviral expression system,Immunoprecipitation assay,ChIP assay	These dual functions of ASCJ9 to suppress PCa proliferation and invasion (via altering STAT3 sumoylation) may help us to develop a better anti-AR compound that may overcome the current antiandrogens unwanted side of increasing the metastasis to better suppress the castration-resistant PCa progression. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These dual functions of ASCJ9 to suppress PCa proliferation and invasion (via altering STAT3 sumoylation) may help us to develop a better anti-AR compound that may overcome the current antiandrogens unwanted side of increasing the metastasis to better suppress the castration-resistant PCa progression. 	Immunohistochemical staining	These dual functions of ASCJ9 to suppress PCa proliferation and invasion (via altering STAT3 sumoylation) may help us to develop a better anti-AR compound that may overcome the current antiandrogens unwanted side of increasing the metastasis to better suppress the castration-resistant PCa progression. 	STAT3		Cell Invasion Assay,3D invasion assay,Quantitative PCR,Western Blot,Transient transfection,Lentiviral expression system,Immunoprecipitation assay,ChIP assay	These dual functions of ASCJ9 to suppress PCa proliferation and invasion (via altering STAT3 sumoylation) may help us to develop a better anti-AR compound that may overcome the current antiandrogens unwanted side of increasing the metastasis to better suppress the castration-resistant PCa progression. 			
29425513	chr8	38139436	38141436	STAR	"Organoid technology, in combi_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_nation with the user-friendly nature of STAR, will facilitate basic research into human adult stem cell
biology."	human		High+Lowthroughput	Specific Labeling of Stem Cell Activity in Human Colorectal Organoids Using an ASCL2-Responsive Minigene	是	无	colorectal cancer 	Human Colorectal Organoids Stem Cell 	E_01_0709	Cell Transfection,Dual-Luciferase Assay,RNA Sequencing,Orthotopic Xenotransplantation of Organoids, FACS analysis	"Organoid technology, in combi_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_nation with the user-friendly nature of STAR, will facilitate basic research into human adult stem cell
biology."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Organoid technology, in combi_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_nation with the user-friendly nature of STAR, will facilitate basic research into human adult stem cell
biology."	Immunohistochemical staining	"Organoid technology, in combi_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_nation with the user-friendly nature of STAR, will facilitate basic research into human adult stem cell
biology."	STAR		Cell Transfection,Dual-Luciferase Assay,RNA Sequencing,Orthotopic Xenotransplantation of Organoids, FACS analysis	"Organoid technology, in combi_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_nation with the user-friendly nature of STAR, will facilitate basic research into human adult stem cell
biology."			
29421235	chr11	112670302	112672302	Sox9	We identified Tead, Sox9, Smad, Tcf, Meis, Rbpj, and Runx1 as the main cardiac fibroblasts TF families. Our analysis shows that in both cell types, distal enhancers, containing concentrated combinatorial clusters of multiple tissue expressed TFs recognition motifs, are combinatorically clustered around tissue specific genes. This model for tissue specific gene expression in the heart supports the general billboard model for enhancer organization. 	mouses		High+Lowthroughput	Analysis of rat cardiac myocytes and fibroblasts identifies combinatorial enhancer organization and transcription factor families	否	无	nothing	rat cardiac myocytes ，rat cardiac  fibroblasts 	E_02_0416	Immunofluorescent analysis,ATAC-seq,RNA-seq, ChIP-seq	We identified Tead, Sox9, Smad, Tcf, Meis, Rbpj, and Runx1 as the main cardiac fibroblasts TF families. Our analysis shows that in both cell types, distal enhancers, containing concentrated combinatorial clusters of multiple tissue expressed TFs recognition motifs, are combinatorically clustered around tissue specific genes. This model for tissue specific gene expression in the heart supports the general billboard model for enhancer organization. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identified Tead, Sox9, Smad, Tcf, Meis, Rbpj, and Runx1 as the main cardiac fibroblasts TF families. Our analysis shows that in both cell types, distal enhancers, containing concentrated combinatorial clusters of multiple tissue expressed TFs recognition motifs, are combinatorically clustered around tissue specific genes. This model for tissue specific gene expression in the heart supports the general billboard model for enhancer organization. 		We identified Tead, Sox9, Smad, Tcf, Meis, Rbpj, and Runx1 as the main cardiac fibroblasts TF families. Our analysis shows that in both cell types, distal enhancers, containing concentrated combinatorial clusters of multiple tissue expressed TFs recognition motifs, are combinatorically clustered around tissue specific genes. This model for tissue specific gene expression in the heart supports the general billboard model for enhancer organization. 	Immunohistochemical staining	We identified Tead, Sox9, Smad, Tcf, Meis, Rbpj, and Runx1 as the main cardiac fibroblasts TF families. Our analysis shows that in both cell types, distal enhancers, containing concentrated combinatorial clusters of multiple tissue expressed TFs recognition motifs, are combinatorically clustered around tissue specific genes. This model for tissue specific gene expression in the heart supports the general billboard model for enhancer organization. 			Immunofluorescent analysis,ATAC-seq,RNA-seq, ChIP-seq				Sox9
29421235	chr16	92395634	92397634	Runx1	We identified Tead, Sox9, Smad, Tcf, Meis, Rbpj, and Runx1 as the main cardiac fibroblasts TF families. Our analysis shows that in both cell types, distal enhancers, containing concentrated combinatorial clusters of multiple tissue expressed TFs recognition motifs, are combinatorically clustered around tissue specific genes. This model for tissue specific gene expression in the heart supports the general billboard model for enhancer organization. 	mouses		High+Lowthroughput	Analysis of rat cardiac myocytes and fibroblasts identifies combinatorial enhancer organization and transcription factor families	否	无	nothing	rat cardiac myocytes ，rat cardiac  fibroblasts 	E_02_0416	Immunofluorescent analysis,ATAC-seq,RNA-seq, ChIP-seq	We identified Tead, Sox9, Smad, Tcf, Meis, Rbpj, and Runx1 as the main cardiac fibroblasts TF families. Our analysis shows that in both cell types, distal enhancers, containing concentrated combinatorial clusters of multiple tissue expressed TFs recognition motifs, are combinatorically clustered around tissue specific genes. This model for tissue specific gene expression in the heart supports the general billboard model for enhancer organization. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identified Tead, Sox9, Smad, Tcf, Meis, Rbpj, and Runx1 as the main cardiac fibroblasts TF families. Our analysis shows that in both cell types, distal enhancers, containing concentrated combinatorial clusters of multiple tissue expressed TFs recognition motifs, are combinatorically clustered around tissue specific genes. This model for tissue specific gene expression in the heart supports the general billboard model for enhancer organization. 		We identified Tead, Sox9, Smad, Tcf, Meis, Rbpj, and Runx1 as the main cardiac fibroblasts TF families. Our analysis shows that in both cell types, distal enhancers, containing concentrated combinatorial clusters of multiple tissue expressed TFs recognition motifs, are combinatorically clustered around tissue specific genes. This model for tissue specific gene expression in the heart supports the general billboard model for enhancer organization. 	Immunohistochemical staining	We identified Tead, Sox9, Smad, Tcf, Meis, Rbpj, and Runx1 as the main cardiac fibroblasts TF families. Our analysis shows that in both cell types, distal enhancers, containing concentrated combinatorial clusters of multiple tissue expressed TFs recognition motifs, are combinatorically clustered around tissue specific genes. This model for tissue specific gene expression in the heart supports the general billboard model for enhancer organization. 			Immunofluorescent analysis,ATAC-seq,RNA-seq, ChIP-seq				Runx1
29420098	chr19	49673051	49675051	PRMT1	In this study, we demonstrate for the first time that the ability of TGFβ to inhibit TLR-NFκB signaling is mediated by protein arginine methyltransferase 1 (PRMT1) induced Smad6 methylation. 	human		High+Lowthroughput	Smad6 Methylation Represses NFκB Activation and Periodontal Inflammation	否	无	Periodontal inflammation	HaCaT cell	E_01_0710	immunoblotting	In this study, we demonstrate for the first time that the ability of TGFβ to inhibit TLR-NFκB signaling is mediated by protein arginine methyltransferase 1 (PRMT1) induced Smad6 methylation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we demonstrate for the first time that the ability of TGFβ to inhibit TLR-NFκB signaling is mediated by protein arginine methyltransferase 1 (PRMT1) induced Smad6 methylation. 		In this study, we demonstrate for the first time that the ability of TGFβ to inhibit TLR-NFκB signaling is mediated by protein arginine methyltransferase 1 (PRMT1) induced Smad6 methylation. 	Immunohistochemical staining	In this study, we demonstrate for the first time that the ability of TGFβ to inhibit TLR-NFκB signaling is mediated by protein arginine methyltransferase 1 (PRMT1) induced Smad6 methylation. 			immunoblotting				PRMT1
29418037	chr6	31572730	31574730	TNF	Expression of IL-1 and TNF , pro-inflammatory cytokines important for wound healing, was significantly decreased in the transgenic mice, prior to delayed healing.	mouse		High+Lowthroughput	Constitutive overexpression of periostin delays wound healing in mouse skin	否	无	nothing	mutant lymphoma cell	E_02_0417	Immunohistochemistry,Quantitative RT-PCR	Expression of IL-1 and TNF , pro-inflammatory cytokines important for wound healing, was significantly decreased in the transgenic mice, prior to delayed healing.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Expression of IL-1 and TNF , pro-inflammatory cytokines important for wound healing, was significantly decreased in the transgenic mice, prior to delayed healing.		Expression of IL-1 and TNF , pro-inflammatory cytokines important for wound healing, was significantly decreased in the transgenic mice, prior to delayed healing.	Immunohistochemical staining	Expression of IL-1 and TNF , pro-inflammatory cytokines important for wound healing, was significantly decreased in the transgenic mice, prior to delayed healing.			Immunohistochemistry,Quantitative RT-PCR				TNF
29416002	chr7	148804302	148806302	EZH2	Overall, these findings revealed that EZH2 affects ACD of VSMCs and the pathologic process of AD via regulating ATG5 and ATG7 expression and MEK ERK1/2 signaling. Our hitherto unrecognized findings indicate that EZH2 activation has therapeutic or preventive potential for AD. 	human		High+Lowthroughput	EZH2 inhibits autophagic cell death of aortic vascular smooth muscle cells to affect aortic dissection	否	无	dissection of aorta 	blood vessel smooth muscle cell	E_01_0711	Western blot，Real-time PCR，Immunofluorescence analysis，Flow cytometry	Overall, these findings revealed that EZH2 affects ACD of VSMCs and the pathologic process of AD via regulating ATG5 and ATG7 expression and MEK ERK1/2 signaling. Our hitherto unrecognized findings indicate that EZH2 activation has therapeutic or preventive potential for AD. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Overall, these findings revealed that EZH2 affects ACD of VSMCs and the pathologic process of AD via regulating ATG5 and ATG7 expression and MEK ERK1/2 signaling. Our hitherto unrecognized findings indicate that EZH2 activation has therapeutic or preventive potential for AD. 	Immunohistochemical staining	Overall, these findings revealed that EZH2 affects ACD of VSMCs and the pathologic process of AD via regulating ATG5 and ATG7 expression and MEK ERK1/2 signaling. Our hitherto unrecognized findings indicate that EZH2 activation has therapeutic or preventive potential for AD. 	EZH2		Western blot，Real-time PCR，Immunofluorescence analysis，Flow cytometry	Overall, these findings revealed that EZH2 affects ACD of VSMCs and the pathologic process of AD via regulating ATG5 and ATG7 expression and MEK ERK1/2 signaling. Our hitherto unrecognized findings indicate that EZH2 activation has therapeutic or preventive potential for AD. 			
29415998	chr7	117284540	117286540	CFTR	In conclusion, our study showed that Hcy activates autophagy by inhibition of CFTR expression via interaction between H3K27me3 and DNA methylation in the mouse liver. These findings provide new insight into the mechanism of Hcyinduced autophagy in liver injury 	human	Liver tissue	High+Lowthroughput	Homocysteine activates autophagy by inhibition of CFTR expression via interaction between DNA methylation and H3K27me3 in mouse liver	否	无	Liver injury	HL-7702 cell	E_01_0712	Quantitative real-time PCR,Western blot,Chromatin immunoprecipitation (ChIP) assays,Bisulfite sequencing,RNA interference	In conclusion, our study showed that Hcy activates autophagy by inhibition of CFTR expression via interaction between H3K27me3 and DNA methylation in the mouse liver. These findings provide new insight into the mechanism of Hcyinduced autophagy in liver injury 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In conclusion, our study showed that Hcy activates autophagy by inhibition of CFTR expression via interaction between H3K27me3 and DNA methylation in the mouse liver. These findings provide new insight into the mechanism of Hcyinduced autophagy in liver injury 	Immunohistochemical staining	In conclusion, our study showed that Hcy activates autophagy by inhibition of CFTR expression via interaction between H3K27me3 and DNA methylation in the mouse liver. These findings provide new insight into the mechanism of Hcyinduced autophagy in liver injury 	CFTR		Quantitative real-time PCR,Western blot,Chromatin immunoprecipitation (ChIP) assays,Bisulfite sequencing,RNA interference	In conclusion, our study showed that Hcy activates autophagy by inhibition of CFTR expression via interaction between H3K27me3 and DNA methylation in the mouse liver. These findings provide new insight into the mechanism of Hcyinduced autophagy in liver injury 			
29413899	chr1	212562611	212564611	ATF3	Collectively, the results document that ATF3 expression in normal and transformed human liver originates from the canonical promoter A that responds to multiple stress signals. 	human		High+Lowthroughput	Regulation of the ATF3 gene by a single promoter in response to amino acid availability and endoplasmic reticulum stress in human primary hepatocytes and hepatoma cells	否	无	inflammation	HCC cell	E_01_0713	Protein isolation and immunoblotting,RNA isolation,RT-qPCR, Chromatin immunoprecipitation (ChIP)	Collectively, the results document that ATF3 expression in normal and transformed human liver originates from the canonical promoter A that responds to multiple stress signals. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Collectively, the results document that ATF3 expression in normal and transformed human liver originates from the canonical promoter A that responds to multiple stress signals. 		Collectively, the results document that ATF3 expression in normal and transformed human liver originates from the canonical promoter A that responds to multiple stress signals. 	Immunohistochemical staining	Collectively, the results document that ATF3 expression in normal and transformed human liver originates from the canonical promoter A that responds to multiple stress signals. 			Protein isolation and immunoblotting,RNA isolation,RT-qPCR, Chromatin immunoprecipitation (ChIP)				ATF3
29413056	chr7	55016381	55018381	EGFR	This study demonstrated that ILF3 plays an oncogenic like role in maintaining the EGFR-mediated cellular pathway, and can be a therapeutic target to improve the therapeutic efficacy of afatinib. Our results suggested that YM155, an ILF3 inhibitor, has the potential for utilization in cancer therapy against EGFR-positive lung cancers 	human		High+Lowthroughput	EGFR-mediated interleukin enhancer-binding factor 3 contributes to formation and survival of cancer stem-like tumorspheres as a therapeutic target against EGFR-positive non-small cell lung cancer	否	无	Non small cell lung cancer	HCC827 cell ，A549  cell	E_01_0714	mRNA extraction,Quantitative PCR,Gene knockdown, Western blotting,Cell viability, RNAseq	This study demonstrated that ILF3 plays an oncogenic like role in maintaining the EGFR-mediated cellular pathway, and can be a therapeutic target to improve the therapeutic efficacy of afatinib. Our results suggested that YM155, an ILF3 inhibitor, has the potential for utilization in cancer therapy against EGFR-positive lung cancers 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			This study demonstrated that ILF3 plays an oncogenic like role in maintaining the EGFR-mediated cellular pathway, and can be a therapeutic target to improve the therapeutic efficacy of afatinib. Our results suggested that YM155, an ILF3 inhibitor, has the potential for utilization in cancer therapy against EGFR-positive lung cancers 	Immunohistochemical staining	This study demonstrated that ILF3 plays an oncogenic like role in maintaining the EGFR-mediated cellular pathway, and can be a therapeutic target to improve the therapeutic efficacy of afatinib. Our results suggested that YM155, an ILF3 inhibitor, has the potential for utilization in cancer therapy against EGFR-positive lung cancers 	EGFR		mRNA extraction,Quantitative PCR,Gene knockdown, Western blotting,Cell viability, RNAseq	This study demonstrated that ILF3 plays an oncogenic like role in maintaining the EGFR-mediated cellular pathway, and can be a therapeutic target to improve the therapeutic efficacy of afatinib. Our results suggested that YM155, an ILF3 inhibitor, has the potential for utilization in cancer therapy against EGFR-positive lung cancers 			
29377931	chr17	85989752	85991752	Six2	Nephron progenitor number determines nephron endowment; a reduced nephron count is linked to the onset of kidney disease. Several transcriptional regulators including Six2, Wt1, Osr1, Sall1, Eya1, Pax2, and Hox11 paralogues are required for specification and/or maintenance of nephron progenitors. 	mouse		High+Lowthroughput	Transcriptional regulatory control of mammalian nephron progenitors revealed by multi-factor cistromic analysis and genetic studies	否	无	kidney disease 	mammalian nephron progenitors	E_02_0418	ChIP-seq,4C-seq,Genomic Regions Enrichment of Annotations Tool (GREAT) analysis,Fluorescence-activated cell sorting,RNA-seq,qPCR,Electrophoretic mobility shift assay (EMSA),Immunoprecipitations,Immunoprecipitations	Nephron progenitor number determines nephron endowment; a reduced nephron count is linked to the onset of kidney disease. Several transcriptional regulators including Six2, Wt1, Osr1, Sall1, Eya1, Pax2, and Hox11 paralogues are required for specification and/or maintenance of nephron progenitors. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Nephron progenitor number determines nephron endowment; a reduced nephron count is linked to the onset of kidney disease. Several transcriptional regulators including Six2, Wt1, Osr1, Sall1, Eya1, Pax2, and Hox11 paralogues are required for specification and/or maintenance of nephron progenitors. 		Nephron progenitor number determines nephron endowment; a reduced nephron count is linked to the onset of kidney disease. Several transcriptional regulators including Six2, Wt1, Osr1, Sall1, Eya1, Pax2, and Hox11 paralogues are required for specification and/or maintenance of nephron progenitors. 	Immunohistochemical staining	Nephron progenitor number determines nephron endowment; a reduced nephron count is linked to the onset of kidney disease. Several transcriptional regulators including Six2, Wt1, Osr1, Sall1, Eya1, Pax2, and Hox11 paralogues are required for specification and/or maintenance of nephron progenitors. 			ChIP-seq,4C-seq,Genomic Regions Enrichment of Annotations Tool (GREAT) analysis,Fluorescence-activated cell sorting,RNA-seq,qPCR,Electrophoretic mobility shift assay (EMSA),Immunoprecipitations,Immunoprecipitations				Six2
29374067	chr13	26129178	26131178	RNF6	TLE3 expression abolished the oncogenic effects of RNF6,and RNF6 plays a pivotal oncogenic role in colorectal tumorigenesis. 	human		High+Lowthroughput	RNF6 Promotes Colorectal Cancer by Activating the Wnt/β-Catenin Pathway via Ubiquitination of TLE3	否	无	colorectal cancer 		E_01_0715	DNA extraction,DNA copy number Real-time PCR,Co-immunoprecipitation,mass spectrometry,Ubiquitination Assay,Luciferase reporter activity analysis	TLE3 expression abolished the oncogenic effects of RNF6,and RNF6 plays a pivotal oncogenic role in colorectal tumorigenesis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	TLE3 expression abolished the oncogenic effects of RNF6,and RNF6 plays a pivotal oncogenic role in colorectal tumorigenesis. 		TLE3 expression abolished the oncogenic effects of RNF6,and RNF6 plays a pivotal oncogenic role in colorectal tumorigenesis. 	Immunohistochemical staining	TLE3 expression abolished the oncogenic effects of RNF6,and RNF6 plays a pivotal oncogenic role in colorectal tumorigenesis. 			DNA extraction,DNA copy number Real-time PCR,Co-immunoprecipitation,mass spectrometry,Ubiquitination Assay,Luciferase reporter activity analysis				RNF6
29374067	chr15	70045127	70047127	TLE3	TLE3 expression abolished the oncogenic effects of RNF6,and RNF6 plays a pivotal oncogenic role in colorectal tumorigenesis. 	human		High+Lowthroughput	RNF6 Promotes Colorectal Cancer by Activating the Wnt/β-Catenin Pathway via Ubiquitination of TLE3	否	无	colorectal cancer 		E_01_0715	DNA extraction,DNA copy number Real-time PCR,Co-immunoprecipitation,mass spectrometry,Ubiquitination Assay,Luciferase reporter activity analysis	TLE3 expression abolished the oncogenic effects of RNF6,and RNF6 plays a pivotal oncogenic role in colorectal tumorigenesis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			TLE3 expression abolished the oncogenic effects of RNF6,and RNF6 plays a pivotal oncogenic role in colorectal tumorigenesis. 	Immunohistochemical staining	TLE3 expression abolished the oncogenic effects of RNF6,and RNF6 plays a pivotal oncogenic role in colorectal tumorigenesis. 	TLE3		DNA extraction,DNA copy number Real-time PCR,Co-immunoprecipitation,mass spectrometry,Ubiquitination Assay,Luciferase reporter activity analysis	TLE3 expression abolished the oncogenic effects of RNF6,and RNF6 plays a pivotal oncogenic role in colorectal tumorigenesis. 			
29373533	chr13	40552808	40554808	FOXO1	These results indicate that a plant flavonoid orientin suppressed the expression of the Pparγ gene through repression of C/ebpδ expression and inhibition of the phosphoinositide 3-kinase /Akt-FOXO1 signaling in adipocytes. 	human		High+Lowthroughput	Suppression of Fatty Acid and Triglyceride Synthesis by the Flavonoid Orientin through Decrease of C/EBPδ Expression and Inhibition of PI3K/Akt-FOXO1 Signaling in Adipocytes	否	无	Obesity	3T3-L1 cell	E_01_0716	Cytotoxicity Assay,Quantitative PCR,Western Blot,Cell Proliferation Assay,Chromatin Immunoprecipitation Assay	These results indicate that a plant flavonoid orientin suppressed the expression of the Pparγ gene through repression of C/ebpδ expression and inhibition of the phosphoinositide 3-kinase /Akt-FOXO1 signaling in adipocytes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			These results indicate that a plant flavonoid orientin suppressed the expression of the Pparγ gene through repression of C/ebpδ expression and inhibition of the phosphoinositide 3-kinase /Akt-FOXO1 signaling in adipocytes. 	Immunohistochemical staining	These results indicate that a plant flavonoid orientin suppressed the expression of the Pparγ gene through repression of C/ebpδ expression and inhibition of the phosphoinositide 3-kinase /Akt-FOXO1 signaling in adipocytes. 	FOXO1		Cytotoxicity Assay,Quantitative PCR,Western Blot,Cell Proliferation Assay,Chromatin Immunoprecipitation Assay	These results indicate that a plant flavonoid orientin suppressed the expression of the Pparγ gene through repression of C/ebpδ expression and inhibition of the phosphoinositide 3-kinase /Akt-FOXO1 signaling in adipocytes. 			
29369995	chr9	92410003	92412003	OMD	Proteome analysis validated by immunohistochemistry may pro_x005f_x0002_vide insight into the mechanism of cranial suture patency and disease from an osteoclast perspective. The authors results suggest a role of inflammatory mediators in nonsyndromic craniosynostosis. Col6A1 may aid in the regulation of suture patency, and OMD may be involved in premature fusion. Additional validation studies are required.	human		High+Lowthroughput	Whole-Proteome Analysis of Human Craniosynostotic Tissue Suggests a Link between Inflammatory Signaling and Osteoclast Activation in Human Cranial Suture Patency	否	无	Craniosynostosis		E_01_0717	Liquid Chromatography–Tandem Mass Spectrometry Analysis,	Proteome analysis validated by immunohistochemistry may pro_x005f_x0002_vide insight into the mechanism of cranial suture patency and disease from an osteoclast perspective. The authors results suggest a role of inflammatory mediators in nonsyndromic craniosynostosis. Col6A1 may aid in the regulation of suture patency, and OMD may be involved in premature fusion. Additional validation studies are required.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Proteome analysis validated by immunohistochemistry may pro_x005f_x0002_vide insight into the mechanism of cranial suture patency and disease from an osteoclast perspective. The authors results suggest a role of inflammatory mediators in nonsyndromic craniosynostosis. Col6A1 may aid in the regulation of suture patency, and OMD may be involved in premature fusion. Additional validation studies are required.		Proteome analysis validated by immunohistochemistry may pro_x005f_x0002_vide insight into the mechanism of cranial suture patency and disease from an osteoclast perspective. The authors results suggest a role of inflammatory mediators in nonsyndromic craniosynostosis. Col6A1 may aid in the regulation of suture patency, and OMD may be involved in premature fusion. Additional validation studies are required.	Immunohistochemical staining	Proteome analysis validated by immunohistochemistry may pro_x005f_x0002_vide insight into the mechanism of cranial suture patency and disease from an osteoclast perspective. The authors results suggest a role of inflammatory mediators in nonsyndromic craniosynostosis. Col6A1 may aid in the regulation of suture patency, and OMD may be involved in premature fusion. Additional validation studies are required.			Liquid Chromatography–Tandem Mass Spectrometry Analysis,				OMD
29369390	chr13	27957641	27959641	CDX2	This study reaffirms the importance of the Wnt signaling pathway in the tumorigenesis of pilomatrical tumors, and introduces CDX2 as a possible regulator and marker of pilomatrical tumorigenesis. LEF-1 and CDX2 performed at least as well as β-catenin, if not better when taking into account expression pattern, as a diagnostic marker for pilomatrical carcinoma, and should be considered in the workup of ambiguous primitive-appearing cutaneous tumors.	human		High+Lowthroughput	CDX2 and LEF-1 expression in pilomatrical tumors and their utility in the diagnosis of pilomatrical carcinoma	否	无	Hairy tumors	squamous cell	E_01_0718	Immunohistochemical analysis	This study reaffirms the importance of the Wnt signaling pathway in the tumorigenesis of pilomatrical tumors, and introduces CDX2 as a possible regulator and marker of pilomatrical tumorigenesis. LEF-1 and CDX2 performed at least as well as β-catenin, if not better when taking into account expression pattern, as a diagnostic marker for pilomatrical carcinoma, and should be considered in the workup of ambiguous primitive-appearing cutaneous tumors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			This study reaffirms the importance of the Wnt signaling pathway in the tumorigenesis of pilomatrical tumors, and introduces CDX2 as a possible regulator and marker of pilomatrical tumorigenesis. LEF-1 and CDX2 performed at least as well as β-catenin, if not better when taking into account expression pattern, as a diagnostic marker for pilomatrical carcinoma, and should be considered in the workup of ambiguous primitive-appearing cutaneous tumors.	Immunohistochemical staining	This study reaffirms the importance of the Wnt signaling pathway in the tumorigenesis of pilomatrical tumors, and introduces CDX2 as a possible regulator and marker of pilomatrical tumorigenesis. LEF-1 and CDX2 performed at least as well as β-catenin, if not better when taking into account expression pattern, as a diagnostic marker for pilomatrical carcinoma, and should be considered in the workup of ambiguous primitive-appearing cutaneous tumors.	CDX2		Immunohistochemical analysis	This study reaffirms the importance of the Wnt signaling pathway in the tumorigenesis of pilomatrical tumors, and introduces CDX2 as a possible regulator and marker of pilomatrical tumorigenesis. LEF-1 and CDX2 performed at least as well as β-catenin, if not better when taking into account expression pattern, as a diagnostic marker for pilomatrical carcinoma, and should be considered in the workup of ambiguous primitive-appearing cutaneous tumors.			
30218753	chr7	148804161	148806161	EZH2	EZH2 overexpression was significantly associated with higher tumor cell proliferation (r=0.582, P=0.000), advanced stage (P=0.012), and predicted poorer overall survival (OS) (P=0.016) in ENKTL. 	human		High+Lowthroughput	Aberrant differential expression of EZH2 and H3K27me3 in extranodal NK/T-cell lymphoma, nasal type, is associated with disease progression and prognosis.	否		cancer	tumor cell	E_01_0719	Immunohistochemistry (IHC), chip PCR, Weston blot, flow cytometry	EZH2 overexpression was significantly associated with higher tumor cell proliferation (r=0.582, P=0.000), advanced stage (P=0.012), and predicted poorer overall survival (OS) (P=0.016) in ENKTL. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2 overexpression was significantly associated with higher tumor cell proliferation (r=0.582, P=0.000), advanced stage (P=0.012), and predicted poorer overall survival (OS) (P=0.016) in ENKTL. 	Immunohistochemical staining	EZH2 overexpression was significantly associated with higher tumor cell proliferation (r=0.582, P=0.000), advanced stage (P=0.012), and predicted poorer overall survival (OS) (P=0.016) in ENKTL. 	EZH2		免疫组化(IHC),ChIP-PCR ,weston blot,流式细胞术	EZH2 overexpression was significantly associated with higher tumor cell proliferation (r=0.582, P=0.000), advanced stage (P=0.012), and predicted poorer overall survival (OS) (P=0.016) in ENKTL. 			
30218754	chr7	148804774	148806774	EZH2	EZH2 overexpression was significantly associated with higher tumor cell proliferation (r=0.582, P=0.000), advanced stage (P=0.012), and predicted poorer overall survival (OS) (P=0.016) in ENKTL. 	human		High+Lowthroughput	Aberrant differential expression of EZH2 and H3K27me3 in extranodal NK/T-cell lymphoma, nasal type, is associated with disease progression and prognosis.	否		cancer	T cell	E_01_0720	Immunohistochemistry (IHC), chip PCR, Weston blot, flow cytometry	EZH2 overexpression was significantly associated with higher tumor cell proliferation (r=0.582, P=0.000), advanced stage (P=0.012), and predicted poorer overall survival (OS) (P=0.016) in ENKTL. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2 overexpression was significantly associated with higher tumor cell proliferation (r=0.582, P=0.000), advanced stage (P=0.012), and predicted poorer overall survival (OS) (P=0.016) in ENKTL. 	Immunohistochemical staining	EZH2 overexpression was significantly associated with higher tumor cell proliferation (r=0.582, P=0.000), advanced stage (P=0.012), and predicted poorer overall survival (OS) (P=0.016) in ENKTL. 	EZH2		免疫组化(IHC),ChIP-PCR ,weston blot,流式细胞术	EZH2 overexpression was significantly associated with higher tumor cell proliferation (r=0.582, P=0.000), advanced stage (P=0.012), and predicted poorer overall survival (OS) (P=0.016) in ENKTL. 			
30218403	chr1	247413468	247415468	NLRP3	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.                                                                                                                                                                            The enhancement of phospho-signal transducer and activator of transcription 3 (p-STAT3), degradation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) as well as the overexpression of fibroblast growth factor 2 (FGF2) resulting from LPS/ATP treatment, and subsequent IL-1β maturation could also be compensated by BHB. 	human,large,mouse		High+Lowthroughput	The Beta-Hydroxybutyrate Suppresses the Migration of Glioma Cells by Inhibition of NLRP3 Inflammasome.	否		Gliomas	C6 cell	E_02_0419	weston blot,GPCR,qPCR	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.                                                                                                                                                                            The enhancement of phospho-signal transducer and activator of transcription 3 (p-STAT3), degradation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) as well as the overexpression of fibroblast growth factor 2 (FGF2) resulting from LPS/ATP treatment, and subsequent IL-1β maturation could also be compensated by BHB. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.                                                                                                                                                                            The enhancement of phospho-signal transducer and activator of transcription 3 (p-STAT3), degradation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) as well as the overexpression of fibroblast growth factor 2 (FGF2) resulting from LPS/ATP treatment, and subsequent IL-1β maturation could also be compensated by BHB. 		Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.                                                                                                                                                                            The enhancement of phospho-signal transducer and activator of transcription 3 (p-STAT3), degradation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) as well as the overexpression of fibroblast growth factor 2 (FGF2) resulting from LPS/ATP treatment, and subsequent IL-1β maturation could also be compensated by BHB. 	Immunohistochemical staining	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.                                                                                                                                                                            The enhancement of phospho-signal transducer and activator of transcription 3 (p-STAT3), degradation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) as well as the overexpression of fibroblast growth factor 2 (FGF2) resulting from LPS/ATP treatment, and subsequent IL-1β maturation could also be compensated by BHB. 			weston blot,GPCR,qPCR				NLRP3
30218403	chr4	122823861	122825861	FGF2	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.                                                                                                                                                                            The enhancement of phospho-signal transducer and activator of transcription 3 (p-STAT3), degradation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) as well as the overexpression of fibroblast growth factor 2 (FGF2) resulting from LPS/ATP treatment, and subsequent IL-1β maturation could also be compensated by BHB. 	human,large,mouse		High+Lowthroughput	The Beta-Hydroxybutyrate Suppresses the Migration of Glioma Cells by Inhibition of NLRP3 Inflammasome.	否		Gliomas	C6 cell	E_02_0419	weston blot,GPCR,qPCR	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.                                                                                                                                                                            The enhancement of phospho-signal transducer and activator of transcription 3 (p-STAT3), degradation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) as well as the overexpression of fibroblast growth factor 2 (FGF2) resulting from LPS/ATP treatment, and subsequent IL-1β maturation could also be compensated by BHB. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.                                                                                                                                                                            The enhancement of phospho-signal transducer and activator of transcription 3 (p-STAT3), degradation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) as well as the overexpression of fibroblast growth factor 2 (FGF2) resulting from LPS/ATP treatment, and subsequent IL-1β maturation could also be compensated by BHB. 		Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.                                                                                                                                                                            The enhancement of phospho-signal transducer and activator of transcription 3 (p-STAT3), degradation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) as well as the overexpression of fibroblast growth factor 2 (FGF2) resulting from LPS/ATP treatment, and subsequent IL-1β maturation could also be compensated by BHB. 	Immunohistochemical staining	Beta-hydroxybutyrate (BHB) is a ketone body that has recently been reported to exert anti-inflammatory effects via inhibition of NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome.                                                                                                                                                                            The enhancement of phospho-signal transducer and activator of transcription 3 (p-STAT3), degradation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IκBα) as well as the overexpression of fibroblast growth factor 2 (FGF2) resulting from LPS/ATP treatment, and subsequent IL-1β maturation could also be compensated by BHB. 			weston blot,GPCR,qPCR				FGF2
30217595	chr5	93580158	93582158	NR2F1	NR2F1 is temporally and spatially regulated during development and required for patterning and regionalization in the nervous system, including sensory hair cell organization in the auditory epithelium of the cochlea.	human,mouse		High+Lowthroughput	A spontaneous mouse deletion in Mctp1 uncovers a long-range cis-regulatory region crucial for NR2F1 function during inner ear development.	否		deaf	sensory hair cell	E_02_0420	RNA SEQ, gene knockdown, immunofluorescence staining, RT qPCR	NR2F1 is temporally and spatially regulated during development and required for patterning and regionalization in the nervous system, including sensory hair cell organization in the auditory epithelium of the cochlea.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	NR2F1 is temporally and spatially regulated during development and required for patterning and regionalization in the nervous system, including sensory hair cell organization in the auditory epithelium of the cochlea.		NR2F1 is temporally and spatially regulated during development and required for patterning and regionalization in the nervous system, including sensory hair cell organization in the auditory epithelium of the cochlea.	Immunohistochemical staining	NR2F1 is temporally and spatially regulated during development and required for patterning and regionalization in the nervous system, including sensory hair cell organization in the auditory epithelium of the cochlea.			RNA-seq,基因敲降,免疫荧光染色，RT-qPCR				NR2F1
30217225	chr3	133743403	133745403	TF	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	human		High+Lowthroughput	Genomic analysis of transcriptional networks directing progression of cell states during MGE development.	否				E_01_0721	RT qPCR, in situ hybridization analysis, gene knockdown, chip SEQ, immunofluorescence staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.		Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Immunohistochemical staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.			RT-qPCR,原位杂交分析,基因敲降,ChIP-seq ,免疫荧光染色				TF
30217225	chr9	122199438	122201438	LHX6	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	human		High+Lowthroughput	Genomic analysis of transcriptional networks directing progression of cell states during MGE development.	否				E_01_0721	RT qPCR, in situ hybridization analysis, gene knockdown, chip SEQ, immunofluorescence staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.		Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Immunohistochemical staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.			RT-qPCR,原位杂交分析,基因敲降,ChIP-seq ,免疫荧光染色				LHX6
30217225	chr1	75126101	75128101	LHX8	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	human		High+Lowthroughput	Genomic analysis of transcriptional networks directing progression of cell states during MGE development.	否				E_01_0721	RT qPCR, in situ hybridization analysis, gene knockdown, chip SEQ, immunofluorescence staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.		Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.	Immunohistochemical staining	Background Homeodomain (HD) transcription factor (TF) NKX2 1 critical for the regional specification of the medial ganglionic eminence (MGE) as well as promoting the GABAergic and cholinergic neuron fates via the induction of TFs such as LHX6 and LHX8.			RT-qPCR,原位杂交分析,基因敲降,ChIP-seq ,免疫荧光染色				LHX8
30216693	chr2	132414057	132416057	GPR39	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	human,mouse	adipose tissue	High+Lowthroughput	Improvement of Duchenne muscular dystrophy phenotype following obestatin treatment.	否		Duchenne muscular dystrophy (DMD)	satellite cell	E_02_0421	Real ‐ time PCR, Weston blot, immunofluorescence staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).		Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).	Immunohistochemical staining	Methods and results Using a multidisciplinary approach, we characterized the ageing related preproghrelin/GPR39 expression patterns in tibialis anterior (TA) muscles of 4 , 8 , and 18 week old mdx mice (n = 3/group) and established the effects of obestatin administration at this level in 8 week old mdx mice (n = 5/group).			real‐time PCR,weston blot,免疫荧光染色				GPR39
30214582	chr6	31572964	31574964	TNF	The activation of NF-κB promotes tumor necrosis factor (TNF)-α to produce VEGF and positively regulate the expression of mRNA and proteins in the VEGF pathway (21). 	human,mouse		High+Lowthroughput	Osthole attenuates angiogenesis in an orthotopic mouse model of hepatocellular carcinoma via the downregulation of nuclear factor-κB and vascular endothelial growth factor.	否		Hepatocellular carcinoma, tumour	HCC cell	E_02_0422	Immunohistochemistry (IHC), Weston blot	The activation of NF-κB promotes tumor necrosis factor (TNF)-α to produce VEGF and positively regulate the expression of mRNA and proteins in the VEGF pathway (21). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The activation of NF-κB promotes tumor necrosis factor (TNF)-α to produce VEGF and positively regulate the expression of mRNA and proteins in the VEGF pathway (21). 		The activation of NF-κB promotes tumor necrosis factor (TNF)-α to produce VEGF and positively regulate the expression of mRNA and proteins in the VEGF pathway (21). 	Immunohistochemical staining	The activation of NF-κB promotes tumor necrosis factor (TNF)-α to produce VEGF and positively regulate the expression of mRNA and proteins in the VEGF pathway (21). 			免疫组化(IHC),weston blot				TNF
30214574	chr1	1612343	1614343	MIB2	The present study demonstrated that mRNA and protein levels of E3 ubiquitin-protein ligase 2 (MIB2) were markedly upregulated in glioma cell lines and clinical samples. 	human		High+Lowthroughput	Ectopic expression of E3 ubiquitin-protein ligase 2 in glioma and enhances resistance to apoptosis through activating nuclear factor κ-light-chain-enhancer of B cells.	否		Tumor glioma	Glioma cell	E_01_0722	RT qPCR, gene knockdown, Weston blot	The present study demonstrated that mRNA and protein levels of E3 ubiquitin-protein ligase 2 (MIB2) were markedly upregulated in glioma cell lines and clinical samples. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present study demonstrated that mRNA and protein levels of E3 ubiquitin-protein ligase 2 (MIB2) were markedly upregulated in glioma cell lines and clinical samples. 		The present study demonstrated that mRNA and protein levels of E3 ubiquitin-protein ligase 2 (MIB2) were markedly upregulated in glioma cell lines and clinical samples. 	Immunohistochemical staining	The present study demonstrated that mRNA and protein levels of E3 ubiquitin-protein ligase 2 (MIB2) were markedly upregulated in glioma cell lines and clinical samples. 			RT-qPCR,基因敲降,weston blot				MIB2
30212590	chr16	10863348	10865348	CIITA	Conclusion Our experiments demonstrate for the first time that differential CTCF binding at XL9 is accompanied by uncoupled MHC-II expression as well as transcriptional and epigenetic alterations of the MHC-II regulator CIITA in septic patients. 	human		High+Lowthroughput	Impact of human sepsis on CCCTC-binding factor associated monocyte transcriptional response of Major Histocompatibility Complex II components.	否		Immunosuppressed patients, sepsis	T cell	E_01_0723	ChIP-seq,PCR	Conclusion Our experiments demonstrate for the first time that differential CTCF binding at XL9 is accompanied by uncoupled MHC-II expression as well as transcriptional and epigenetic alterations of the MHC-II regulator CIITA in septic patients. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Conclusion Our experiments demonstrate for the first time that differential CTCF binding at XL9 is accompanied by uncoupled MHC-II expression as well as transcriptional and epigenetic alterations of the MHC-II regulator CIITA in septic patients. 		Conclusion Our experiments demonstrate for the first time that differential CTCF binding at XL9 is accompanied by uncoupled MHC-II expression as well as transcriptional and epigenetic alterations of the MHC-II regulator CIITA in septic patients. 	Immunohistochemical staining	Conclusion Our experiments demonstrate for the first time that differential CTCF binding at XL9 is accompanied by uncoupled MHC-II expression as well as transcriptional and epigenetic alterations of the MHC-II regulator CIITA in septic patients. 			ChIP-seq,PCR				CIITA
30212590	chr16	67559766	67561766	CTCF	Conclusion Our experiments demonstrate for the first time that differential CTCF binding at XL9 is accompanied by uncoupled MHC-II expression as well as transcriptional and epigenetic alterations of the MHC-II regulator CIITA in septic patients. 	human		High+Lowthroughput	Impact of human sepsis on CCCTC-binding factor associated monocyte transcriptional response of Major Histocompatibility Complex II components.	否		Immunosuppressed patients, sepsis	T cell	E_01_0723	ChIP-seq,PCR	Conclusion Our experiments demonstrate for the first time that differential CTCF binding at XL9 is accompanied by uncoupled MHC-II expression as well as transcriptional and epigenetic alterations of the MHC-II regulator CIITA in septic patients. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Conclusion Our experiments demonstrate for the first time that differential CTCF binding at XL9 is accompanied by uncoupled MHC-II expression as well as transcriptional and epigenetic alterations of the MHC-II regulator CIITA in septic patients. 	Immunohistochemical staining	Conclusion Our experiments demonstrate for the first time that differential CTCF binding at XL9 is accompanied by uncoupled MHC-II expression as well as transcriptional and epigenetic alterations of the MHC-II regulator CIITA in septic patients. 	CTCF		ChIP-seq,PCR	Conclusion Our experiments demonstrate for the first time that differential CTCF binding at XL9 is accompanied by uncoupled MHC-II expression as well as transcriptional and epigenetic alterations of the MHC-II regulator CIITA in septic patients. 			
30212242	chr6	117450516	117452516	DCBLD1	Rs6942067 showed allele-specific luciferase expression and expression quantitative trait loci analysis indicates that it influences expression of DCBLD1, a gene that encodes an unknown membrane protein and is overexpressed in LUAD. 	human		High+Lowthroughput	Positional integration of lung adenocarcinoma susceptibility loci with primary human alveolar epithelial cell epigenomes.	是	rs6942067	Lung adenocarcinoma, autoimmune disease, Alzheimer's disease, diabetes, breast, prostate and colon cancer	epithelial cell of alveolus of lung	E_01_0724	ChIP-seq,FAIRE-seq, qPCR	Rs6942067 showed allele-specific luciferase expression and expression quantitative trait loci analysis indicates that it influences expression of DCBLD1, a gene that encodes an unknown membrane protein and is overexpressed in LUAD. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Rs6942067 showed allele-specific luciferase expression and expression quantitative trait loci analysis indicates that it influences expression of DCBLD1, a gene that encodes an unknown membrane protein and is overexpressed in LUAD. 		Rs6942067 showed allele-specific luciferase expression and expression quantitative trait loci analysis indicates that it influences expression of DCBLD1, a gene that encodes an unknown membrane protein and is overexpressed in LUAD. 	Immunohistochemical staining	Rs6942067 showed allele-specific luciferase expression and expression quantitative trait loci analysis indicates that it influences expression of DCBLD1, a gene that encodes an unknown membrane protein and is overexpressed in LUAD. 			ChIP-seq,FAIRE-seq, qPCR				DCBLD1
30209133	chr22	39516890	39518890	ATF4	We recently reported that activation of the activating transcription factor 4 (ATF4) pathway through the saturated fatty acid (SFA)-induced endoplasmic reticulum (ER) stress response plays a causative role in CKD-associated vascular calcification.                                                                                                                                                                                                                   Moreover, selective CDK9 inhibitors and CRISPR/Cas9-mediated CDK9 reduction blocked SFA-mediated induction of CHOP expression, whereas inhibitors of other CDK isoforms did not.            	mouse,human		High+Lowthroughput	The CDK9-cyclin T1 complex mediates saturated fatty acid-induced vascular calcification by inducing expression of the transcription factor CHOP	否		Vascular calcification	smooth muscle cell	E_02_0423	QRT PCR, Weston blot, gene knockdown	We recently reported that activation of the activating transcription factor 4 (ATF4) pathway through the saturated fatty acid (SFA)-induced endoplasmic reticulum (ER) stress response plays a causative role in CKD-associated vascular calcification.                                                                                                                                                                                                                   Moreover, selective CDK9 inhibitors and CRISPR/Cas9-mediated CDK9 reduction blocked SFA-mediated induction of CHOP expression, whereas inhibitors of other CDK isoforms did not.            	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We recently reported that activation of the activating transcription factor 4 (ATF4) pathway through the saturated fatty acid (SFA)-induced endoplasmic reticulum (ER) stress response plays a causative role in CKD-associated vascular calcification.                                                                                                                                                                                                                   Moreover, selective CDK9 inhibitors and CRISPR/Cas9-mediated CDK9 reduction blocked SFA-mediated induction of CHOP expression, whereas inhibitors of other CDK isoforms did not.            		We recently reported that activation of the activating transcription factor 4 (ATF4) pathway through the saturated fatty acid (SFA)-induced endoplasmic reticulum (ER) stress response plays a causative role in CKD-associated vascular calcification.                                                                                                                                                                                                                   Moreover, selective CDK9 inhibitors and CRISPR/Cas9-mediated CDK9 reduction blocked SFA-mediated induction of CHOP expression, whereas inhibitors of other CDK isoforms did not.            	Immunohistochemical staining	We recently reported that activation of the activating transcription factor 4 (ATF4) pathway through the saturated fatty acid (SFA)-induced endoplasmic reticulum (ER) stress response plays a causative role in CKD-associated vascular calcification.                                                                                                                                                                                                                   Moreover, selective CDK9 inhibitors and CRISPR/Cas9-mediated CDK9 reduction blocked SFA-mediated induction of CHOP expression, whereas inhibitors of other CDK isoforms did not.            			qRT-PCR,weston blot,基因敲降				ATF4
30209133	chr9	127782900	127784900	CDK9	We recently reported that activation of the activating transcription factor 4 (ATF4) pathway through the saturated fatty acid (SFA)-induced endoplasmic reticulum (ER) stress response plays a causative role in CKD-associated vascular calcification.                                                                                                                                                                                                                   Moreover, selective CDK9 inhibitors and CRISPR/Cas9-mediated CDK9 reduction blocked SFA-mediated induction of CHOP expression, whereas inhibitors of other CDK isoforms did not.            	mouse,human		High+Lowthroughput	The CDK9-cyclin T1 complex mediates saturated fatty acid-induced vascular calcification by inducing expression of the transcription factor CHOP	否		Vascular calcification	smooth muscle cell	E_02_0423	QRT PCR, Weston blot, gene knockdown	We recently reported that activation of the activating transcription factor 4 (ATF4) pathway through the saturated fatty acid (SFA)-induced endoplasmic reticulum (ER) stress response plays a causative role in CKD-associated vascular calcification.                                                                                                                                                                                                                   Moreover, selective CDK9 inhibitors and CRISPR/Cas9-mediated CDK9 reduction blocked SFA-mediated induction of CHOP expression, whereas inhibitors of other CDK isoforms did not.            	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We recently reported that activation of the activating transcription factor 4 (ATF4) pathway through the saturated fatty acid (SFA)-induced endoplasmic reticulum (ER) stress response plays a causative role in CKD-associated vascular calcification.                                                                                                                                                                                                                   Moreover, selective CDK9 inhibitors and CRISPR/Cas9-mediated CDK9 reduction blocked SFA-mediated induction of CHOP expression, whereas inhibitors of other CDK isoforms did not.            		We recently reported that activation of the activating transcription factor 4 (ATF4) pathway through the saturated fatty acid (SFA)-induced endoplasmic reticulum (ER) stress response plays a causative role in CKD-associated vascular calcification.                                                                                                                                                                                                                   Moreover, selective CDK9 inhibitors and CRISPR/Cas9-mediated CDK9 reduction blocked SFA-mediated induction of CHOP expression, whereas inhibitors of other CDK isoforms did not.            	Immunohistochemical staining	We recently reported that activation of the activating transcription factor 4 (ATF4) pathway through the saturated fatty acid (SFA)-induced endoplasmic reticulum (ER) stress response plays a causative role in CKD-associated vascular calcification.                                                                                                                                                                                                                   Moreover, selective CDK9 inhibitors and CRISPR/Cas9-mediated CDK9 reduction blocked SFA-mediated induction of CHOP expression, whereas inhibitors of other CDK isoforms did not.            			qRT-PCR,weston blot,基因敲降				CDK9
30208322	chr1	247413632	247415632	NLRP3	Emerging evidence suggests that the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in hepatocytes plays a role in the pathogenesis of liver diseases (Szabo and Csak, 2012; Szabo and Petrasek, 2015).                                                                                                                                                                                                                                                Fxr deficiency in mice augmented the ability of ER stress to induce NLRP3 and thioredoxin-interacting protein (TXNIP), whereas FXR ligand activation prevented it, ameliorating liver injury. 	mouse,human,hepatitis,B,virus,(HBV)		High+Lowthroughput	FXR Inhibits Endoplasmic Reticulum Stress-Induced NLRP3 Inflammasome in Hepatocytes and Ameliorates Liver Injury	否		Non alcoholic fatty liver disease, inflammation, liver fibrosis	hepatocyte	E_02_0424	qRT-PCR,weston blot	Emerging evidence suggests that the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in hepatocytes plays a role in the pathogenesis of liver diseases (Szabo and Csak, 2012; Szabo and Petrasek, 2015).                                                                                                                                                                                                                                                Fxr deficiency in mice augmented the ability of ER stress to induce NLRP3 and thioredoxin-interacting protein (TXNIP), whereas FXR ligand activation prevented it, ameliorating liver injury. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Emerging evidence suggests that the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in hepatocytes plays a role in the pathogenesis of liver diseases (Szabo and Csak, 2012; Szabo and Petrasek, 2015).                                                                                                                                                                                                                                                Fxr deficiency in mice augmented the ability of ER stress to induce NLRP3 and thioredoxin-interacting protein (TXNIP), whereas FXR ligand activation prevented it, ameliorating liver injury. 		Emerging evidence suggests that the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in hepatocytes plays a role in the pathogenesis of liver diseases (Szabo and Csak, 2012; Szabo and Petrasek, 2015).                                                                                                                                                                                                                                                Fxr deficiency in mice augmented the ability of ER stress to induce NLRP3 and thioredoxin-interacting protein (TXNIP), whereas FXR ligand activation prevented it, ameliorating liver injury. 	Immunohistochemical staining	Emerging evidence suggests that the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in hepatocytes plays a role in the pathogenesis of liver diseases (Szabo and Csak, 2012; Szabo and Petrasek, 2015).                                                                                                                                                                                                                                                Fxr deficiency in mice augmented the ability of ER stress to induce NLRP3 and thioredoxin-interacting protein (TXNIP), whereas FXR ligand activation prevented it, ameliorating liver injury. 			qRT-PCR,weston blot				NLRP3
30208322	chr1	145989675	145991675	TXNIP	Emerging evidence suggests that the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in hepatocytes plays a role in the pathogenesis of liver diseases (Szabo and Csak, 2012; Szabo and Petrasek, 2015).                                                                                                                                                                                                                                                Fxr deficiency in mice augmented the ability of ER stress to induce NLRP3 and thioredoxin-interacting protein (TXNIP), whereas FXR ligand activation prevented it, ameliorating liver injury. 	mouse,human,hepatitis,B,virus,(HBV)		High+Lowthroughput	FXR Inhibits Endoplasmic Reticulum Stress-Induced NLRP3 Inflammasome in Hepatocytes and Ameliorates Liver Injury	否		Non alcoholic fatty liver disease, inflammation, liver fibrosis	hepatocyte	E_02_0424	qRT-PCR,weston blot	Emerging evidence suggests that the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in hepatocytes plays a role in the pathogenesis of liver diseases (Szabo and Csak, 2012; Szabo and Petrasek, 2015).                                                                                                                                                                                                                                                Fxr deficiency in mice augmented the ability of ER stress to induce NLRP3 and thioredoxin-interacting protein (TXNIP), whereas FXR ligand activation prevented it, ameliorating liver injury. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Emerging evidence suggests that the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in hepatocytes plays a role in the pathogenesis of liver diseases (Szabo and Csak, 2012; Szabo and Petrasek, 2015).                                                                                                                                                                                                                                                Fxr deficiency in mice augmented the ability of ER stress to induce NLRP3 and thioredoxin-interacting protein (TXNIP), whereas FXR ligand activation prevented it, ameliorating liver injury. 		Emerging evidence suggests that the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in hepatocytes plays a role in the pathogenesis of liver diseases (Szabo and Csak, 2012; Szabo and Petrasek, 2015).                                                                                                                                                                                                                                                Fxr deficiency in mice augmented the ability of ER stress to induce NLRP3 and thioredoxin-interacting protein (TXNIP), whereas FXR ligand activation prevented it, ameliorating liver injury. 	Immunohistochemical staining	Emerging evidence suggests that the NACHT, LRR, and PYD domains-containing protein 3 (NLRP3) inflammasome in hepatocytes plays a role in the pathogenesis of liver diseases (Szabo and Csak, 2012; Szabo and Petrasek, 2015).                                                                                                                                                                                                                                                Fxr deficiency in mice augmented the ability of ER stress to induce NLRP3 and thioredoxin-interacting protein (TXNIP), whereas FXR ligand activation prevented it, ameliorating liver injury. 			qRT-PCR,weston blot				TXNIP
30206934	chr20	6765006	6767006	BMP2	Not only gene expression was affected, tension force was also able to induce ATP release, which subse- quently could promote osteogenesis by osteoblasts (Kariya et al., 2015; Sun et al., 2013). This promoting effect was proposed to be due to a stimulated expression of BMP2, 4, and 5 (Ayala Peña, Scolaro, &Santillán, 2013). 	human,mouse		High+Lowthroughput	Cyclic tensile force stimulates BMP9 synthesis and in vitro mineralization by human periodontal ligament cells	否			periodontal ligament cell	E_02_0425	RT‐PCR	Not only gene expression was affected, tension force was also able to induce ATP release, which subse- quently could promote osteogenesis by osteoblasts (Kariya et al., 2015; Sun et al., 2013). This promoting effect was proposed to be due to a stimulated expression of BMP2, 4, and 5 (Ayala Peña, Scolaro, &Santillán, 2013). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Not only gene expression was affected, tension force was also able to induce ATP release, which subse- quently could promote osteogenesis by osteoblasts (Kariya et al., 2015; Sun et al., 2013). This promoting effect was proposed to be due to a stimulated expression of BMP2, 4, and 5 (Ayala Peña, Scolaro, &Santillán, 2013). 		Not only gene expression was affected, tension force was also able to induce ATP release, which subse- quently could promote osteogenesis by osteoblasts (Kariya et al., 2015; Sun et al., 2013). This promoting effect was proposed to be due to a stimulated expression of BMP2, 4, and 5 (Ayala Peña, Scolaro, &Santillán, 2013). 	Immunohistochemical staining	Not only gene expression was affected, tension force was also able to induce ATP release, which subse- quently could promote osteogenesis by osteoblasts (Kariya et al., 2015; Sun et al., 2013). This promoting effect was proposed to be due to a stimulated expression of BMP2, 4, and 5 (Ayala Peña, Scolaro, &Santillán, 2013). 			RT‐PCR				BMP2
30205834	chr14	92041650	92043650	ATXN3	Methods We first examined a role for intracellular astrocytic responses in a Drosophila model for Spinocerebellar ataxia type 3 (SCA3, also known as Machado Joseph disease), a disease caused by expansion of the polyglutamine (polyQ) stretch in the ATXN3 gene. 	mouse		High+Lowthroughput	Inhibition of NF-κB in astrocytes is sufficient to delay neurodegeneration induced by proteotoxicity in neurons	否		Neurodegenerative diseases, Alzheimer's disease	Astrocyte	E_02_0426	RT qPCR, Weston BOT, gene knockdown	Methods We first examined a role for intracellular astrocytic responses in a Drosophila model for Spinocerebellar ataxia type 3 (SCA3, also known as Machado Joseph disease), a disease caused by expansion of the polyglutamine (polyQ) stretch in the ATXN3 gene. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Methods We first examined a role for intracellular astrocytic responses in a Drosophila model for Spinocerebellar ataxia type 3 (SCA3, also known as Machado Joseph disease), a disease caused by expansion of the polyglutamine (polyQ) stretch in the ATXN3 gene. 		Methods We first examined a role for intracellular astrocytic responses in a Drosophila model for Spinocerebellar ataxia type 3 (SCA3, also known as Machado Joseph disease), a disease caused by expansion of the polyglutamine (polyQ) stretch in the ATXN3 gene. 	Immunohistochemical staining	Methods We first examined a role for intracellular astrocytic responses in a Drosophila model for Spinocerebellar ataxia type 3 (SCA3, also known as Machado Joseph disease), a disease caused by expansion of the polyglutamine (polyQ) stretch in the ATXN3 gene. 			RT-qPCR,weston bot,基因敲降				ATXN3
30205135	chr17	82075582	82077582	FASN	Kahweol preferentially inhibited cell proliferation and induced cell death through the induction of a caspase 3-dependent pathway in HER2-overexpression breast cancer cell lines.                             Furthermore, we found that blocking Akt signaling through kahweol treatment significantly reduced FASN expression and subsequently suppressed cell proliferation in HER2- overexpressing cancer cells.	human		High+Lowthroughput	Kahweol inhibits proliferation and induces apoptosis by suppressing fatty acid synthase in HER2-overexpressing cancer cells	否		mammary cancer	breast cancer cell	E_01_0725	qRT-PCR,weston blot	Kahweol preferentially inhibited cell proliferation and induced cell death through the induction of a caspase 3-dependent pathway in HER2-overexpression breast cancer cell lines.                             Furthermore, we found that blocking Akt signaling through kahweol treatment significantly reduced FASN expression and subsequently suppressed cell proliferation in HER2- overexpressing cancer cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Kahweol preferentially inhibited cell proliferation and induced cell death through the induction of a caspase 3-dependent pathway in HER2-overexpression breast cancer cell lines.                             Furthermore, we found that blocking Akt signaling through kahweol treatment significantly reduced FASN expression and subsequently suppressed cell proliferation in HER2- overexpressing cancer cells.		Kahweol preferentially inhibited cell proliferation and induced cell death through the induction of a caspase 3-dependent pathway in HER2-overexpression breast cancer cell lines.                             Furthermore, we found that blocking Akt signaling through kahweol treatment significantly reduced FASN expression and subsequently suppressed cell proliferation in HER2- overexpressing cancer cells.	Immunohistochemical staining	Kahweol preferentially inhibited cell proliferation and induced cell death through the induction of a caspase 3-dependent pathway in HER2-overexpression breast cancer cell lines.                             Furthermore, we found that blocking Akt signaling through kahweol treatment significantly reduced FASN expression and subsequently suppressed cell proliferation in HER2- overexpressing cancer cells.			qRT-PCR,weston blot				FASN
30203098	chr12	102392859	102394859	IGF1	In the present study, fermented corn-soybean meal significantly improved average daily gain and gain:food ratio (P < 0.05). Fermented feed (FF) significantly increased insulin-like growth factor 1 (IGF1) transcription in liver (P < 0.05).	mouse		High+Lowthroughput	Fermented corn-soybean meal elevated IGF1 levels in grower-finisher pigs	否				E_02_0427	weston blot,Real-time PCR	In the present study, fermented corn-soybean meal significantly improved average daily gain and gain:food ratio (P < 0.05). Fermented feed (FF) significantly increased insulin-like growth factor 1 (IGF1) transcription in liver (P < 0.05).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, fermented corn-soybean meal significantly improved average daily gain and gain:food ratio (P < 0.05). Fermented feed (FF) significantly increased insulin-like growth factor 1 (IGF1) transcription in liver (P < 0.05).		In the present study, fermented corn-soybean meal significantly improved average daily gain and gain:food ratio (P < 0.05). Fermented feed (FF) significantly increased insulin-like growth factor 1 (IGF1) transcription in liver (P < 0.05).	Immunohistochemical staining	In the present study, fermented corn-soybean meal significantly improved average daily gain and gain:food ratio (P < 0.05). Fermented feed (FF) significantly increased insulin-like growth factor 1 (IGF1) transcription in liver (P < 0.05).			weston blot,Real-time PCR				IGF1
30201991	chr3	119521370	119523370	CD80	For example, CTLA-4 can inhibit T cell activation intrinsically by outcompeting CD28 for binding to CD80 and CD86, while PD-1 engagement by PD-L1 or PD-L2 triggers an inhibitory signal. 	human		High+Lowthroughput	An immunoregulatory and tissue-residency program modulated by c-MAF in human T(H)17 cells	否		chronic inflammation 		E_01_0726	RNA SEQ, chip SEQ, qPCR, chip qPCR, flow cytometry	For example, CTLA-4 can inhibit T cell activation intrinsically by outcompeting CD28 for binding to CD80 and CD86, while PD-1 engagement by PD-L1 or PD-L2 triggers an inhibitory signal. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			For example, CTLA-4 can inhibit T cell activation intrinsically by outcompeting CD28 for binding to CD80 and CD86, while PD-1 engagement by PD-L1 or PD-L2 triggers an inhibitory signal. 	Immunohistochemical staining	For example, CTLA-4 can inhibit T cell activation intrinsically by outcompeting CD28 for binding to CD80 and CD86, while PD-1 engagement by PD-L1 or PD-L2 triggers an inhibitory signal. 	CD80		RNA-seq,ChIP-seq,qPCR, ChIP-qPCR,流式细胞术	For example, CTLA-4 can inhibit T cell activation intrinsically by outcompeting CD28 for binding to CD80 and CD86, while PD-1 engagement by PD-L1 or PD-L2 triggers an inhibitory signal. 			
30201991	chr3	122052619	122054619	CD86	For example, CTLA-4 can inhibit T cell activation intrinsically by outcompeting CD28 for binding to CD80 and CD86, while PD-1 engagement by PD-L1 or PD-L2 triggers an inhibitory signal. 	human		High+Lowthroughput	An immunoregulatory and tissue-residency program modulated by c-MAF in human T(H)17 cells	否		chronic inflammation 		E_01_0726	RNA SEQ, chip SEQ, qPCR, chip qPCR, flow cytometry	For example, CTLA-4 can inhibit T cell activation intrinsically by outcompeting CD28 for binding to CD80 and CD86, while PD-1 engagement by PD-L1 or PD-L2 triggers an inhibitory signal. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			For example, CTLA-4 can inhibit T cell activation intrinsically by outcompeting CD28 for binding to CD80 and CD86, while PD-1 engagement by PD-L1 or PD-L2 triggers an inhibitory signal. 	Immunohistochemical staining	For example, CTLA-4 can inhibit T cell activation intrinsically by outcompeting CD28 for binding to CD80 and CD86, while PD-1 engagement by PD-L1 or PD-L2 triggers an inhibitory signal. 	CD86		RNA-seq,ChIP-seq,qPCR, ChIP-qPCR,流式细胞术	For example, CTLA-4 can inhibit T cell activation intrinsically by outcompeting CD28 for binding to CD80 and CD86, while PD-1 engagement by PD-L1 or PD-L2 triggers an inhibitory signal. 			
30201766	chr22	35603362	35605362	MB	It was proposed that the Drosophila amnesiac gene (amn) is required for consolidation of aversive memory in the dorsal paired medial (DPM) neurons, a pair of large neurons that broadly innervate the mushroom bodies (MB), the fly center for olfactory learning and memory (Waddell et al., 2000). 	human,Drosophila,fly		High+Lowthroughput	Amnesiac Is Required in the Adult Mushroom Body for Memory Formation	否		Amnesia		E_02_0428	Immunofluorescence staining, qPCR	It was proposed that the Drosophila amnesiac gene (amn) is required for consolidation of aversive memory in the dorsal paired medial (DPM) neurons, a pair of large neurons that broadly innervate the mushroom bodies (MB), the fly center for olfactory learning and memory (Waddell et al., 2000). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	It was proposed that the Drosophila amnesiac gene (amn) is required for consolidation of aversive memory in the dorsal paired medial (DPM) neurons, a pair of large neurons that broadly innervate the mushroom bodies (MB), the fly center for olfactory learning and memory (Waddell et al., 2000). 		It was proposed that the Drosophila amnesiac gene (amn) is required for consolidation of aversive memory in the dorsal paired medial (DPM) neurons, a pair of large neurons that broadly innervate the mushroom bodies (MB), the fly center for olfactory learning and memory (Waddell et al., 2000). 	Immunohistochemical staining	It was proposed that the Drosophila amnesiac gene (amn) is required for consolidation of aversive memory in the dorsal paired medial (DPM) neurons, a pair of large neurons that broadly innervate the mushroom bodies (MB), the fly center for olfactory learning and memory (Waddell et al., 2000). 			免疫荧光染色, qPCR 				MB
30200840	chr2	38740810	38742810	SRSF7	Mutagenesis of the minigene delineates the cis-acting enhancer element for SRSF2 within exon 6 to single nucleotide resolution and reveals that the combined activity of SRSF2 and SRSF7 is required for oscillating U2af26 AS.	mouse,human		High+Lowthroughput	Characterization of cis-acting elements that control oscillating alternative splicing	否			N2Acell	E_02_0429	RNA-Seq,RT-PCR,	Mutagenesis of the minigene delineates the cis-acting enhancer element for SRSF2 within exon 6 to single nucleotide resolution and reveals that the combined activity of SRSF2 and SRSF7 is required for oscillating U2af26 AS.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mutagenesis of the minigene delineates the cis-acting enhancer element for SRSF2 within exon 6 to single nucleotide resolution and reveals that the combined activity of SRSF2 and SRSF7 is required for oscillating U2af26 AS.		Mutagenesis of the minigene delineates the cis-acting enhancer element for SRSF2 within exon 6 to single nucleotide resolution and reveals that the combined activity of SRSF2 and SRSF7 is required for oscillating U2af26 AS.	Immunohistochemical staining	Mutagenesis of the minigene delineates the cis-acting enhancer element for SRSF2 within exon 6 to single nucleotide resolution and reveals that the combined activity of SRSF2 and SRSF7 is required for oscillating U2af26 AS.			RNA-Seq,RT-PCR,				SRSF7
30200414	chr18	55219748	55221748	TCF4	Wnt Effector TCF4 Is Dispensable for Wnt Signaling in Human Cancer Cells.However, in human cells, the TCF4 role is redundant with the related T-cell factor 1 (TCF1) and lymphoid enhancer-binding factor 1 (LEF1) transcription factors. 	mouse,human		High+Lowthroughput	Wnt Effector TCF4 Is Dispensable for Wnt Signaling in Human Cancer Cells	否		Colorectal cancer, adenomatous colorectal polyposis	TA cell	E_02_0430	ChIP-seq,qRT-PCR,weston blot	Wnt Effector TCF4 Is Dispensable for Wnt Signaling in Human Cancer Cells.However, in human cells, the TCF4 role is redundant with the related T-cell factor 1 (TCF1) and lymphoid enhancer-binding factor 1 (LEF1) transcription factors. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Wnt Effector TCF4 Is Dispensable for Wnt Signaling in Human Cancer Cells.However, in human cells, the TCF4 role is redundant with the related T-cell factor 1 (TCF1) and lymphoid enhancer-binding factor 1 (LEF1) transcription factors. 		Wnt Effector TCF4 Is Dispensable for Wnt Signaling in Human Cancer Cells.However, in human cells, the TCF4 role is redundant with the related T-cell factor 1 (TCF1) and lymphoid enhancer-binding factor 1 (LEF1) transcription factors. 	Immunohistochemical staining	Wnt Effector TCF4 Is Dispensable for Wnt Signaling in Human Cancer Cells.However, in human cells, the TCF4 role is redundant with the related T-cell factor 1 (TCF1) and lymphoid enhancer-binding factor 1 (LEF1) transcription factors. 			ChIP-seq,qRT-PCR,weston blot				TCF4
30200414	chr4	108044921	108046921	LEF1	Wnt Effector TCF4 Is Dispensable for Wnt Signaling in Human Cancer Cells.However, in human cells, the TCF4 role is redundant with the related T-cell factor 1 (TCF1) and lymphoid enhancer-binding factor 1 (LEF1) transcription factors. 	mouse,human		High+Lowthroughput	Wnt Effector TCF4 Is Dispensable for Wnt Signaling in Human Cancer Cells	否		Colorectal cancer, adenomatous colorectal polyposis	TA cell	E_02_0430	ChIP-seq,qRT-PCR,weston blot	Wnt Effector TCF4 Is Dispensable for Wnt Signaling in Human Cancer Cells.However, in human cells, the TCF4 role is redundant with the related T-cell factor 1 (TCF1) and lymphoid enhancer-binding factor 1 (LEF1) transcription factors. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Wnt Effector TCF4 Is Dispensable for Wnt Signaling in Human Cancer Cells.However, in human cells, the TCF4 role is redundant with the related T-cell factor 1 (TCF1) and lymphoid enhancer-binding factor 1 (LEF1) transcription factors. 		Wnt Effector TCF4 Is Dispensable for Wnt Signaling in Human Cancer Cells.However, in human cells, the TCF4 role is redundant with the related T-cell factor 1 (TCF1) and lymphoid enhancer-binding factor 1 (LEF1) transcription factors. 	Immunohistochemical staining	Wnt Effector TCF4 Is Dispensable for Wnt Signaling in Human Cancer Cells.However, in human cells, the TCF4 role is redundant with the related T-cell factor 1 (TCF1) and lymphoid enhancer-binding factor 1 (LEF1) transcription factors. 			ChIP-seq,qRT-PCR,weston blot				LEF1
30199902	chr10	88951016	88953016	FAS	Lipid synthesis pro- teins such as fatty acid synthase (FAS) and sterol regulatory ele-ment-binding protein (SREBP) are involved in fatty acid and cho- lesterol synthesis, and contribute toward lipid homeostasis.	mouse		High+Lowthroughput	2,6-Dimethoxy-1,4-benzoquinone Inhibits 3T3-L1 Adipocyte Differentiation via Regulation of AMPK and mTORC1	否		Obesity		E_02_0431	weston blot	Lipid synthesis pro- teins such as fatty acid synthase (FAS) and sterol regulatory ele-ment-binding protein (SREBP) are involved in fatty acid and cho- lesterol synthesis, and contribute toward lipid homeostasis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Lipid synthesis pro- teins such as fatty acid synthase (FAS) and sterol regulatory ele-ment-binding protein (SREBP) are involved in fatty acid and cho- lesterol synthesis, and contribute toward lipid homeostasis.		Lipid synthesis pro- teins such as fatty acid synthase (FAS) and sterol regulatory ele-ment-binding protein (SREBP) are involved in fatty acid and cho- lesterol synthesis, and contribute toward lipid homeostasis.	Immunohistochemical staining	Lipid synthesis pro- teins such as fatty acid synthase (FAS) and sterol regulatory ele-ment-binding protein (SREBP) are involved in fatty acid and cho- lesterol synthesis, and contribute toward lipid homeostasis.			weston blot				FAS
30196018	chr11	27652477	27654477	BDNF	Moreover, SAK3 administration (0.5 mg/kg, p.o.) antagonized the reduction of calcium/calmodulin-dependent protein kinase II (CaMKII) and CaMKIV phosphorylation levels, thereby rescuing the decreased levels of cAMP response element- binding protein (CREB)/brain derived neurotrophic factor (BDNF) signaling in the OBX DG.	human,mouse		High+Lowthroughput	T-type calcium channel enhancer SAK3 produces anti-depressant-like effects by promoting adult hippocampal neurogenesis in olfactory bulbectomized mice	否		depression	neural progenitor cell	E_02_0432	qPCR,weston blot	Moreover, SAK3 administration (0.5 mg/kg, p.o.) antagonized the reduction of calcium/calmodulin-dependent protein kinase II (CaMKII) and CaMKIV phosphorylation levels, thereby rescuing the decreased levels of cAMP response element- binding protein (CREB)/brain derived neurotrophic factor (BDNF) signaling in the OBX DG.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, SAK3 administration (0.5 mg/kg, p.o.) antagonized the reduction of calcium/calmodulin-dependent protein kinase II (CaMKII) and CaMKIV phosphorylation levels, thereby rescuing the decreased levels of cAMP response element- binding protein (CREB)/brain derived neurotrophic factor (BDNF) signaling in the OBX DG.		Moreover, SAK3 administration (0.5 mg/kg, p.o.) antagonized the reduction of calcium/calmodulin-dependent protein kinase II (CaMKII) and CaMKIV phosphorylation levels, thereby rescuing the decreased levels of cAMP response element- binding protein (CREB)/brain derived neurotrophic factor (BDNF) signaling in the OBX DG.	Immunohistochemical staining	Moreover, SAK3 administration (0.5 mg/kg, p.o.) antagonized the reduction of calcium/calmodulin-dependent protein kinase II (CaMKII) and CaMKIV phosphorylation levels, thereby rescuing the decreased levels of cAMP response element- binding protein (CREB)/brain derived neurotrophic factor (BDNF) signaling in the OBX DG.			qPCR,weston blot				BDNF
30195779	chrX	103771144	103773144	PLP1	DNA variants of the proteolipid protein 1 gene (PLP1) that shift PLP1/DM20 alternative splicing away from the PLP1 form toward DM20 cause the allelic X-linked leukodystrophies Pelizaeus-Merzbacher disease (PMD), spastic paraplegia 2 (SPG2), and hypomyelination of early myelinating structures (HEMS).	human,mouse		High+Lowthroughput	Morpholino Antisense Oligomers as a Potential Therapeutic Option for the Correction of Alternative Splicing in PMD, SPG2, and HEMS	否		Spastic paraplegia	Oligodendrocytes	E_02_0433	RT-PCR	DNA variants of the proteolipid protein 1 gene (PLP1) that shift PLP1/DM20 alternative splicing away from the PLP1 form toward DM20 cause the allelic X-linked leukodystrophies Pelizaeus-Merzbacher disease (PMD), spastic paraplegia 2 (SPG2), and hypomyelination of early myelinating structures (HEMS).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	DNA variants of the proteolipid protein 1 gene (PLP1) that shift PLP1/DM20 alternative splicing away from the PLP1 form toward DM20 cause the allelic X-linked leukodystrophies Pelizaeus-Merzbacher disease (PMD), spastic paraplegia 2 (SPG2), and hypomyelination of early myelinating structures (HEMS).		DNA variants of the proteolipid protein 1 gene (PLP1) that shift PLP1/DM20 alternative splicing away from the PLP1 form toward DM20 cause the allelic X-linked leukodystrophies Pelizaeus-Merzbacher disease (PMD), spastic paraplegia 2 (SPG2), and hypomyelination of early myelinating structures (HEMS).	Immunohistochemical staining	DNA variants of the proteolipid protein 1 gene (PLP1) that shift PLP1/DM20 alternative splicing away from the PLP1 form toward DM20 cause the allelic X-linked leukodystrophies Pelizaeus-Merzbacher disease (PMD), spastic paraplegia 2 (SPG2), and hypomyelination of early myelinating structures (HEMS).			RT-PCR				PLP1
30195778	chr1	156460686	156462686	MEF2D	This indicates that lncR-D63785 acts as a competitive endogenous RNA (ceRNA) of miR-422a and promotes chemoresistance by blocking miR-422-dependent suppression of MEF2D.	human	Gastric cancer tissues	High+Lowthroughput	The Long Noncoding RNA D63785 Regulates Chemotherapy Sensitivity in Human Gastric Cancer by Targeting miR-422a	否		gastric cancer	gastric cancer cell	E_01_0727	Real time qPCR, Weston blot, immunofluorescence staining, gene knockdown	This indicates that lncR-D63785 acts as a competitive endogenous RNA (ceRNA) of miR-422a and promotes chemoresistance by blocking miR-422-dependent suppression of MEF2D.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This indicates that lncR-D63785 acts as a competitive endogenous RNA (ceRNA) of miR-422a and promotes chemoresistance by blocking miR-422-dependent suppression of MEF2D.		This indicates that lncR-D63785 acts as a competitive endogenous RNA (ceRNA) of miR-422a and promotes chemoresistance by blocking miR-422-dependent suppression of MEF2D.	Immunohistochemical staining	This indicates that lncR-D63785 acts as a competitive endogenous RNA (ceRNA) of miR-422a and promotes chemoresistance by blocking miR-422-dependent suppression of MEF2D.			real-time qPCR,weston blot,免疫荧光染色,基因敲降				MEF2D
30195603	chr12	6531538	6533538	GAPDH	Conclusions: Our findings reveal GAPDH/Siah1 signaling cascades as a novel therapeutic target for ischemic SCI and identify WIN55212-2 with the potential to treat ischemic SCI by targeting this pathway. 	mouse		High+Lowthroughput	Inhibiting a spinal cord signaling pathway protects against ischemia injury in rats	否		Ischemic spinal cord injury	leukocyte	E_02_0434	Weston blot, CO immunoprecipitation, ELISA	Conclusions: Our findings reveal GAPDH/Siah1 signaling cascades as a novel therapeutic target for ischemic SCI and identify WIN55212-2 with the potential to treat ischemic SCI by targeting this pathway. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Conclusions: Our findings reveal GAPDH/Siah1 signaling cascades as a novel therapeutic target for ischemic SCI and identify WIN55212-2 with the potential to treat ischemic SCI by targeting this pathway. 		Conclusions: Our findings reveal GAPDH/Siah1 signaling cascades as a novel therapeutic target for ischemic SCI and identify WIN55212-2 with the potential to treat ischemic SCI by targeting this pathway. 	Immunohistochemical staining	Conclusions: Our findings reveal GAPDH/Siah1 signaling cascades as a novel therapeutic target for ischemic SCI and identify WIN55212-2 with the potential to treat ischemic SCI by targeting this pathway. 			weston blot,共同免疫沉淀法,酶联免疫吸附法				GAPDH
30195387	chr8	81475654	81477654	FABP4	Diazinon has been known to induce neurotoxic effects mainly through the inhibition of acetylcholinesterase (AChE).                                                                          Diazinon significantly induced protein expression of transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), their downstream proteins, fatty acid synthase (FASN), acetyl CoA carboxylase (ACC), fatty acid-binding protein 4 (FABP4), lipoprotein lipase (LPL), adiponectin and perilipin in dose and time-dependent manners. 	human,mouse		High+Lowthroughput	Diazinon exposure activated transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ) and induced adipogenesis in 3T3-L1 preadipocytes	否		Obesity	3T3‑L1 adipocytes	E_02_0435	RT-PCR, immunofluorescence light staining, Western blot	Diazinon has been known to induce neurotoxic effects mainly through the inhibition of acetylcholinesterase (AChE).                                                                          Diazinon significantly induced protein expression of transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), their downstream proteins, fatty acid synthase (FASN), acetyl CoA carboxylase (ACC), fatty acid-binding protein 4 (FABP4), lipoprotein lipase (LPL), adiponectin and perilipin in dose and time-dependent manners. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Diazinon has been known to induce neurotoxic effects mainly through the inhibition of acetylcholinesterase (AChE).                                                                          Diazinon significantly induced protein expression of transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), their downstream proteins, fatty acid synthase (FASN), acetyl CoA carboxylase (ACC), fatty acid-binding protein 4 (FABP4), lipoprotein lipase (LPL), adiponectin and perilipin in dose and time-dependent manners. 		Diazinon has been known to induce neurotoxic effects mainly through the inhibition of acetylcholinesterase (AChE).                                                                          Diazinon significantly induced protein expression of transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), their downstream proteins, fatty acid synthase (FASN), acetyl CoA carboxylase (ACC), fatty acid-binding protein 4 (FABP4), lipoprotein lipase (LPL), adiponectin and perilipin in dose and time-dependent manners. 	Immunohistochemical staining	Diazinon has been known to induce neurotoxic effects mainly through the inhibition of acetylcholinesterase (AChE).                                                                          Diazinon significantly induced protein expression of transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), their downstream proteins, fatty acid synthase (FASN), acetyl CoA carboxylase (ACC), fatty acid-binding protein 4 (FABP4), lipoprotein lipase (LPL), adiponectin and perilipin in dose and time-dependent manners. 			RT-PCR,免疫荧光光染色,Western Blot				FABP4
30195387	chr17	82076134	82078134	FASN	Diazinon has been known to induce neurotoxic effects mainly through the inhibition of acetylcholinesterase (AChE).                                                                          Diazinon significantly induced protein expression of transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), their downstream proteins, fatty acid synthase (FASN), acetyl CoA carboxylase (ACC), fatty acid-binding protein 4 (FABP4), lipoprotein lipase (LPL), adiponectin and perilipin in dose and time-dependent manners. 	human,mouse		High+Lowthroughput	Diazinon exposure activated transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ) and induced adipogenesis in 3T3-L1 preadipocytes	否		Obesity	3T3‑L1 adipocytes	E_02_0435	RT-PCR, immunofluorescence light staining, Western blot	Diazinon has been known to induce neurotoxic effects mainly through the inhibition of acetylcholinesterase (AChE).                                                                          Diazinon significantly induced protein expression of transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), their downstream proteins, fatty acid synthase (FASN), acetyl CoA carboxylase (ACC), fatty acid-binding protein 4 (FABP4), lipoprotein lipase (LPL), adiponectin and perilipin in dose and time-dependent manners. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Diazinon has been known to induce neurotoxic effects mainly through the inhibition of acetylcholinesterase (AChE).                                                                          Diazinon significantly induced protein expression of transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), their downstream proteins, fatty acid synthase (FASN), acetyl CoA carboxylase (ACC), fatty acid-binding protein 4 (FABP4), lipoprotein lipase (LPL), adiponectin and perilipin in dose and time-dependent manners. 		Diazinon has been known to induce neurotoxic effects mainly through the inhibition of acetylcholinesterase (AChE).                                                                          Diazinon significantly induced protein expression of transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), their downstream proteins, fatty acid synthase (FASN), acetyl CoA carboxylase (ACC), fatty acid-binding protein 4 (FABP4), lipoprotein lipase (LPL), adiponectin and perilipin in dose and time-dependent manners. 	Immunohistochemical staining	Diazinon has been known to induce neurotoxic effects mainly through the inhibition of acetylcholinesterase (AChE).                                                                          Diazinon significantly induced protein expression of transcriptional factors CCAAT-enhancer-binding proteins α (C/EBPα) and peroxisome proliferator-activated receptor γ (PPARγ), their downstream proteins, fatty acid synthase (FASN), acetyl CoA carboxylase (ACC), fatty acid-binding protein 4 (FABP4), lipoprotein lipase (LPL), adiponectin and perilipin in dose and time-dependent manners. 			RT-PCR,免疫荧光光染色,Western Blot				FASN
30194633	chr18	59217178	59219178	GRP	At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux.	human		High+Lowthroughput	Palmitic acid induces human osteoblast-like Saos-2 cell apoptosis via endoplasmic reticulum stress and autophagy	否			Saos-2 cell	E_01_0728	Flow cytometry, Weston blot, statistical analysis, mcherry-gfp-lc3 analysis, and immunofluorescence light staining	At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux.		At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux.	Immunohistochemical staining	At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux.			流式细胞术,weston blot,统计分析,mCherry-GFP-LC3 analysis,免疫荧光光染色				GRP
30194633	chr19	48952001	48954001	BAX	At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux.	human		High+Lowthroughput	Palmitic acid induces human osteoblast-like Saos-2 cell apoptosis via endoplasmic reticulum stress and autophagy	否			Saos-2 cell	E_01_0728	Flow cytometry, Weston blot, statistical analysis, mcherry-gfp-lc3 analysis, and immunofluorescence light staining	At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux.		At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux.	Immunohistochemical staining	At the same time, PA induced the expression of ER stress marker genes (glucose-regulated protein 78 (GRP78) and CCAAT/enhancer binding protein homologous protein (CHOP)), altered autophagy-related gene expression (microtubule-associated protein 1 light chain 3 (LC3), ATG5, p62, and Beclin), promoted apoptosis-related gene expression (Caspase 3 and BAX), and affected autophagic flux.			流式细胞术,weston blot,统计分析,mCherry-GFP-LC3 analysis,免疫荧光光染色				BAX
30193323	chrX	48518970	48520970	EBP	The adipogenesis-related downstream mediators of the PI3K/ AKT cascade, that is, forkhead box protein O1 (FOXO1) and mammalian target of rapamycin (mTOR), also were measured by Western blotting.                                                                                                                                                      After adipogenic differentiation and idelalisib treatment, cells were stained with Oil Red O and the levels of peroxisome proliferator activator c (PPARc) and CCAAT-enhancer binding proteins (C/EBP) a/b were determined by Western blot analyses.	human		High+Lowthroughput	Inhibitory Effect of Idelalisib, a Selective Phosphatidylinositol 3-Kinase δ Inhibitor, on Adipogenesis in an In Vitro Model of Graves' Orbitopathy	否		Graves ophthalmopathy (go), graphene oxide	fibroblast	E_01_0729	Weston blot, ELISA, Western blot	The adipogenesis-related downstream mediators of the PI3K/ AKT cascade, that is, forkhead box protein O1 (FOXO1) and mammalian target of rapamycin (mTOR), also were measured by Western blotting.                                                                                                                                                      After adipogenic differentiation and idelalisib treatment, cells were stained with Oil Red O and the levels of peroxisome proliferator activator c (PPARc) and CCAAT-enhancer binding proteins (C/EBP) a/b were determined by Western blot analyses.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The adipogenesis-related downstream mediators of the PI3K/ AKT cascade, that is, forkhead box protein O1 (FOXO1) and mammalian target of rapamycin (mTOR), also were measured by Western blotting.                                                                                                                                                      After adipogenic differentiation and idelalisib treatment, cells were stained with Oil Red O and the levels of peroxisome proliferator activator c (PPARc) and CCAAT-enhancer binding proteins (C/EBP) a/b were determined by Western blot analyses.		The adipogenesis-related downstream mediators of the PI3K/ AKT cascade, that is, forkhead box protein O1 (FOXO1) and mammalian target of rapamycin (mTOR), also were measured by Western blotting.                                                                                                                                                      After adipogenic differentiation and idelalisib treatment, cells were stained with Oil Red O and the levels of peroxisome proliferator activator c (PPARc) and CCAAT-enhancer binding proteins (C/EBP) a/b were determined by Western blot analyses.	Immunohistochemical staining	The adipogenesis-related downstream mediators of the PI3K/ AKT cascade, that is, forkhead box protein O1 (FOXO1) and mammalian target of rapamycin (mTOR), also were measured by Western blotting.                                                                                                                                                      After adipogenic differentiation and idelalisib treatment, cells were stained with Oil Red O and the levels of peroxisome proliferator activator c (PPARc) and CCAAT-enhancer binding proteins (C/EBP) a/b were determined by Western blot analyses.			weston blot,酶联免疫吸附法,免疫印迹法				EBP
30191958	chr16	30955149	30957149	SETD1A	The histone H3 lysine 4-specific methyltransferase SETD1A is associated with transcription activation and is considered a key epigenetic regulator that modulates the cell cycle and metastasis in triple-negative breast cancer cells.	human	Mammary tissue	High+Lowthroughput	Aberrant expression of SETD1A promotes survival and migration of estrogen receptor α-positive breast cancer cells	否		mammary cancer	MCF-7 cell	E_01_0730	RT qPCR, faire qPCR, mRNA SEQ, RNA SEQ, Weston BOT, gene knockdown	The histone H3 lysine 4-specific methyltransferase SETD1A is associated with transcription activation and is considered a key epigenetic regulator that modulates the cell cycle and metastasis in triple-negative breast cancer cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The histone H3 lysine 4-specific methyltransferase SETD1A is associated with transcription activation and is considered a key epigenetic regulator that modulates the cell cycle and metastasis in triple-negative breast cancer cells.		The histone H3 lysine 4-specific methyltransferase SETD1A is associated with transcription activation and is considered a key epigenetic regulator that modulates the cell cycle and metastasis in triple-negative breast cancer cells.	Immunohistochemical staining	The histone H3 lysine 4-specific methyltransferase SETD1A is associated with transcription activation and is considered a key epigenetic regulator that modulates the cell cycle and metastasis in triple-negative breast cancer cells.			RT-qPCR, FAIRE-qPCR,mRNA-seq,RNA-seq,weston bot,基因敲降				SETD1A
30191953	chr3	181709352	181711352	SOX2	Overexpression of miR 302/367 cluster in MDA MB 231 and SK BR 3 breast cancer cells upregulated expression of miR 302/367 members and also some core pluripotency factors including OCT4A, SOX2 and NANOG, induced mesenchymal to epithelial transition, suppressed invasion, proliferation, and induced apoptosis in the both cell lines.	human,mouse		High+Lowthroughput	Vitamin C counteracts miR-302/367-induced reprogramming of human breast cancer cells and restores their invasive and proliferative capacity	否		mammary cancer	breast cancer cell	E_02_0436	Flow cytometry, real ‐ time PCR, Western blot	Overexpression of miR 302/367 cluster in MDA MB 231 and SK BR 3 breast cancer cells upregulated expression of miR 302/367 members and also some core pluripotency factors including OCT4A, SOX2 and NANOG, induced mesenchymal to epithelial transition, suppressed invasion, proliferation, and induced apoptosis in the both cell lines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Overexpression of miR 302/367 cluster in MDA MB 231 and SK BR 3 breast cancer cells upregulated expression of miR 302/367 members and also some core pluripotency factors including OCT4A, SOX2 and NANOG, induced mesenchymal to epithelial transition, suppressed invasion, proliferation, and induced apoptosis in the both cell lines.		Overexpression of miR 302/367 cluster in MDA MB 231 and SK BR 3 breast cancer cells upregulated expression of miR 302/367 members and also some core pluripotency factors including OCT4A, SOX2 and NANOG, induced mesenchymal to epithelial transition, suppressed invasion, proliferation, and induced apoptosis in the both cell lines.	Immunohistochemical staining	Overexpression of miR 302/367 cluster in MDA MB 231 and SK BR 3 breast cancer cells upregulated expression of miR 302/367 members and also some core pluripotency factors including OCT4A, SOX2 and NANOG, induced mesenchymal to epithelial transition, suppressed invasion, proliferation, and induced apoptosis in the both cell lines.			流式细胞术,real‐time PCR,westoon blot				SOX2
30190462	chr3	189628438	189630438	TP63	Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 	human		High+Lowthroughput	Co-activation of super-enhancer-driven CCAT1 by TP63 and SOX2 promotes squamous cancer progression	否		Squamous cell carcinomas (SCCs)	squamous cell	E_01_0731	qRT-PCR,weston blot,RNA-seq,plasmid transfection,ChIP-seq	Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 	Immunohistochemical staining	Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 	TP63		qRT-PCR,weston blot,RNA-seq,plasmid transfection,ChIP-seq	Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 			
30190462	chr3	181709340	181711340	SOX2	Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 	human		High+Lowthroughput	Co-activation of super-enhancer-driven CCAT1 by TP63 and SOX2 promotes squamous cancer progression	否		Squamous cell carcinomas (SCCs)	squamous cell	E_01_0731	qRT-PCR,weston blot,RNA-seq,plasmid transfection,ChIP-seq	Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 	Immunohistochemical staining	Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 	SOX2		qRT-PCR,weston blot,RNA-seq,plasmid transfection,ChIP-seq	Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 			
30190462	chr7	55016806	55018806	EGFR	Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 	human		High+Lowthroughput	Co-activation of super-enhancer-driven CCAT1 by TP63 and SOX2 promotes squamous cancer progression	否		Squamous cell carcinomas (SCCs)	squamous cell	E_01_0731	qRT-PCR,weston blot,RNA-seq,plasmid transfection,ChIP-seq	Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 	Immunohistochemical staining	Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 	EGFR		qRT-PCR,weston blot,RNA-seq,plasmid transfection,ChIP-seq	Here, epigenomic profilings of different types of SCCs reveal that TP63 and SOX2 cooperatively and lineage-specifically regulate long non-coding RNA (lncRNA) CCAT1 expression, through activation of its super-enhancers and promoter.Silencing of CCAT1 substantially reduces cellular growth both in vitro and in vivo, phenotyping the effect of inhibiting either TP63 or SOX2.                                                                                                                                                              ChIRP analysis shows that CCAT1 forms a complex with TP63 and SOX2, which regulates EGFR expression by binding to the super-enhancers of EGFR, thereby activating both MEK/ERK1/2 and PI3K/AKT signaling pathways. 			
30190126	chr17	49596074	49598074	SPOP	 Notably, SPOP inhibits NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity and its target genes expression via FADD. 	human		High+Lowthroughput	SPOP promotes FADD degradation and inhibits NF-κB activity in non-small cell lung cancer	否		Non small cell lung cancer	NSCLC cell	E_01_0732	Statistical analysis, Weston blot, RT qPCR	 Notably, SPOP inhibits NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity and its target genes expression via FADD. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 Notably, SPOP inhibits NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity and its target genes expression via FADD. 		 Notably, SPOP inhibits NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity and its target genes expression via FADD. 	Immunohistochemical staining	 Notably, SPOP inhibits NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity and its target genes expression via FADD. 			统计分析,weston blot,RT-qPCR				SPOP
30190126	chr11	70200700	70202700	FADD	 Notably, SPOP inhibits NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity and its target genes expression via FADD. 	human		High+Lowthroughput	SPOP promotes FADD degradation and inhibits NF-κB activity in non-small cell lung cancer	否		Non small cell lung cancer	NSCLC cell	E_01_0732	Statistical analysis, Weston blot, RT qPCR	 Notably, SPOP inhibits NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity and its target genes expression via FADD. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 Notably, SPOP inhibits NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity and its target genes expression via FADD. 		 Notably, SPOP inhibits NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity and its target genes expression via FADD. 	Immunohistochemical staining	 Notably, SPOP inhibits NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) activity and its target genes expression via FADD. 			统计分析,weston blot,RT-qPCR				FADD
30187766	chr9	117701087	117703087	TLR4	 Results: We identified significantly decreased STC1 expression in TLR4 knockout mouse lungs and primary lung endothelium isolated from TLR4 knockout mice. Overexpression of STC1 was associated with endothelial cytoprotection while decreased or insufficient expression was associated with increased oxidant-induced injury and death.	mouse,human		High+Lowthroughput	Endothelial Stanniocalcin 1 Maintains Mitochondrial Bioenergetics and Prevents Oxidant-Induced Lung Injury via Toll-Like Receptor 4	否		Acute lung injury (ALI)	endothelial cell	E_02_0437	RT-PCR, Weston blot, immunofluorescence light staining, gene knockdown	 Results: We identified significantly decreased STC1 expression in TLR4 knockout mouse lungs and primary lung endothelium isolated from TLR4 knockout mice. Overexpression of STC1 was associated with endothelial cytoprotection while decreased or insufficient expression was associated with increased oxidant-induced injury and death.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 Results: We identified significantly decreased STC1 expression in TLR4 knockout mouse lungs and primary lung endothelium isolated from TLR4 knockout mice. Overexpression of STC1 was associated with endothelial cytoprotection while decreased or insufficient expression was associated with increased oxidant-induced injury and death.		 Results: We identified significantly decreased STC1 expression in TLR4 knockout mouse lungs and primary lung endothelium isolated from TLR4 knockout mice. Overexpression of STC1 was associated with endothelial cytoprotection while decreased or insufficient expression was associated with increased oxidant-induced injury and death.	Immunohistochemical staining	 Results: We identified significantly decreased STC1 expression in TLR4 knockout mouse lungs and primary lung endothelium isolated from TLR4 knockout mice. Overexpression of STC1 was associated with endothelial cytoprotection while decreased or insufficient expression was associated with increased oxidant-induced injury and death.			RT-PCR,weston blot,免疫荧光光染色,基因敲降				TLR4
30187766	chr8	23839381	23841381	STC1	 Results: We identified significantly decreased STC1 expression in TLR4 knockout mouse lungs and primary lung endothelium isolated from TLR4 knockout mice. Overexpression of STC1 was associated with endothelial cytoprotection while decreased or insufficient expression was associated with increased oxidant-induced injury and death.	mouse,human		High+Lowthroughput	Endothelial Stanniocalcin 1 Maintains Mitochondrial Bioenergetics and Prevents Oxidant-Induced Lung Injury via Toll-Like Receptor 4	否		Acute lung injury (ALI)	endothelial cell	E_02_0437	RT-PCR, Weston blot, immunofluorescence light staining, gene knockdown	 Results: We identified significantly decreased STC1 expression in TLR4 knockout mouse lungs and primary lung endothelium isolated from TLR4 knockout mice. Overexpression of STC1 was associated with endothelial cytoprotection while decreased or insufficient expression was associated with increased oxidant-induced injury and death.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 Results: We identified significantly decreased STC1 expression in TLR4 knockout mouse lungs and primary lung endothelium isolated from TLR4 knockout mice. Overexpression of STC1 was associated with endothelial cytoprotection while decreased or insufficient expression was associated with increased oxidant-induced injury and death.		 Results: We identified significantly decreased STC1 expression in TLR4 knockout mouse lungs and primary lung endothelium isolated from TLR4 knockout mice. Overexpression of STC1 was associated with endothelial cytoprotection while decreased or insufficient expression was associated with increased oxidant-induced injury and death.	Immunohistochemical staining	 Results: We identified significantly decreased STC1 expression in TLR4 knockout mouse lungs and primary lung endothelium isolated from TLR4 knockout mice. Overexpression of STC1 was associated with endothelial cytoprotection while decreased or insufficient expression was associated with increased oxidant-induced injury and death.			RT-PCR,weston blot,免疫荧光光染色,基因敲降				STC1
30186385	chr7	148804832	148806832	EZH2	Additionally, predictions with TargetScan software indicated that the 3 -untranslated regions of enhancer of zeste homolog 2 (EZH2) and histone deacetylase (HDAC9) mRNAs are targeted by miR-101-3p. 	mouse,human		High+Lowthroughput	MicroRNA-101-3p inhibits proliferation in retinoblastoma cells by targeting EZH2 and HDAC9	否		Retinoblastoma	Y79 cell	E_02_0438	RT qPCR, Weston blot, MTT assay, flow cytometry, statistical analysis	Additionally, predictions with TargetScan software indicated that the 3 -untranslated regions of enhancer of zeste homolog 2 (EZH2) and histone deacetylase (HDAC9) mRNAs are targeted by miR-101-3p. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, predictions with TargetScan software indicated that the 3 -untranslated regions of enhancer of zeste homolog 2 (EZH2) and histone deacetylase (HDAC9) mRNAs are targeted by miR-101-3p. 		Additionally, predictions with TargetScan software indicated that the 3 -untranslated regions of enhancer of zeste homolog 2 (EZH2) and histone deacetylase (HDAC9) mRNAs are targeted by miR-101-3p. 	Immunohistochemical staining	Additionally, predictions with TargetScan software indicated that the 3 -untranslated regions of enhancer of zeste homolog 2 (EZH2) and histone deacetylase (HDAC9) mRNAs are targeted by miR-101-3p. 			RT-qPCR,weston blot,MTT assay,流式细胞术,统计分析				EZH2
30186385	chr7	18083932	18085932	HDAC9	Additionally, predictions with TargetScan software indicated that the 3 -untranslated regions of enhancer of zeste homolog 2 (EZH2) and histone deacetylase (HDAC9) mRNAs are targeted by miR-101-3p. 	mouse,human		High+Lowthroughput	MicroRNA-101-3p inhibits proliferation in retinoblastoma cells by targeting EZH2 and HDAC9	否		Retinoblastoma	Y79 cell	E_02_0438	RT qPCR, Weston blot, MTT assay, flow cytometry, statistical analysis	Additionally, predictions with TargetScan software indicated that the 3 -untranslated regions of enhancer of zeste homolog 2 (EZH2) and histone deacetylase (HDAC9) mRNAs are targeted by miR-101-3p. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, predictions with TargetScan software indicated that the 3 -untranslated regions of enhancer of zeste homolog 2 (EZH2) and histone deacetylase (HDAC9) mRNAs are targeted by miR-101-3p. 		Additionally, predictions with TargetScan software indicated that the 3 -untranslated regions of enhancer of zeste homolog 2 (EZH2) and histone deacetylase (HDAC9) mRNAs are targeted by miR-101-3p. 	Immunohistochemical staining	Additionally, predictions with TargetScan software indicated that the 3 -untranslated regions of enhancer of zeste homolog 2 (EZH2) and histone deacetylase (HDAC9) mRNAs are targeted by miR-101-3p. 			RT-qPCR,weston blot,MTT assay,流式细胞术,统计分析				HDAC9
30185805	chr6	124838893	124840893	Cd4	 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.	human,mouse		High+Lowthroughput	Stage-specific epigenetic regulation of CD4 expression by coordinated enhancer elements during T cell development	否			T cell	E_02_0439	Flow cytometry, statistical analysis, real time quantitative PCR	 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.		 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.	Immunohistochemical staining	 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.			流式细胞术,统计分析,Real-time quantitative PCR				Cd4
30185805	chr10	68557686	68559686	TET1	 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.	human,mouse		High+Lowthroughput	Stage-specific epigenetic regulation of CD4 expression by coordinated enhancer elements during T cell development	否			T cell	E_02_0439	Flow cytometry, statistical analysis, real time quantitative PCR	 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.		 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.	Immunohistochemical staining	 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.			流式细胞术,统计分析,Real-time quantitative PCR				TET1
30185805	chr2	73982554	73984554	TET3	 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.	human,mouse		High+Lowthroughput	Stage-specific epigenetic regulation of CD4 expression by coordinated enhancer elements during T cell development	否			T cell	E_02_0439	Flow cytometry, statistical analysis, real time quantitative PCR	 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.		 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.	Immunohistochemical staining	 Here we show that two stage-specific Cd4 cis-elements, the pre- viously characterized enhancer E4p and a novel enhancer E4m, coordinately promote Cd4 transcription in mature thymic MHC-II-specific T cells, in part through the canonical Wnt pathway.Specifically, E4p licenses E4m to orchestrate DNA demethylation by TET1 and TET3, which in turn poises the Cd4 locus for transcription in peripheral T cells.			流式细胞术,统计分析,Real-time quantitative PCR				TET3
30185787	chr6	124838963	124840963	Cd4	An intronic silencer, S4, in the Cd4 gene has been shown to be responsible for the helper-lineage-specific expression of CD4;	human		High+Lowthroughput	Runx-dependent and silencer-independent repression of a maturation enhancer in the Cd4 gene	否			T cell	E_01_0733	ATAC SEQ, chip SEQ, chip qPCR, quantitative RT-PCR, flow cytometry	An intronic silencer, S4, in the Cd4 gene has been shown to be responsible for the helper-lineage-specific expression of CD4;	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	An intronic silencer, S4, in the Cd4 gene has been shown to be responsible for the helper-lineage-specific expression of CD4;		An intronic silencer, S4, in the Cd4 gene has been shown to be responsible for the helper-lineage-specific expression of CD4;	Immunohistochemical staining	An intronic silencer, S4, in the Cd4 gene has been shown to be responsible for the helper-lineage-specific expression of CD4;			ATAC-Seq,ChIP-Seq,ChIP-qPCR ,Quantitative RT-PCR,流式细胞术				Cd4
30182035	chr2	60447469	60449469	BCL11A	In addition, BCL11A enhancer modification in mobilized CD34+ cells from patients with b-thalassemia major resulted in a readily detectable g-globin increase with a preferential increase in G-gamma, leading to an improved phenotype and, likely, a survival advantage for maturing erythroid cells after editing.	human		High+Lowthroughput	Disruption of the BCL11A Erythroid Enhancer Reactivates Fetal Hemoglobin in Erythroid Cells of Patients with β-Thalassemia Major	否		B-globin thalassemia	progenitor cell	E_01_0734	Miseq deep sequencing, QRT PCR, immunofluorescence staining	In addition, BCL11A enhancer modification in mobilized CD34+ cells from patients with b-thalassemia major resulted in a readily detectable g-globin increase with a preferential increase in G-gamma, leading to an improved phenotype and, likely, a survival advantage for maturing erythroid cells after editing.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, BCL11A enhancer modification in mobilized CD34+ cells from patients with b-thalassemia major resulted in a readily detectable g-globin increase with a preferential increase in G-gamma, leading to an improved phenotype and, likely, a survival advantage for maturing erythroid cells after editing.		In addition, BCL11A enhancer modification in mobilized CD34+ cells from patients with b-thalassemia major resulted in a readily detectable g-globin increase with a preferential increase in G-gamma, leading to an improved phenotype and, likely, a survival advantage for maturing erythroid cells after editing.	Immunohistochemical staining	In addition, BCL11A enhancer modification in mobilized CD34+ cells from patients with b-thalassemia major resulted in a readily detectable g-globin increase with a preferential increase in G-gamma, leading to an improved phenotype and, likely, a survival advantage for maturing erythroid cells after editing.			MiSeq Deep Sequencing,qRT-PCR,免疫荧光染色				BCL11A
30176898	chr22	39517104	39519104	ATF4	Importantly, CA activated endoplasmic reticulum (ER) stress-associated two pro-apoptotic signaling pathways, as evidenced by increased protein levels of typical ER stress markers including IRE-1/ASK1/JNK and PERK/eIF2α/ATF4/CHOP. Meanwhile, CHOP induced expression increased Tribbles 3 (TRIB3) level, which lead to AKT inactivation and PCa cell death.	human		High+Lowthroughput	Corosolic acid, a natural triterpenoid, induces ER stress-dependent apoptosis in human castration resistant prostate cancer cells via activation of IRE-1/JNK, PERK/CHOP and TRIB3	否		Prostate cancer (CRPC)		E_01_0735	Real time PCR, Western blot, immunofluorescence light staining, gene transfection, statistical analysis, MTT assay, flow cytometry	Importantly, CA activated endoplasmic reticulum (ER) stress-associated two pro-apoptotic signaling pathways, as evidenced by increased protein levels of typical ER stress markers including IRE-1/ASK1/JNK and PERK/eIF2α/ATF4/CHOP. Meanwhile, CHOP induced expression increased Tribbles 3 (TRIB3) level, which lead to AKT inactivation and PCa cell death.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Importantly, CA activated endoplasmic reticulum (ER) stress-associated two pro-apoptotic signaling pathways, as evidenced by increased protein levels of typical ER stress markers including IRE-1/ASK1/JNK and PERK/eIF2α/ATF4/CHOP. Meanwhile, CHOP induced expression increased Tribbles 3 (TRIB3) level, which lead to AKT inactivation and PCa cell death.	Immunohistochemical staining	Importantly, CA activated endoplasmic reticulum (ER) stress-associated two pro-apoptotic signaling pathways, as evidenced by increased protein levels of typical ER stress markers including IRE-1/ASK1/JNK and PERK/eIF2α/ATF4/CHOP. Meanwhile, CHOP induced expression increased Tribbles 3 (TRIB3) level, which lead to AKT inactivation and PCa cell death.	ATF4		Real-time PCR,western blot,免疫荧光光染色,基因转染,统计分析,MTT法,流式细胞术	Importantly, CA activated endoplasmic reticulum (ER) stress-associated two pro-apoptotic signaling pathways, as evidenced by increased protein levels of typical ER stress markers including IRE-1/ASK1/JNK and PERK/eIF2α/ATF4/CHOP. Meanwhile, CHOP induced expression increased Tribbles 3 (TRIB3) level, which lead to AKT inactivation and PCa cell death.			
30176898	chr20	360115	362115	TRIB3	Importantly, CA activated endoplasmic reticulum (ER) stress-associated two pro-apoptotic signaling pathways, as evidenced by increased protein levels of typical ER stress markers including IRE-1/ASK1/JNK and PERK/eIF2α/ATF4/CHOP. Meanwhile, CHOP induced expression increased Tribbles 3 (TRIB3) level, which lead to AKT inactivation and PCa cell death.	human		High+Lowthroughput	Corosolic acid, a natural triterpenoid, induces ER stress-dependent apoptosis in human castration resistant prostate cancer cells via activation of IRE-1/JNK, PERK/CHOP and TRIB3	否		Prostate cancer (CRPC)		E_01_0735	Real time PCR, Western blot, immunofluorescence light staining, gene transfection, statistical analysis, MTT assay, flow cytometry	Importantly, CA activated endoplasmic reticulum (ER) stress-associated two pro-apoptotic signaling pathways, as evidenced by increased protein levels of typical ER stress markers including IRE-1/ASK1/JNK and PERK/eIF2α/ATF4/CHOP. Meanwhile, CHOP induced expression increased Tribbles 3 (TRIB3) level, which lead to AKT inactivation and PCa cell death.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Importantly, CA activated endoplasmic reticulum (ER) stress-associated two pro-apoptotic signaling pathways, as evidenced by increased protein levels of typical ER stress markers including IRE-1/ASK1/JNK and PERK/eIF2α/ATF4/CHOP. Meanwhile, CHOP induced expression increased Tribbles 3 (TRIB3) level, which lead to AKT inactivation and PCa cell death.		Importantly, CA activated endoplasmic reticulum (ER) stress-associated two pro-apoptotic signaling pathways, as evidenced by increased protein levels of typical ER stress markers including IRE-1/ASK1/JNK and PERK/eIF2α/ATF4/CHOP. Meanwhile, CHOP induced expression increased Tribbles 3 (TRIB3) level, which lead to AKT inactivation and PCa cell death.	Immunohistochemical staining	Importantly, CA activated endoplasmic reticulum (ER) stress-associated two pro-apoptotic signaling pathways, as evidenced by increased protein levels of typical ER stress markers including IRE-1/ASK1/JNK and PERK/eIF2α/ATF4/CHOP. Meanwhile, CHOP induced expression increased Tribbles 3 (TRIB3) level, which lead to AKT inactivation and PCa cell death.			Real-time PCR,western blot,免疫荧光光染色,基因转染,统计分析,MTT法,流式细胞术				TRIB3
30176159	chr9	36830723	36832723	PAX5	Epstein-Barr virus (EBV) expresses an abundant nuclear noncoding RNA called EBER2, which interacts with and acts as a guide RNA for the host transcription factor PAX5.	mouse		High+Lowthroughput	Identification of host RNAs that interact with EBV noncoding RNA EBER2	否				E_02_0440	qRT-PCR,RNA-seq,ChIP-seq	Epstein-Barr virus (EBV) expresses an abundant nuclear noncoding RNA called EBER2, which interacts with and acts as a guide RNA for the host transcription factor PAX5.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Epstein-Barr virus (EBV) expresses an abundant nuclear noncoding RNA called EBER2, which interacts with and acts as a guide RNA for the host transcription factor PAX5.		Epstein-Barr virus (EBV) expresses an abundant nuclear noncoding RNA called EBER2, which interacts with and acts as a guide RNA for the host transcription factor PAX5.	Immunohistochemical staining	Epstein-Barr virus (EBV) expresses an abundant nuclear noncoding RNA called EBER2, which interacts with and acts as a guide RNA for the host transcription factor PAX5.			qRT-PCR,RNA-seq,ChIP-seq				PAX5
30174670	chr20	38343789	38345789	LBP	LBP can raise both from IVD-induced damage of dorsal root ganglions (DRG) and from nociceptive stimulation of DRGs by molecules released from the degenerated IVD (7 9). Indeed, severity of DDD correlates with increased expression of inflammation mediators/markers in the IVD tissue (10), including interleukin-1 beta (IL-1β) (11), tumor necrosis factor-alpha (TNF-α) (12), interleukin-6 (IL-6), and interleukin-8 (IL-8) (13).	human		High+Lowthroughput	p38 MAPK Facilitates Crosstalk Between Endoplasmic Reticulum Stress and IL-6 Release in the Intervertebral Disc	否		Degenerative disc disease, inflammation, neurodegenerative disease, type 2 diabetes, rheumatoid arthritis		E_01_0736	Enzyme-Linked Immunosorbent Assay,Metabolic Activity Assay (MTT),RT-qPCR 	LBP can raise both from IVD-induced damage of dorsal root ganglions (DRG) and from nociceptive stimulation of DRGs by molecules released from the degenerated IVD (7 9). Indeed, severity of DDD correlates with increased expression of inflammation mediators/markers in the IVD tissue (10), including interleukin-1 beta (IL-1β) (11), tumor necrosis factor-alpha (TNF-α) (12), interleukin-6 (IL-6), and interleukin-8 (IL-8) (13).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	LBP can raise both from IVD-induced damage of dorsal root ganglions (DRG) and from nociceptive stimulation of DRGs by molecules released from the degenerated IVD (7 9). Indeed, severity of DDD correlates with increased expression of inflammation mediators/markers in the IVD tissue (10), including interleukin-1 beta (IL-1β) (11), tumor necrosis factor-alpha (TNF-α) (12), interleukin-6 (IL-6), and interleukin-8 (IL-8) (13).		LBP can raise both from IVD-induced damage of dorsal root ganglions (DRG) and from nociceptive stimulation of DRGs by molecules released from the degenerated IVD (7 9). Indeed, severity of DDD correlates with increased expression of inflammation mediators/markers in the IVD tissue (10), including interleukin-1 beta (IL-1β) (11), tumor necrosis factor-alpha (TNF-α) (12), interleukin-6 (IL-6), and interleukin-8 (IL-8) (13).	Immunohistochemical staining	LBP can raise both from IVD-induced damage of dorsal root ganglions (DRG) and from nociceptive stimulation of DRGs by molecules released from the degenerated IVD (7 9). Indeed, severity of DDD correlates with increased expression of inflammation mediators/markers in the IVD tissue (10), including interleukin-1 beta (IL-1β) (11), tumor necrosis factor-alpha (TNF-α) (12), interleukin-6 (IL-6), and interleukin-8 (IL-8) (13).			Enzyme-Linked Immunosorbent Assay,Metabolic Activity Assay (MTT),RT-qPCR 				LBP
30174670	chr15	40402996	40404996	IVD	LBP can raise both from IVD-induced damage of dorsal root ganglions (DRG) and from nociceptive stimulation of DRGs by molecules released from the degenerated IVD (7 9). Indeed, severity of DDD correlates with increased expression of inflammation mediators/markers in the IVD tissue (10), including interleukin-1 beta (IL-1β) (11), tumor necrosis factor-alpha (TNF-α) (12), interleukin-6 (IL-6), and interleukin-8 (IL-8) (13).	human		High+Lowthroughput	p38 MAPK Facilitates Crosstalk Between Endoplasmic Reticulum Stress and IL-6 Release in the Intervertebral Disc	否		Degenerative disc disease, inflammation, neurodegenerative disease, type 2 diabetes, rheumatoid arthritis		E_01_0736	Enzyme-Linked Immunosorbent Assay,Metabolic Activity Assay (MTT),RT-qPCR 	LBP can raise both from IVD-induced damage of dorsal root ganglions (DRG) and from nociceptive stimulation of DRGs by molecules released from the degenerated IVD (7 9). Indeed, severity of DDD correlates with increased expression of inflammation mediators/markers in the IVD tissue (10), including interleukin-1 beta (IL-1β) (11), tumor necrosis factor-alpha (TNF-α) (12), interleukin-6 (IL-6), and interleukin-8 (IL-8) (13).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	LBP can raise both from IVD-induced damage of dorsal root ganglions (DRG) and from nociceptive stimulation of DRGs by molecules released from the degenerated IVD (7 9). Indeed, severity of DDD correlates with increased expression of inflammation mediators/markers in the IVD tissue (10), including interleukin-1 beta (IL-1β) (11), tumor necrosis factor-alpha (TNF-α) (12), interleukin-6 (IL-6), and interleukin-8 (IL-8) (13).		LBP can raise both from IVD-induced damage of dorsal root ganglions (DRG) and from nociceptive stimulation of DRGs by molecules released from the degenerated IVD (7 9). Indeed, severity of DDD correlates with increased expression of inflammation mediators/markers in the IVD tissue (10), including interleukin-1 beta (IL-1β) (11), tumor necrosis factor-alpha (TNF-α) (12), interleukin-6 (IL-6), and interleukin-8 (IL-8) (13).	Immunohistochemical staining	LBP can raise both from IVD-induced damage of dorsal root ganglions (DRG) and from nociceptive stimulation of DRGs by molecules released from the degenerated IVD (7 9). Indeed, severity of DDD correlates with increased expression of inflammation mediators/markers in the IVD tissue (10), including interleukin-1 beta (IL-1β) (11), tumor necrosis factor-alpha (TNF-α) (12), interleukin-6 (IL-6), and interleukin-8 (IL-8) (13).			Enzyme-Linked Immunosorbent Assay,Metabolic Activity Assay (MTT),RT-qPCR 				IVD
30173509	chr10	88950916	88952916	FAS	The antibodies for phospho-AMP-activated protein kinase alpha (p-AMPKα,73 Thr 172), AMPKα, phospho-acetyl-CoA carboxylase (p-ACC, Ser 79), ACC, fatty acid74 synthase (FAS), elongation of very long-chain fatty acids protein 6 (ELOVL 6), stearoyl-CoA75 desaturase-1 (SCD1), peroxisome proliferator-activated receptor gamma (PPAR-γ),76 CCAAT/enhancer-binding protein alpha (C/EBP-α), TATA-binding protein (TBP), and β-77 actin were from Cell Signaling Technology (Danvers, MA, USA).	mouse,human		High+Lowthroughput	Antiobesity Effect of Tricin, a Methylated Cereal Flavone, in High-Fat-Diet-Induced Obese Mice	否		Obesity, diabetes, hypertension, CVD	fat cell	E_02_0441	Statistical analysis, Weston blot	The antibodies for phospho-AMP-activated protein kinase alpha (p-AMPKα,73 Thr 172), AMPKα, phospho-acetyl-CoA carboxylase (p-ACC, Ser 79), ACC, fatty acid74 synthase (FAS), elongation of very long-chain fatty acids protein 6 (ELOVL 6), stearoyl-CoA75 desaturase-1 (SCD1), peroxisome proliferator-activated receptor gamma (PPAR-γ),76 CCAAT/enhancer-binding protein alpha (C/EBP-α), TATA-binding protein (TBP), and β-77 actin were from Cell Signaling Technology (Danvers, MA, USA).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The antibodies for phospho-AMP-activated protein kinase alpha (p-AMPKα,73 Thr 172), AMPKα, phospho-acetyl-CoA carboxylase (p-ACC, Ser 79), ACC, fatty acid74 synthase (FAS), elongation of very long-chain fatty acids protein 6 (ELOVL 6), stearoyl-CoA75 desaturase-1 (SCD1), peroxisome proliferator-activated receptor gamma (PPAR-γ),76 CCAAT/enhancer-binding protein alpha (C/EBP-α), TATA-binding protein (TBP), and β-77 actin were from Cell Signaling Technology (Danvers, MA, USA).		The antibodies for phospho-AMP-activated protein kinase alpha (p-AMPKα,73 Thr 172), AMPKα, phospho-acetyl-CoA carboxylase (p-ACC, Ser 79), ACC, fatty acid74 synthase (FAS), elongation of very long-chain fatty acids protein 6 (ELOVL 6), stearoyl-CoA75 desaturase-1 (SCD1), peroxisome proliferator-activated receptor gamma (PPAR-γ),76 CCAAT/enhancer-binding protein alpha (C/EBP-α), TATA-binding protein (TBP), and β-77 actin were from Cell Signaling Technology (Danvers, MA, USA).	Immunohistochemical staining	The antibodies for phospho-AMP-activated protein kinase alpha (p-AMPKα,73 Thr 172), AMPKα, phospho-acetyl-CoA carboxylase (p-ACC, Ser 79), ACC, fatty acid74 synthase (FAS), elongation of very long-chain fatty acids protein 6 (ELOVL 6), stearoyl-CoA75 desaturase-1 (SCD1), peroxisome proliferator-activated receptor gamma (PPAR-γ),76 CCAAT/enhancer-binding protein alpha (C/EBP-α), TATA-binding protein (TBP), and β-77 actin were from Cell Signaling Technology (Danvers, MA, USA).			统计分析,weston blot				FAS
30173509	chr10	112147016	112149016	GPAM	The antibodies for phospho-AMP-activated protein kinase alpha (p-AMPKα,73 Thr 172), AMPKα, phospho-acetyl-CoA carboxylase (p-ACC, Ser 79), ACC, fatty acid74 synthase (FAS), elongation of very long-chain fatty acids protein 6 (ELOVL 6), stearoyl-CoA75 desaturase-1 (SCD1), peroxisome proliferator-activated receptor gamma (PPAR-γ),76 CCAAT/enhancer-binding protein alpha (C/EBP-α), TATA-binding protein (TBP), and β-77 actin were from Cell Signaling Technology (Danvers, MA, USA).	mouse,human		High+Lowthroughput	Antiobesity Effect of Tricin, a Methylated Cereal Flavone, in High-Fat-Diet-Induced Obese Mice	否		Obesity, diabetes, hypertension, CVD	fat cell	E_02_0441	Statistical analysis, Weston blot	The antibodies for phospho-AMP-activated protein kinase alpha (p-AMPKα,73 Thr 172), AMPKα, phospho-acetyl-CoA carboxylase (p-ACC, Ser 79), ACC, fatty acid74 synthase (FAS), elongation of very long-chain fatty acids protein 6 (ELOVL 6), stearoyl-CoA75 desaturase-1 (SCD1), peroxisome proliferator-activated receptor gamma (PPAR-γ),76 CCAAT/enhancer-binding protein alpha (C/EBP-α), TATA-binding protein (TBP), and β-77 actin were from Cell Signaling Technology (Danvers, MA, USA).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The antibodies for phospho-AMP-activated protein kinase alpha (p-AMPKα,73 Thr 172), AMPKα, phospho-acetyl-CoA carboxylase (p-ACC, Ser 79), ACC, fatty acid74 synthase (FAS), elongation of very long-chain fatty acids protein 6 (ELOVL 6), stearoyl-CoA75 desaturase-1 (SCD1), peroxisome proliferator-activated receptor gamma (PPAR-γ),76 CCAAT/enhancer-binding protein alpha (C/EBP-α), TATA-binding protein (TBP), and β-77 actin were from Cell Signaling Technology (Danvers, MA, USA).		The antibodies for phospho-AMP-activated protein kinase alpha (p-AMPKα,73 Thr 172), AMPKα, phospho-acetyl-CoA carboxylase (p-ACC, Ser 79), ACC, fatty acid74 synthase (FAS), elongation of very long-chain fatty acids protein 6 (ELOVL 6), stearoyl-CoA75 desaturase-1 (SCD1), peroxisome proliferator-activated receptor gamma (PPAR-γ),76 CCAAT/enhancer-binding protein alpha (C/EBP-α), TATA-binding protein (TBP), and β-77 actin were from Cell Signaling Technology (Danvers, MA, USA).	Immunohistochemical staining	The antibodies for phospho-AMP-activated protein kinase alpha (p-AMPKα,73 Thr 172), AMPKα, phospho-acetyl-CoA carboxylase (p-ACC, Ser 79), ACC, fatty acid74 synthase (FAS), elongation of very long-chain fatty acids protein 6 (ELOVL 6), stearoyl-CoA75 desaturase-1 (SCD1), peroxisome proliferator-activated receptor gamma (PPAR-γ),76 CCAAT/enhancer-binding protein alpha (C/EBP-α), TATA-binding protein (TBP), and β-77 actin were from Cell Signaling Technology (Danvers, MA, USA).			统计分析,weston blot				GPAM
30172905	chr19	5555467	5557467	TINCR	As we know, Terminal differentiation-induced ncRNA (TINCR) is required in somatic tissue differentiation.	human	adipose tissue	High+Lowthroughput	LncRNA TINCR/miR-31-5p/C/EBP-α feedback loop modulates the adipogenic differentiation process in human adipose tissue-derived mesenchymal stem cells	否		Obesity	mesenchymal stem cell	E_01_0737	Real-time PC,RNA Immunoprecipitation (RIP), Chromatin immunoprecipitation (ChIP),weston blot	As we know, Terminal differentiation-induced ncRNA (TINCR) is required in somatic tissue differentiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	As we know, Terminal differentiation-induced ncRNA (TINCR) is required in somatic tissue differentiation.		As we know, Terminal differentiation-induced ncRNA (TINCR) is required in somatic tissue differentiation.	Immunohistochemical staining	As we know, Terminal differentiation-induced ncRNA (TINCR) is required in somatic tissue differentiation.			Real-time PC,RNA Immunoprecipitation (RIP), Chromatin immunoprecipitation (ChIP),weston blot				TINCR
30170702	chr9	81580913	81582913	TLE1	5 Recently, IHC labelling for the transducin-like enhancer of split 1 (TLE1) has been proposed as a marker for diagnosis of synovial sarcoma.	human		High+Lowthroughput	Pleural malignant mesothelioma versus pleuropulmonary synovial sarcoma: a clinicopathological study of 22 cases with molecular analysis and survival data	否		Malignant neoplasm, spindle cell carcinoma of the lung		E_01_0738	RT-PCR, immunofluorescence light staining, fluorescence in situ hybridization (FISH)	5 Recently, IHC labelling for the transducin-like enhancer of split 1 (TLE1) has been proposed as a marker for diagnosis of synovial sarcoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			5 Recently, IHC labelling for the transducin-like enhancer of split 1 (TLE1) has been proposed as a marker for diagnosis of synovial sarcoma.	Immunohistochemical staining	5 Recently, IHC labelling for the transducin-like enhancer of split 1 (TLE1) has been proposed as a marker for diagnosis of synovial sarcoma.	TLE1		RT-PCR,免疫荧光光染色,荧光原位杂交(FISH)	5 Recently, IHC labelling for the transducin-like enhancer of split 1 (TLE1) has been proposed as a marker for diagnosis of synovial sarcoma.			
30169732	chr7	16913181	16915181	AHR	Using MC-deficient KitW-sh/W-sh mice and Mas-TRECK mice, which carries a diphtheria toxin (DT)-induced MC deletion system based on il4 enhancer elements, we demonstrate here that MCs are involved in the induction of house dust mite (HDM)-induced AHR. 	human,mouse		High+Lowthroughput	Allergin-1 on mast cells suppresses house dust mite-induced airway hyperresponsiveness in mice	否		asthma	mast cell	E_02_0442	Degranulation assay, flow cytometry, ELISA	Using MC-deficient KitW-sh/W-sh mice and Mas-TRECK mice, which carries a diphtheria toxin (DT)-induced MC deletion system based on il4 enhancer elements, we demonstrate here that MCs are involved in the induction of house dust mite (HDM)-induced AHR. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Using MC-deficient KitW-sh/W-sh mice and Mas-TRECK mice, which carries a diphtheria toxin (DT)-induced MC deletion system based on il4 enhancer elements, we demonstrate here that MCs are involved in the induction of house dust mite (HDM)-induced AHR. 		Using MC-deficient KitW-sh/W-sh mice and Mas-TRECK mice, which carries a diphtheria toxin (DT)-induced MC deletion system based on il4 enhancer elements, we demonstrate here that MCs are involved in the induction of house dust mite (HDM)-induced AHR. 	Immunohistochemical staining	Using MC-deficient KitW-sh/W-sh mice and Mas-TRECK mice, which carries a diphtheria toxin (DT)-induced MC deletion system based on il4 enhancer elements, we demonstrate here that MCs are involved in the induction of house dust mite (HDM)-induced AHR. 			Degranulation assay,流式细胞术,ELISA法				AHR
30168706	chr5	102751294	102753294	PAM	 In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. 	human		High+Lowthroughput	Fenoprofen-An Old Drug Rediscovered as a Biased Allosteric Enhancer for Melanocortin Receptors	否		Obesity, chronic inflammation	pigment cell	E_01_0739	Western blot, statistical analysis	 In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			 In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. 	Immunohistochemical staining	 In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. 	MYCBP2		western blot,统计分析	 In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations. 			
30168706	chr16	89909594	89911594	MC1R	In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations.                                                                                                  Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8.	human		High+Lowthroughput	Fenoprofen-An Old Drug Rediscovered as a Biased Allosteric Enhancer for Melanocortin Receptors	否		Obesity, chronic inflammation	HEK293T	E_01_0739	Western blot, statistical analysis	In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations.                                                                                                  Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations.                                                                                                  Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8.		In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations.                                                                                                  Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8.	Immunohistochemical staining	In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations.                                                                                                  Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8.			western blot,统计分析				MC1R
30168706	chr18	13879155	13881155	MC2R	In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations.                                                                                                  Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8.	human		High+Lowthroughput	Fenoprofen-An Old Drug Rediscovered as a Biased Allosteric Enhancer for Melanocortin Receptors	否		Obesity, chronic inflammation	HEK293T	E_01_0739	Western blot, statistical analysis	In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations.                                                                                                  Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations.                                                                                                  Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8.	Immunohistochemical staining	In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations.                                                                                                  Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8.	MC2R		western blot,统计分析	In addition, fenoprofen induced biased signaling at MC3-5R, as it selectively31 activated ERK1/2 cascade but not the canonical cAMP signaling. Notably, fenoprofen32 stimulated biased signaling at MC3-5R, but not at MC1R, hence acting selectively33 among this highly conserved family of receptors. Moreover, PAM activity and biased34 signaling induced by fenoprofen were observed not only at wild-type but also at35 naturally occurring mutant MC3Rs, suggesting that this biased allosteric enhancer36 action might constitute as novel therapeutic opportunity for obese patients harboring37 these mutations.                                                                                                  Extensive studies spanning87 decades have elucidated well-established functions of melanocortins mediated by cell88 surface receptors named MC1R (MSH receptor), MC2R (ACTH receptor), MC3R and89 MC4R (neural MCRs), and MC5R 7, 8.			
30166330	chr13	83649673	83651673	Mef2c	Tbx1 occupies the anterior heart field (AHF) enhancer of the Mef2c gene, which encodes a key cardiac differentiation transcription factor.	human,mouse		High+Lowthroughput	Tbx1 represses Mef2c gene expression and is correlated with histone 3 deacetylation of the anterior heart field enhancer	否		22q11.2 deletion syndrome	myoblast cell	E_02_0443	Immunofluorescence and alkaline phosphatase activity assay, QRT PCR, CO IP, statistical analysis	Tbx1 occupies the anterior heart field (AHF) enhancer of the Mef2c gene, which encodes a key cardiac differentiation transcription factor.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Tbx1 occupies the anterior heart field (AHF) enhancer of the Mef2c gene, which encodes a key cardiac differentiation transcription factor.		Tbx1 occupies the anterior heart field (AHF) enhancer of the Mef2c gene, which encodes a key cardiac differentiation transcription factor.	Immunohistochemical staining	Tbx1 occupies the anterior heart field (AHF) enhancer of the Mef2c gene, which encodes a key cardiac differentiation transcription factor.			Immunofluorescence and alkaline phosphatase activity assay,qRT-PCR,Co-IP,统计分析				Mef2c
30166330	chr16	18397004	18399004	Tbx1	Tbx1 occupies the anterior heart field (AHF) enhancer of the Mef2c gene, which encodes a key cardiac differentiation transcription factor.	human,mouse		High+Lowthroughput	Tbx1 represses Mef2c gene expression and is correlated with histone 3 deacetylation of the anterior heart field enhancer	否		22q11.2 deletion syndrome	myoblast cell	E_02_0443	Immunofluorescence and alkaline phosphatase activity assay, QRT PCR, CO IP, statistical analysis	Tbx1 occupies the anterior heart field (AHF) enhancer of the Mef2c gene, which encodes a key cardiac differentiation transcription factor.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Tbx1 occupies the anterior heart field (AHF) enhancer of the Mef2c gene, which encodes a key cardiac differentiation transcription factor.		Tbx1 occupies the anterior heart field (AHF) enhancer of the Mef2c gene, which encodes a key cardiac differentiation transcription factor.	Immunohistochemical staining	Tbx1 occupies the anterior heart field (AHF) enhancer of the Mef2c gene, which encodes a key cardiac differentiation transcription factor.			Immunofluorescence and alkaline phosphatase activity assay,qRT-PCR,Co-IP,统计分析				Tbx1
30165902	chr13	109749894	109751894	IRS2	hMSCs were transfected by miR-431 or small interfering RNA (siRNA) for insulin receptor substance 2 (IRS2).	human		High+Lowthroughput	miR-431 inhibits adipogenic differentiation of human bone marrow-derived mesenchymal stem cells via targeting insulin receptor substance 2	否		Type 2 diabetes, adipocyte cancer	mesenchymal stem cell	E_01_0740	qRT-PCR,weston blot	hMSCs were transfected by miR-431 or small interfering RNA (siRNA) for insulin receptor substance 2 (IRS2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	hMSCs were transfected by miR-431 or small interfering RNA (siRNA) for insulin receptor substance 2 (IRS2).		hMSCs were transfected by miR-431 or small interfering RNA (siRNA) for insulin receptor substance 2 (IRS2).	Immunohistochemical staining	hMSCs were transfected by miR-431 or small interfering RNA (siRNA) for insulin receptor substance 2 (IRS2).			qRT-PCR,weston blot				IRS2
30161129	chr3	123607146	123609146	MYLK	We previously reported that MYLKP1, the pseudogene of MYLK that encodes myosin light chain kinase (MLCK), is highly expressed in lung and colon cancer cell lines and tissues but not in normal lung or colon.	human		High+Lowthroughput	Single nucleotide polymorphisms in the MYLKP1 pseudogene are associated with increased colon cancer risk in African Americans	是		Colon cancer, lung cancer	Colon cell	E_01_0741	MYLKP1 luciferase assay,PCR differential detection	We previously reported that MYLKP1, the pseudogene of MYLK that encodes myosin light chain kinase (MLCK), is highly expressed in lung and colon cancer cell lines and tissues but not in normal lung or colon.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We previously reported that MYLKP1, the pseudogene of MYLK that encodes myosin light chain kinase (MLCK), is highly expressed in lung and colon cancer cell lines and tissues but not in normal lung or colon.		We previously reported that MYLKP1, the pseudogene of MYLK that encodes myosin light chain kinase (MLCK), is highly expressed in lung and colon cancer cell lines and tissues but not in normal lung or colon.	Immunohistochemical staining	We previously reported that MYLKP1, the pseudogene of MYLK that encodes myosin light chain kinase (MLCK), is highly expressed in lung and colon cancer cell lines and tissues but not in normal lung or colon.			MYLKP1 luciferase assay,PCR differential detection				MYLK
30160785	chr6	43168442	43170442	SRF	The synergistic apoptosis and regression of tumor growth were also observed in xenograft tumors when SRF and TRAIL were administered to tumor-bearing mice. 	human,mouse		High+Lowthroughput	Ferroptosis-inducing agents enhance TRAIL-induced apoptosis through upregulation of death receptor 5	否		Colon cancer	LS174T cell	E_02_0444	Weston blot, immunofluorescence light staining, statistical analysis	The synergistic apoptosis and regression of tumor growth were also observed in xenograft tumors when SRF and TRAIL were administered to tumor-bearing mice. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The synergistic apoptosis and regression of tumor growth were also observed in xenograft tumors when SRF and TRAIL were administered to tumor-bearing mice. 		The synergistic apoptosis and regression of tumor growth were also observed in xenograft tumors when SRF and TRAIL were administered to tumor-bearing mice. 	Immunohistochemical staining	The synergistic apoptosis and regression of tumor growth were also observed in xenograft tumors when SRF and TRAIL were administered to tumor-bearing mice. 			weston blot,免疫荧光光染色,统计分析				SRF
30158339	chr4	70515658	70517658	AMTN	AMTN-deficient mice have a hypo- mineralized inner enamel and structural defects in the outer enamel due to delayed expression of kallikrein-4 (8). During JE regeneration after gingivectomy, ODAM is first expressed at the leading edge of the wound and AMTN expression appears later, suggesting ODAM and AMTN have coordinated tasks at the cell-tooth interface (9). AMTN can promote hydroxyapatite mineralizati.	mouse		High+Lowthroughput	IL-1β and TNF-α regulate mouse amelotin gene transcription in gingival epithelial cells	否		tumour	ameloblast	E_02_0445	Real time polymerase chain reaction (PCR), Weston blot, luciferase assays, gel shift assays, chromatin immunoprecipitation (chip) assays, statistical analysis	AMTN-deficient mice have a hypo- mineralized inner enamel and structural defects in the outer enamel due to delayed expression of kallikrein-4 (8). During JE regeneration after gingivectomy, ODAM is first expressed at the leading edge of the wound and AMTN expression appears later, suggesting ODAM and AMTN have coordinated tasks at the cell-tooth interface (9). AMTN can promote hydroxyapatite mineralizati.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	AMTN-deficient mice have a hypo- mineralized inner enamel and structural defects in the outer enamel due to delayed expression of kallikrein-4 (8). During JE regeneration after gingivectomy, ODAM is first expressed at the leading edge of the wound and AMTN expression appears later, suggesting ODAM and AMTN have coordinated tasks at the cell-tooth interface (9). AMTN can promote hydroxyapatite mineralizati.		AMTN-deficient mice have a hypo- mineralized inner enamel and structural defects in the outer enamel due to delayed expression of kallikrein-4 (8). During JE regeneration after gingivectomy, ODAM is first expressed at the leading edge of the wound and AMTN expression appears later, suggesting ODAM and AMTN have coordinated tasks at the cell-tooth interface (9). AMTN can promote hydroxyapatite mineralizati.	Immunohistochemical staining	AMTN-deficient mice have a hypo- mineralized inner enamel and structural defects in the outer enamel due to delayed expression of kallikrein-4 (8). During JE regeneration after gingivectomy, ODAM is first expressed at the leading edge of the wound and AMTN expression appears later, suggesting ODAM and AMTN have coordinated tasks at the cell-tooth interface (9). AMTN can promote hydroxyapatite mineralizati.			Real-time polymerase chain reaction (PCR),weston blot,Luciferase assays,Gel shift assays,Chromatin immunoprecipitation (ChIP) assays,统计分析				AMTN
30158147	chr19	47816826	47818826	CRX	Cone-rod homeobox (CRX) is a paired-like homeodomain transcription factor (TF) and a master regulator of photoreceptor development in vertebrates. 	mouse		High+Lowthroughput	A massively parallel reporter assay reveals context-dependent activity of homeodomain binding sites in vivo	否			B cell	E_02_0446	PCR,ChIP-seq,CRE-seq assay	Cone-rod homeobox (CRX) is a paired-like homeodomain transcription factor (TF) and a master regulator of photoreceptor development in vertebrates. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cone-rod homeobox (CRX) is a paired-like homeodomain transcription factor (TF) and a master regulator of photoreceptor development in vertebrates. 		Cone-rod homeobox (CRX) is a paired-like homeodomain transcription factor (TF) and a master regulator of photoreceptor development in vertebrates. 	Immunohistochemical staining	Cone-rod homeobox (CRX) is a paired-like homeodomain transcription factor (TF) and a master regulator of photoreceptor development in vertebrates. 			PCR,ChIP-seq,CRE-seq assay				CRX
30158147	chr3	133743373	133745373	TF	Cone-rod homeobox (CRX) is a paired-like homeodomain transcription factor (TF) and a master regulator of photoreceptor development in vertebrates. 	mouse		High+Lowthroughput	A massively parallel reporter assay reveals context-dependent activity of homeodomain binding sites in vivo	否			B cell	E_02_0446	PCR,ChIP-seq,CRE-seq assay	Cone-rod homeobox (CRX) is a paired-like homeodomain transcription factor (TF) and a master regulator of photoreceptor development in vertebrates. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cone-rod homeobox (CRX) is a paired-like homeodomain transcription factor (TF) and a master regulator of photoreceptor development in vertebrates. 		Cone-rod homeobox (CRX) is a paired-like homeodomain transcription factor (TF) and a master regulator of photoreceptor development in vertebrates. 	Immunohistochemical staining	Cone-rod homeobox (CRX) is a paired-like homeodomain transcription factor (TF) and a master regulator of photoreceptor development in vertebrates. 			PCR,ChIP-seq,CRE-seq assay				TF
30157915	chr3	133743588	133745588	TF	Pairwise comparisons between cell lines demonstrate a strong association between modulation of A/B compartmentalization, differential gene expression and transcription factor (TF) binding events. 	human		High+Lowthroughput	Genomic meta-analysis of the interplay between 3D chromatin organization and gene expression programs under basal and stress conditions	否		mammary cancer	stem cell	E_01_0742	Chip SEQ, RNA SEQ, flow cytometry	Pairwise comparisons between cell lines demonstrate a strong association between modulation of A/B compartmentalization, differential gene expression and transcription factor (TF) binding events. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Pairwise comparisons between cell lines demonstrate a strong association between modulation of A/B compartmentalization, differential gene expression and transcription factor (TF) binding events. 		Pairwise comparisons between cell lines demonstrate a strong association between modulation of A/B compartmentalization, differential gene expression and transcription factor (TF) binding events. 	Immunohistochemical staining	Pairwise comparisons between cell lines demonstrate a strong association between modulation of A/B compartmentalization, differential gene expression and transcription factor (TF) binding events. 			ChIP-seq,RNA-seq,流式细胞术				TF
30157475	chr7	148804409	148806409	EZH2	RNA immunopreciptation (RIP) analysis was performed to examine whether SNHG6 could bind to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit), and chromatin immunoprecipitation (ChIP) assay was conducted to examine whether SNHG6 could repress p21 transcription by recruiting EZH2 to the p21 promoter.                                             Results: Here we found that SNHG6 was upregulated and its expression levels were positively correlated with advanced tumor stage in colorectal cancer. 	human,mouse		High+Lowthroughput	SNHG6 Promotes Tumor Growth via Repression of P21 in Colorectal Cancer	否		colorectal cancer 	Human colorectal carcinoma cell	E_02_0447	Real time PCR, immunohistochemistry, Weston blot, chromatin immunoprecipitation (chip) assay, and flow cytometry	RNA immunopreciptation (RIP) analysis was performed to examine whether SNHG6 could bind to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit), and chromatin immunoprecipitation (ChIP) assay was conducted to examine whether SNHG6 could repress p21 transcription by recruiting EZH2 to the p21 promoter.                                             Results: Here we found that SNHG6 was upregulated and its expression levels were positively correlated with advanced tumor stage in colorectal cancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RNA immunopreciptation (RIP) analysis was performed to examine whether SNHG6 could bind to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit), and chromatin immunoprecipitation (ChIP) assay was conducted to examine whether SNHG6 could repress p21 transcription by recruiting EZH2 to the p21 promoter.                                             Results: Here we found that SNHG6 was upregulated and its expression levels were positively correlated with advanced tumor stage in colorectal cancer. 		RNA immunopreciptation (RIP) analysis was performed to examine whether SNHG6 could bind to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit), and chromatin immunoprecipitation (ChIP) assay was conducted to examine whether SNHG6 could repress p21 transcription by recruiting EZH2 to the p21 promoter.                                             Results: Here we found that SNHG6 was upregulated and its expression levels were positively correlated with advanced tumor stage in colorectal cancer. 	Immunohistochemical staining	RNA immunopreciptation (RIP) analysis was performed to examine whether SNHG6 could bind to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit), and chromatin immunoprecipitation (ChIP) assay was conducted to examine whether SNHG6 could repress p21 transcription by recruiting EZH2 to the p21 promoter.                                             Results: Here we found that SNHG6 was upregulated and its expression levels were positively correlated with advanced tumor stage in colorectal cancer. 			real-time PCR ,免疫组化,weston blot,染色质免疫沉淀(ChIP)测定,流式细胞术				EZH2
30157475	chr8	66917586	66919586	SNHG6	RNA immunopreciptation (RIP) analysis was performed to examine whether SNHG6 could bind to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit), and chromatin immunoprecipitation (ChIP) assay was conducted to examine whether SNHG6 could repress p21 transcription by recruiting EZH2 to the p21 promoter.                                             Results: Here we found that SNHG6 was upregulated and its expression levels were positively correlated with advanced tumor stage in colorectal cancer. 	human,mouse		High+Lowthroughput	SNHG6 Promotes Tumor Growth via Repression of P21 in Colorectal Cancer	否		colorectal cancer 	Human colorectal carcinoma cell	E_02_0447	Real time PCR, immunohistochemistry, Weston blot, chromatin immunoprecipitation (chip) assay, and flow cytometry	RNA immunopreciptation (RIP) analysis was performed to examine whether SNHG6 could bind to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit), and chromatin immunoprecipitation (ChIP) assay was conducted to examine whether SNHG6 could repress p21 transcription by recruiting EZH2 to the p21 promoter.                                             Results: Here we found that SNHG6 was upregulated and its expression levels were positively correlated with advanced tumor stage in colorectal cancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RNA immunopreciptation (RIP) analysis was performed to examine whether SNHG6 could bind to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit), and chromatin immunoprecipitation (ChIP) assay was conducted to examine whether SNHG6 could repress p21 transcription by recruiting EZH2 to the p21 promoter.                                             Results: Here we found that SNHG6 was upregulated and its expression levels were positively correlated with advanced tumor stage in colorectal cancer. 		RNA immunopreciptation (RIP) analysis was performed to examine whether SNHG6 could bind to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit), and chromatin immunoprecipitation (ChIP) assay was conducted to examine whether SNHG6 could repress p21 transcription by recruiting EZH2 to the p21 promoter.                                             Results: Here we found that SNHG6 was upregulated and its expression levels were positively correlated with advanced tumor stage in colorectal cancer. 	Immunohistochemical staining	RNA immunopreciptation (RIP) analysis was performed to examine whether SNHG6 could bind to EZH2 (enhancer of zeste 2 polycomb repressive complex 2 subunit), and chromatin immunoprecipitation (ChIP) assay was conducted to examine whether SNHG6 could repress p21 transcription by recruiting EZH2 to the p21 promoter.                                             Results: Here we found that SNHG6 was upregulated and its expression levels were positively correlated with advanced tumor stage in colorectal cancer. 			real-time PCR ,免疫组化,weston blot,染色质免疫沉淀(ChIP)测定,流式细胞术				SNHG6
30157244	chr6	137489826	137491826	OLIG3	OLIG3 and FIP1L1 have specific roles in transcription and may effect expression of other genes.	human		High+Lowthroughput	Whole exome sequencing in Finnish families identifies new candidate genes for osteoarthritis	是		Osteoarthritis (OA)	GM12878 cell	E_01_0743	Whole exome sequencing,PCR	OLIG3 and FIP1L1 have specific roles in transcription and may effect expression of other genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	OLIG3 and FIP1L1 have specific roles in transcription and may effect expression of other genes.		OLIG3 and FIP1L1 have specific roles in transcription and may effect expression of other genes.	Immunohistochemical staining	OLIG3 and FIP1L1 have specific roles in transcription and may effect expression of other genes.			Whole exome sequencing,PCR				OLIG3
30157244	chr4	53374689	53376689	FIP1L1	OLIG3 and FIP1L1 have specific roles in transcription and may effect expression of other genes.	human		High+Lowthroughput	Whole exome sequencing in Finnish families identifies new candidate genes for osteoarthritis	是		Osteoarthritis (OA)	GM12878 cell	E_01_0743	Whole exome sequencing,PCR	OLIG3 and FIP1L1 have specific roles in transcription and may effect expression of other genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	OLIG3 and FIP1L1 have specific roles in transcription and may effect expression of other genes.		OLIG3 and FIP1L1 have specific roles in transcription and may effect expression of other genes.	Immunohistochemical staining	OLIG3 and FIP1L1 have specific roles in transcription and may effect expression of other genes.			Whole exome sequencing,PCR				FIP1L1
30155966	chr2	239045155	239047155	HDAC4	HDAC4 enhancer DNA methylation data were obtained from a previous MethylRAD seq.	mouse,human		High+Lowthroughput	Correlation between HDAC4 enhancer DNA methylation and mRNA expression during palatal fusion induced by all-trans retinoic acid	是			epithelial cell	E_02_0448	MS ‐ PCR, real ‐ time PCR, statistical analysis, methylrad ‐ seq	HDAC4 enhancer DNA methylation data were obtained from a previous MethylRAD seq.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HDAC4 enhancer DNA methylation data were obtained from a previous MethylRAD seq.		HDAC4 enhancer DNA methylation data were obtained from a previous MethylRAD seq.	Immunohistochemical staining	HDAC4 enhancer DNA methylation data were obtained from a previous MethylRAD seq.			MS‐PCR,real‐time PCR,统计分析,methylRAD-seq				HDAC4
30154946	chr17	44900435	44902435	GFAP	In the same way, we observed an increment in interleukin-1β, TNF-α, and GFAP, indicative of exacerbated inflammatory processes by the combination of MS and Aβ1 42.	mouse		High+Lowthroughput	Metabolic Syndrome Exacerbates the Recognition Memory Impairment and Oxidative-Inflammatory Response in Rats with an Intrahippocampal Injection of Amyloid Beta 1-42	否		Alzheimer's disease (AD), atherosclerosis, cardiovascular disease, type 2 diabetes mellitus (T2DM) and metabolic syndrome (MS), obesity	microglial cell	E_02_0449	Immunofluorescence staining, statistical analysis, PCR	In the same way, we observed an increment in interleukin-1β, TNF-α, and GFAP, indicative of exacerbated inflammatory processes by the combination of MS and Aβ1 42.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the same way, we observed an increment in interleukin-1β, TNF-α, and GFAP, indicative of exacerbated inflammatory processes by the combination of MS and Aβ1 42.		In the same way, we observed an increment in interleukin-1β, TNF-α, and GFAP, indicative of exacerbated inflammatory processes by the combination of MS and Aβ1 42.	Immunohistochemical staining	In the same way, we observed an increment in interleukin-1β, TNF-α, and GFAP, indicative of exacerbated inflammatory processes by the combination of MS and Aβ1 42.			免疫荧光染色,统计分析,PCR				GFAP
30154726	chr10	88950948	88952948	FAS	The mRNA expression of CCAAT/enhancer-binding protein α (C/EBPα) and fatty acid synthase (FAS), FAS activity, and the content of glycerol and triglyceride (TG) were decreased in the muscle by 509.6 and 1007.5 mg/kg VC diets.	mouse		High+Lowthroughput	Investigation of the Lipid-Lowering Effect of Vitamin C Through GSK-3β/β-Catenin Signaling in Zebrafish	否		Atherosclerosis, coronary heart disease, obesity	ZF4 cell	E_02_0450	Real time PCR, Weston blot, statistical analysis, and immunofluorescence staining	The mRNA expression of CCAAT/enhancer-binding protein α (C/EBPα) and fatty acid synthase (FAS), FAS activity, and the content of glycerol and triglyceride (TG) were decreased in the muscle by 509.6 and 1007.5 mg/kg VC diets.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The mRNA expression of CCAAT/enhancer-binding protein α (C/EBPα) and fatty acid synthase (FAS), FAS activity, and the content of glycerol and triglyceride (TG) were decreased in the muscle by 509.6 and 1007.5 mg/kg VC diets.		The mRNA expression of CCAAT/enhancer-binding protein α (C/EBPα) and fatty acid synthase (FAS), FAS activity, and the content of glycerol and triglyceride (TG) were decreased in the muscle by 509.6 and 1007.5 mg/kg VC diets.	Immunohistochemical staining	The mRNA expression of CCAAT/enhancer-binding protein α (C/EBPα) and fatty acid synthase (FAS), FAS activity, and the content of glycerol and triglyceride (TG) were decreased in the muscle by 509.6 and 1007.5 mg/kg VC diets.			real-time PCR,weston blot,统计分析,免疫荧光染色				FAS
30154449	chr12	53959572	53961572	HOTAIR	Furthermore, functional studies revealed a pivotal role for HOTAIR in the epithelial-to-mesenchymal transition, as this RNA is causal for the repressive activity of the master factor SNAIL on epithelial genes.                                                                                                                                                                            We recently demonstrated that HOTAIR expression is induced in hepatocytes undergoing EMT and functions to bridge, in specific chromatin sites, the interaction between EZH2 and Snail. In other words, the EMT master factor Snail (i.e., sufficient to trigger and orchestrate the transition) conveys the Polycomb catalytic subunit to specific sites by means of a direct interaction with HOTAIR.	human		High+Lowthroughput	The lncRNA HOTAIR transcription is controlled by HNF4α-induced chromatin topology modulation	否		Gastrointestinal cancer, hepatocellular carcinoma	epithelial cell	E_01_0744	RT qPCR, chromatin immunoprecipitation (chip) analysis, statistical analysis, Weston blot	Furthermore, functional studies revealed a pivotal role for HOTAIR in the epithelial-to-mesenchymal transition, as this RNA is causal for the repressive activity of the master factor SNAIL on epithelial genes.                                                                                                                                                                            We recently demonstrated that HOTAIR expression is induced in hepatocytes undergoing EMT and functions to bridge, in specific chromatin sites, the interaction between EZH2 and Snail. In other words, the EMT master factor Snail (i.e., sufficient to trigger and orchestrate the transition) conveys the Polycomb catalytic subunit to specific sites by means of a direct interaction with HOTAIR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Furthermore, functional studies revealed a pivotal role for HOTAIR in the epithelial-to-mesenchymal transition, as this RNA is causal for the repressive activity of the master factor SNAIL on epithelial genes.                                                                                                                                                                            We recently demonstrated that HOTAIR expression is induced in hepatocytes undergoing EMT and functions to bridge, in specific chromatin sites, the interaction between EZH2 and Snail. In other words, the EMT master factor Snail (i.e., sufficient to trigger and orchestrate the transition) conveys the Polycomb catalytic subunit to specific sites by means of a direct interaction with HOTAIR.	Immunohistochemical staining	Furthermore, functional studies revealed a pivotal role for HOTAIR in the epithelial-to-mesenchymal transition, as this RNA is causal for the repressive activity of the master factor SNAIL on epithelial genes.                                                                                                                                                                            We recently demonstrated that HOTAIR expression is induced in hepatocytes undergoing EMT and functions to bridge, in specific chromatin sites, the interaction between EZH2 and Snail. In other words, the EMT master factor Snail (i.e., sufficient to trigger and orchestrate the transition) conveys the Polycomb catalytic subunit to specific sites by means of a direct interaction with HOTAIR.	HOTAIR		RT-qPCR,Chromatin immunoprecipitation (ChIP) analysis,统计分析,weston blot	Furthermore, functional studies revealed a pivotal role for HOTAIR in the epithelial-to-mesenchymal transition, as this RNA is causal for the repressive activity of the master factor SNAIL on epithelial genes.                                                                                                                                                                            We recently demonstrated that HOTAIR expression is induced in hepatocytes undergoing EMT and functions to bridge, in specific chromatin sites, the interaction between EZH2 and Snail. In other words, the EMT master factor Snail (i.e., sufficient to trigger and orchestrate the transition) conveys the Polycomb catalytic subunit to specific sites by means of a direct interaction with HOTAIR.			
30154449	chr7	148804504	148806504	EZH2	Furthermore, functional studies revealed a pivotal role for HOTAIR in the epithelial-to-mesenchymal transition, as this RNA is causal for the repressive activity of the master factor SNAIL on epithelial genes.                                                                                                                                                                            We recently demonstrated that HOTAIR expression is induced in hepatocytes undergoing EMT and functions to bridge, in specific chromatin sites, the interaction between EZH2 and Snail. In other words, the EMT master factor Snail (i.e., sufficient to trigger and orchestrate the transition) conveys the Polycomb catalytic subunit to specific sites by means of a direct interaction with HOTAIR.	human		High+Lowthroughput	The lncRNA HOTAIR transcription is controlled by HNF4α-induced chromatin topology modulation	否		Gastrointestinal cancer, hepatocellular carcinoma	epithelial cell	E_01_0744	RT qPCR, chromatin immunoprecipitation (chip) analysis, statistical analysis, Weston blot	Furthermore, functional studies revealed a pivotal role for HOTAIR in the epithelial-to-mesenchymal transition, as this RNA is causal for the repressive activity of the master factor SNAIL on epithelial genes.                                                                                                                                                                            We recently demonstrated that HOTAIR expression is induced in hepatocytes undergoing EMT and functions to bridge, in specific chromatin sites, the interaction between EZH2 and Snail. In other words, the EMT master factor Snail (i.e., sufficient to trigger and orchestrate the transition) conveys the Polycomb catalytic subunit to specific sites by means of a direct interaction with HOTAIR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Furthermore, functional studies revealed a pivotal role for HOTAIR in the epithelial-to-mesenchymal transition, as this RNA is causal for the repressive activity of the master factor SNAIL on epithelial genes.                                                                                                                                                                            We recently demonstrated that HOTAIR expression is induced in hepatocytes undergoing EMT and functions to bridge, in specific chromatin sites, the interaction between EZH2 and Snail. In other words, the EMT master factor Snail (i.e., sufficient to trigger and orchestrate the transition) conveys the Polycomb catalytic subunit to specific sites by means of a direct interaction with HOTAIR.	Immunohistochemical staining	Furthermore, functional studies revealed a pivotal role for HOTAIR in the epithelial-to-mesenchymal transition, as this RNA is causal for the repressive activity of the master factor SNAIL on epithelial genes.                                                                                                                                                                            We recently demonstrated that HOTAIR expression is induced in hepatocytes undergoing EMT and functions to bridge, in specific chromatin sites, the interaction between EZH2 and Snail. In other words, the EMT master factor Snail (i.e., sufficient to trigger and orchestrate the transition) conveys the Polycomb catalytic subunit to specific sites by means of a direct interaction with HOTAIR.	EZH2		RT-qPCR,Chromatin immunoprecipitation (ChIP) analysis,统计分析,weston blot	Furthermore, functional studies revealed a pivotal role for HOTAIR in the epithelial-to-mesenchymal transition, as this RNA is causal for the repressive activity of the master factor SNAIL on epithelial genes.                                                                                                                                                                            We recently demonstrated that HOTAIR expression is induced in hepatocytes undergoing EMT and functions to bridge, in specific chromatin sites, the interaction between EZH2 and Snail. In other words, the EMT master factor Snail (i.e., sufficient to trigger and orchestrate the transition) conveys the Polycomb catalytic subunit to specific sites by means of a direct interaction with HOTAIR.			
30153568	chr5	88714138	88716138	MEF2C	Furthermore, there were no statistically significant differences in cell viability, metabolic activity, population doubling time, and myocyte enhancer factor 2 (MEF2C) expression between cell cultures established from freshly harvested and one year-stored frozen tissue specimens. 	human,mouse		High+Lowthroughput	Establishment of primary myoblast cell cultures from cryopreserved skeletal muscle biopsies to serve as a tool in related research & development studies	否		Neuromuscular disorders	myocyte	E_02_0451	Real time RT-PCR, immunofluorescence staining, statistical analysis	Furthermore, there were no statistically significant differences in cell viability, metabolic activity, population doubling time, and myocyte enhancer factor 2 (MEF2C) expression between cell cultures established from freshly harvested and one year-stored frozen tissue specimens. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, there were no statistically significant differences in cell viability, metabolic activity, population doubling time, and myocyte enhancer factor 2 (MEF2C) expression between cell cultures established from freshly harvested and one year-stored frozen tissue specimens. 		Furthermore, there were no statistically significant differences in cell viability, metabolic activity, population doubling time, and myocyte enhancer factor 2 (MEF2C) expression between cell cultures established from freshly harvested and one year-stored frozen tissue specimens. 	Immunohistochemical staining	Furthermore, there were no statistically significant differences in cell viability, metabolic activity, population doubling time, and myocyte enhancer factor 2 (MEF2C) expression between cell cultures established from freshly harvested and one year-stored frozen tissue specimens. 			real-time RT-PCR,免疫荧光染色,统计分析				MEF2C
30151761	chr8	22111886	22113886	HR	Prior to the genome editing era, the conventional knock-in strategy based on homologous recombination (HR) was the only option avail- able, but it had limitations in mouse embryonic stem cells because intrinsic HR at a target site occurs with extremely low frequency in somatic cells. 	mouse		High+Lowthroughput	A Simple Knock-In System for Xenopus via Microhomology Mediated End Joining Repair	否			embryonic stem cell	E_02_0452	PCR, gene knockdown	Prior to the genome editing era, the conventional knock-in strategy based on homologous recombination (HR) was the only option avail- able, but it had limitations in mouse embryonic stem cells because intrinsic HR at a target site occurs with extremely low frequency in somatic cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Prior to the genome editing era, the conventional knock-in strategy based on homologous recombination (HR) was the only option avail- able, but it had limitations in mouse embryonic stem cells because intrinsic HR at a target site occurs with extremely low frequency in somatic cells. 		Prior to the genome editing era, the conventional knock-in strategy based on homologous recombination (HR) was the only option avail- able, but it had limitations in mouse embryonic stem cells because intrinsic HR at a target site occurs with extremely low frequency in somatic cells. 	Immunohistochemical staining	Prior to the genome editing era, the conventional knock-in strategy based on homologous recombination (HR) was the only option avail- able, but it had limitations in mouse embryonic stem cells because intrinsic HR at a target site occurs with extremely low frequency in somatic cells. 			PCR,基因敲降				HR
30150754	chr16	67559736	67561736	CTCF	Examination of chromatin interaction around functional elements such as promoters and CTCF binding sites within 2000 bp regions at a 10-bp resolution revealed a clear pattern of separation of interaction domains anchored at promoters of actively transcribed genes and at CTCF binding sites (Fig. 2c).	human		High+Lowthroughput	Trac-looping measures genome structure and chromatin accessibility	否			CD4+T cell	E_01_0745	ATAC-seq,PCR,3D fluorescence in situ hybridization (FISH)	Examination of chromatin interaction around functional elements such as promoters and CTCF binding sites within 2000 bp regions at a 10-bp resolution revealed a clear pattern of separation of interaction domains anchored at promoters of actively transcribed genes and at CTCF binding sites (Fig. 2c).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Examination of chromatin interaction around functional elements such as promoters and CTCF binding sites within 2000 bp regions at a 10-bp resolution revealed a clear pattern of separation of interaction domains anchored at promoters of actively transcribed genes and at CTCF binding sites (Fig. 2c).	Immunohistochemical staining	Examination of chromatin interaction around functional elements such as promoters and CTCF binding sites within 2000 bp regions at a 10-bp resolution revealed a clear pattern of separation of interaction domains anchored at promoters of actively transcribed genes and at CTCF binding sites (Fig. 2c).	CTCF		ATAC-seq,PCR,3D fluorescence in situ hybridization (FISH)	Examination of chromatin interaction around functional elements such as promoters and CTCF binding sites within 2000 bp regions at a 10-bp resolution revealed a clear pattern of separation of interaction domains anchored at promoters of actively transcribed genes and at CTCF binding sites (Fig. 2c).			
30150059	chr7	148804095	148806095	EZH2	Enhancer of zeste homolog 2 (EZH2), an oncogene responsible for the tri-methylation of histone H3 at lysine 27 (H3K27me3), was identified to be overexpressed in approximate 70 90% of HCC cases, which prompted us to investigate whether or how AR regulates EZH2 expression.	human		High+Lowthroughput	Androgen receptor drives hepatocellular carcinogenesis by activating enhancer of zeste homolog 2-mediated Wnt/β-catenin signaling	否		Hepatocellular carcinoma (HCC)	LO2 cell	E_01_0746	Quantitative RT-PCR, chromatin immunoprecipitation, immunoblotting, gene knockdown, Weston blot	Enhancer of zeste homolog 2 (EZH2), an oncogene responsible for the tri-methylation of histone H3 at lysine 27 (H3K27me3), was identified to be overexpressed in approximate 70 90% of HCC cases, which prompted us to investigate whether or how AR regulates EZH2 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2 (EZH2), an oncogene responsible for the tri-methylation of histone H3 at lysine 27 (H3K27me3), was identified to be overexpressed in approximate 70 90% of HCC cases, which prompted us to investigate whether or how AR regulates EZH2 expression.	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2), an oncogene responsible for the tri-methylation of histone H3 at lysine 27 (H3K27me3), was identified to be overexpressed in approximate 70 90% of HCC cases, which prompted us to investigate whether or how AR regulates EZH2 expression.	EZH2		Quantitative RT-PCR,染色质免疫沉淀,免疫印迹法,基因敲降,weston blot	Enhancer of zeste homolog 2 (EZH2), an oncogene responsible for the tri-methylation of histone H3 at lysine 27 (H3K27me3), was identified to be overexpressed in approximate 70 90% of HCC cases, which prompted us to investigate whether or how AR regulates EZH2 expression.			
30149809	chr13	63009830	63011830	Fbp1	However, functional studies of cis-regulatory elements have been restricted to a small number of sequences that were originally identified by promoter analysis of ecdysone-induced genes. For example, Hsp27, Eip28/29, Fbp1, and Sgs-4 are induced directly by ecdysone and contain an EcRE in their basal promoter region [36 38]. 	mouse		High+Lowthroughput	The genome-wide transcriptional regulatory landscape of ecdysone in the silkworm	否			embryonic cell 	E_02_0453	RNA-seq,ChIP-seq,PCR	However, functional studies of cis-regulatory elements have been restricted to a small number of sequences that were originally identified by promoter analysis of ecdysone-induced genes. For example, Hsp27, Eip28/29, Fbp1, and Sgs-4 are induced directly by ecdysone and contain an EcRE in their basal promoter region [36 38]. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, functional studies of cis-regulatory elements have been restricted to a small number of sequences that were originally identified by promoter analysis of ecdysone-induced genes. For example, Hsp27, Eip28/29, Fbp1, and Sgs-4 are induced directly by ecdysone and contain an EcRE in their basal promoter region [36 38]. 		However, functional studies of cis-regulatory elements have been restricted to a small number of sequences that were originally identified by promoter analysis of ecdysone-induced genes. For example, Hsp27, Eip28/29, Fbp1, and Sgs-4 are induced directly by ecdysone and contain an EcRE in their basal promoter region [36 38]. 	Immunohistochemical staining	However, functional studies of cis-regulatory elements have been restricted to a small number of sequences that were originally identified by promoter analysis of ecdysone-induced genes. For example, Hsp27, Eip28/29, Fbp1, and Sgs-4 are induced directly by ecdysone and contain an EcRE in their basal promoter region [36 38]. 			RNA-seq,ChIP-seq,PCR				Fbp1
30149019	chr8	18388409	18390409	NAT2	Genetic polymorphisms of NAT2 modify drug efficacy and toxicity and susceptibility to diseases such as cancer and type 2 diabetes.                                                              The N-acetylation capacity of NAT2 in the presence of SIRT1 enhancer was significantly decreased (p<0.001), conversely, the transient silencing of SIRT1 resulted in an increase of N-acetylation capacity (p<0.001). 	human,mouse		High+Lowthroughput	Expression and genotype-dependent catalytic activity of N-acetyltransferase 2 (NAT2) in human peripheral blood mononuclear cells and its modulation by Sirtuin 1	是	rs1041983,rs1801280, rs1799930 , rs1799929,rs1208,rs1799931 	Cancer, type 2 diabetes	CD3+ cell	E_02_0454	Statistical analysis, PCR	Genetic polymorphisms of NAT2 modify drug efficacy and toxicity and susceptibility to diseases such as cancer and type 2 diabetes.                                                              The N-acetylation capacity of NAT2 in the presence of SIRT1 enhancer was significantly decreased (p<0.001), conversely, the transient silencing of SIRT1 resulted in an increase of N-acetylation capacity (p<0.001). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genetic polymorphisms of NAT2 modify drug efficacy and toxicity and susceptibility to diseases such as cancer and type 2 diabetes.                                                              The N-acetylation capacity of NAT2 in the presence of SIRT1 enhancer was significantly decreased (p<0.001), conversely, the transient silencing of SIRT1 resulted in an increase of N-acetylation capacity (p<0.001). 		Genetic polymorphisms of NAT2 modify drug efficacy and toxicity and susceptibility to diseases such as cancer and type 2 diabetes.                                                              The N-acetylation capacity of NAT2 in the presence of SIRT1 enhancer was significantly decreased (p<0.001), conversely, the transient silencing of SIRT1 resulted in an increase of N-acetylation capacity (p<0.001). 	Immunohistochemical staining	Genetic polymorphisms of NAT2 modify drug efficacy and toxicity and susceptibility to diseases such as cancer and type 2 diabetes.                                                              The N-acetylation capacity of NAT2 in the presence of SIRT1 enhancer was significantly decreased (p<0.001), conversely, the transient silencing of SIRT1 resulted in an increase of N-acetylation capacity (p<0.001). 			统计分析,PCR 				NAT2
30149019	chr10	67882103	67884103	SIRT1	Genetic polymorphisms of NAT2 modify drug efficacy and toxicity and susceptibility to diseases such as cancer and type 2 diabetes.                                                              The N-acetylation capacity of NAT2 in the presence of SIRT1 enhancer was significantly decreased (p<0.001), conversely, the transient silencing of SIRT1 resulted in an increase of N-acetylation capacity (p<0.001). 	human,mouse		High+Lowthroughput	Expression and genotype-dependent catalytic activity of N-acetyltransferase 2 (NAT2) in human peripheral blood mononuclear cells and its modulation by Sirtuin 1	是	rs1041983,rs1801280, rs1799930 , rs1799929,rs1208,rs1799931 	Cancer, type 2 diabetes	CD3+ cell	E_02_0454	Statistical analysis, PCR	Genetic polymorphisms of NAT2 modify drug efficacy and toxicity and susceptibility to diseases such as cancer and type 2 diabetes.                                                              The N-acetylation capacity of NAT2 in the presence of SIRT1 enhancer was significantly decreased (p<0.001), conversely, the transient silencing of SIRT1 resulted in an increase of N-acetylation capacity (p<0.001). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genetic polymorphisms of NAT2 modify drug efficacy and toxicity and susceptibility to diseases such as cancer and type 2 diabetes.                                                              The N-acetylation capacity of NAT2 in the presence of SIRT1 enhancer was significantly decreased (p<0.001), conversely, the transient silencing of SIRT1 resulted in an increase of N-acetylation capacity (p<0.001). 		Genetic polymorphisms of NAT2 modify drug efficacy and toxicity and susceptibility to diseases such as cancer and type 2 diabetes.                                                              The N-acetylation capacity of NAT2 in the presence of SIRT1 enhancer was significantly decreased (p<0.001), conversely, the transient silencing of SIRT1 resulted in an increase of N-acetylation capacity (p<0.001). 	Immunohistochemical staining	Genetic polymorphisms of NAT2 modify drug efficacy and toxicity and susceptibility to diseases such as cancer and type 2 diabetes.                                                              The N-acetylation capacity of NAT2 in the presence of SIRT1 enhancer was significantly decreased (p<0.001), conversely, the transient silencing of SIRT1 resulted in an increase of N-acetylation capacity (p<0.001). 			统计分析,PCR 				SIRT1
30148699	chr6	41733756	41735756	PGC	However, the levels of other mitochon- drial transcription factors (mtTF) such as PPAR-c coactivator (PGC)-1a and mtTFA were decreased by 32% and 35%, re- spectively, relative to untreated 3T3-L1 cells, although only the latter was statistically significant (Fig. 5B D). 	mouse,human		High+Lowthroughput	Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032 Cell Extracts Inhibit Adipogenesis in 3T3-L1 and HepG2 Cells	否		Obesity	3T3-L1 cell	E_02_0455	PCR, statistical analysis	However, the levels of other mitochon- drial transcription factors (mtTF) such as PPAR-c coactivator (PGC)-1a and mtTFA were decreased by 32% and 35%, re- spectively, relative to untreated 3T3-L1 cells, although only the latter was statistically significant (Fig. 5B D). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, the levels of other mitochon- drial transcription factors (mtTF) such as PPAR-c coactivator (PGC)-1a and mtTFA were decreased by 32% and 35%, re- spectively, relative to untreated 3T3-L1 cells, although only the latter was statistically significant (Fig. 5B D). 		However, the levels of other mitochon- drial transcription factors (mtTF) such as PPAR-c coactivator (PGC)-1a and mtTFA were decreased by 32% and 35%, re- spectively, relative to untreated 3T3-L1 cells, although only the latter was statistically significant (Fig. 5B D). 	Immunohistochemical staining	However, the levels of other mitochon- drial transcription factors (mtTF) such as PPAR-c coactivator (PGC)-1a and mtTFA were decreased by 32% and 35%, re- spectively, relative to untreated 3T3-L1 cells, although only the latter was statistically significant (Fig. 5B D). 			PCR,统计分析				PGC
30146478	chr11	111838889	111839334	SOX9	SRY-box 9 (SOX9) is a master transcription factor that regulates cartilage development.                                                                                               CRISPR/dCas9-ChIP-mass spectrometry analysis further implicated STAT3 in acting at the enhancer to regulate SOX9 expression.	mouse		Low+High throughput	Combinatorial CRISPR/Cas9 Approach to Elucidate a Far-Upstream Enhancer Complex for Tissue-Specific Sox9 Expression	否	--	--	chondroblast	E_02_0456	ChIP-qPCR	We next performed the ChIP-qPCR using anti-H3K4me1 and H3K27ac antibody in all five regions and found that RCSE regions were significantly enriched in both H3K4me1 and H3K27ac ChIP, suggesting the potential enhancer.	Enhancer	3C	PCR	These data suggest that there is a long-range interaction between the Sox9 promoter and RCSE region in primary chondrocytes.	2010306G03Rik,AV220920,mKIAA4243	TG mice with the Sox9 promoter and 43 RCSE region.These data suggest that the RCSE region functions as a costal- and sternum cartilage-specific Enhancer.	Transgenic mice	TG mice with the Sox9 promoter and 43 RCSE region.These data suggest that the RCSE region functions as a costal- and sternum cartilage-specific Enhancer.	Stat3	1110034C02Rik,AW109958,Aprf	Luciferase Reporter Assay,Immunostaining	Furthermore, transcription factors that regulate Sox9 expres sion were screened using a CRISPR/Cas9-chromatin immuno precipitation (ChIP)-mass spectrometry (MS) system targeting the RCSE region in chondrocytes; signal transducer and acti vator of transcription 3 (Stat3) was identified as a transacting fac tor for the Sox9 Enhancer.	--	--	Sox9
30146478	chr11	111838889	111839334	STAT3	SRY-box 9 (SOX9) is a master transcription factor that regulates cartilage development.                                                                                               CRISPR/dCas9-ChIP-mass spectrometry analysis further implicated STAT3 in acting at the enhancer to regulate SOX9 expression.	mouse		Low+High throughput	Combinatorial CRISPR/Cas9 Approach to Elucidate a Far-Upstream Enhancer Complex for Tissue-Specific Sox9 Expression	否	--	--	chondroblast	E_02_0456	ChIP-qPCR	We next performed the ChIP-qPCR using anti-H3K4me1 and H3K27ac antibody in all five regions and found that RCSE regions were significantly enriched in both H3K4me1 and H3K27ac ChIP, suggesting the potential enhancer.	Enhancer	3C	PCR	These data suggest that there is a long-range interaction between the Sox9 promoter and RCSE region in primary chondrocytes.	2010306G03Rik,AV220920,mKIAA4243	TG mice with the Sox9 promoter and 43 RCSE region.These data suggest that the RCSE region functions as a costal- and sternum cartilage-specific Enhancer.	Transgenic mice	TG mice with the Sox9 promoter and 43 RCSE region.These data suggest that the RCSE region functions as a costal- and sternum cartilage-specific Enhancer.	Stat3	1110034C02Rik,AW109958,Aprf	Luciferase Reporter Assay,Immunostaining	Furthermore, transcription factors that regulate Sox9 expres sion were screened using a CRISPR/Cas9-chromatin immuno precipitation (ChIP)-mass spectrometry (MS) system targeting the RCSE region in chondrocytes; signal transducer and acti vator of transcription 3 (Stat3) was identified as a transacting fac tor for the Sox9 Enhancer.	--	--	Sox9
30146411	chr16	48121715	48123715	Dppa2	Hernandez et al. identify chromatin-associated factors Dppa2 and Dppa4 as the key components mediating the reset of somatic chromatin to a pluripotent configuration.	mouse,human		High+Lowthroughput	Dppa2/4 Facilitate Epigenetic Remodeling during Reprogramming to Pluripotency	否			fibroblast	E_02_0457	Flow cytometry, immunofluorescence light staining, PCR, RNA SEQ, chip seq	Hernandez et al. identify chromatin-associated factors Dppa2 and Dppa4 as the key components mediating the reset of somatic chromatin to a pluripotent configuration.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hernandez et al. identify chromatin-associated factors Dppa2 and Dppa4 as the key components mediating the reset of somatic chromatin to a pluripotent configuration.		Hernandez et al. identify chromatin-associated factors Dppa2 and Dppa4 as the key components mediating the reset of somatic chromatin to a pluripotent configuration.	Immunohistochemical staining	Hernandez et al. identify chromatin-associated factors Dppa2 and Dppa4 as the key components mediating the reset of somatic chromatin to a pluripotent configuration.			流式细胞术,免疫荧光光染色,PCR,RNA-seq ,ChIP-Seq				Dppa2
30146411	chr16	48101037	48103037	Dppa4	Hernandez et al. identify chromatin-associated factors Dppa2 and Dppa4 as the key components mediating the reset of somatic chromatin to a pluripotent configuration.	mouse,human		High+Lowthroughput	Dppa2/4 Facilitate Epigenetic Remodeling during Reprogramming to Pluripotency	否			fibroblast	E_02_0457	Flow cytometry, immunofluorescence light staining, PCR, RNA SEQ, chip seq	Hernandez et al. identify chromatin-associated factors Dppa2 and Dppa4 as the key components mediating the reset of somatic chromatin to a pluripotent configuration.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hernandez et al. identify chromatin-associated factors Dppa2 and Dppa4 as the key components mediating the reset of somatic chromatin to a pluripotent configuration.		Hernandez et al. identify chromatin-associated factors Dppa2 and Dppa4 as the key components mediating the reset of somatic chromatin to a pluripotent configuration.	Immunohistochemical staining	Hernandez et al. identify chromatin-associated factors Dppa2 and Dppa4 as the key components mediating the reset of somatic chromatin to a pluripotent configuration.			流式细胞术,免疫荧光光染色,PCR,RNA-seq ,ChIP-Seq				Dppa4
30146317	chr15	76897064	76899064	Mb	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 	human,mouse		High+Lowthroughput	The Evf2 Ultraconserved Enhancer lncRNA Functionally and Spatially Organizes Megabase Distant Genes in the Developing Forebrain	否				E_02_0458	QRT PCR, chipseq, statistical analysis, immunofluorescence staining	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 		Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 	Immunohistochemical staining	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 			qRT-PCR, ChIPseq,统计分析,免疫荧光染色				Mb
30146317	chr6	18845842	18847842	Lsm8	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 	human,mouse		High+Lowthroughput	The Evf2 Ultraconserved Enhancer lncRNA Functionally and Spatially Organizes Megabase Distant Genes in the Developing Forebrain	否				E_02_0458	QRT PCR, chipseq, statistical analysis, immunofluorescence staining	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 		Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 	Immunohistochemical staining	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 			qRT-PCR, ChIPseq,统计分析,免疫荧光染色				Lsm8
30146317	chr6	34328827	34330827	Akr1b8	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 	human,mouse		High+Lowthroughput	The Evf2 Ultraconserved Enhancer lncRNA Functionally and Spatially Organizes Megabase Distant Genes in the Developing Forebrain	否				E_02_0458	QRT PCR, chipseq, statistical analysis, immunofluorescence staining	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 		Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 	Immunohistochemical staining	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 			qRT-PCR, ChIPseq,统计分析,免疫荧光染色				Akr1b8
30146317	chr5	28658801	28660801	Shh	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 	human,mouse		High+Lowthroughput	The Evf2 Ultraconserved Enhancer lncRNA Functionally and Spatially Organizes Megabase Distant Genes in the Developing Forebrain	否				E_02_0458	QRT PCR, chipseq, statistical analysis, immunofluorescence staining	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 		Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 	Immunohistochemical staining	Gene regulation requires selective targeting of DNA regulatory enhancers over megabase (Mb) distances.                                                                               Transgene expression of Evf2 activates Lsm8 (12Mb distant), but fails to repress Akr1b8, supporting trans-activation and long-range cis repression.                                       Early studies showed regulatory interactions between the sonic hedgehog (Shh) limb Enh (ZRS) and the Shh gene, despite 1Mb distance (Lettice et al., 2003). 			qRT-PCR, ChIPseq,统计分析,免疫荧光染色				Shh
30146162	chr5	69232175	69234175	CDK7	We show that blocking CKIα together with CDK7 and/or CDK9 synergistically stabilize p53, deprive leukemia cells of survival and proliferation-maintaining SE-driven oncogenes, and induce apoptosis.	mouse,human		High+Lowthroughput	Small Molecules Co-targeting CKIα and the Transcriptional Kinases CDK7/9 Control AML in Preclinical Models	否		leukemia	leukemic cell	E_02_0459	RT-PCR,ChIP-seq,weston blot  	We show that blocking CKIα together with CDK7 and/or CDK9 synergistically stabilize p53, deprive leukemia cells of survival and proliferation-maintaining SE-driven oncogenes, and induce apoptosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We show that blocking CKIα together with CDK7 and/or CDK9 synergistically stabilize p53, deprive leukemia cells of survival and proliferation-maintaining SE-driven oncogenes, and induce apoptosis.		We show that blocking CKIα together with CDK7 and/or CDK9 synergistically stabilize p53, deprive leukemia cells of survival and proliferation-maintaining SE-driven oncogenes, and induce apoptosis.	Immunohistochemical staining	We show that blocking CKIα together with CDK7 and/or CDK9 synergistically stabilize p53, deprive leukemia cells of survival and proliferation-maintaining SE-driven oncogenes, and induce apoptosis.			RT-PCR,ChIP-seq,weston blot  				CDK7
30146162	chr9	127783255	127785255	CDK9	We show that blocking CKIα together with CDK7 and/or CDK9 synergistically stabilize p53, deprive leukemia cells of survival and proliferation-maintaining SE-driven oncogenes, and induce apoptosis.	mouse,human		High+Lowthroughput	Small Molecules Co-targeting CKIα and the Transcriptional Kinases CDK7/9 Control AML in Preclinical Models	否		leukemia	leukemic cell	E_02_0459	RT-PCR,ChIP-seq,weston blot  	We show that blocking CKIα together with CDK7 and/or CDK9 synergistically stabilize p53, deprive leukemia cells of survival and proliferation-maintaining SE-driven oncogenes, and induce apoptosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We show that blocking CKIα together with CDK7 and/or CDK9 synergistically stabilize p53, deprive leukemia cells of survival and proliferation-maintaining SE-driven oncogenes, and induce apoptosis.		We show that blocking CKIα together with CDK7 and/or CDK9 synergistically stabilize p53, deprive leukemia cells of survival and proliferation-maintaining SE-driven oncogenes, and induce apoptosis.	Immunohistochemical staining	We show that blocking CKIα together with CDK7 and/or CDK9 synergistically stabilize p53, deprive leukemia cells of survival and proliferation-maintaining SE-driven oncogenes, and induce apoptosis.			RT-PCR,ChIP-seq,weston blot  				CDK9
30145643	chr1	161763665	161765665	ATF6	The UPR is mediated by three main sensors embedded in the ER membrane Activating transcription factor 6 (ATF6), Inositol-requiring enzyme 1 (IRE1) and Protein Kinase R-like ER kinase (PERK) [3].                                                                                                                                                                    Activated IRE1 splices an intron from XBP1 mRNA allowing it to be translated into a functional transcription factor (XBP1s), which has several downstream targets involved in the UPR [11,12]. 	human		High+Lowthroughput	GIV/Girdin promotes cell survival during endoplasmic reticulum stress	否		Cancer, diabetes		E_01_0747	Weston blot, statistical analysis	The UPR is mediated by three main sensors embedded in the ER membrane Activating transcription factor 6 (ATF6), Inositol-requiring enzyme 1 (IRE1) and Protein Kinase R-like ER kinase (PERK) [3].                                                                                                                                                                    Activated IRE1 splices an intron from XBP1 mRNA allowing it to be translated into a functional transcription factor (XBP1s), which has several downstream targets involved in the UPR [11,12]. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The UPR is mediated by three main sensors embedded in the ER membrane Activating transcription factor 6 (ATF6), Inositol-requiring enzyme 1 (IRE1) and Protein Kinase R-like ER kinase (PERK) [3].                                                                                                                                                                    Activated IRE1 splices an intron from XBP1 mRNA allowing it to be translated into a functional transcription factor (XBP1s), which has several downstream targets involved in the UPR [11,12]. 	Immunohistochemical staining	The UPR is mediated by three main sensors embedded in the ER membrane Activating transcription factor 6 (ATF6), Inositol-requiring enzyme 1 (IRE1) and Protein Kinase R-like ER kinase (PERK) [3].                                                                                                                                                                    Activated IRE1 splices an intron from XBP1 mRNA allowing it to be translated into a functional transcription factor (XBP1s), which has several downstream targets involved in the UPR [11,12]. 	ATF6		weston blot,统计分析	The UPR is mediated by three main sensors embedded in the ER membrane Activating transcription factor 6 (ATF6), Inositol-requiring enzyme 1 (IRE1) and Protein Kinase R-like ER kinase (PERK) [3].                                                                                                                                                                    Activated IRE1 splices an intron from XBP1 mRNA allowing it to be translated into a functional transcription factor (XBP1s), which has several downstream targets involved in the UPR [11,12]. 			
30145643	chr22	28792293	28794293	XBP1	The UPR is mediated by three main sensors embedded in the ER membrane Activating transcription factor 6 (ATF6), Inositol-requiring enzyme 1 (IRE1) and Protein Kinase R-like ER kinase (PERK) [3].                                                                                                                                                                    Activated IRE1 splices an intron from XBP1 mRNA allowing it to be translated into a functional transcription factor (XBP1s), which has several downstream targets involved in the UPR [11,12]. 	human		High+Lowthroughput	GIV/Girdin promotes cell survival during endoplasmic reticulum stress	否		Cancer, diabetes		E_01_0747	Weston blot, statistical analysis	The UPR is mediated by three main sensors embedded in the ER membrane Activating transcription factor 6 (ATF6), Inositol-requiring enzyme 1 (IRE1) and Protein Kinase R-like ER kinase (PERK) [3].                                                                                                                                                                    Activated IRE1 splices an intron from XBP1 mRNA allowing it to be translated into a functional transcription factor (XBP1s), which has several downstream targets involved in the UPR [11,12]. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The UPR is mediated by three main sensors embedded in the ER membrane Activating transcription factor 6 (ATF6), Inositol-requiring enzyme 1 (IRE1) and Protein Kinase R-like ER kinase (PERK) [3].                                                                                                                                                                    Activated IRE1 splices an intron from XBP1 mRNA allowing it to be translated into a functional transcription factor (XBP1s), which has several downstream targets involved in the UPR [11,12]. 	Immunohistochemical staining	The UPR is mediated by three main sensors embedded in the ER membrane Activating transcription factor 6 (ATF6), Inositol-requiring enzyme 1 (IRE1) and Protein Kinase R-like ER kinase (PERK) [3].                                                                                                                                                                    Activated IRE1 splices an intron from XBP1 mRNA allowing it to be translated into a functional transcription factor (XBP1s), which has several downstream targets involved in the UPR [11,12]. 	XBP1		weston blot,统计分析	The UPR is mediated by three main sensors embedded in the ER membrane Activating transcription factor 6 (ATF6), Inositol-requiring enzyme 1 (IRE1) and Protein Kinase R-like ER kinase (PERK) [3].                                                                                                                                                                    Activated IRE1 splices an intron from XBP1 mRNA allowing it to be translated into a functional transcription factor (XBP1s), which has several downstream targets involved in the UPR [11,12]. 			
30145202	chr6	151653890	151655890	ESR1	Abstract Breast cancer is the most prevalent type of malignancy in women with ~1.7 million new cases diagnosed annually, of which the majority express ERα (ESR1), a ligand- dependent transcription factor.                                                                                                                                                          Here, we show that CUTE controls CUEDC1 expression, and that this interaction is essential for ERα-mediated cell proliferation.	human		High+Lowthroughput	CUEDC1 is a primary target of ERα essential for the growth of breast cancer cells	否		mammary cancer	HEK293T	E_01_0748	qPCR,weston blot,GRO-seq，DNA-seq,RNA-seq,ChIP-seq	Abstract Breast cancer is the most prevalent type of malignancy in women with ~1.7 million new cases diagnosed annually, of which the majority express ERα (ESR1), a ligand- dependent transcription factor.                                                                                                                                                          Here, we show that CUTE controls CUEDC1 expression, and that this interaction is essential for ERα-mediated cell proliferation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Abstract Breast cancer is the most prevalent type of malignancy in women with ~1.7 million new cases diagnosed annually, of which the majority express ERα (ESR1), a ligand- dependent transcription factor.                                                                                                                                                          Here, we show that CUTE controls CUEDC1 expression, and that this interaction is essential for ERα-mediated cell proliferation.	Immunohistochemical staining	Abstract Breast cancer is the most prevalent type of malignancy in women with ~1.7 million new cases diagnosed annually, of which the majority express ERα (ESR1), a ligand- dependent transcription factor.                                                                                                                                                          Here, we show that CUTE controls CUEDC1 expression, and that this interaction is essential for ERα-mediated cell proliferation.	ESR1		qPCR,weston blot,GRO-seq，DNA-seq,RNA-seq,ChIP-seq	Abstract Breast cancer is the most prevalent type of malignancy in women with ~1.7 million new cases diagnosed annually, of which the majority express ERα (ESR1), a ligand- dependent transcription factor.                                                                                                                                                          Here, we show that CUTE controls CUEDC1 expression, and that this interaction is essential for ERα-mediated cell proliferation.			
30145202	chr17	57858176	57860176	CUEDC1	Abstract Breast cancer is the most prevalent type of malignancy in women with ~1.7 million new cases diagnosed annually, of which the majority express ERα (ESR1), a ligand- dependent transcription factor.                                                                                                                                                          Here, we show that CUTE controls CUEDC1 expression, and that this interaction is essential for ERα-mediated cell proliferation.	human		High+Lowthroughput	CUEDC1 is a primary target of ERα essential for the growth of breast cancer cells	否		mammary cancer	HEK293T	E_01_0748	qPCR,weston blot,GRO-seq，DNA-seq,RNA-seq,ChIP-seq	Abstract Breast cancer is the most prevalent type of malignancy in women with ~1.7 million new cases diagnosed annually, of which the majority express ERα (ESR1), a ligand- dependent transcription factor.                                                                                                                                                          Here, we show that CUTE controls CUEDC1 expression, and that this interaction is essential for ERα-mediated cell proliferation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Abstract Breast cancer is the most prevalent type of malignancy in women with ~1.7 million new cases diagnosed annually, of which the majority express ERα (ESR1), a ligand- dependent transcription factor.                                                                                                                                                          Here, we show that CUTE controls CUEDC1 expression, and that this interaction is essential for ERα-mediated cell proliferation.		Abstract Breast cancer is the most prevalent type of malignancy in women with ~1.7 million new cases diagnosed annually, of which the majority express ERα (ESR1), a ligand- dependent transcription factor.                                                                                                                                                          Here, we show that CUTE controls CUEDC1 expression, and that this interaction is essential for ERα-mediated cell proliferation.	Immunohistochemical staining	Abstract Breast cancer is the most prevalent type of malignancy in women with ~1.7 million new cases diagnosed annually, of which the majority express ERα (ESR1), a ligand- dependent transcription factor.                                                                                                                                                          Here, we show that CUTE controls CUEDC1 expression, and that this interaction is essential for ERα-mediated cell proliferation.			qPCR,weston blot,GRO-seq，DNA-seq,RNA-seq,ChIP-seq				CUEDC1
30143575	chr9	973683	975683	DMRT3	We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).	human,mouse		High+Lowthroughput	DMRT5, DMRT3, and EMX2 Cooperatively Repress Gsx2 at the Pallium-Subpallium Boundary to Maintain Cortical Identity in Dorsal Telencephalic Progenitors	否		Telencephalic developmental defects	progenitor cell	E_02_0460	RNA SEQ, QRT PCR, statistical analysis, immunofluorescence staining, gene knockdown	We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).		We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).	Immunohistochemical staining	We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).			RNA-seq,qRT-PCR,统计分析,免疫荧光染色,基因敲降				DMRT3
30143575	chr4	54097254	54099254	GSX2	We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).	human,mouse		High+Lowthroughput	DMRT5, DMRT3, and EMX2 Cooperatively Repress Gsx2 at the Pallium-Subpallium Boundary to Maintain Cortical Identity in Dorsal Telencephalic Progenitors	否		Telencephalic developmental defects	progenitor cell	E_02_0460	RNA SEQ, QRT PCR, statistical analysis, immunofluorescence staining, gene knockdown	We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).		We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).	Immunohistochemical staining	We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).			RNA-seq,qRT-PCR,统计分析,免疫荧光染色,基因敲降				GSX2
30143575	chr1	50414891	50416891	DMRTA2	We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).	human,mouse		High+Lowthroughput	DMRT5, DMRT3, and EMX2 Cooperatively Repress Gsx2 at the Pallium-Subpallium Boundary to Maintain Cortical Identity in Dorsal Telencephalic Progenitors	否		Telencephalic developmental defects	progenitor cell	E_02_0460	RNA SEQ, QRT PCR, statistical analysis, immunofluorescence staining, gene knockdown	We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).		We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).	Immunohistochemical staining	We find that DMRT3 and DMRT5 act as critical regulators of progenitor cell dorsoventral identity by repressing ventralizing regulators.                                                          Conditional overexpression of Dmrt5 throughout the telencephalon produces gene expression and structural defects that are highly consistent with reduced GSX2 activity.                    Related to this study, a loss-of-function mutation in the human DMRT5/DMRTA2 gene has been found to be associated with microcephaly (Urquhart et al., 2016).			RNA-seq,qRT-PCR,统计分析,免疫荧光染色,基因敲降				DMRTA2
30141986	chr18	47806131	47808131	SMAD2	LVAD support was associated with CaMKIIδ activation, increased nuclear myocyte enhancer factor 2,  sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05).                                 Active CaMKIIδ activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33).	human	Myocardial tissue	High+Lowthroughput	Structural and functional cardiac profile after prolonged duration of mechanical unloading: potential implications for myocardial recovery	否		heart disease	cardiac muscle cell (sensu Arthopoda)	E_01_0749	weston blot,RNA sequencing analysis	LVAD support was associated with CaMKIIδ activation, increased nuclear myocyte enhancer factor 2,  sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05).                                 Active CaMKIIδ activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			LVAD support was associated with CaMKIIδ activation, increased nuclear myocyte enhancer factor 2,  sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05).                                 Active CaMKIIδ activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33).	Immunohistochemical staining	LVAD support was associated with CaMKIIδ activation, increased nuclear myocyte enhancer factor 2,  sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05).                                 Active CaMKIIδ activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33).	SMAD2		weston blot,RNA sequencing analysis	LVAD support was associated with CaMKIIδ activation, increased nuclear myocyte enhancer factor 2,  sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05).                                 Active CaMKIIδ activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33).			
30141986	chr17	44073646	44075646	HDAC5	LVAD support was associated with CaMKIIδ activation, increased nuclear myocyte enhancer factor 2,  sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05).                                 Active CaMKIIδ activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33).	human	Myocardial tissue	High+Lowthroughput	Structural and functional cardiac profile after prolonged duration of mechanical unloading: potential implications for myocardial recovery	否		heart disease	cardiac muscle cell (sensu Arthopoda)	E_01_0749	weston blot,RNA sequencing analysis	LVAD support was associated with CaMKIIδ activation, increased nuclear myocyte enhancer factor 2,  sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05).                                 Active CaMKIIδ activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	LVAD support was associated with CaMKIIδ activation, increased nuclear myocyte enhancer factor 2,  sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05).                                 Active CaMKIIδ activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33).		LVAD support was associated with CaMKIIδ activation, increased nuclear myocyte enhancer factor 2,  sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05).                                 Active CaMKIIδ activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33).	Immunohistochemical staining	LVAD support was associated with CaMKIIδ activation, increased nuclear myocyte enhancer factor 2,  sustained histone deacetylase-4 phosphorylation, increased circulating and cardiac myostatin (MSTN) and MSTN signaling mediated by SMAD2, ongoing structural protein dysregulation and sustained fibrosis and apoptosis (all P < 0.05).                                 Active CaMKIIδ activates class IIa histone deacetylases (HDACs), HDAC4 and HDAC5, which in turn activate the myocyte enhancer factor 2 (MEF2) transcription factor (3). MEF2 drives the expression of fetal cardiac and stress response genes, including the negative growth factor regulator myostatin (MSTN) (33).			weston blot,RNA sequencing analysis				HDAC5
30140372	chr1	173855894	173857894	GAS5	The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 	human		High+Lowthroughput	Lyophilized human cells stored at room temperature preserve multiple RNA species at excellent quality for RNA sequencing	否				E_01_0750	RT qPCR, RNA SEQ, statistical analysis	The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 	Immunohistochemical staining	The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 	GAS5		RT-qPCR,RNA-Seq,统计分析	The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 			
30140372	chr22	30966430	30968430	TUG1	The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 	human		High+Lowthroughput	Lyophilized human cells stored at room temperature preserve multiple RNA species at excellent quality for RNA sequencing	否				E_01_0750	RT qPCR, RNA SEQ, statistical analysis	The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 		The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 	Immunohistochemical staining	The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 			RT-qPCR,RNA-Seq,统计分析				TUG1
30140372	chr11	65495229	65497229	MALAT1	The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 	human		High+Lowthroughput	Lyophilized human cells stored at room temperature preserve multiple RNA species at excellent quality for RNA sequencing	否				E_01_0750	RT qPCR, RNA SEQ, statistical analysis	The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 	Immunohistochemical staining	The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 	MALAT1		RT-qPCR,RNA-Seq,统计分析	The abundance of the selected mRNAs with various expression levels, as well as enhancer-associated RNAs and cancer biomarker long non-coding RNAs (MALAT1, GAS5 and TUG1), were not significantly different between the two groups as assessed by RT-qPCR. 			
30139998	chr20	30244800	30316534	RNF2	Here, we show that RNF2, encoding RING1B, and canonical PRC1 (cPRC1) genes are overexpressed in breast cancer.                                                                                  BMI1, encoding for PCGF4, is the best studied PRC1 gene in cancer to date.	human		Low+High throughput	Polycomb complexes associate with enhancers and promote oncogenic transcriptional programs in cancer through multiple mechanisms	否	--	Breast Cancer	mammary gland epithelial cell	E_02_0461	ChIP-qPCR,ChIP-seq,Luciferase Reporter Assay	In contrast to the broad RING1B ChIP-seq signals in pluripotent cells, RING1B peaks in the breast cell lines were narrow, resembling ChIP-seq signals of transcription factors. Therefore, we assessed whether RING1B is recruited to specific transcription factor-binding sites at SEs.	Super-Enhancer	--	qRT-PCR	Indeed,we observed RING1B recruitment at SE regions near BCL2L1 in MDA-MB-231 and ESR1 in T47D23.	BCL-XL/S,BCL2L,BCLX,Bcl-X,PPP1R52	RING1B regulates Enhancer activity and gene transcription not only by promoting the expression of oncogenes but also by regulating chromatin accessibility.	ATAC-seq	"RING1B was recruited to regions targeted by transcription factors and its depletion deregulated breast cancer signaling pathways as well as FOXA1 and ERα localization to chromatin, we next hypothesized that RING1B regulates transcriptional programs in breast cancer by orchestrating chromatin accessibility. To test
this, we performed transposase-accessible chromatin sequencing (ATAC-seq)35 in RING1B-depleted cells.These results indicate that RING1B depletion affects chromatin
accessibility at enhancer regions."	RNF2	BAP-1,BAP1,DING,HIPI3,RING1B,RING2	ChIP-qPCR	RING1B, H3K27me3 and H3K27ac ChIP-qPCR of RIN1GB-containing enhancers in control and RING1B-depleted T47D cells. IgG antibody was used as a negative control. As additional control, RING1B ChIP-qPCR were performed using a different RING1B antibody from the one used for ChIP-seq.	--	--	BCL2L1
30139998	chr20	30244800	30316534	PRC1	Here, we show that RNF2, encoding RING1B, and canonical PRC1 (cPRC1) genes are overexpressed in breast cancer.                                                                                  BMI1, encoding for PCGF4, is the best studied PRC1 gene in cancer to date.	human		Low+High throughput	Polycomb complexes associate with enhancers and promote oncogenic transcriptional programs in cancer through multiple mechanisms	否	--	Breast Cancer	mammary gland epithelial cell	E_02_0461	ChIP-qPCR,ChIP-seq,Luciferase Reporter Assay	In contrast to the broad RING1B ChIP-seq signals in pluripotent cells, RING1B peaks in the breast cell lines were narrow, resembling ChIP-seq signals of transcription factors. Therefore, we assessed whether RING1B is recruited to specific transcription factor-binding sites at SEs.	Super-Enhancer	--	qRT-PCR	Indeed,we observed RING1B recruitment at SE regions near BCL2L1 in MDA-MB-231 and ESR1 in T47D23.	BCL-XL/S,BCL2L,BCLX,Bcl-X,PPP1R52	RING1B regulates Enhancer activity and gene transcription not only by promoting the expression of oncogenes but also by regulating chromatin accessibility.	ATAC-seq	"RING1B was recruited to regions targeted by transcription factors and its depletion deregulated breast cancer signaling pathways as well as FOXA1 and ERα localization to chromatin, we next hypothesized that RING1B regulates transcriptional programs in breast cancer by orchestrating chromatin accessibility. To test
this, we performed transposase-accessible chromatin sequencing (ATAC-seq)35 in RING1B-depleted cells.These results indicate that RING1B depletion affects chromatin
accessibility at enhancer regions."	RNF2	BAP-1,BAP1,DING,HIPI3,RING1B,RING2	ChIP-qPCR	RING1B, H3K27me3 and H3K27ac ChIP-qPCR of RIN1GB-containing enhancers in control and RING1B-depleted T47D cells. IgG antibody was used as a negative control. As additional control, RING1B ChIP-qPCR were performed using a different RING1B antibody from the one used for ChIP-seq.	--	--	BCL2L1
30139998	chr20	30244800	30316534	BMI1	Here, we show that RNF2, encoding RING1B, and canonical PRC1 (cPRC1) genes are overexpressed in breast cancer.                                                                                  BMI1, encoding for PCGF4, is the best studied PRC1 gene in cancer to date.	human		Low+High throughput	Polycomb complexes associate with enhancers and promote oncogenic transcriptional programs in cancer through multiple mechanisms	否	--	Breast Cancer	mammary gland epithelial cell	E_02_0461	ChIP-qPCR,ChIP-seq,Luciferase Reporter Assay	In contrast to the broad RING1B ChIP-seq signals in pluripotent cells, RING1B peaks in the breast cell lines were narrow, resembling ChIP-seq signals of transcription factors. Therefore, we assessed whether RING1B is recruited to specific transcription factor-binding sites at SEs.	Super-Enhancer	--	qRT-PCR	Indeed,we observed RING1B recruitment at SE regions near BCL2L1 in MDA-MB-231 and ESR1 in T47D23.	BCL-XL/S,BCL2L,BCLX,Bcl-X,PPP1R52	RING1B regulates Enhancer activity and gene transcription not only by promoting the expression of oncogenes but also by regulating chromatin accessibility.	ATAC-seq	"RING1B was recruited to regions targeted by transcription factors and its depletion deregulated breast cancer signaling pathways as well as FOXA1 and ERα localization to chromatin, we next hypothesized that RING1B regulates transcriptional programs in breast cancer by orchestrating chromatin accessibility. To test
this, we performed transposase-accessible chromatin sequencing (ATAC-seq)35 in RING1B-depleted cells.These results indicate that RING1B depletion affects chromatin
accessibility at enhancer regions."	RNF2	BAP-1,BAP1,DING,HIPI3,RING1B,RING2	ChIP-qPCR	RING1B, H3K27me3 and H3K27ac ChIP-qPCR of RIN1GB-containing enhancers in control and RING1B-depleted T47D cells. IgG antibody was used as a negative control. As additional control, RING1B ChIP-qPCR were performed using a different RING1B antibody from the one used for ChIP-seq.	--	--	BCL2L1
30139328	chr18	38066274	38068274	Hdac3	Applied to wildtype and histone deacetylase 3 (Hdac3) knockout mouse livers, NRSA showed that HDAC3 regulates RNA polymerase recruitment through both proximal (promoter) and distal (enhancer) regulatory elements. 	mouse,human		High+Lowthroughput	Nascent RNA sequencing analysis provides insights into enhancer-mediated gene regulation	否		leukemia	K562 cell	E_02_0462	PCR, pro SEQ, gro SEQ, nascent RNA sequencing analysis, chip seq	Applied to wildtype and histone deacetylase 3 (Hdac3) knockout mouse livers, NRSA showed that HDAC3 regulates RNA polymerase recruitment through both proximal (promoter) and distal (enhancer) regulatory elements. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Applied to wildtype and histone deacetylase 3 (Hdac3) knockout mouse livers, NRSA showed that HDAC3 regulates RNA polymerase recruitment through both proximal (promoter) and distal (enhancer) regulatory elements. 		Applied to wildtype and histone deacetylase 3 (Hdac3) knockout mouse livers, NRSA showed that HDAC3 regulates RNA polymerase recruitment through both proximal (promoter) and distal (enhancer) regulatory elements. 	Immunohistochemical staining	Applied to wildtype and histone deacetylase 3 (Hdac3) knockout mouse livers, NRSA showed that HDAC3 regulates RNA polymerase recruitment through both proximal (promoter) and distal (enhancer) regulatory elements. 			PCR,PRO-seq,GRO-seq,新生RNA测序分析,ChIP-seq				Hdac3
30138574	chr1	161763471	161765471	ATF6	Furthermore, 4-PBA diminished the expression32 of ERS markers (GRP78, CHOP, PERK, ATF6 and IRE1α) in vital organs of AP rats.	mouse		High+Lowthroughput	Inhibition of endoplasmic reticulum stress by 4-phenylbutyric acid prevents vital organ injury in rat acute pancreatitis	否		acute pancreatitis	Beta cell	E_02_0463	Real time PCR, immunofluorescence staining, statistical analysis	Furthermore, 4-PBA diminished the expression32 of ERS markers (GRP78, CHOP, PERK, ATF6 and IRE1α) in vital organs of AP rats.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, 4-PBA diminished the expression32 of ERS markers (GRP78, CHOP, PERK, ATF6 and IRE1α) in vital organs of AP rats.		Furthermore, 4-PBA diminished the expression32 of ERS markers (GRP78, CHOP, PERK, ATF6 and IRE1α) in vital organs of AP rats.	Immunohistochemical staining	Furthermore, 4-PBA diminished the expression32 of ERS markers (GRP78, CHOP, PERK, ATF6 and IRE1α) in vital organs of AP rats.			real-time PCR,免疫荧光染色,统计分析				ATF6
30137413	chr21	37362767	37364767	DYRK1A	DYRK1A, dual-specificity tyrosine phosphorylation-regulated kinase 1A, which is linked to mental retardation and microcephaly, is a member of the CMGC group of kinases.	humanmouse		High+Lowthroughput	DYRK1A interacts with histone acetyl transferase p300 and CBP and localizes to enhancers	否		Mental retardation, microcephaly		E_02_0464	Chip SEQ, RT qPCR, statistical analysis, Weston blot, gene knockdown	DYRK1A, dual-specificity tyrosine phosphorylation-regulated kinase 1A, which is linked to mental retardation and microcephaly, is a member of the CMGC group of kinases.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	DYRK1A, dual-specificity tyrosine phosphorylation-regulated kinase 1A, which is linked to mental retardation and microcephaly, is a member of the CMGC group of kinases.		DYRK1A, dual-specificity tyrosine phosphorylation-regulated kinase 1A, which is linked to mental retardation and microcephaly, is a member of the CMGC group of kinases.	Immunohistochemical staining	DYRK1A, dual-specificity tyrosine phosphorylation-regulated kinase 1A, which is linked to mental retardation and microcephaly, is a member of the CMGC group of kinases.			ChIP-Seq,RT-qPCR,统计分析,weston blot,基因敲降				DYRK1A
30136421	chr19	10130546	10132546	DNMT1	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	human	Liver cancer liver tissues	High+Lowthroughput	Integrating the Epigenome to Identify Drivers of Hepatocellular Carcinoma	否		Hepatocellular carcinoma (HCC), cirrhosis, hepatitis B	hepatocyte	E_01_0751	qRT-PCR ,ChIP-seq,RNA-seq	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	Immunohistochemical staining	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	DNMT1		qRT-PCR ,ChIP-seq,RNA-seq	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).			
30136421	chr2	25225067	25227067	DNMT3A	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	human	Liver cancer liver tissues	High+Lowthroughput	Integrating the Epigenome to Identify Drivers of Hepatocellular Carcinoma	否		Hepatocellular carcinoma (HCC), cirrhosis, hepatitis B	hepatocyte	E_01_0751	qRT-PCR ,ChIP-seq,RNA-seq	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	Immunohistochemical staining	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	DNMT3A		qRT-PCR ,ChIP-seq,RNA-seq	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).			
30136421	chr10	68557795	68559795	TET1	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	human	Liver cancer liver tissues	High+Lowthroughput	Integrating the Epigenome to Identify Drivers of Hepatocellular Carcinoma	否		Hepatocellular carcinoma (HCC), cirrhosis, hepatitis B	hepatocyte	E_01_0751	qRT-PCR ,ChIP-seq,RNA-seq	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	Immunohistochemical staining	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	TET1		qRT-PCR ,ChIP-seq,RNA-seq	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).			
30136421	chr2	73982342	73984342	TET3	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	human	Liver cancer liver tissues	High+Lowthroughput	Integrating the Epigenome to Identify Drivers of Hepatocellular Carcinoma	否		Hepatocellular carcinoma (HCC), cirrhosis, hepatitis B	hepatocyte	E_01_0751	qRT-PCR ,ChIP-seq,RNA-seq	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).		While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	Immunohistochemical staining	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).			qRT-PCR ,ChIP-seq,RNA-seq				TET3
30136421	chr4	105142898	105144898	TET2	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	human	Liver cancer liver tissues	High+Lowthroughput	Integrating the Epigenome to Identify Drivers of Hepatocellular Carcinoma	否		Hepatocellular carcinoma (HCC), cirrhosis, hepatitis B	hepatocyte	E_01_0751	qRT-PCR ,ChIP-seq,RNA-seq	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).		While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).	Immunohistochemical staining	While it is likely that etiologic risk exposures drive HCC through both genetic and epigenetic mechanisms, epigenetic modifications appear to be profoundly disrupted preceding detectable malignancy (5, 6). Epigenetic marks on the DNA, including 5-methylcytosine (5mC, mediated by the DNA methyltransferases DNMT1, DNMT3A, and DNMT3B) and 5-hydroxymethylcytosine (5hmC, mediated by the ten-eleven translocation family TET1, TET2, and TET3), are critical regulators of development that frequently become deregulated in and directly contribute to tumorigenesis (7).			qRT-PCR ,ChIP-seq,RNA-seq				TET2
30135326	chr8	132864317	132866317	TG	Rg1 significantly reduced liver weight, serum alanine aminotransferase (A LT), aspartate aminotransferase (AST), triglyceride (TG), liver fr ee fatty acids (FFAs) and malondialdehyde (MDA) levels, and increased superoxide dismutase (SOD) activity.	mouse,human		High+Lowthroughput	Ginsenoside Rg1 Protects against Non-alcoholic Fatty Liver Disease by Ameliorating Lipid Peroxidation, Endoplasmic Reticulum Stress, and Inflammasome Activation	否		Non alcoholic fatty liver disease (NaF LD), liver fibrosis, cirrhosis, hepatocellular carcinoma	B cell	E_02_0465	QPCR, ELISA, Weston blot, statistical analysis	Rg1 significantly reduced liver weight, serum alanine aminotransferase (A LT), aspartate aminotransferase (AST), triglyceride (TG), liver fr ee fatty acids (FFAs) and malondialdehyde (MDA) levels, and increased superoxide dismutase (SOD) activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Rg1 significantly reduced liver weight, serum alanine aminotransferase (A LT), aspartate aminotransferase (AST), triglyceride (TG), liver fr ee fatty acids (FFAs) and malondialdehyde (MDA) levels, and increased superoxide dismutase (SOD) activity.		Rg1 significantly reduced liver weight, serum alanine aminotransferase (A LT), aspartate aminotransferase (AST), triglyceride (TG), liver fr ee fatty acids (FFAs) and malondialdehyde (MDA) levels, and increased superoxide dismutase (SOD) activity.	Immunohistochemical staining	Rg1 significantly reduced liver weight, serum alanine aminotransferase (A LT), aspartate aminotransferase (AST), triglyceride (TG), liver fr ee fatty acids (FFAs) and malondialdehyde (MDA) levels, and increased superoxide dismutase (SOD) activity.			qPCR,ELISA,weston blot,统计分析				TG
30134807	chr13	30453788	30455788	HMGB1	Background High mobility group box 1 (HMGB1) protein is a central endogenous inflammatory mediator contributing to the pathogenesis of several inflammatory disorders.                  However, full length HMGB1 and Δ30 HMGB1 formed complexes with PGN, a known TLR2 ligand, and synergistically potentiated the inflammatory response in PBMCs.	human		High+Lowthroughput	Ligation of free HMGB1 to TLR2 in the absence of ligand is negatively regulated by the C-terminal tail domain	否		inflammation	macrophage	E_01_0752	Statistical analysis, ELISA method	Background High mobility group box 1 (HMGB1) protein is a central endogenous inflammatory mediator contributing to the pathogenesis of several inflammatory disorders.                  However, full length HMGB1 and Δ30 HMGB1 formed complexes with PGN, a known TLR2 ligand, and synergistically potentiated the inflammatory response in PBMCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background High mobility group box 1 (HMGB1) protein is a central endogenous inflammatory mediator contributing to the pathogenesis of several inflammatory disorders.                  However, full length HMGB1 and Δ30 HMGB1 formed complexes with PGN, a known TLR2 ligand, and synergistically potentiated the inflammatory response in PBMCs.		Background High mobility group box 1 (HMGB1) protein is a central endogenous inflammatory mediator contributing to the pathogenesis of several inflammatory disorders.                  However, full length HMGB1 and Δ30 HMGB1 formed complexes with PGN, a known TLR2 ligand, and synergistically potentiated the inflammatory response in PBMCs.	Immunohistochemical staining	Background High mobility group box 1 (HMGB1) protein is a central endogenous inflammatory mediator contributing to the pathogenesis of several inflammatory disorders.                  However, full length HMGB1 and Δ30 HMGB1 formed complexes with PGN, a known TLR2 ligand, and synergistically potentiated the inflammatory response in PBMCs.			统计分析,elisa法				HMGB1
30134807	chr4	153681555	153683555	TLR2	Background High mobility group box 1 (HMGB1) protein is a central endogenous inflammatory mediator contributing to the pathogenesis of several inflammatory disorders.                  However, full length HMGB1 and Δ30 HMGB1 formed complexes with PGN, a known TLR2 ligand, and synergistically potentiated the inflammatory response in PBMCs.	human		High+Lowthroughput	Ligation of free HMGB1 to TLR2 in the absence of ligand is negatively regulated by the C-terminal tail domain	否		inflammation	macrophage	E_01_0752	Statistical analysis, ELISA method	Background High mobility group box 1 (HMGB1) protein is a central endogenous inflammatory mediator contributing to the pathogenesis of several inflammatory disorders.                  However, full length HMGB1 and Δ30 HMGB1 formed complexes with PGN, a known TLR2 ligand, and synergistically potentiated the inflammatory response in PBMCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Background High mobility group box 1 (HMGB1) protein is a central endogenous inflammatory mediator contributing to the pathogenesis of several inflammatory disorders.                  However, full length HMGB1 and Δ30 HMGB1 formed complexes with PGN, a known TLR2 ligand, and synergistically potentiated the inflammatory response in PBMCs.	Immunohistochemical staining	Background High mobility group box 1 (HMGB1) protein is a central endogenous inflammatory mediator contributing to the pathogenesis of several inflammatory disorders.                  However, full length HMGB1 and Δ30 HMGB1 formed complexes with PGN, a known TLR2 ligand, and synergistically potentiated the inflammatory response in PBMCs.	TLR2		统计分析,elisa法	Background High mobility group box 1 (HMGB1) protein is a central endogenous inflammatory mediator contributing to the pathogenesis of several inflammatory disorders.                  However, full length HMGB1 and Δ30 HMGB1 formed complexes with PGN, a known TLR2 ligand, and synergistically potentiated the inflammatory response in PBMCs.			
30134174	chr20	47206665	47208665	ZMYND8	Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.	human		High+Lowthroughput	Positive Regulation of Transcription by Human ZMYND8 through Its Association with P-TEFb Complex	否			293T cell	E_01_0753	Chip SEQ, QRT PCR, Weston blot, analysis of immunoprecipitation reactions, statistical analysis	Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.		Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.	Immunohistochemical staining	Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.			ChIP-seq,qRT-PCR,weston blot,免疫沉淀反应分析,统计分析				ZMYND8
30134174	chrX	53173820	53175820	KDM5C	Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.	human		High+Lowthroughput	Positive Regulation of Transcription by Human ZMYND8 through Its Association with P-TEFb Complex	否			293T cell	E_01_0753	Chip SEQ, QRT PCR, Weston blot, analysis of immunoprecipitation reactions, statistical analysis	Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.	Immunohistochemical staining	Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.	KDM5C		ChIP-seq,qRT-PCR,weston blot,免疫沉淀反应分析,统计分析	Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.			
30134174	chr9	127783018	127785018	CDK9	Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.	human		High+Lowthroughput	Positive Regulation of Transcription by Human ZMYND8 through Its Association with P-TEFb Complex	否			293T cell	E_01_0753	Chip SEQ, QRT PCR, Weston blot, analysis of immunoprecipitation reactions, statistical analysis	Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.	Immunohistochemical staining	Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.	CDK9		ChIP-seq,qRT-PCR,weston blot,免疫沉淀反应分析,统计分析	Physiologically, we further show that the ZMYND8 P-TEFb complex-mediated transcriptional activation is required for All-Trans Retinoic Acid (ATRA)-mediated differentiation of neuronal precursor cells.                                                                                                                                                                                    Through its interaction with KDM5C, ZMYND8 also suppresses enhancer over-expression by maintaining H3K4me1 enhancer signature (Shen et al., 2016).                                                  Among all the positive regulators of transcription, human P-TEFb complex, a heterodimer of CyclinT1/T2 and cyclin-dependent kinase 9 (CDK9) (Peng et al., 1998), plays a major role in activating target gene expression.			
30132567	chr14	49641316	49643316	POLE2	Furthermore, knockdown of POLE2 expression inhibited A549 and NCI-H1299 cell proliferation and apoptosis.	human		High+Lowthroughput	Knockdown of POLE2 expression suppresses lung adenocarcinoma cell malignant phenotypes in?vitro	否		Lung adenocarcinoma	A549 cell	E_01_0754	QRT PCR, Weston blot, statistical analysis	Furthermore, knockdown of POLE2 expression inhibited A549 and NCI-H1299 cell proliferation and apoptosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, knockdown of POLE2 expression inhibited A549 and NCI-H1299 cell proliferation and apoptosis.		Furthermore, knockdown of POLE2 expression inhibited A549 and NCI-H1299 cell proliferation and apoptosis.	Immunohistochemical staining	Furthermore, knockdown of POLE2 expression inhibited A549 and NCI-H1299 cell proliferation and apoptosis.			qRT-PCR,weston blot,统计分析				POLE2
30132536	chr6	31572566	31574566	TNF	TRAIL has reduced toxicicity compared with other members of the tumor necrosis factor (TNF) protein family, such as TNFα and Fas ligand (CD95L) (3). Pre-clinical trials have determined that TRAIL effectively inhibits tumor growth without inducing toxicity in both mice and non-human primates (4,5).	human,mouse		High+Lowthroughput	3?Bromopyruvate sensitizes human breast cancer cells to TRAIL?induced apoptosis via the phosphorylated AMPK?mediated upregulation of DR5	否		mammary cancer	MCF-7 cell	E_02_0466	ATP quantification, Weston blot, statistical analysis	TRAIL has reduced toxicicity compared with other members of the tumor necrosis factor (TNF) protein family, such as TNFα and Fas ligand (CD95L) (3). Pre-clinical trials have determined that TRAIL effectively inhibits tumor growth without inducing toxicity in both mice and non-human primates (4,5).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	TRAIL has reduced toxicicity compared with other members of the tumor necrosis factor (TNF) protein family, such as TNFα and Fas ligand (CD95L) (3). Pre-clinical trials have determined that TRAIL effectively inhibits tumor growth without inducing toxicity in both mice and non-human primates (4,5).		TRAIL has reduced toxicicity compared with other members of the tumor necrosis factor (TNF) protein family, such as TNFα and Fas ligand (CD95L) (3). Pre-clinical trials have determined that TRAIL effectively inhibits tumor growth without inducing toxicity in both mice and non-human primates (4,5).	Immunohistochemical staining	TRAIL has reduced toxicicity compared with other members of the tumor necrosis factor (TNF) protein family, such as TNFα and Fas ligand (CD95L) (3). Pre-clinical trials have determined that TRAIL effectively inhibits tumor growth without inducing toxicity in both mice and non-human primates (4,5).			ATP quantification,weston blot,统计分析				TNF
30131420	chr12	106988606	106990606	CRY1	he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 	mouse		High+Lowthroughput	Photoexcited CRYPTOCHROME1 Interacts with Dephosphorylated BES1 to Regulate Brassinosteroid Signaling and Photomorphogenesis in Arabidopsis	否				E_02_0467	BiFC Assays,Co-IP Assays,RT-qPCR,ChIP-qPCR,RNA-Seq,weston blot	he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 		he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 	Immunohistochemical staining	he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 			BiFC Assays,Co-IP Assays,RT-qPCR,ChIP-qPCR,RNA-Seq,weston blot				CRY1
30131420	chr11	45844577	45846577	CRY2	he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 	mouse		High+Lowthroughput	Photoexcited CRYPTOCHROME1 Interacts with Dephosphorylated BES1 to Regulate Brassinosteroid Signaling and Photomorphogenesis in Arabidopsis	否				E_02_0467	BiFC Assays,Co-IP Assays,RT-qPCR,ChIP-qPCR,RNA-Seq,weston blot	he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 		he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 	Immunohistochemical staining	he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 			BiFC Assays,Co-IP Assays,RT-qPCR,ChIP-qPCR,RNA-Seq,weston blot				CRY2
30131420	chr1	175941922	175943922	COP1	he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 	mouse		High+Lowthroughput	Photoexcited CRYPTOCHROME1 Interacts with Dephosphorylated BES1 to Regulate Brassinosteroid Signaling and Photomorphogenesis in Arabidopsis	否				E_02_0467	BiFC Assays,Co-IP Assays,RT-qPCR,ChIP-qPCR,RNA-Seq,weston blot	he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 		he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 	Immunohistochemical staining	he signaling mechanism by which Arabidopsis thaliana cryptochromes CRY1 and CRY2 promote photomorphogenesis involves direct interactions with COP1, a RING motif-containing E3 ubiquitin ligase, and its enhancer SPA1. 			BiFC Assays,Co-IP Assays,RT-qPCR,ChIP-qPCR,RNA-Seq,weston blot				COP1
30131250	chr7	148804336	148806336	EZH2	Enhancer of Zeste 2 (EZH2) is the key enzymatic factor in Polycomb Repressive Complex 2 (PRC2), a transcriptional repressor which contributes to oncogenesis.                                                 We found that PHF19 transcript and protein levels were significantly elevated in human glioma tumors, which was negatively associated with expression of the anti-PHF19 microRNA miR-124a.	human,mouse		High+Lowthroughput	microRNA-124a suppresses PHF19 over-expression, EZH2 hyper-activation, and aberrant cell proliferation in human glioma	否		Gliomas	Glioma cell	E_02_0468	qRT-PCR,weston blot,	Enhancer of Zeste 2 (EZH2) is the key enzymatic factor in Polycomb Repressive Complex 2 (PRC2), a transcriptional repressor which contributes to oncogenesis.                                                 We found that PHF19 transcript and protein levels were significantly elevated in human glioma tumors, which was negatively associated with expression of the anti-PHF19 microRNA miR-124a.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of Zeste 2 (EZH2) is the key enzymatic factor in Polycomb Repressive Complex 2 (PRC2), a transcriptional repressor which contributes to oncogenesis.                                                 We found that PHF19 transcript and protein levels were significantly elevated in human glioma tumors, which was negatively associated with expression of the anti-PHF19 microRNA miR-124a.		Enhancer of Zeste 2 (EZH2) is the key enzymatic factor in Polycomb Repressive Complex 2 (PRC2), a transcriptional repressor which contributes to oncogenesis.                                                 We found that PHF19 transcript and protein levels were significantly elevated in human glioma tumors, which was negatively associated with expression of the anti-PHF19 microRNA miR-124a.	Immunohistochemical staining	Enhancer of Zeste 2 (EZH2) is the key enzymatic factor in Polycomb Repressive Complex 2 (PRC2), a transcriptional repressor which contributes to oncogenesis.                                                 We found that PHF19 transcript and protein levels were significantly elevated in human glioma tumors, which was negatively associated with expression of the anti-PHF19 microRNA miR-124a.			qRT-PCR,weston blot,				EZH2
30131250	chr9	120852845	120854845	PHF19	Enhancer of Zeste 2 (EZH2) is the key enzymatic factor in Polycomb Repressive Complex 2 (PRC2), a transcriptional repressor which contributes to oncogenesis.                                                 We found that PHF19 transcript and protein levels were significantly elevated in human glioma tumors, which was negatively associated with expression of the anti-PHF19 microRNA miR-124a.	human,mouse		High+Lowthroughput	microRNA-124a suppresses PHF19 over-expression, EZH2 hyper-activation, and aberrant cell proliferation in human glioma	否		Gliomas	Glioma cell	E_02_0468	qRT-PCR,weston blot,	Enhancer of Zeste 2 (EZH2) is the key enzymatic factor in Polycomb Repressive Complex 2 (PRC2), a transcriptional repressor which contributes to oncogenesis.                                                 We found that PHF19 transcript and protein levels were significantly elevated in human glioma tumors, which was negatively associated with expression of the anti-PHF19 microRNA miR-124a.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of Zeste 2 (EZH2) is the key enzymatic factor in Polycomb Repressive Complex 2 (PRC2), a transcriptional repressor which contributes to oncogenesis.                                                 We found that PHF19 transcript and protein levels were significantly elevated in human glioma tumors, which was negatively associated with expression of the anti-PHF19 microRNA miR-124a.		Enhancer of Zeste 2 (EZH2) is the key enzymatic factor in Polycomb Repressive Complex 2 (PRC2), a transcriptional repressor which contributes to oncogenesis.                                                 We found that PHF19 transcript and protein levels were significantly elevated in human glioma tumors, which was negatively associated with expression of the anti-PHF19 microRNA miR-124a.	Immunohistochemical staining	Enhancer of Zeste 2 (EZH2) is the key enzymatic factor in Polycomb Repressive Complex 2 (PRC2), a transcriptional repressor which contributes to oncogenesis.                                                 We found that PHF19 transcript and protein levels were significantly elevated in human glioma tumors, which was negatively associated with expression of the anti-PHF19 microRNA miR-124a.			qRT-PCR,weston blot,				PHF19
30130256	chr11	98040271	98042271	Med1	Using renin cells at various stages of stimulation, we identified regions in the genome where the chromatin is open for transcription, mapped histone modifications characteristic of active enhancers such as H3K27ac, and tracked deposition of transcriptional activators such as Med1, whose deletion results in ablation of renin expression and low blood pressure.	human,mouse		High+Lowthroughput	Super-enhancers maintain renin-expressing cell identity and memory to preserve multi-system homeostasis	否			As4.1 cell	E_02_0469	QRT PCR, ATAC SEQ, chip SEQ, RNA SEQ, statistical analysis	Using renin cells at various stages of stimulation, we identified regions in the genome where the chromatin is open for transcription, mapped histone modifications characteristic of active enhancers such as H3K27ac, and tracked deposition of transcriptional activators such as Med1, whose deletion results in ablation of renin expression and low blood pressure.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Using renin cells at various stages of stimulation, we identified regions in the genome where the chromatin is open for transcription, mapped histone modifications characteristic of active enhancers such as H3K27ac, and tracked deposition of transcriptional activators such as Med1, whose deletion results in ablation of renin expression and low blood pressure.		Using renin cells at various stages of stimulation, we identified regions in the genome where the chromatin is open for transcription, mapped histone modifications characteristic of active enhancers such as H3K27ac, and tracked deposition of transcriptional activators such as Med1, whose deletion results in ablation of renin expression and low blood pressure.	Immunohistochemical staining	Using renin cells at various stages of stimulation, we identified regions in the genome where the chromatin is open for transcription, mapped histone modifications characteristic of active enhancers such as H3K27ac, and tracked deposition of transcriptional activators such as Med1, whose deletion results in ablation of renin expression and low blood pressure.			qRT-PCR,ATAC-Seq,ChIP-Seq,RNA-Seq,统计分析				Med1
30127913	chr1	212033036	212035036	DTL	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.	human		High+Lowthroughput	Potential biomarkers of HCC based on gene expression and DNA methylation profiles	否		Hepatocellular carcinoma	endothelial cell	E_01_0755	RT qPCR, statistical analysis	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.		The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.	Immunohistochemical staining	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.			RT-qPCR,统计分析				DTL
30127913	chr5	172765310	172767310	DUSP1	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.	human		High+Lowthroughput	Potential biomarkers of HCC based on gene expression and DNA methylation profiles	否		Hepatocellular carcinoma	endothelial cell	E_01_0755	RT qPCR, statistical analysis	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.		The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.	Immunohistochemical staining	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.			RT-qPCR,统计分析				DUSP1
30127913	chr14	35398894	35400894	NFKBIA	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.	human		High+Lowthroughput	Potential biomarkers of HCC based on gene expression and DNA methylation profiles	否		Hepatocellular carcinoma	endothelial cell	E_01_0755	RT qPCR, statistical analysis	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.	Immunohistochemical staining	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.	NFKBIA		RT-qPCR,统计分析	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.			
30127913	chr12	93567415	93569415	SOCS2	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.	human		High+Lowthroughput	Potential biomarkers of HCC based on gene expression and DNA methylation profiles	否		Hepatocellular carcinoma	endothelial cell	E_01_0755	RT qPCR, statistical analysis	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.		The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.	Immunohistochemical staining	The present study suggested that DTL, DUSP1, NFKBIA and SOCS2 may be potential biomarkers of HCC, and the tumor protein p53 signaling , forkhead box O1 signaling and metabolic pathways may serve roles in the pathogenesis of HCC.			RT-qPCR,统计分析				SOCS2
30127433	chr16	67559500	67561500	CTCF	Go to: Introduction Cohesin is a multiprotein complex that cooperates with the sequence-specific DNA binding protein CTCF in forming key features of 3D genome organization such as topologically associated domains (TADs), contact domains and chromatin loops.	human		High+Lowthroughput	Control of inducible gene expression links cohesin to hematopoietic progenitor self-renewal and differentiation	否		Acute myeloid leukemia	macrophage	E_01_0756	RT-PCR,ChIP-PCR,RNA-seq,FACS analysis,GRO-seq,ATAC-seq,ChIP-seq	Go to: Introduction Cohesin is a multiprotein complex that cooperates with the sequence-specific DNA binding protein CTCF in forming key features of 3D genome organization such as topologically associated domains (TADs), contact domains and chromatin loops.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Go to: Introduction Cohesin is a multiprotein complex that cooperates with the sequence-specific DNA binding protein CTCF in forming key features of 3D genome organization such as topologically associated domains (TADs), contact domains and chromatin loops.	Immunohistochemical staining	Go to: Introduction Cohesin is a multiprotein complex that cooperates with the sequence-specific DNA binding protein CTCF in forming key features of 3D genome organization such as topologically associated domains (TADs), contact domains and chromatin loops.	CTCF		RT-PCR,ChIP-PCR,RNA-seq,FACS analysis,GRO-seq,ATAC-seq,ChIP-seq	Go to: Introduction Cohesin is a multiprotein complex that cooperates with the sequence-specific DNA binding protein CTCF in forming key features of 3D genome organization such as topologically associated domains (TADs), contact domains and chromatin loops.			
30127357	chr17	71648774	71650774	Smchd1	Structural maintenance of chromosomes hinge domain contain- ing 1 (Smchd1) is a noncanonical SMC protein12 that is similar to the canonical SMC proteins13 15 in that it dimerizes and interacts with nucleic acids through its hinge domain 16,17 .                                                                                                                                    At all Smchd1 targets, chromosome conformation at differ- ent scales plays a role in regulating gene expression.	human,mouse		High+Lowthroughput	Smchd1 regulates long-range chromatin interactions on the inactive X chromosome and at Hox clusters	是			293 cell	E_02_0470	Chip SEQ, immunofluorescence staining, RT qPCR, Weston blot	Structural maintenance of chromosomes hinge domain contain- ing 1 (Smchd1) is a noncanonical SMC protein12 that is similar to the canonical SMC proteins13 15 in that it dimerizes and interacts with nucleic acids through its hinge domain 16,17 .                                                                                                                                    At all Smchd1 targets, chromosome conformation at differ- ent scales plays a role in regulating gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Structural maintenance of chromosomes hinge domain contain- ing 1 (Smchd1) is a noncanonical SMC protein12 that is similar to the canonical SMC proteins13 15 in that it dimerizes and interacts with nucleic acids through its hinge domain 16,17 .                                                                                                                                    At all Smchd1 targets, chromosome conformation at differ- ent scales plays a role in regulating gene expression.		Structural maintenance of chromosomes hinge domain contain- ing 1 (Smchd1) is a noncanonical SMC protein12 that is similar to the canonical SMC proteins13 15 in that it dimerizes and interacts with nucleic acids through its hinge domain 16,17 .                                                                                                                                    At all Smchd1 targets, chromosome conformation at differ- ent scales plays a role in regulating gene expression.	Immunohistochemical staining	Structural maintenance of chromosomes hinge domain contain- ing 1 (Smchd1) is a noncanonical SMC protein12 that is similar to the canonical SMC proteins13 15 in that it dimerizes and interacts with nucleic acids through its hinge domain 16,17 .                                                                                                                                    At all Smchd1 targets, chromosome conformation at differ- ent scales plays a role in regulating gene expression.			ChIP-seq,免疫荧光染色,RT-qPCR,weston blot				Smchd1
30127245	chr3	49826074	49828074	TRAIP	TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 	human,mouse		High+Lowthroughput	In Vitro Inhibitory Mechanism Effect of TRAIP on the Function of TRAF2 Revealed by Characterization of Interaction Domains	否			B cell	E_02_0471	Real time PCR, mals, native PAGE shift assay	TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 		TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 	Immunohistochemical staining	TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 			Real-Time PCR,MALS,Native-PAGE转移分析				TRAIP
30127245	chr9	136879188	136881188	TRAF2	TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 	human,mouse		High+Lowthroughput	In Vitro Inhibitory Mechanism Effect of TRAIP on the Function of TRAF2 Revealed by Characterization of Interaction Domains	否			B cell	E_02_0471	Real time PCR, mals, native PAGE shift assay	TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 		TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 	Immunohistochemical staining	TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 			Real-Time PCR,MALS,Native-PAGE转移分析				TRAF2
30127245	chr9	120899960	120901960	TRAF1	TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 	human,mouse		High+Lowthroughput	In Vitro Inhibitory Mechanism Effect of TRAIP on the Function of TRAF2 Revealed by Characterization of Interaction Domains	否			B cell	E_02_0471	Real time PCR, mals, native PAGE shift assay	TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 		TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 	Immunohistochemical staining	TRAF-interacting protein (TRAIP), a negative regulator of TNF-induced-nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activation, inhibits adaptor protein TRAF2 by direct interaction and is critical in apoptosis, cell proliferation, antiviral response, and embryonic development.                                                        Characterization of the TRAF-N domains of TRAF1 and TRAF2, the tentative TRAIP-binding region of TRAFs, suggested the molecular basis of the inhibitory effect of TRAIP on TRAF2 in NF-κB signaling. 			Real-Time PCR,MALS,Native-PAGE转移分析				TRAF1
30126893	chr10	8042438	8044438	GATA3	Haploid deficiency of the human GATA3 gene leads to a dominantly inherited condition known as HDR (hypoparathyroidism, neural sensory deafness, and renal defect) syndrome (12), underscoring a prominent role for GATA3 in specifying normal developmental programing in the affected tissues.	human,mouse		High+Lowthroughput	A Gata3 3' Distal Otic Vesicle Enhancer Directs Inner Ear-Specific Gata3 Expression	是		Neurosensory deafness		E_02_0472	PCR,Histological analysis	Haploid deficiency of the human GATA3 gene leads to a dominantly inherited condition known as HDR (hypoparathyroidism, neural sensory deafness, and renal defect) syndrome (12), underscoring a prominent role for GATA3 in specifying normal developmental programing in the affected tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Haploid deficiency of the human GATA3 gene leads to a dominantly inherited condition known as HDR (hypoparathyroidism, neural sensory deafness, and renal defect) syndrome (12), underscoring a prominent role for GATA3 in specifying normal developmental programing in the affected tissues.		Haploid deficiency of the human GATA3 gene leads to a dominantly inherited condition known as HDR (hypoparathyroidism, neural sensory deafness, and renal defect) syndrome (12), underscoring a prominent role for GATA3 in specifying normal developmental programing in the affected tissues.	Immunohistochemical staining	Haploid deficiency of the human GATA3 gene leads to a dominantly inherited condition known as HDR (hypoparathyroidism, neural sensory deafness, and renal defect) syndrome (12), underscoring a prominent role for GATA3 in specifying normal developmental programing in the affected tissues.			PCR,Histological analysis				GATA3
30126161	chr8	84014206	84016206	Ucp1	H3K27 acetylation was also seen within Ucp1 promoter upon isoproterenol addition, favouring open chromatin for Ucp1 transcriptional activation.                                                             In contrast, HDAC3 mRNA and protein levels were simultaneously downregulated upon isoproterenol addition, resulting in reduced recruitment of HDAC3 to the Ucp1 enhancer region, causing an increased H3K27 acetylation for Ucp1 upregulation. 	human,mouse	adipose tissue	High+Lowthroughput	β-adrenergic Receptor Stimulation Revealed a Novel Regulatory Pathway via Suppressing Histone Deacetylase 3 to Induce Uncoupling Protein 1 Expression in Mice Beige Adipocyte	否		Obesity		E_02_0473	Real time PCR, chromatin immunoprecipitation (chip), statistical analysis, Weston blot	H3K27 acetylation was also seen within Ucp1 promoter upon isoproterenol addition, favouring open chromatin for Ucp1 transcriptional activation.                                                             In contrast, HDAC3 mRNA and protein levels were simultaneously downregulated upon isoproterenol addition, resulting in reduced recruitment of HDAC3 to the Ucp1 enhancer region, causing an increased H3K27 acetylation for Ucp1 upregulation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	H3K27 acetylation was also seen within Ucp1 promoter upon isoproterenol addition, favouring open chromatin for Ucp1 transcriptional activation.                                                             In contrast, HDAC3 mRNA and protein levels were simultaneously downregulated upon isoproterenol addition, resulting in reduced recruitment of HDAC3 to the Ucp1 enhancer region, causing an increased H3K27 acetylation for Ucp1 upregulation. 		H3K27 acetylation was also seen within Ucp1 promoter upon isoproterenol addition, favouring open chromatin for Ucp1 transcriptional activation.                                                             In contrast, HDAC3 mRNA and protein levels were simultaneously downregulated upon isoproterenol addition, resulting in reduced recruitment of HDAC3 to the Ucp1 enhancer region, causing an increased H3K27 acetylation for Ucp1 upregulation. 	Immunohistochemical staining	H3K27 acetylation was also seen within Ucp1 promoter upon isoproterenol addition, favouring open chromatin for Ucp1 transcriptional activation.                                                             In contrast, HDAC3 mRNA and protein levels were simultaneously downregulated upon isoproterenol addition, resulting in reduced recruitment of HDAC3 to the Ucp1 enhancer region, causing an increased H3K27 acetylation for Ucp1 upregulation. 			real-time PCR,Chromatin Immunoprecipitation (ChIP) ,统计分析,weston blot				Ucp1
30125982	chr10	30705623	30707623	Hey2	Hairy and enhancer of split related with YRPW motif 2 (Hey2), also known as cardiovascular helix loop helix factor 1 (CHF1), is a member of the hairy and enhancer of split related (HESR) family of basic helix loop helix (bHLH) type transcription factors.22	human,large,mouse		High+Lowthroughput	microRNA-146a and Hey2 form a mutual negative feedback loop to regulate the inflammatory response in chronic apical periodontitis	否		Chronic periapical periodontitis (CAP)	MC3T3-E1 cell	E_02_0474	Real ‐ time PCR, ELISA, Weston blot, chromatin immunoprecipitation (chip)	Hairy and enhancer of split related with YRPW motif 2 (Hey2), also known as cardiovascular helix loop helix factor 1 (CHF1), is a member of the hairy and enhancer of split related (HESR) family of basic helix loop helix (bHLH) type transcription factors.22	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Hairy and enhancer of split related with YRPW motif 2 (Hey2), also known as cardiovascular helix loop helix factor 1 (CHF1), is a member of the hairy and enhancer of split related (HESR) family of basic helix loop helix (bHLH) type transcription factors.22		Hairy and enhancer of split related with YRPW motif 2 (Hey2), also known as cardiovascular helix loop helix factor 1 (CHF1), is a member of the hairy and enhancer of split related (HESR) family of basic helix loop helix (bHLH) type transcription factors.22	Immunohistochemical staining	Hairy and enhancer of split related with YRPW motif 2 (Hey2), also known as cardiovascular helix loop helix factor 1 (CHF1), is a member of the hairy and enhancer of split related (HESR) family of basic helix loop helix (bHLH) type transcription factors.22			Real‐time PCR,ELISA,weston blot,染色质免疫沉淀(ChIP)				Hey2
30125275	chr17	42310564	42312564	STAT3	Niclosamide has been reported to competitively inhibit the mTOR (mammalian target of rapamycin), STAT3 (signal transducer and activator of transcription 3), and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) signaling pathways; however, selective inhibitors of those pathways did not reduce DENV infection. 	mouse		High+Lowthroughput	The antiparasitic drug niclosamide inhibits dengue virus infection by interfering with endosomal acidification independent of mTOR	否			A549 cell	E_02_0475	ELISA, Weston blot, statistical analysis, immunofluorescence light staining	Niclosamide has been reported to competitively inhibit the mTOR (mammalian target of rapamycin), STAT3 (signal transducer and activator of transcription 3), and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) signaling pathways; however, selective inhibitors of those pathways did not reduce DENV infection. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Niclosamide has been reported to competitively inhibit the mTOR (mammalian target of rapamycin), STAT3 (signal transducer and activator of transcription 3), and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) signaling pathways; however, selective inhibitors of those pathways did not reduce DENV infection. 		Niclosamide has been reported to competitively inhibit the mTOR (mammalian target of rapamycin), STAT3 (signal transducer and activator of transcription 3), and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) signaling pathways; however, selective inhibitors of those pathways did not reduce DENV infection. 	Immunohistochemical staining	Niclosamide has been reported to competitively inhibit the mTOR (mammalian target of rapamycin), STAT3 (signal transducer and activator of transcription 3), and NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) signaling pathways; however, selective inhibitors of those pathways did not reduce DENV infection. 			ELISA,weston blot,统计分析,免疫荧光光染色				STAT3
30124855	chr1	145667850	145669850	PDZK1	siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	human,zebrafish		High+Lowthroughput	A non-coding genetic variant maximally associated with serum urate levels is functionally linked to HNF4A-dependent PDZK1 expression	是	rs1967017,rs1471633	hyperuricemia	HEK293 cell	E_02_0476	Quantitative PCR, immunoblot analysis, chip PCR, statistical analysis, Weston blot	siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 		siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	Immunohistochemical staining	siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 			Quantitative PCR,Immunoblot analysis, ChIP-PCR,统计分析,weston blot				PDZK1
30124855	chr20	44352999	44354999	HNF4A	siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	human,zebrafish		High+Lowthroughput	A non-coding genetic variant maximally associated with serum urate levels is functionally linked to HNF4A-dependent PDZK1 expression	是	rs1967017,rs1471633	hyperuricemia	HEK293 cell	E_02_0476	Quantitative PCR, immunoblot analysis, chip PCR, statistical analysis, Weston blot	siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 		siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 	Immunohistochemical staining	siRNA depletion of HNF4A reduced endogenous PDZK1 expression in HepG2 cells. 			Quantitative PCR,Immunoblot analysis, ChIP-PCR,统计分析,weston blot				HNF4A
30123075	chr11	73215337	73217337	P2RY2	P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 	human		High+Lowthroughput	Enhancer RNA - P2RY2e induced by estrogen promotes malignant behaviors of bladder cancer	否		Breast, bladder, stomach, pancreas, prostate, lung	T24 cell	E_01_0757	RT qPCR, flow cytometry, ELISA, statistical analysis	P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 		P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 	Immunohistochemical staining	P2RY2 enhancer RNA (P2RY2e) is an estrogen-responsive eRNA and involved in the development of breast cancer. 			RT-qPCR,流式细胞术,ELISA,统计分析				P2RY2
30122536	chr8	144288649	144290649	HSF1	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.	human,Drosophila,melanogaster		High+Lowthroughput	Architectural Proteins and Pluripotency Factors Cooperate to Orchestrate the Transcriptional Response of hESCs to Temperature Stress	否			embryonic stem cell	E_02_0477	EU-seq,HiChIP,ChIP-Seq,ATAC-seq,APA metaplot analysis 	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.		We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.	Immunohistochemical staining	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.			EU-seq,HiChIP,ChIP-Seq,ATAC-seq,APA metaplot analysis 				HSF1
30122536	chr12	7785009	7787009	NANOG	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.	human,Drosophila,melanogaster		High+Lowthroughput	Architectural Proteins and Pluripotency Factors Cooperate to Orchestrate the Transcriptional Response of hESCs to Temperature Stress	否			embryonic stem cell	E_02_0477	EU-seq,HiChIP,ChIP-Seq,ATAC-seq,APA metaplot analysis 	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.		We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.	Immunohistochemical staining	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.			EU-seq,HiChIP,ChIP-Seq,ATAC-seq,APA metaplot analysis 				NANOG
30122536	chr9	107481906	107483906	KLF4	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.	human,Drosophila,melanogaster		High+Lowthroughput	Architectural Proteins and Pluripotency Factors Cooperate to Orchestrate the Transcriptional Response of hESCs to Temperature Stress	否			embryonic stem cell	E_02_0477	EU-seq,HiChIP,ChIP-Seq,ATAC-seq,APA metaplot analysis 	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.		We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.	Immunohistochemical staining	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.			EU-seq,HiChIP,ChIP-Seq,ATAC-seq,APA metaplot analysis 				KLF4
30122536	chr8	116843283	116845283	RAD21	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.	human,Drosophila,melanogaster		High+Lowthroughput	Architectural Proteins and Pluripotency Factors Cooperate to Orchestrate the Transcriptional Response of hESCs to Temperature Stress	否			embryonic stem cell	E_02_0477	EU-seq,HiChIP,ChIP-Seq,ATAC-seq,APA metaplot analysis 	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.		We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.	Immunohistochemical staining	We find that temperature stress results in the activation or decommissioning of thousands of enhancers. This process involves alterations in the occupancy of transcription factors HSF1, AP-1, NANOG, KLF4, and OCT4, accompanied by nucleosome remodeling by BRG1 and changes in H3K27ac.  Furthermore, redistribution of RAD21 and CTCF results in the formation and disassembly of interactions mediated by these two proteins.			EU-seq,HiChIP,ChIP-Seq,ATAC-seq,APA metaplot analysis 				RAD21
30121393	chr12	102954801	102956801	ASCL1	ABSTRACT Introduction: A subgroup of lung adenocarcinoma shows neuroendocrine differentiation and expression of achaete- scute family bHLH transcription factor 1 (ASCL1), common to high-grade neuroendocrine tumors, small-cell lung can- cer and large cell neuroendocrine carcinoma. 	human		High+Lowthroughput	An Integrative Analysis of Transcriptome and Epigenome Features of ASCL1-Positive Lung Adenocarcinomas	否		Lung adenocarcinoma, lung squamous cell carcinoma	tumor cell	E_01_0758	RNA-seq,RT-PCR	ABSTRACT Introduction: A subgroup of lung adenocarcinoma shows neuroendocrine differentiation and expression of achaete- scute family bHLH transcription factor 1 (ASCL1), common to high-grade neuroendocrine tumors, small-cell lung can- cer and large cell neuroendocrine carcinoma. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			ABSTRACT Introduction: A subgroup of lung adenocarcinoma shows neuroendocrine differentiation and expression of achaete- scute family bHLH transcription factor 1 (ASCL1), common to high-grade neuroendocrine tumors, small-cell lung can- cer and large cell neuroendocrine carcinoma. 	Immunohistochemical staining	ABSTRACT Introduction: A subgroup of lung adenocarcinoma shows neuroendocrine differentiation and expression of achaete- scute family bHLH transcription factor 1 (ASCL1), common to high-grade neuroendocrine tumors, small-cell lung can- cer and large cell neuroendocrine carcinoma. 	ASCL1		RNA-seq,RT-PCR	ABSTRACT Introduction: A subgroup of lung adenocarcinoma shows neuroendocrine differentiation and expression of achaete- scute family bHLH transcription factor 1 (ASCL1), common to high-grade neuroendocrine tumors, small-cell lung can- cer and large cell neuroendocrine carcinoma. 			
30119690	chr16	86422446	86426834	FOXF1	Conclusions Our study elucidates a novel cascade mediated by AP-1 and FOXF1 that regulates oncogene-induced senescence and further demonstrates the power of CRISPR-based functional genomic screens in deciphering the function of non-coding regulatory elements in the genome.	human		Low+High throughput	Functional CRISPR screen identifies AP1-associated enhancer regulating FOXF1 to modulate oncogene-induced senescence	否	--	--		E_02_0478	ChIP-seq,Luciferase Reporter Assay,CRISPR/Cas9	Notably, two of these five sgRNAs,sgRNAs-AP169 and sgRNA-AP171, are independent sgRNAs that target the same enhancer region,hence increasing the confidence that these are true-positive hits. ENCODE ChIP-seq data confirmed a strong binding of both FOS and JUN to this region.	Enhancer	CRISPR/Cas9	qRT-PCR	Furthermore,we identified FOXF1 as the tar_x0002_get gene of this Enhancer and demonstrated that it regu_x0002_lates the senescence phenotype.	ACDMPV,FKHL5,FREAC1	We identify FOXF1 as the gene regulated by this enhancer and demonstrate that FOXF1 mediates EnhAP1-OIS1 effect on the senescence phenotype.	qRT-PCR,Western blot	the physical interactions between EnhAP1-OIS1 and the promoter region of FOXF1 were significantly stronger , suggesting a robust transcriptional regulation of EnhAP1-OIS1.	JUN	AP-1,AP1,c-Jun,cJUN,p39	CRISPR/Cas9,Luciferase Reporter Assay	We thus constructed a CRISPR-Cas9 sgRNA library designed to target senescence-induced Enhancers that are putatively regulated by AP-1 and used it in a functional screen.That screen was confined to regions that are directly bound by p53 as detected by p53 chromatin immunoprecipitation-sequencing (ChIP-seq) analysis and therefore missed Enhancers that are critical for OIS enforcement and are regulated by other TFs, in either a p53-dependent or -independent manner.	--	--	FOXF1
30119259	chr7	148804464	148806464	EZH2	Mechanistic investigations showed that HOXD-AS1 epigenetically repressed p57 through re- cruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p57.                                              MALAT1	human		High+Lowthroughput	Long noncoding RNA HOXD-AS1 aggravates osteosarcoma carcinogenesis through epigenetically inhibiting p57 via EZH2	否		Osteosarcoma	osteosarcoma cell	E_01_0759	RT-PCR, Weston blot, statistical analysis	Mechanistic investigations showed that HOXD-AS1 epigenetically repressed p57 through re- cruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p57.                                              MALAT1	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mechanistic investigations showed that HOXD-AS1 epigenetically repressed p57 through re- cruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p57.                                              MALAT1	Immunohistochemical staining	Mechanistic investigations showed that HOXD-AS1 epigenetically repressed p57 through re- cruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p57.                                              MALAT1	EZH2		RT-PCR,weston blot,统计分析	Mechanistic investigations showed that HOXD-AS1 epigenetically repressed p57 through re- cruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p57.                                              MALAT1			
30119259	chr11	65494967	65496967	MALAT1	Mechanistic investigations showed that HOXD-AS1 epigenetically repressed p57 through re- cruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p57.                                              MALAT1	human		High+Lowthroughput	Long noncoding RNA HOXD-AS1 aggravates osteosarcoma carcinogenesis through epigenetically inhibiting p57 via EZH2	否		Osteosarcoma	osteosarcoma cell	E_01_0759	RT-PCR, Weston blot, statistical analysis	Mechanistic investigations showed that HOXD-AS1 epigenetically repressed p57 through re- cruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p57.                                              MALAT1	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mechanistic investigations showed that HOXD-AS1 epigenetically repressed p57 through re- cruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p57.                                              MALAT1	Immunohistochemical staining	Mechanistic investigations showed that HOXD-AS1 epigenetically repressed p57 through re- cruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p57.                                              MALAT1	MALAT1		RT-PCR,weston blot,统计分析	Mechanistic investigations showed that HOXD-AS1 epigenetically repressed p57 through re- cruiting enhancer of zeste homolog 2 (EZH2) to the promoter of p57.                                              MALAT1			
30118678	chr11	67116871	67118871	KDM2A	Surprisingly, these basally-active estrogen-repressed (BAER) enhancers are decommissioned by ERα-dependent recruitment of the histone demethylase, KDM2A, functioning independently of its demethylase activity.                                                                                                                                                      While indirectly bound ERα recruits coactivators to these enhancers in a ligand-dependent fashion, the repression events, unexpectedly, reflect the availability of the ERα DNA binding domain (DBD) to interact with the histone demethylase, KDM2A, which, even in the absence of its demethylase function, serves to recruit the ubiquitin ligase NEDD4 to these enhancers, resulting ubiquitylation and dismissal of Pol II and consequent inhibition of these enhancer activities. 	human		High+Lowthroughput	Dismissal of RNA Polymerase II Underlies a Large Ligand-Induced Enhancer Decommissioning Program	否		mammary cancer	MCF7 cell	E_01_0760	RT-qPCR,GRO-seq,ChIP-seq,ChIP-qPCR ,weston blot,PRO-seq 	Surprisingly, these basally-active estrogen-repressed (BAER) enhancers are decommissioned by ERα-dependent recruitment of the histone demethylase, KDM2A, functioning independently of its demethylase activity.                                                                                                                                                      While indirectly bound ERα recruits coactivators to these enhancers in a ligand-dependent fashion, the repression events, unexpectedly, reflect the availability of the ERα DNA binding domain (DBD) to interact with the histone demethylase, KDM2A, which, even in the absence of its demethylase function, serves to recruit the ubiquitin ligase NEDD4 to these enhancers, resulting ubiquitylation and dismissal of Pol II and consequent inhibition of these enhancer activities. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Surprisingly, these basally-active estrogen-repressed (BAER) enhancers are decommissioned by ERα-dependent recruitment of the histone demethylase, KDM2A, functioning independently of its demethylase activity.                                                                                                                                                      While indirectly bound ERα recruits coactivators to these enhancers in a ligand-dependent fashion, the repression events, unexpectedly, reflect the availability of the ERα DNA binding domain (DBD) to interact with the histone demethylase, KDM2A, which, even in the absence of its demethylase function, serves to recruit the ubiquitin ligase NEDD4 to these enhancers, resulting ubiquitylation and dismissal of Pol II and consequent inhibition of these enhancer activities. 		Surprisingly, these basally-active estrogen-repressed (BAER) enhancers are decommissioned by ERα-dependent recruitment of the histone demethylase, KDM2A, functioning independently of its demethylase activity.                                                                                                                                                      While indirectly bound ERα recruits coactivators to these enhancers in a ligand-dependent fashion, the repression events, unexpectedly, reflect the availability of the ERα DNA binding domain (DBD) to interact with the histone demethylase, KDM2A, which, even in the absence of its demethylase function, serves to recruit the ubiquitin ligase NEDD4 to these enhancers, resulting ubiquitylation and dismissal of Pol II and consequent inhibition of these enhancer activities. 	Immunohistochemical staining	Surprisingly, these basally-active estrogen-repressed (BAER) enhancers are decommissioned by ERα-dependent recruitment of the histone demethylase, KDM2A, functioning independently of its demethylase activity.                                                                                                                                                      While indirectly bound ERα recruits coactivators to these enhancers in a ligand-dependent fashion, the repression events, unexpectedly, reflect the availability of the ERα DNA binding domain (DBD) to interact with the histone demethylase, KDM2A, which, even in the absence of its demethylase function, serves to recruit the ubiquitin ligase NEDD4 to these enhancers, resulting ubiquitylation and dismissal of Pol II and consequent inhibition of these enhancer activities. 			RT-qPCR,GRO-seq,ChIP-seq,ChIP-qPCR ,weston blot,PRO-seq 				KDM2A
30116320	chr7	45108174	45110174	Bax	The results revealed that baicalin administration increased cell viability and decreased LDH levels, most notably at a dosage of 100 mol/l. Baicalin pretreatment also downregulated the expression of caspase 3, cleaved caspase 3 and Bax, while upregulating the expression of Bcl-2.	human		High+Lowthroughput	Baicalin attenuates liver hypoxia/reoxygenation injury by inducing autophagy	否		B cell lymphoma	LO2 cell	E_01_0761	RT qPCR, Weston blot, statistical analysis, flow cytometry	The results revealed that baicalin administration increased cell viability and decreased LDH levels, most notably at a dosage of 100 mol/l. Baicalin pretreatment also downregulated the expression of caspase 3, cleaved caspase 3 and Bax, while upregulating the expression of Bcl-2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The results revealed that baicalin administration increased cell viability and decreased LDH levels, most notably at a dosage of 100 mol/l. Baicalin pretreatment also downregulated the expression of caspase 3, cleaved caspase 3 and Bax, while upregulating the expression of Bcl-2.		The results revealed that baicalin administration increased cell viability and decreased LDH levels, most notably at a dosage of 100 mol/l. Baicalin pretreatment also downregulated the expression of caspase 3, cleaved caspase 3 and Bax, while upregulating the expression of Bcl-2.	Immunohistochemical staining	The results revealed that baicalin administration increased cell viability and decreased LDH levels, most notably at a dosage of 100 mol/l. Baicalin pretreatment also downregulated the expression of caspase 3, cleaved caspase 3 and Bax, while upregulating the expression of Bcl-2.			RT-qPCR,weston blot,统计分析,流式细胞术				Bax
30115916	chr1	175705483	175707483	Exo1	Although, we previously confirmed that the overexpression of exonuclease 1 (Exo1) enhanced the efficiency of PITCh knock-in9, we attempted to enhance the efficiency further to secure robust gene knock-ins at various genomic loci. We newly identified CtIP as a strong MMEJ enhancer by genetic screening (Supplementary Fig. 1).	human,mouse		High+Lowthroughput	Biased genome editing using the local accumulation of DSB repair molecules system	是			stem cell	E_02_0479	Flow cytometry, statistical analysis, gene knockdown, immunofluorescence staining	Although, we previously confirmed that the overexpression of exonuclease 1 (Exo1) enhanced the efficiency of PITCh knock-in9, we attempted to enhance the efficiency further to secure robust gene knock-ins at various genomic loci. We newly identified CtIP as a strong MMEJ enhancer by genetic screening (Supplementary Fig. 1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Although, we previously confirmed that the overexpression of exonuclease 1 (Exo1) enhanced the efficiency of PITCh knock-in9, we attempted to enhance the efficiency further to secure robust gene knock-ins at various genomic loci. We newly identified CtIP as a strong MMEJ enhancer by genetic screening (Supplementary Fig. 1).		Although, we previously confirmed that the overexpression of exonuclease 1 (Exo1) enhanced the efficiency of PITCh knock-in9, we attempted to enhance the efficiency further to secure robust gene knock-ins at various genomic loci. We newly identified CtIP as a strong MMEJ enhancer by genetic screening (Supplementary Fig. 1).	Immunohistochemical staining	Although, we previously confirmed that the overexpression of exonuclease 1 (Exo1) enhanced the efficiency of PITCh knock-in9, we attempted to enhance the efficiency further to secure robust gene knock-ins at various genomic loci. We newly identified CtIP as a strong MMEJ enhancer by genetic screening (Supplementary Fig. 1).			流式细胞术,统计分析,基因敲降,免疫荧光染色				Exo1
30110655	chrX	20724142	20726142	Syn1	The six elements included the human cytomegalovirus immediate early core promoter element (hCPE), three synthetic enhancer element (SEE1, SEE2, Syn1), human cytomegalovirus immediate early enhancer (hCMV-IEE), and a regulatory element isolated from CHO-K1 genomic DNA (C77).	mouse		High+Lowthroughput	Enhanced transgene expression using cis-acting elements combined with the EF1 promoter in a mammalian expression system	否				E_02_0480	ELISA, real time (q) PCR analyses, statistical analysis	The six elements included the human cytomegalovirus immediate early core promoter element (hCPE), three synthetic enhancer element (SEE1, SEE2, Syn1), human cytomegalovirus immediate early enhancer (hCMV-IEE), and a regulatory element isolated from CHO-K1 genomic DNA (C77).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The six elements included the human cytomegalovirus immediate early core promoter element (hCPE), three synthetic enhancer element (SEE1, SEE2, Syn1), human cytomegalovirus immediate early enhancer (hCMV-IEE), and a regulatory element isolated from CHO-K1 genomic DNA (C77).		The six elements included the human cytomegalovirus immediate early core promoter element (hCPE), three synthetic enhancer element (SEE1, SEE2, Syn1), human cytomegalovirus immediate early enhancer (hCMV-IEE), and a regulatory element isolated from CHO-K1 genomic DNA (C77).	Immunohistochemical staining	The six elements included the human cytomegalovirus immediate early core promoter element (hCPE), three synthetic enhancer element (SEE1, SEE2, Syn1), human cytomegalovirus immediate early enhancer (hCMV-IEE), and a regulatory element isolated from CHO-K1 genomic DNA (C77).			ELISA,Real-time (q)PCR analyses,统计分析				Syn1
30109252	chr20	5112272	5114272	PCNA	PCNA	human,mouse		High+Lowthroughput	Gankyrin Promotes Tumor-Suppressor Protein Degradation to Drive Hepatocyte Proliferation	否		Hepatocellular carcinoma	Huh6 cell	E_02_0481	RT-PCR, Weston blot, statistical analysis	PCNA	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	PCNA		PCNA	Immunohistochemical staining	PCNA			RT-PCR,weston blot,统计分析				PCNA
30108282	chr9	21999744	22001744	CDKN2B	Variants in the long noncoding RNA (lncRNA) gene CDKN2B-AS1 (CDKN2B antisense RNA 1; ANRIL) are genome-wide associated with type 2 diabetes (T2D), atherosclerosis, and several forms of cancer.                                                                                                                                                                                         Direct binding of CDKN2B-AS1 transcripts to RBMS1 was shown by RNA immunoprecipitation. RBMS1 encodes a cell cycle suppressor. 	human		High+Lowthroughput	Linear isoforms of the long noncoding RNA CDKN2B-AS1 regulate the c-myc-enhancer binding factor RBMS1	是	rs564398,rs10811661, rs7593730,rs10217586	Type 2 diabetes (T2D), atherosclerosis, coronary heart disease	T-Rex HEK293 cell	E_01_0762	weston blot,qRT-PCR,RNA immunoprecipitation (RIP), RNA-seq	Variants in the long noncoding RNA (lncRNA) gene CDKN2B-AS1 (CDKN2B antisense RNA 1; ANRIL) are genome-wide associated with type 2 diabetes (T2D), atherosclerosis, and several forms of cancer.                                                                                                                                                                                         Direct binding of CDKN2B-AS1 transcripts to RBMS1 was shown by RNA immunoprecipitation. RBMS1 encodes a cell cycle suppressor. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Variants in the long noncoding RNA (lncRNA) gene CDKN2B-AS1 (CDKN2B antisense RNA 1; ANRIL) are genome-wide associated with type 2 diabetes (T2D), atherosclerosis, and several forms of cancer.                                                                                                                                                                                         Direct binding of CDKN2B-AS1 transcripts to RBMS1 was shown by RNA immunoprecipitation. RBMS1 encodes a cell cycle suppressor. 		Variants in the long noncoding RNA (lncRNA) gene CDKN2B-AS1 (CDKN2B antisense RNA 1; ANRIL) are genome-wide associated with type 2 diabetes (T2D), atherosclerosis, and several forms of cancer.                                                                                                                                                                                         Direct binding of CDKN2B-AS1 transcripts to RBMS1 was shown by RNA immunoprecipitation. RBMS1 encodes a cell cycle suppressor. 	Immunohistochemical staining	Variants in the long noncoding RNA (lncRNA) gene CDKN2B-AS1 (CDKN2B antisense RNA 1; ANRIL) are genome-wide associated with type 2 diabetes (T2D), atherosclerosis, and several forms of cancer.                                                                                                                                                                                         Direct binding of CDKN2B-AS1 transcripts to RBMS1 was shown by RNA immunoprecipitation. RBMS1 encodes a cell cycle suppressor. 			weston blot,qRT-PCR,RNA immunoprecipitation (RIP), RNA-seq				CDKN2B
30107177	chr10	101128610	101130610	TLX1	Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 	human,mouse		High+Lowthroughput	Cooperative Enhancer Activation by TLX1 and STAT5 Drives Development of NUP214-ABL1/TLX1-Positive T Cell Acute Lymphoblastic Leukemia	否		T-cell acute lymphoblastic leukemia		E_02_0482	QRT PCR, RNA SEQ, chip SEQ, fast ATAC SEQ, Weston blot, flow cytometry, statistical analysis	Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 		Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 	Immunohistochemical staining	Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 			qRT-PCR,RNA-seq,ChIP-seq,Fast-ATAC-seq,weston blot,流式细胞术,统计分析				TLX1
30107177	chr8	127732644	127734644	MYC	Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 	human,mouse		High+Lowthroughput	Cooperative Enhancer Activation by TLX1 and STAT5 Drives Development of NUP214-ABL1/TLX1-Positive T Cell Acute Lymphoblastic Leukemia	否		T-cell acute lymphoblastic leukemia		E_02_0482	QRT PCR, RNA SEQ, chip SEQ, fast ATAC SEQ, Weston blot, flow cytometry, statistical analysis	Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 		Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 	Immunohistochemical staining	Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 			qRT-PCR,RNA-seq,ChIP-seq,Fast-ATAC-seq,weston blot,流式细胞术,统计分析				MYC
30107177	chr18	63120362	63122362	BCL2	Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 	human,mouse		High+Lowthroughput	Cooperative Enhancer Activation by TLX1 and STAT5 Drives Development of NUP214-ABL1/TLX1-Positive T Cell Acute Lymphoblastic Leukemia	否		T-cell acute lymphoblastic leukemia		E_02_0482	QRT PCR, RNA SEQ, chip SEQ, fast ATAC SEQ, Weston blot, flow cytometry, statistical analysis	Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 		Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 	Immunohistochemical staining	Our data show that TLX1 and STAT5 directly cooperate at the transcriptional level through activation of enhancer regions of key proto-oncogenes such as MYC and BCL2. 			qRT-PCR,RNA-seq,ChIP-seq,Fast-ATAC-seq,weston blot,流式细胞术,统计分析				BCL2
30106596	chr5	88714837	88716837	MEF2C	MEF2 (myocyte enhancer factor 2) is a transcription factor that regulates multiple genes that are important during cardiovascular development and for vascular homeostasis (1), with MEF2C known to play a crucial role in regulating endothelial integrity, survival, and angiogenesis (2).                                                                                        Some of the results of these studies have been previously reported in the form of an abstract (5). Methods To investigate the role of endothelial MEF2 function in the pathogenesis of PH, we generated adult mice with inducible, endothelial-specific deletion of the Mef2c allele, using a tamoxifen-responsive Cdh5 promoter driven Cre recombinase crossed to mice with Mef2cfl/fl alleles (henceforth called Mef2cECKO mice) (6, 7).	human,mouse		High+Lowthroughput	Therapeutic Engagement of the Histone Deacetylase IIA-Myocyte Enhancer Factor 2 Axis Improves Experimental Pulmonary Hypertension	否		Pulmonary arterial hypertension	endothelial cell	E_02_0483	Flow cytometry, immunofluorescence light staining	MEF2 (myocyte enhancer factor 2) is a transcription factor that regulates multiple genes that are important during cardiovascular development and for vascular homeostasis (1), with MEF2C known to play a crucial role in regulating endothelial integrity, survival, and angiogenesis (2).                                                                                        Some of the results of these studies have been previously reported in the form of an abstract (5). Methods To investigate the role of endothelial MEF2 function in the pathogenesis of PH, we generated adult mice with inducible, endothelial-specific deletion of the Mef2c allele, using a tamoxifen-responsive Cdh5 promoter driven Cre recombinase crossed to mice with Mef2cfl/fl alleles (henceforth called Mef2cECKO mice) (6, 7).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MEF2 (myocyte enhancer factor 2) is a transcription factor that regulates multiple genes that are important during cardiovascular development and for vascular homeostasis (1), with MEF2C known to play a crucial role in regulating endothelial integrity, survival, and angiogenesis (2).                                                                                        Some of the results of these studies have been previously reported in the form of an abstract (5). Methods To investigate the role of endothelial MEF2 function in the pathogenesis of PH, we generated adult mice with inducible, endothelial-specific deletion of the Mef2c allele, using a tamoxifen-responsive Cdh5 promoter driven Cre recombinase crossed to mice with Mef2cfl/fl alleles (henceforth called Mef2cECKO mice) (6, 7).		MEF2 (myocyte enhancer factor 2) is a transcription factor that regulates multiple genes that are important during cardiovascular development and for vascular homeostasis (1), with MEF2C known to play a crucial role in regulating endothelial integrity, survival, and angiogenesis (2).                                                                                        Some of the results of these studies have been previously reported in the form of an abstract (5). Methods To investigate the role of endothelial MEF2 function in the pathogenesis of PH, we generated adult mice with inducible, endothelial-specific deletion of the Mef2c allele, using a tamoxifen-responsive Cdh5 promoter driven Cre recombinase crossed to mice with Mef2cfl/fl alleles (henceforth called Mef2cECKO mice) (6, 7).	Immunohistochemical staining	MEF2 (myocyte enhancer factor 2) is a transcription factor that regulates multiple genes that are important during cardiovascular development and for vascular homeostasis (1), with MEF2C known to play a crucial role in regulating endothelial integrity, survival, and angiogenesis (2).                                                                                        Some of the results of these studies have been previously reported in the form of an abstract (5). Methods To investigate the role of endothelial MEF2 function in the pathogenesis of PH, we generated adult mice with inducible, endothelial-specific deletion of the Mef2c allele, using a tamoxifen-responsive Cdh5 promoter driven Cre recombinase crossed to mice with Mef2cfl/fl alleles (henceforth called Mef2cECKO mice) (6, 7).			流式细胞术,免疫荧光光染色				MEF2C
30105866	chr17	48721960	48723960	HOXB13	Conversely, knockdown of HOXB13 AS1 resulted in decreased cell proliferation and tumor growth. Mechanistically, we showed that HOXB13 AS1 overexpression increased DNMT3B mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP), epigenetically suppressing HOXB13 expression. 	human		High+Lowthroughput	Long noncoding RNA HOXB13-AS1 regulates HOXB13 gene methylation by interacting with EZH2 in glioma	否		Glioma, breast cancer	Glioma cell	E_01_0763	QRT – PCR, chromatin immunoprecipitation (chip) assay, Weston blot, statistical analysis, gene knockdown	Conversely, knockdown of HOXB13 AS1 resulted in decreased cell proliferation and tumor growth. Mechanistically, we showed that HOXB13 AS1 overexpression increased DNMT3B mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP), epigenetically suppressing HOXB13 expression. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Conversely, knockdown of HOXB13 AS1 resulted in decreased cell proliferation and tumor growth. Mechanistically, we showed that HOXB13 AS1 overexpression increased DNMT3B mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP), epigenetically suppressing HOXB13 expression. 	Immunohistochemical staining	Conversely, knockdown of HOXB13 AS1 resulted in decreased cell proliferation and tumor growth. Mechanistically, we showed that HOXB13 AS1 overexpression increased DNMT3B mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP), epigenetically suppressing HOXB13 expression. 	HOXB13		qRT–PCR,染色质免疫沉淀(ChIP)测定,weston blot,统计分析,基因敲降	Conversely, knockdown of HOXB13 AS1 resulted in decreased cell proliferation and tumor growth. Mechanistically, we showed that HOXB13 AS1 overexpression increased DNMT3B mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP), epigenetically suppressing HOXB13 expression. 			
30105866	chr7	148804600	148806600	EZH2	Conversely, knockdown of HOXB13 AS1 resulted in decreased cell proliferation and tumor growth. Mechanistically, we showed that HOXB13 AS1 overexpression increased DNMT3B mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP), epigenetically suppressing HOXB13 expression. 	human		High+Lowthroughput	Long noncoding RNA HOXB13-AS1 regulates HOXB13 gene methylation by interacting with EZH2 in glioma	否		Glioma, breast cancer	Glioma cell	E_01_0763	QRT – PCR, chromatin immunoprecipitation (chip) assay, Weston blot, statistical analysis, gene knockdown	Conversely, knockdown of HOXB13 AS1 resulted in decreased cell proliferation and tumor growth. Mechanistically, we showed that HOXB13 AS1 overexpression increased DNMT3B mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP), epigenetically suppressing HOXB13 expression. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Conversely, knockdown of HOXB13 AS1 resulted in decreased cell proliferation and tumor growth. Mechanistically, we showed that HOXB13 AS1 overexpression increased DNMT3B mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP), epigenetically suppressing HOXB13 expression. 	Immunohistochemical staining	Conversely, knockdown of HOXB13 AS1 resulted in decreased cell proliferation and tumor growth. Mechanistically, we showed that HOXB13 AS1 overexpression increased DNMT3B mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP), epigenetically suppressing HOXB13 expression. 	EZH2		qRT–PCR,染色质免疫沉淀(ChIP)测定,weston blot,统计分析,基因敲降	Conversely, knockdown of HOXB13 AS1 resulted in decreased cell proliferation and tumor growth. Mechanistically, we showed that HOXB13 AS1 overexpression increased DNMT3B mediated methylation of adjacent gene HOXB13 promoter by binding with the enhancer of zeste homolog 2 (EZH2) using bisulfite sequencing PCR (BSP), epigenetically suppressing HOXB13 expression. 			
30104406	chr3	108955128	108957128	MORC1	We previously demonstrated that the Su(var)3 9 homologs SUVH2 and SUVH9, which are RdDM components, interact with MORC1 and MORC6 and thereby link the RdDM pathway and heterochromatin condensation (Liu et al, 2016). However, it is thought that the RdDM pathway is unlikely to be involved in heterochromatin condensation at the whole genome level. 	human		High+Lowthroughput	The PEAT protein complexes are required for histone deacetylation and heterochromatin silencing	否				E_01_0764	ChIP‐seq,RNA expression analysis,Immunofluorescence assay,,weston blot	We previously demonstrated that the Su(var)3 9 homologs SUVH2 and SUVH9, which are RdDM components, interact with MORC1 and MORC6 and thereby link the RdDM pathway and heterochromatin condensation (Liu et al, 2016). However, it is thought that the RdDM pathway is unlikely to be involved in heterochromatin condensation at the whole genome level. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We previously demonstrated that the Su(var)3 9 homologs SUVH2 and SUVH9, which are RdDM components, interact with MORC1 and MORC6 and thereby link the RdDM pathway and heterochromatin condensation (Liu et al, 2016). However, it is thought that the RdDM pathway is unlikely to be involved in heterochromatin condensation at the whole genome level. 		We previously demonstrated that the Su(var)3 9 homologs SUVH2 and SUVH9, which are RdDM components, interact with MORC1 and MORC6 and thereby link the RdDM pathway and heterochromatin condensation (Liu et al, 2016). However, it is thought that the RdDM pathway is unlikely to be involved in heterochromatin condensation at the whole genome level. 	Immunohistochemical staining	We previously demonstrated that the Su(var)3 9 homologs SUVH2 and SUVH9, which are RdDM components, interact with MORC1 and MORC6 and thereby link the RdDM pathway and heterochromatin condensation (Liu et al, 2016). However, it is thought that the RdDM pathway is unlikely to be involved in heterochromatin condensation at the whole genome level. 			ChIP‐seq,RNA expression analysis,Immunofluorescence assay,,weston blot				MORC1
30103943	chr14	100776331	100778331	MEG3	Knockdown studies of MEG3 and EZH2 by siRNA showed that MEG3/EZH2 negatively regulated osteo- genesis of hDFSCs.	human,mouse	Osteogenic tissues	High+Lowthroughput	Down-regulated lncRNA MEG3 promotes osteogenic differentiation of human dental follicle stem cells by epigenetically regulating Wnt pathway	否			Dental follicle cells	E_02_0484	Gene knockdown, fish, QRT PCR, Weston blot, chromatin immunoprecipitation (chip) - PCR assay, statistical analysis	Knockdown studies of MEG3 and EZH2 by siRNA showed that MEG3/EZH2 negatively regulated osteo- genesis of hDFSCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Knockdown studies of MEG3 and EZH2 by siRNA showed that MEG3/EZH2 negatively regulated osteo- genesis of hDFSCs.		Knockdown studies of MEG3 and EZH2 by siRNA showed that MEG3/EZH2 negatively regulated osteo- genesis of hDFSCs.	Immunohistochemical staining	Knockdown studies of MEG3 and EZH2 by siRNA showed that MEG3/EZH2 negatively regulated osteo- genesis of hDFSCs.			基因敲降,FISH, qRT-PCR,weston blot,Chromatin immunoprecipitation (ChIP)-PCR assay,统计分析				MEG3
30103943	chr7	148804318	148806318	EZH2	Knockdown studies of MEG3 and EZH2 by siRNA showed that MEG3/EZH2 negatively regulated osteo- genesis of hDFSCs.	human,mouse	Osteogenic tissues	High+Lowthroughput	Down-regulated lncRNA MEG3 promotes osteogenic differentiation of human dental follicle stem cells by epigenetically regulating Wnt pathway	否			Dental follicle cells	E_02_0484	Gene knockdown, fish, QRT PCR, Weston blot, chromatin immunoprecipitation (chip) - PCR assay, statistical analysis	Knockdown studies of MEG3 and EZH2 by siRNA showed that MEG3/EZH2 negatively regulated osteo- genesis of hDFSCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Knockdown studies of MEG3 and EZH2 by siRNA showed that MEG3/EZH2 negatively regulated osteo- genesis of hDFSCs.		Knockdown studies of MEG3 and EZH2 by siRNA showed that MEG3/EZH2 negatively regulated osteo- genesis of hDFSCs.	Immunohistochemical staining	Knockdown studies of MEG3 and EZH2 by siRNA showed that MEG3/EZH2 negatively regulated osteo- genesis of hDFSCs.			基因敲降,FISH, qRT-PCR,weston blot,Chromatin immunoprecipitation (ChIP)-PCR assay,统计分析				EZH2
30103804	chr1	150923029	150925029	SETDB1	Results Here, we show that loss of SETDB1 does not result in large-scale H3K9me3 changes at the Xi, but unexpectedly we observed striking decompaction of the Xi territory. 	human		High+Lowthroughput	Loss of SETDB1 decompacts the inactive X chromosome in part through reactivation of an enhancer in the IL1RAPL1 gene	是	rs140261831, rs113985890, rs190632360,rs144991617	Intellectual disability		E_01_0765	RT-PCR, Weston blot, immunofluorescence staining, chip SEQ, RNA SEQ, statistical analysis	Results Here, we show that loss of SETDB1 does not result in large-scale H3K9me3 changes at the Xi, but unexpectedly we observed striking decompaction of the Xi territory. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Results Here, we show that loss of SETDB1 does not result in large-scale H3K9me3 changes at the Xi, but unexpectedly we observed striking decompaction of the Xi territory. 		Results Here, we show that loss of SETDB1 does not result in large-scale H3K9me3 changes at the Xi, but unexpectedly we observed striking decompaction of the Xi territory. 	Immunohistochemical staining	Results Here, we show that loss of SETDB1 does not result in large-scale H3K9me3 changes at the Xi, but unexpectedly we observed striking decompaction of the Xi territory. 			RT-PCR,weston blot,免疫荧光染色,ChIP-Seq,RNA-Seq,统计分析				SETDB1
30102396	chr2	230200488	230202488	SP140	ABSTRACT SP140 locus has been associated with multiple sclerosis (MS) as well as other autoimmune  diseases by genome-wide association studies (GWAS). 	human		High+Lowthroughput	SP140 regulates the expression of immune-related genes associated with multiple sclerosis and other autoimmune diseases by NF-κB inhibition	是	rs28445040	Multiple sclerosis (MS)	B cell	E_01_0766	RNA-Seq,weston blot,ddPCR	ABSTRACT SP140 locus has been associated with multiple sclerosis (MS) as well as other autoimmune  diseases by genome-wide association studies (GWAS). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ABSTRACT SP140 locus has been associated with multiple sclerosis (MS) as well as other autoimmune  diseases by genome-wide association studies (GWAS). 		ABSTRACT SP140 locus has been associated with multiple sclerosis (MS) as well as other autoimmune  diseases by genome-wide association studies (GWAS). 	Immunohistochemical staining	ABSTRACT SP140 locus has been associated with multiple sclerosis (MS) as well as other autoimmune  diseases by genome-wide association studies (GWAS). 			RNA-Seq,weston blot,ddPCR				SP140
30100186	chr9	128680671	128682671	SET	The activity of the catalytic SET domain (Su(var)3 9, Enhancer-of-zeste and Trithorax) is endowed through forming a complex with a set of core proteins that are widely shared from yeast to humans.	human		High+Lowthroughput	Structure and Conformational Dynamics of a COMPASS Histone H3K4 Methyltransferase Complex	否		All, acute lymphoblastic leukaemia	Sf9 cell	E_01_0767	Weston blot, PCR, statistical analysis	The activity of the catalytic SET domain (Su(var)3 9, Enhancer-of-zeste and Trithorax) is endowed through forming a complex with a set of core proteins that are widely shared from yeast to humans.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The activity of the catalytic SET domain (Su(var)3 9, Enhancer-of-zeste and Trithorax) is endowed through forming a complex with a set of core proteins that are widely shared from yeast to humans.		The activity of the catalytic SET domain (Su(var)3 9, Enhancer-of-zeste and Trithorax) is endowed through forming a complex with a set of core proteins that are widely shared from yeast to humans.	Immunohistochemical staining	The activity of the catalytic SET domain (Su(var)3 9, Enhancer-of-zeste and Trithorax) is endowed through forming a complex with a set of core proteins that are widely shared from yeast to humans.			weston blot,PCR,统计分析				SET
30100087	chr12	1968286	1970286	CACNA1C	Genome-wide association studies have strongly and repeatedly linked risk for both of these neuropsychiatric diseases to a 100 kb interval in the third intron of the human calcium channel gene CACNA1C. 	human,chimpanzee		High+Lowthroughput	Characterization of a Human-Specific Tandem Repeat Associated with Bipolar Disorder and Schizophrenia	是	rs2007044, rs1006737, rs4765905, and rs4765913	Bipolar disorder (BD), schizophrenia (SCZ)		E_02_0485	Southern blot,PacBio,PCR	Genome-wide association studies have strongly and repeatedly linked risk for both of these neuropsychiatric diseases to a 100 kb interval in the third intron of the human calcium channel gene CACNA1C. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genome-wide association studies have strongly and repeatedly linked risk for both of these neuropsychiatric diseases to a 100 kb interval in the third intron of the human calcium channel gene CACNA1C. 		Genome-wide association studies have strongly and repeatedly linked risk for both of these neuropsychiatric diseases to a 100 kb interval in the third intron of the human calcium channel gene CACNA1C. 	Immunohistochemical staining	Genome-wide association studies have strongly and repeatedly linked risk for both of these neuropsychiatric diseases to a 100 kb interval in the third intron of the human calcium channel gene CACNA1C. 			Southern blot,PacBio,PCR				CACNA1C
30099761	chr3	13476946	13478946	HDAC11	Histone deacetylases (HDACs) are a vast family divided into four major classes: class I (1, 2, 3, and 8), class II (4, 5, 6, 7, 9 and 10), class III (sirtuin family) and class IV (HDAC11). HDAC inhibition attenuates cardiac hypertrophy through suppression of the mechanistic target of rapamycin complex1 (mTORC1) signaling. HDAC inhibitors upregulate the expression of tuberous sclerosis complex 2 (TSC2), an mTORC1 inhibitor. However, the molecular mechanism underlying HDAC inhibitor- mediated upregulation of TSC2 is unclear.	human,mouse		High+Lowthroughput	Upregulation of C/EBPβ and TSC2 by an HDAC inhibitor CG200745 protects heart from DOCA-induced hypertrophy	否		hypertension	neural cell	E_02_0486	QRT PCR, chromatin immunoprecipitation (chip) assay, Weston blot, statistical analysis	Histone deacetylases (HDACs) are a vast family divided into four major classes: class I (1, 2, 3, and 8), class II (4, 5, 6, 7, 9 and 10), class III (sirtuin family) and class IV (HDAC11). HDAC inhibition attenuates cardiac hypertrophy through suppression of the mechanistic target of rapamycin complex1 (mTORC1) signaling. HDAC inhibitors upregulate the expression of tuberous sclerosis complex 2 (TSC2), an mTORC1 inhibitor. However, the molecular mechanism underlying HDAC inhibitor- mediated upregulation of TSC2 is unclear.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Histone deacetylases (HDACs) are a vast family divided into four major classes: class I (1, 2, 3, and 8), class II (4, 5, 6, 7, 9 and 10), class III (sirtuin family) and class IV (HDAC11). HDAC inhibition attenuates cardiac hypertrophy through suppression of the mechanistic target of rapamycin complex1 (mTORC1) signaling. HDAC inhibitors upregulate the expression of tuberous sclerosis complex 2 (TSC2), an mTORC1 inhibitor. However, the molecular mechanism underlying HDAC inhibitor- mediated upregulation of TSC2 is unclear.		Histone deacetylases (HDACs) are a vast family divided into four major classes: class I (1, 2, 3, and 8), class II (4, 5, 6, 7, 9 and 10), class III (sirtuin family) and class IV (HDAC11). HDAC inhibition attenuates cardiac hypertrophy through suppression of the mechanistic target of rapamycin complex1 (mTORC1) signaling. HDAC inhibitors upregulate the expression of tuberous sclerosis complex 2 (TSC2), an mTORC1 inhibitor. However, the molecular mechanism underlying HDAC inhibitor- mediated upregulation of TSC2 is unclear.	Immunohistochemical staining	Histone deacetylases (HDACs) are a vast family divided into four major classes: class I (1, 2, 3, and 8), class II (4, 5, 6, 7, 9 and 10), class III (sirtuin family) and class IV (HDAC11). HDAC inhibition attenuates cardiac hypertrophy through suppression of the mechanistic target of rapamycin complex1 (mTORC1) signaling. HDAC inhibitors upregulate the expression of tuberous sclerosis complex 2 (TSC2), an mTORC1 inhibitor. However, the molecular mechanism underlying HDAC inhibitor- mediated upregulation of TSC2 is unclear.			qRT-PCR,染色质免疫沉淀(ChIP)测定,weston blot,统计分析				HDAC11
30099761	chr16	2045096	2047096	TSC2	Histone deacetylases (HDACs) are a vast family divided into four major classes: class I (1, 2, 3, and 8), class II (4, 5, 6, 7, 9 and 10), class III (sirtuin family) and class IV (HDAC11). HDAC inhibition attenuates cardiac hypertrophy through suppression of the mechanistic target of rapamycin complex1 (mTORC1) signaling. HDAC inhibitors upregulate the expression of tuberous sclerosis complex 2 (TSC2), an mTORC1 inhibitor. However, the molecular mechanism underlying HDAC inhibitor- mediated upregulation of TSC2 is unclear.	human,mouse		High+Lowthroughput	Upregulation of C/EBPβ and TSC2 by an HDAC inhibitor CG200745 protects heart from DOCA-induced hypertrophy	否		hypertension	neural cell	E_02_0486	QRT PCR, chromatin immunoprecipitation (chip) assay, Weston blot, statistical analysis	Histone deacetylases (HDACs) are a vast family divided into four major classes: class I (1, 2, 3, and 8), class II (4, 5, 6, 7, 9 and 10), class III (sirtuin family) and class IV (HDAC11). HDAC inhibition attenuates cardiac hypertrophy through suppression of the mechanistic target of rapamycin complex1 (mTORC1) signaling. HDAC inhibitors upregulate the expression of tuberous sclerosis complex 2 (TSC2), an mTORC1 inhibitor. However, the molecular mechanism underlying HDAC inhibitor- mediated upregulation of TSC2 is unclear.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Histone deacetylases (HDACs) are a vast family divided into four major classes: class I (1, 2, 3, and 8), class II (4, 5, 6, 7, 9 and 10), class III (sirtuin family) and class IV (HDAC11). HDAC inhibition attenuates cardiac hypertrophy through suppression of the mechanistic target of rapamycin complex1 (mTORC1) signaling. HDAC inhibitors upregulate the expression of tuberous sclerosis complex 2 (TSC2), an mTORC1 inhibitor. However, the molecular mechanism underlying HDAC inhibitor- mediated upregulation of TSC2 is unclear.		Histone deacetylases (HDACs) are a vast family divided into four major classes: class I (1, 2, 3, and 8), class II (4, 5, 6, 7, 9 and 10), class III (sirtuin family) and class IV (HDAC11). HDAC inhibition attenuates cardiac hypertrophy through suppression of the mechanistic target of rapamycin complex1 (mTORC1) signaling. HDAC inhibitors upregulate the expression of tuberous sclerosis complex 2 (TSC2), an mTORC1 inhibitor. However, the molecular mechanism underlying HDAC inhibitor- mediated upregulation of TSC2 is unclear.	Immunohistochemical staining	Histone deacetylases (HDACs) are a vast family divided into four major classes: class I (1, 2, 3, and 8), class II (4, 5, 6, 7, 9 and 10), class III (sirtuin family) and class IV (HDAC11). HDAC inhibition attenuates cardiac hypertrophy through suppression of the mechanistic target of rapamycin complex1 (mTORC1) signaling. HDAC inhibitors upregulate the expression of tuberous sclerosis complex 2 (TSC2), an mTORC1 inhibitor. However, the molecular mechanism underlying HDAC inhibitor- mediated upregulation of TSC2 is unclear.			qRT-PCR,染色质免疫沉淀(ChIP)测定,weston blot,统计分析				TSC2
30099093	chr17	42697287	42699287	EZH1	Moreover, the polycomb-associated H3K27 methyltransferase, EZH1, is regulated by miR-132 and upregulated in the PFC of schizophrenics.	human,mouse		High+Lowthroughput	EZH1 is an antipsychotic-sensitive epigenetic modulator of social and motivational behavior that is dysregulated in schizophrenia	否		Schizophrenia	HEK-293 cells	E_02_0487	qRT-PCR,RNA seq,weston blot	Moreover, the polycomb-associated H3K27 methyltransferase, EZH1, is regulated by miR-132 and upregulated in the PFC of schizophrenics.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, the polycomb-associated H3K27 methyltransferase, EZH1, is regulated by miR-132 and upregulated in the PFC of schizophrenics.		Moreover, the polycomb-associated H3K27 methyltransferase, EZH1, is regulated by miR-132 and upregulated in the PFC of schizophrenics.	Immunohistochemical staining	Moreover, the polycomb-associated H3K27 methyltransferase, EZH1, is regulated by miR-132 and upregulated in the PFC of schizophrenics.			qRT-PCR,RNA seq,weston blot				EZH1
30098338	chr2	113096632	113098632	IL1RN	We specifically targeted regions approximately 4kb, 8kb and 24kb from the IL1RN promoter that do not contain any feature of a regulatory element based on ENCODE H3K27ac and transcription factor ChIP-Seq data (Fig. 1b, Fig.S1a).	human,mouse		High+Lowthroughput	Temporal and Spatial Epigenome Editing Allows Precise Gene Regulation in Mammalian Cells	否		cancer	K562 cell	E_02_0488	Chip qPCR, RT qPCR, chromatin immunoprecipitation reaction, 3-C assay, chip SEQ, DNase - seq	We specifically targeted regions approximately 4kb, 8kb and 24kb from the IL1RN promoter that do not contain any feature of a regulatory element based on ENCODE H3K27ac and transcription factor ChIP-Seq data (Fig. 1b, Fig.S1a).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We specifically targeted regions approximately 4kb, 8kb and 24kb from the IL1RN promoter that do not contain any feature of a regulatory element based on ENCODE H3K27ac and transcription factor ChIP-Seq data (Fig. 1b, Fig.S1a).		We specifically targeted regions approximately 4kb, 8kb and 24kb from the IL1RN promoter that do not contain any feature of a regulatory element based on ENCODE H3K27ac and transcription factor ChIP-Seq data (Fig. 1b, Fig.S1a).	Immunohistochemical staining	We specifically targeted regions approximately 4kb, 8kb and 24kb from the IL1RN promoter that do not contain any feature of a regulatory element based on ENCODE H3K27ac and transcription factor ChIP-Seq data (Fig. 1b, Fig.S1a).			ChIP-qPCR, RT-qPCR,染色质免疫沉淀反应,3-C Assay,ChIP-Seq,DNase- seq				IL1RN
30098214	chr14	100235593	100237593	YY1	Ei and E3 are both required for Igκ gene rearrangement during early stages of B cell development, whereas optimal expression of the rearranged Igκ gene relies on both E3 and Ed. The transcription factor YY1 affects the expression of many genes involved in B cell development, probably by mediating interactions between their enhancers and promoters.Herein, we found that YY1 binds to the E3 enhancer and suppresses Igκ expression in B lymphoma cells by epigenetically modifying the enhancer.                                                                                                                                                                                                                                                                           Knocking down YY1 enhanced Igκ expression, which was associated with increased levels of E2A (encoded by the TCF3 gene) and its binding to the E3 enhancer. 	human,mouse		High+Lowthroughput	YY1 binds to the E3' enhancer and inhibits the expression of the immunoglobulin κ gene via epigenetic modifications	否			B cell	E_02_0489	RT ‐ PCR, Weston blot, flow cytometry, statistical analysis, chromatin immunoprecipitation assays, gene knockdown	Ei and E3 are both required for Igκ gene rearrangement during early stages of B cell development, whereas optimal expression of the rearranged Igκ gene relies on both E3 and Ed. The transcription factor YY1 affects the expression of many genes involved in B cell development, probably by mediating interactions between their enhancers and promoters.Herein, we found that YY1 binds to the E3 enhancer and suppresses Igκ expression in B lymphoma cells by epigenetically modifying the enhancer.                                                                                                                                                                                                                                                                           Knocking down YY1 enhanced Igκ expression, which was associated with increased levels of E2A (encoded by the TCF3 gene) and its binding to the E3 enhancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ei and E3 are both required for Igκ gene rearrangement during early stages of B cell development, whereas optimal expression of the rearranged Igκ gene relies on both E3 and Ed. The transcription factor YY1 affects the expression of many genes involved in B cell development, probably by mediating interactions between their enhancers and promoters.Herein, we found that YY1 binds to the E3 enhancer and suppresses Igκ expression in B lymphoma cells by epigenetically modifying the enhancer.                                                                                                                                                                                                                                                                           Knocking down YY1 enhanced Igκ expression, which was associated with increased levels of E2A (encoded by the TCF3 gene) and its binding to the E3 enhancer. 		Ei and E3 are both required for Igκ gene rearrangement during early stages of B cell development, whereas optimal expression of the rearranged Igκ gene relies on both E3 and Ed. The transcription factor YY1 affects the expression of many genes involved in B cell development, probably by mediating interactions between their enhancers and promoters.Herein, we found that YY1 binds to the E3 enhancer and suppresses Igκ expression in B lymphoma cells by epigenetically modifying the enhancer.                                                                                                                                                                                                                                                                           Knocking down YY1 enhanced Igκ expression, which was associated with increased levels of E2A (encoded by the TCF3 gene) and its binding to the E3 enhancer. 	Immunohistochemical staining	Ei and E3 are both required for Igκ gene rearrangement during early stages of B cell development, whereas optimal expression of the rearranged Igκ gene relies on both E3 and Ed. The transcription factor YY1 affects the expression of many genes involved in B cell development, probably by mediating interactions between their enhancers and promoters.Herein, we found that YY1 binds to the E3 enhancer and suppresses Igκ expression in B lymphoma cells by epigenetically modifying the enhancer.                                                                                                                                                                                                                                                                           Knocking down YY1 enhanced Igκ expression, which was associated with increased levels of E2A (encoded by the TCF3 gene) and its binding to the E3 enhancer. 			RT‐PCR,weston blot,流式细胞术,统计分析,Chromatin immunoprecipitation assays,基因敲降				YY1
30098214	chr19	1606278	1608278	TCF3	Ei and E3 are both required for Igκ gene rearrangement during early stages of B cell development, whereas optimal expression of the rearranged Igκ gene relies on both E3 and Ed. The transcription factor YY1 affects the expression of many genes involved in B cell development, probably by mediating interactions between their enhancers and promoters.Herein, we found that YY1 binds to the E3 enhancer and suppresses Igκ expression in B lymphoma cells by epigenetically modifying the enhancer.                                                                                                                                                                                                                                                                           Knocking down YY1 enhanced Igκ expression, which was associated with increased levels of E2A (encoded by the TCF3 gene) and its binding to the E3 enhancer. 	human,mouse		High+Lowthroughput	YY1 binds to the E3' enhancer and inhibits the expression of the immunoglobulin κ gene via epigenetic modifications	否			B cell	E_02_0489	RT ‐ PCR, Weston blot, flow cytometry, statistical analysis, chromatin immunoprecipitation assays, gene knockdown	Ei and E3 are both required for Igκ gene rearrangement during early stages of B cell development, whereas optimal expression of the rearranged Igκ gene relies on both E3 and Ed. The transcription factor YY1 affects the expression of many genes involved in B cell development, probably by mediating interactions between their enhancers and promoters.Herein, we found that YY1 binds to the E3 enhancer and suppresses Igκ expression in B lymphoma cells by epigenetically modifying the enhancer.                                                                                                                                                                                                                                                                           Knocking down YY1 enhanced Igκ expression, which was associated with increased levels of E2A (encoded by the TCF3 gene) and its binding to the E3 enhancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ei and E3 are both required for Igκ gene rearrangement during early stages of B cell development, whereas optimal expression of the rearranged Igκ gene relies on both E3 and Ed. The transcription factor YY1 affects the expression of many genes involved in B cell development, probably by mediating interactions between their enhancers and promoters.Herein, we found that YY1 binds to the E3 enhancer and suppresses Igκ expression in B lymphoma cells by epigenetically modifying the enhancer.                                                                                                                                                                                                                                                                           Knocking down YY1 enhanced Igκ expression, which was associated with increased levels of E2A (encoded by the TCF3 gene) and its binding to the E3 enhancer. 		Ei and E3 are both required for Igκ gene rearrangement during early stages of B cell development, whereas optimal expression of the rearranged Igκ gene relies on both E3 and Ed. The transcription factor YY1 affects the expression of many genes involved in B cell development, probably by mediating interactions between their enhancers and promoters.Herein, we found that YY1 binds to the E3 enhancer and suppresses Igκ expression in B lymphoma cells by epigenetically modifying the enhancer.                                                                                                                                                                                                                                                                           Knocking down YY1 enhanced Igκ expression, which was associated with increased levels of E2A (encoded by the TCF3 gene) and its binding to the E3 enhancer. 	Immunohistochemical staining	Ei and E3 are both required for Igκ gene rearrangement during early stages of B cell development, whereas optimal expression of the rearranged Igκ gene relies on both E3 and Ed. The transcription factor YY1 affects the expression of many genes involved in B cell development, probably by mediating interactions between their enhancers and promoters.Herein, we found that YY1 binds to the E3 enhancer and suppresses Igκ expression in B lymphoma cells by epigenetically modifying the enhancer.                                                                                                                                                                                                                                                                           Knocking down YY1 enhanced Igκ expression, which was associated with increased levels of E2A (encoded by the TCF3 gene) and its binding to the E3 enhancer. 			RT‐PCR,weston blot,流式细胞术,统计分析,Chromatin immunoprecipitation assays,基因敲降				TCF3
30097586	chr7	44101429	44103429	AEBP1	Adipocyte enhancer binding protein 1 (AEBP1) is a transcriptional repressor that plays a critical role in regulating adipogenesis.	human		High+Lowthroughput	AEBP1 promotes epithelial-mesenchymal transition of gastric cancer cells by activating the NF-κB pathway and predicts poor outcome of the patients	否		Gastric cancer, nonalcoholic fatty liver disease	epithelial cell	E_01_0768	QRT PCR, Weston blot, statistical analysis	Adipocyte enhancer binding protein 1 (AEBP1) is a transcriptional repressor that plays a critical role in regulating adipogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Adipocyte enhancer binding protein 1 (AEBP1) is a transcriptional repressor that plays a critical role in regulating adipogenesis.		Adipocyte enhancer binding protein 1 (AEBP1) is a transcriptional repressor that plays a critical role in regulating adipogenesis.	Immunohistochemical staining	Adipocyte enhancer binding protein 1 (AEBP1) is a transcriptional repressor that plays a critical role in regulating adipogenesis.			qRT-PCR,weston blot,统计分析				AEBP1
30097539	chr3	133743162	133745162	TF	Glucocorticoids are potent steroid hormones that regulate immunity and metabolism by activating the transcription factor (TF) activity of glucocorticoid receptor (GR).                                                                                                                     At these sites, GR also commonly cobinds with certain pioneer factors, such as AP-1 TFs (Biddie et al. 2011) and CEBPB (Grøntved et al. 2013), which are so designated for their ability to bind sequence motifs in condensed chromatin and to remodel chromatin to increase accessibility (Zaret and Carroll 2011). 	human		High+Lowthroughput	Glucocorticoid receptor recruits to enhancers and drives activation by motif-directed binding	否			A549 cell	E_01_0769	ChIP-seq,DNase-seq ,PCR,RNA-seq	Glucocorticoids are potent steroid hormones that regulate immunity and metabolism by activating the transcription factor (TF) activity of glucocorticoid receptor (GR).                                                                                                                     At these sites, GR also commonly cobinds with certain pioneer factors, such as AP-1 TFs (Biddie et al. 2011) and CEBPB (Grøntved et al. 2013), which are so designated for their ability to bind sequence motifs in condensed chromatin and to remodel chromatin to increase accessibility (Zaret and Carroll 2011). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Glucocorticoids are potent steroid hormones that regulate immunity and metabolism by activating the transcription factor (TF) activity of glucocorticoid receptor (GR).                                                                                                                     At these sites, GR also commonly cobinds with certain pioneer factors, such as AP-1 TFs (Biddie et al. 2011) and CEBPB (Grøntved et al. 2013), which are so designated for their ability to bind sequence motifs in condensed chromatin and to remodel chromatin to increase accessibility (Zaret and Carroll 2011). 		Glucocorticoids are potent steroid hormones that regulate immunity and metabolism by activating the transcription factor (TF) activity of glucocorticoid receptor (GR).                                                                                                                     At these sites, GR also commonly cobinds with certain pioneer factors, such as AP-1 TFs (Biddie et al. 2011) and CEBPB (Grøntved et al. 2013), which are so designated for their ability to bind sequence motifs in condensed chromatin and to remodel chromatin to increase accessibility (Zaret and Carroll 2011). 	Immunohistochemical staining	Glucocorticoids are potent steroid hormones that regulate immunity and metabolism by activating the transcription factor (TF) activity of glucocorticoid receptor (GR).                                                                                                                     At these sites, GR also commonly cobinds with certain pioneer factors, such as AP-1 TFs (Biddie et al. 2011) and CEBPB (Grøntved et al. 2013), which are so designated for their ability to bind sequence motifs in condensed chromatin and to remodel chromatin to increase accessibility (Zaret and Carroll 2011). 			ChIP-seq,DNase-seq ,PCR,RNA-seq				TF
30096897	chr1	180629337	180631337	XPR1	The E-MLVs use the CAT-1 receptor [4], and all X/P-MLVs use the XPR1 receptor [5,6,7]. There are functionally distinct XPR1 variants in the genus Mus, but the majority of mouse strains carry Xpr1n, which allows for the infection of P-MLVs but not X-MLVs [8].	mouse,human		High+Lowthroughput	Xenotropic Mouse Gammaretroviruses Isolated from Pre-Leukemic Tissues Include a Recombinant	否		leukemia		E_02_0490	PCR	The E-MLVs use the CAT-1 receptor [4], and all X/P-MLVs use the XPR1 receptor [5,6,7]. There are functionally distinct XPR1 variants in the genus Mus, but the majority of mouse strains carry Xpr1n, which allows for the infection of P-MLVs but not X-MLVs [8].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The E-MLVs use the CAT-1 receptor [4], and all X/P-MLVs use the XPR1 receptor [5,6,7]. There are functionally distinct XPR1 variants in the genus Mus, but the majority of mouse strains carry Xpr1n, which allows for the infection of P-MLVs but not X-MLVs [8].		The E-MLVs use the CAT-1 receptor [4], and all X/P-MLVs use the XPR1 receptor [5,6,7]. There are functionally distinct XPR1 variants in the genus Mus, but the majority of mouse strains carry Xpr1n, which allows for the infection of P-MLVs but not X-MLVs [8].	Immunohistochemical staining	The E-MLVs use the CAT-1 receptor [4], and all X/P-MLVs use the XPR1 receptor [5,6,7]. There are functionally distinct XPR1 variants in the genus Mus, but the majority of mouse strains carry Xpr1n, which allows for the infection of P-MLVs but not X-MLVs [8].			PCR				XPR1
30092404	chr7	148804297	148806297	EZH2	Mechanistically, LINC00460 repressed Krüppel-like factor 2 (KLF2) transcription by binding to enhancer of zeste homolog 2 (EZH2).	human		High+Lowthroughput	A Novel lncRNA, LINC00460, Affects Cell Proliferation and Apoptosis by Regulating KLF2 and CUL4A Expression in Colorectal Cancer	否		Human colorectal cancer (CRC), acute myeloid leukemia		E_01_0770	Real time qPCR, Western blot, flow cytometry, statistical analysis	Mechanistically, LINC00460 repressed Krüppel-like factor 2 (KLF2) transcription by binding to enhancer of zeste homolog 2 (EZH2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mechanistically, LINC00460 repressed Krüppel-like factor 2 (KLF2) transcription by binding to enhancer of zeste homolog 2 (EZH2).	Immunohistochemical staining	Mechanistically, LINC00460 repressed Krüppel-like factor 2 (KLF2) transcription by binding to enhancer of zeste homolog 2 (EZH2).	EZH2		Real-Time qPCR,western Blot,流式细胞术,统计分析	Mechanistically, LINC00460 repressed Krüppel-like factor 2 (KLF2) transcription by binding to enhancer of zeste homolog 2 (EZH2).			
30087711	chr10	31315956	31317956	ZEB1	Objective: Recent studies have shown that cancer-associated fibroblasts (CAFs) and the epithelial-mesenchymal transition (EMT) play important roles in the progression and metastasis of CRC.                                                            The expression of CAF-related markers, including α-smooth muscle actin, CD10, podoplanin, fibroblast specific protein 1, and adipocyte enhancer-binding protein 1, and EMT-related proteins [zinc finger protein SNAI2 (ZEB1) and twist-related protein 1 (TWIST1) in SiCRC with (n = 29) or without (n = 80) lymph node metastasis was examined by immunohistochemistry.	human		High+Lowthroughput	Analysis of the expression of cancer-associated fibroblast- and EMT-related proteins in submucosal invasive colorectal cancer	否		colorectal cancer 	fibroblast	E_01_0771	Immunohistochemistry, hierarchical clustering analysis	Objective: Recent studies have shown that cancer-associated fibroblasts (CAFs) and the epithelial-mesenchymal transition (EMT) play important roles in the progression and metastasis of CRC.                                                            The expression of CAF-related markers, including α-smooth muscle actin, CD10, podoplanin, fibroblast specific protein 1, and adipocyte enhancer-binding protein 1, and EMT-related proteins [zinc finger protein SNAI2 (ZEB1) and twist-related protein 1 (TWIST1) in SiCRC with (n = 29) or without (n = 80) lymph node metastasis was examined by immunohistochemistry.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Objective: Recent studies have shown that cancer-associated fibroblasts (CAFs) and the epithelial-mesenchymal transition (EMT) play important roles in the progression and metastasis of CRC.                                                            The expression of CAF-related markers, including α-smooth muscle actin, CD10, podoplanin, fibroblast specific protein 1, and adipocyte enhancer-binding protein 1, and EMT-related proteins [zinc finger protein SNAI2 (ZEB1) and twist-related protein 1 (TWIST1) in SiCRC with (n = 29) or without (n = 80) lymph node metastasis was examined by immunohistochemistry.	Immunohistochemical staining	Objective: Recent studies have shown that cancer-associated fibroblasts (CAFs) and the epithelial-mesenchymal transition (EMT) play important roles in the progression and metastasis of CRC.                                                            The expression of CAF-related markers, including α-smooth muscle actin, CD10, podoplanin, fibroblast specific protein 1, and adipocyte enhancer-binding protein 1, and EMT-related proteins [zinc finger protein SNAI2 (ZEB1) and twist-related protein 1 (TWIST1) in SiCRC with (n = 29) or without (n = 80) lymph node metastasis was examined by immunohistochemistry.	ZEB1		免疫组化,层次聚类分析	Objective: Recent studies have shown that cancer-associated fibroblasts (CAFs) and the epithelial-mesenchymal transition (EMT) play important roles in the progression and metastasis of CRC.                                                            The expression of CAF-related markers, including α-smooth muscle actin, CD10, podoplanin, fibroblast specific protein 1, and adipocyte enhancer-binding protein 1, and EMT-related proteins [zinc finger protein SNAI2 (ZEB1) and twist-related protein 1 (TWIST1) in SiCRC with (n = 29) or without (n = 80) lymph node metastasis was examined by immunohistochemistry.			
30087711	chr7	19018106	19020106	TWIST1	Objective: Recent studies have shown that cancer-associated fibroblasts (CAFs) and the epithelial-mesenchymal transition (EMT) play important roles in the progression and metastasis of CRC.                                                            The expression of CAF-related markers, including α-smooth muscle actin, CD10, podoplanin, fibroblast specific protein 1, and adipocyte enhancer-binding protein 1, and EMT-related proteins [zinc finger protein SNAI2 (ZEB1) and twist-related protein 1 (TWIST1) in SiCRC with (n = 29) or without (n = 80) lymph node metastasis was examined by immunohistochemistry.	human		High+Lowthroughput	Analysis of the expression of cancer-associated fibroblast- and EMT-related proteins in submucosal invasive colorectal cancer	否		colorectal cancer 	fibroblast	E_01_0771	Immunohistochemistry, hierarchical clustering analysis	Objective: Recent studies have shown that cancer-associated fibroblasts (CAFs) and the epithelial-mesenchymal transition (EMT) play important roles in the progression and metastasis of CRC.                                                            The expression of CAF-related markers, including α-smooth muscle actin, CD10, podoplanin, fibroblast specific protein 1, and adipocyte enhancer-binding protein 1, and EMT-related proteins [zinc finger protein SNAI2 (ZEB1) and twist-related protein 1 (TWIST1) in SiCRC with (n = 29) or without (n = 80) lymph node metastasis was examined by immunohistochemistry.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Objective: Recent studies have shown that cancer-associated fibroblasts (CAFs) and the epithelial-mesenchymal transition (EMT) play important roles in the progression and metastasis of CRC.                                                            The expression of CAF-related markers, including α-smooth muscle actin, CD10, podoplanin, fibroblast specific protein 1, and adipocyte enhancer-binding protein 1, and EMT-related proteins [zinc finger protein SNAI2 (ZEB1) and twist-related protein 1 (TWIST1) in SiCRC with (n = 29) or without (n = 80) lymph node metastasis was examined by immunohistochemistry.	Immunohistochemical staining	Objective: Recent studies have shown that cancer-associated fibroblasts (CAFs) and the epithelial-mesenchymal transition (EMT) play important roles in the progression and metastasis of CRC.                                                            The expression of CAF-related markers, including α-smooth muscle actin, CD10, podoplanin, fibroblast specific protein 1, and adipocyte enhancer-binding protein 1, and EMT-related proteins [zinc finger protein SNAI2 (ZEB1) and twist-related protein 1 (TWIST1) in SiCRC with (n = 29) or without (n = 80) lymph node metastasis was examined by immunohistochemistry.	TWIST1		免疫组化,层次聚类分析	Objective: Recent studies have shown that cancer-associated fibroblasts (CAFs) and the epithelial-mesenchymal transition (EMT) play important roles in the progression and metastasis of CRC.                                                            The expression of CAF-related markers, including α-smooth muscle actin, CD10, podoplanin, fibroblast specific protein 1, and adipocyte enhancer-binding protein 1, and EMT-related proteins [zinc finger protein SNAI2 (ZEB1) and twist-related protein 1 (TWIST1) in SiCRC with (n = 29) or without (n = 80) lymph node metastasis was examined by immunohistochemistry.			
30087389	chr15	40841317	40843317	SPINT1	The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 	human		High+Lowthroughput	Intestinal regulation of suppression of tumorigenicity 14 (ST14) and serine peptidase inhibitor, Kunitz type -1 (SPINT1) by transcription factor CDX2	否		Inflammatory bowel disease, allergic disease, malignancy	Caco-2 cell	E_01_0772	Chip PCR, RT-PCR, chip SEQ, statistical analysis	The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 		The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 	Immunohistochemical staining	The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 			ChIP-PCR,RT-PCR,ChIP-seq,统计分析				SPINT1
30087389	chr11	130157100	130159100	ST14	The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 	human		High+Lowthroughput	Intestinal regulation of suppression of tumorigenicity 14 (ST14) and serine peptidase inhibitor, Kunitz type -1 (SPINT1) by transcription factor CDX2	否		Inflammatory bowel disease, allergic disease, malignancy	Caco-2 cell	E_01_0772	Chip PCR, RT-PCR, chip SEQ, statistical analysis	The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 		The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 	Immunohistochemical staining	The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 			ChIP-PCR,RT-PCR,ChIP-seq,统计分析				ST14
30087389	chr13	27958050	27960050	CDX2	The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 	human		High+Lowthroughput	Intestinal regulation of suppression of tumorigenicity 14 (ST14) and serine peptidase inhibitor, Kunitz type -1 (SPINT1) by transcription factor CDX2	否		Inflammatory bowel disease, allergic disease, malignancy	Caco-2 cell	E_01_0772	Chip PCR, RT-PCR, chip SEQ, statistical analysis	The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 	Immunohistochemical staining	The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 	CDX2		ChIP-PCR,RT-PCR,ChIP-seq,统计分析	The type II membrane-anchored serine protease, matriptase, encoded by suppression of tumorgenicity-14 (ST14) regulates the integrity of the intestinal epithelial barrier in concert with its inhibitor, HAI-1 encoded by serine peptidase inhibitor, Kunitz type -1 (SPINT1).In this study, we show that CDX2 has a dual function in regulating both ST14 and SPINT1, gene expression in intestinal cells. 			
30085311	chr19	19142788	19144788	MEF2B	Broiler growth is related to skeletal muscle develop- ment which is regulated by myogenic regulatory factors including myogenic differentiation factor 1 (MyoD1), myogenic factor 5 (Myf5), muscle regulator 4 (MRF4), myogenin (MyoG), myocyte enhancer factor 2 family of transcription factors (MEF2A, B, C, D), as well as myostatin (MSTN) (Hennebry et al., 2009; Townley-Tilson et al., 2010). 	mouse		High+Lowthroughput	Betaine improves the growth performance and muscle growth of partridge shank broiler chickens via altering myogenic gene expression and insulin-like growth factor-1 signaling pathway	否			C2C12 cell	E_02_0491	Real time PCR, IGF-1 enzyme linked immunosorbent assay, Western blot, and statistical analysis	Broiler growth is related to skeletal muscle develop- ment which is regulated by myogenic regulatory factors including myogenic differentiation factor 1 (MyoD1), myogenic factor 5 (Myf5), muscle regulator 4 (MRF4), myogenin (MyoG), myocyte enhancer factor 2 family of transcription factors (MEF2A, B, C, D), as well as myostatin (MSTN) (Hennebry et al., 2009; Townley-Tilson et al., 2010). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Broiler growth is related to skeletal muscle develop- ment which is regulated by myogenic regulatory factors including myogenic differentiation factor 1 (MyoD1), myogenic factor 5 (Myf5), muscle regulator 4 (MRF4), myogenin (MyoG), myocyte enhancer factor 2 family of transcription factors (MEF2A, B, C, D), as well as myostatin (MSTN) (Hennebry et al., 2009; Townley-Tilson et al., 2010). 		Broiler growth is related to skeletal muscle develop- ment which is regulated by myogenic regulatory factors including myogenic differentiation factor 1 (MyoD1), myogenic factor 5 (Myf5), muscle regulator 4 (MRF4), myogenin (MyoG), myocyte enhancer factor 2 family of transcription factors (MEF2A, B, C, D), as well as myostatin (MSTN) (Hennebry et al., 2009; Townley-Tilson et al., 2010). 	Immunohistochemical staining	Broiler growth is related to skeletal muscle develop- ment which is regulated by myogenic regulatory factors including myogenic differentiation factor 1 (MyoD1), myogenic factor 5 (Myf5), muscle regulator 4 (MRF4), myogenin (MyoG), myocyte enhancer factor 2 family of transcription factors (MEF2A, B, C, D), as well as myostatin (MSTN) (Hennebry et al., 2009; Townley-Tilson et al., 2010). 			real-time PCR,IGF-1 Enzyme-Linked Immunosorbent Assay,western blot,统计分析				MEF2B
30085311	chr10	107316559	107318559	Myf5	Broiler growth is related to skeletal muscle develop- ment which is regulated by myogenic regulatory factors including myogenic differentiation factor 1 (MyoD1), myogenic factor 5 (Myf5), muscle regulator 4 (MRF4), myogenin (MyoG), myocyte enhancer factor 2 family of transcription factors (MEF2A, B, C, D), as well as myostatin (MSTN) (Hennebry et al., 2009; Townley-Tilson et al., 2010). 	mouse		High+Lowthroughput	Betaine improves the growth performance and muscle growth of partridge shank broiler chickens via altering myogenic gene expression and insulin-like growth factor-1 signaling pathway	否			C2C12 cell	E_02_0491	Real time PCR, IGF-1 enzyme linked immunosorbent assay, Western blot, and statistical analysis	Broiler growth is related to skeletal muscle develop- ment which is regulated by myogenic regulatory factors including myogenic differentiation factor 1 (MyoD1), myogenic factor 5 (Myf5), muscle regulator 4 (MRF4), myogenin (MyoG), myocyte enhancer factor 2 family of transcription factors (MEF2A, B, C, D), as well as myostatin (MSTN) (Hennebry et al., 2009; Townley-Tilson et al., 2010). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Broiler growth is related to skeletal muscle develop- ment which is regulated by myogenic regulatory factors including myogenic differentiation factor 1 (MyoD1), myogenic factor 5 (Myf5), muscle regulator 4 (MRF4), myogenin (MyoG), myocyte enhancer factor 2 family of transcription factors (MEF2A, B, C, D), as well as myostatin (MSTN) (Hennebry et al., 2009; Townley-Tilson et al., 2010). 		Broiler growth is related to skeletal muscle develop- ment which is regulated by myogenic regulatory factors including myogenic differentiation factor 1 (MyoD1), myogenic factor 5 (Myf5), muscle regulator 4 (MRF4), myogenin (MyoG), myocyte enhancer factor 2 family of transcription factors (MEF2A, B, C, D), as well as myostatin (MSTN) (Hennebry et al., 2009; Townley-Tilson et al., 2010). 	Immunohistochemical staining	Broiler growth is related to skeletal muscle develop- ment which is regulated by myogenic regulatory factors including myogenic differentiation factor 1 (MyoD1), myogenic factor 5 (Myf5), muscle regulator 4 (MRF4), myogenin (MyoG), myocyte enhancer factor 2 family of transcription factors (MEF2A, B, C, D), as well as myostatin (MSTN) (Hennebry et al., 2009; Townley-Tilson et al., 2010). 			real-time PCR,IGF-1 Enzyme-Linked Immunosorbent Assay,western blot,统计分析				Myf5
30084829	chr14	100776351	100778351	MEG3	In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 	mouse,human		High+Lowthroughput	The Dysregulation of the DLK1-MEG3 Locus in Islets From Patients With Type 2 Diabetes Is Mimicked by Targeted Epimutation of Its Promoter With TALE-DNMT Constructs	是	rs3783355	Type 2 diabetes mellitus (T2DM)		E_02_0492	ChIP-PCR,4C-Seq,RT-PCR	In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 		In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 	Immunohistochemical staining	In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 			ChIP-PCR,4C-Seq,RT-PCR				MEG3
30084829	chr20	22578390	22580390	FOXA2	In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 	mouse,human		High+Lowthroughput	The Dysregulation of the DLK1-MEG3 Locus in Islets From Patients With Type 2 Diabetes Is Mimicked by Targeted Epimutation of Its Promoter With TALE-DNMT Constructs	是	rs3783355	Type 2 diabetes mellitus (T2DM)		E_02_0492	ChIP-PCR,4C-Seq,RT-PCR	In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 		In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 	Immunohistochemical staining	In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 			ChIP-PCR,4C-Seq,RT-PCR				FOXA2
30084829	chr13	27917344	27919344	PDX1	In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 	mouse,human		High+Lowthroughput	The Dysregulation of the DLK1-MEG3 Locus in Islets From Patients With Type 2 Diabetes Is Mimicked by Targeted Epimutation of Its Promoter With TALE-DNMT Constructs	是	rs3783355	Type 2 diabetes mellitus (T2DM)		E_02_0492	ChIP-PCR,4C-Seq,RT-PCR	In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 		In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 	Immunohistochemical staining	In this study, using targeted epigenetic modifiers, we prove that increased methylation at the promoter of Meg3 in mouse βTC6 β-cells results in decreased transcription of the maternal transcripts associated with this locus.                                                                                                                                                                                                                                                                                                                                                                                                  Using circular chromosome conformation capture followed by high-throughput sequencing, we demonstrate that the promoter of MEG3 physically interacts with this novel enhancer and other putative regulatory elements in this imprinted region in human islets. Remarkably, this enhancer is bound in an allele-specific manner by the transcription factors FOXA2, PDX1, and NKX2.2. 			ChIP-PCR,4C-Seq,RT-PCR				PDX1
30084155	chr16	86507365	86509365	FOXF1	Alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is a rare, lethal, neonatal developmental lung disorder caused by point mutations or copy-number variant (CNV) deletions of FOXF1 or its distant tissue-specific enhancer. 	human		High+Lowthroughput	LINE- and Alu-containing genomic instability hotspot at 16q24.1 associated with recurrent and nonrecurrent CNV deletions causative for ACDMPV	是		Alveolar capillary dysplasia with misalignment of pulmonary veins (acdmpv)	germ line cell	E_01_0773	PCR	Alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is a rare, lethal, neonatal developmental lung disorder caused by point mutations or copy-number variant (CNV) deletions of FOXF1 or its distant tissue-specific enhancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is a rare, lethal, neonatal developmental lung disorder caused by point mutations or copy-number variant (CNV) deletions of FOXF1 or its distant tissue-specific enhancer. 	Immunohistochemical staining	Alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is a rare, lethal, neonatal developmental lung disorder caused by point mutations or copy-number variant (CNV) deletions of FOXF1 or its distant tissue-specific enhancer. 	FOXF1		PCR	Alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) is a rare, lethal, neonatal developmental lung disorder caused by point mutations or copy-number variant (CNV) deletions of FOXF1 or its distant tissue-specific enhancer. 			
30082743	chr10	67882384	67884384	SIRT1	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.	human		High+Lowthroughput	DBC1 regulates Wnt/β-catenin-mediated expression of MACC1, a key regulator of cancer progression, in colon cancer	否		Colon cancer 1 (MACC1), breast cancer	Cancer Stem Cell	E_01_0774	QRT PCR, chip SEQ, chip qPCR, immunofluorescence staining, statistical analysis	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.	Immunohistochemical staining	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.	SIRT1		qRT-PCR,ChIP-seq,ChIP-qPCR,免疫荧光染色,统计分析	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.			
30082743	chr5	141617941	141619941	HDAC3	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.	human		High+Lowthroughput	DBC1 regulates Wnt/β-catenin-mediated expression of MACC1, a key regulator of cancer progression, in colon cancer	否		Colon cancer 1 (MACC1), breast cancer	Cancer Stem Cell	E_01_0774	QRT PCR, chip SEQ, chip qPCR, immunofluorescence staining, statistical analysis	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.		We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.	Immunohistochemical staining	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.			qRT-PCR,ChIP-seq,ChIP-qPCR,免疫荧光染色,统计分析				HDAC3
30082743	chrX	48692379	48694379	SUV39H1	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.	human		High+Lowthroughput	DBC1 regulates Wnt/β-catenin-mediated expression of MACC1, a key regulator of cancer progression, in colon cancer	否		Colon cancer 1 (MACC1), breast cancer	Cancer Stem Cell	E_01_0774	QRT PCR, chip SEQ, chip qPCR, immunofluorescence staining, statistical analysis	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.		We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.	Immunohistochemical staining	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.			qRT-PCR,ChIP-seq,ChIP-qPCR,免疫荧光染色,统计分析				SUV39H1
30082743	chr12	68805197	68807197	MDM2	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.	human		High+Lowthroughput	DBC1 regulates Wnt/β-catenin-mediated expression of MACC1, a key regulator of cancer progression, in colon cancer	否		Colon cancer 1 (MACC1), breast cancer	Cancer Stem Cell	E_01_0774	QRT PCR, chip SEQ, chip qPCR, immunofluorescence staining, statistical analysis	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.		We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.	Immunohistochemical staining	We and others have recently shown that DBC1 plays a key role in multiple oncogenic signaling pathways by acting as a transcriptional coactivator for estrogen receptor, PEA3/ETV4, LEF1-β-catenin, androgen receptor, and androgen receptor variant 7 and by functioning as an inhibitor of epigenetic modifiers such as SIRT1, HDAC3, SUV39H1, MDM2, and CHIP7 14.			qRT-PCR,ChIP-seq,ChIP-qPCR,免疫荧光染色,统计分析				MDM2
30082728	chr8	115405258	115407258	TRPS1	We show that TRPS1 globally regulates YAP-dependent transcription by binding to a large set of joint genomic sites, mainly enhancers.	human,mouse		High+Lowthroughput	TRPS1 shapes YAP/TEAD-dependent transcription in breast cancer cells	否		Colon cancer, breast cancer	mammary gland epithelial cell	E_02_0493	QRT PCR, Western blot, chromatin immunoprecipitation (chip), chip SEQ, 4C SEQ, ATAC SEQ, immunofluorescence staining, statistical analysis	We show that TRPS1 globally regulates YAP-dependent transcription by binding to a large set of joint genomic sites, mainly enhancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We show that TRPS1 globally regulates YAP-dependent transcription by binding to a large set of joint genomic sites, mainly enhancers.		We show that TRPS1 globally regulates YAP-dependent transcription by binding to a large set of joint genomic sites, mainly enhancers.	Immunohistochemical staining	We show that TRPS1 globally regulates YAP-dependent transcription by binding to a large set of joint genomic sites, mainly enhancers.			qRT-PCR,western blot,染色质免疫沉淀(ChIP),ChIP-Seq,4C-Seq,ATAC-Seq,免疫荧光染色,统计分析				TRPS1
30082223	chr11	32384746	32386746	WT1	The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.	human		High+Lowthroughput	Wilms Tumor 1 Expression at Diagnosis Correlates With Genetic Abnormalities and Polymorphism But Is Not Independently Prognostic in Acute Myelogenous Leukemia: A?Hokkaido Leukemia Net Study	是	rs16754	Acute myeloid leukemia (AML)	K562 cell	E_01_0775	Statistical analysis, PCR	The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.		The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.	Immunohistochemical staining	The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.			统计分析,PCR				WT1
30082223	chr5	171384586	171386586	NPM1	The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.	human		High+Lowthroughput	Wilms Tumor 1 Expression at Diagnosis Correlates With Genetic Abnormalities and Polymorphism But Is Not Independently Prognostic in Acute Myelogenous Leukemia: A?Hokkaido Leukemia Net Study	是	rs16754	Acute myeloid leukemia (AML)	K562 cell	E_01_0775	Statistical analysis, PCR	The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.		The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.	Immunohistochemical staining	The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.			统计分析,PCR				NPM1
30082223	chr19	33297318	33299318	CEBPA	The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.	human		High+Lowthroughput	Wilms Tumor 1 Expression at Diagnosis Correlates With Genetic Abnormalities and Polymorphism But Is Not Independently Prognostic in Acute Myelogenous Leukemia: A?Hokkaido Leukemia Net Study	是	rs16754	Acute myeloid leukemia (AML)	K562 cell	E_01_0775	Statistical analysis, PCR	The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.	Immunohistochemical staining	The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.	CEBPA		统计分析,PCR	The WT1 protein is a unique transcription factor that can activate or repress target promoters depending on the cellular cofactors it binds to.3 More than 70% of patients with acute myelogenous leukemia (AML) will have overexpression of WT1 at diagnosis. 4-7 Whether the WT1 transcript levels at diagnosis are predictive of the outcomes of AML patients is controversial.			
30081852	chr5	5137696	5139696	ADAMTS16	Conclusions We identified ADAMTS16 as novel gene with cancer-specific promoter hypermethylation in CRC, LC and SCC patients implicating ADAMTS16 as potential biomarker for these tumors.	human	Tumor tissues	High+Lowthroughput	Aberrant DNA methylation of ADAMTS16 in colorectal and other epithelial cancers	是		Oral squamous cell carcinoma (SCC), lung cancer	HT29 cell	E_01_0776	Western blot, immunohistochemical analysis, statistical analysis	Conclusions We identified ADAMTS16 as novel gene with cancer-specific promoter hypermethylation in CRC, LC and SCC patients implicating ADAMTS16 as potential biomarker for these tumors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Conclusions We identified ADAMTS16 as novel gene with cancer-specific promoter hypermethylation in CRC, LC and SCC patients implicating ADAMTS16 as potential biomarker for these tumors.		Conclusions We identified ADAMTS16 as novel gene with cancer-specific promoter hypermethylation in CRC, LC and SCC patients implicating ADAMTS16 as potential biomarker for these tumors.	Immunohistochemical staining	Conclusions We identified ADAMTS16 as novel gene with cancer-specific promoter hypermethylation in CRC, LC and SCC patients implicating ADAMTS16 as potential biomarker for these tumors.			western blot,免疫组化分析,统计分析				ADAMTS16
30081852	chr5	179107998	179109998	ADAMTS2	Conclusions We identified ADAMTS16 as novel gene with cancer-specific promoter hypermethylation in CRC, LC and SCC patients implicating ADAMTS16 as potential biomarker for these tumors.	human	Tumor tissues	High+Lowthroughput	Aberrant DNA methylation of ADAMTS16 in colorectal and other epithelial cancers	是		Oral squamous cell carcinoma (SCC), lung cancer	HT29 cell	E_01_0776	Western blot, immunohistochemical analysis, statistical analysis	Conclusions We identified ADAMTS16 as novel gene with cancer-specific promoter hypermethylation in CRC, LC and SCC patients implicating ADAMTS16 as potential biomarker for these tumors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Conclusions We identified ADAMTS16 as novel gene with cancer-specific promoter hypermethylation in CRC, LC and SCC patients implicating ADAMTS16 as potential biomarker for these tumors.		Conclusions We identified ADAMTS16 as novel gene with cancer-specific promoter hypermethylation in CRC, LC and SCC patients implicating ADAMTS16 as potential biomarker for these tumors.	Immunohistochemical staining	Conclusions We identified ADAMTS16 as novel gene with cancer-specific promoter hypermethylation in CRC, LC and SCC patients implicating ADAMTS16 as potential biomarker for these tumors.			western blot,免疫组化分析,统计分析				ADAMTS2
30081710	chr6	114617420	114619420	Atg7	Atg7 knockdown suppressed neonatal satellite cell (nSC) proliferation and differentiation, downregulating the GH-IGF1 functions. When we disrupted autophagy, NFE2L2/NRF2 (nuclear factor, erythroid 2 like 2) accumulated in muscle and nSCs and negatively modulated DDIT3/CHOP (DNA-damage inducible transcript 3) expression.	human,mouse		High+Lowthroughput	Autophagy controls neonatal myogenesis by regulating the GH-IGF1 system through a NFE2L2- and DDIT3-mediated mechanism	否			C2C12 cell	E_02_0494	RT qPCR, Western blot, immunofluorescence staining, statistical analysis	Atg7 knockdown suppressed neonatal satellite cell (nSC) proliferation and differentiation, downregulating the GH-IGF1 functions. When we disrupted autophagy, NFE2L2/NRF2 (nuclear factor, erythroid 2 like 2) accumulated in muscle and nSCs and negatively modulated DDIT3/CHOP (DNA-damage inducible transcript 3) expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Atg7 knockdown suppressed neonatal satellite cell (nSC) proliferation and differentiation, downregulating the GH-IGF1 functions. When we disrupted autophagy, NFE2L2/NRF2 (nuclear factor, erythroid 2 like 2) accumulated in muscle and nSCs and negatively modulated DDIT3/CHOP (DNA-damage inducible transcript 3) expression.		Atg7 knockdown suppressed neonatal satellite cell (nSC) proliferation and differentiation, downregulating the GH-IGF1 functions. When we disrupted autophagy, NFE2L2/NRF2 (nuclear factor, erythroid 2 like 2) accumulated in muscle and nSCs and negatively modulated DDIT3/CHOP (DNA-damage inducible transcript 3) expression.	Immunohistochemical staining	Atg7 knockdown suppressed neonatal satellite cell (nSC) proliferation and differentiation, downregulating the GH-IGF1 functions. When we disrupted autophagy, NFE2L2/NRF2 (nuclear factor, erythroid 2 like 2) accumulated in muscle and nSCs and negatively modulated DDIT3/CHOP (DNA-damage inducible transcript 3) expression.			RT-qPCR,western blot,免疫荧光染色,统计分析				Atg7
30081710	chr2	177224378	177226378	NFE2L2	Atg7 knockdown suppressed neonatal satellite cell (nSC) proliferation and differentiation, downregulating the GH-IGF1 functions. When we disrupted autophagy, NFE2L2/NRF2 (nuclear factor, erythroid 2 like 2) accumulated in muscle and nSCs and negatively modulated DDIT3/CHOP (DNA-damage inducible transcript 3) expression.	human,mouse		High+Lowthroughput	Autophagy controls neonatal myogenesis by regulating the GH-IGF1 system through a NFE2L2- and DDIT3-mediated mechanism	否			C2C12 cell	E_02_0494	RT qPCR, Western blot, immunofluorescence staining, statistical analysis	Atg7 knockdown suppressed neonatal satellite cell (nSC) proliferation and differentiation, downregulating the GH-IGF1 functions. When we disrupted autophagy, NFE2L2/NRF2 (nuclear factor, erythroid 2 like 2) accumulated in muscle and nSCs and negatively modulated DDIT3/CHOP (DNA-damage inducible transcript 3) expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Atg7 knockdown suppressed neonatal satellite cell (nSC) proliferation and differentiation, downregulating the GH-IGF1 functions. When we disrupted autophagy, NFE2L2/NRF2 (nuclear factor, erythroid 2 like 2) accumulated in muscle and nSCs and negatively modulated DDIT3/CHOP (DNA-damage inducible transcript 3) expression.		Atg7 knockdown suppressed neonatal satellite cell (nSC) proliferation and differentiation, downregulating the GH-IGF1 functions. When we disrupted autophagy, NFE2L2/NRF2 (nuclear factor, erythroid 2 like 2) accumulated in muscle and nSCs and negatively modulated DDIT3/CHOP (DNA-damage inducible transcript 3) expression.	Immunohistochemical staining	Atg7 knockdown suppressed neonatal satellite cell (nSC) proliferation and differentiation, downregulating the GH-IGF1 functions. When we disrupted autophagy, NFE2L2/NRF2 (nuclear factor, erythroid 2 like 2) accumulated in muscle and nSCs and negatively modulated DDIT3/CHOP (DNA-damage inducible transcript 3) expression.			RT-qPCR,western blot,免疫荧光染色,统计分析				NFE2L2
30081225	chr5	122060306	122062306	LOX	Expression of mediators of cholesterol transport, namely the lectin-like oxidized low-density lipoprotein receptor (LOX)-1 and ATP-binding cassette transporter (ABCA)-1, inflammatory markers tumor necrosis factor (TNF)-α and interleukin (IL)-1β/IL-6, nuclear-factor kappa-light-chain-enhancer of activated B cells (NF-κB), intracellular/vascular adhesion molecule(s) (VCAM-1, ICAM-1), and miRNAs (miR-221/ 21/ 1), associated with cardiovascular disease (CVD), were analyzed in cardiac tissue and coronary vasculature.	mouse,human		High+Lowthroughput	The effects of subacute inhaled multi-walled carbon nanotube exposure on signaling pathways associated with cholesterol transport and inflammatory markers in the vasculature of wild-type mice	否		Atherosclerosis, coronary artery disease (CAD)	B cell	E_02_0495	RT-PCR, immunofluorescence staining	Expression of mediators of cholesterol transport, namely the lectin-like oxidized low-density lipoprotein receptor (LOX)-1 and ATP-binding cassette transporter (ABCA)-1, inflammatory markers tumor necrosis factor (TNF)-α and interleukin (IL)-1β/IL-6, nuclear-factor kappa-light-chain-enhancer of activated B cells (NF-κB), intracellular/vascular adhesion molecule(s) (VCAM-1, ICAM-1), and miRNAs (miR-221/ 21/ 1), associated with cardiovascular disease (CVD), were analyzed in cardiac tissue and coronary vasculature.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Expression of mediators of cholesterol transport, namely the lectin-like oxidized low-density lipoprotein receptor (LOX)-1 and ATP-binding cassette transporter (ABCA)-1, inflammatory markers tumor necrosis factor (TNF)-α and interleukin (IL)-1β/IL-6, nuclear-factor kappa-light-chain-enhancer of activated B cells (NF-κB), intracellular/vascular adhesion molecule(s) (VCAM-1, ICAM-1), and miRNAs (miR-221/ 21/ 1), associated with cardiovascular disease (CVD), were analyzed in cardiac tissue and coronary vasculature.		Expression of mediators of cholesterol transport, namely the lectin-like oxidized low-density lipoprotein receptor (LOX)-1 and ATP-binding cassette transporter (ABCA)-1, inflammatory markers tumor necrosis factor (TNF)-α and interleukin (IL)-1β/IL-6, nuclear-factor kappa-light-chain-enhancer of activated B cells (NF-κB), intracellular/vascular adhesion molecule(s) (VCAM-1, ICAM-1), and miRNAs (miR-221/ 21/ 1), associated with cardiovascular disease (CVD), were analyzed in cardiac tissue and coronary vasculature.	Immunohistochemical staining	Expression of mediators of cholesterol transport, namely the lectin-like oxidized low-density lipoprotein receptor (LOX)-1 and ATP-binding cassette transporter (ABCA)-1, inflammatory markers tumor necrosis factor (TNF)-α and interleukin (IL)-1β/IL-6, nuclear-factor kappa-light-chain-enhancer of activated B cells (NF-κB), intracellular/vascular adhesion molecule(s) (VCAM-1, ICAM-1), and miRNAs (miR-221/ 21/ 1), associated with cardiovascular disease (CVD), were analyzed in cardiac tissue and coronary vasculature.			RT-PCR,免疫荧光染色				LOX
30080426	chr8	63165731	63167731	YTHDF3	Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 	human,mouse		High+Lowthroughput	Expression of circular RNAs during C2C12 myoblast differentiation and prediction of coding potential based on the number of open reading frames and N6-methyladenosine motifs	否		Hepatocellular carcinoma	C2C12 cell	E_02_0496	QRT-PCR, statistical analysis	Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 		Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 	Immunohistochemical staining	Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 			QRT-PCR,统计分析				YTHDF3
30080426	chr11	67088028	67090028	Myh1	Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 	human,mouse		High+Lowthroughput	Expression of circular RNAs during C2C12 myoblast differentiation and prediction of coding potential based on the number of open reading frames and N6-methyladenosine motifs	否		Hepatocellular carcinoma	C2C12 cell	E_02_0496	QRT-PCR, statistical analysis	Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 		Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 	Immunohistochemical staining	Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 			QRT-PCR,统计分析				Myh1
30080426	chr14	55205228	55207228	Myh7	Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 	human,mouse		High+Lowthroughput	Expression of circular RNAs during C2C12 myoblast differentiation and prediction of coding potential based on the number of open reading frames and N6-methyladenosine motifs	否		Hepatocellular carcinoma	C2C12 cell	E_02_0496	QRT-PCR, statistical analysis	Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 		Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 	Immunohistochemical staining	Recently, it was reported that m6A motif was sufficient to drive translation initiation in circRNAs; and m6A motif-driven translation required eukaryotic translation initiation factor 4 gamma 2 (eIF4G2) and m6A reader YTH domain family protein 3 (YTHDF3) in human cells [21].                                                                                                                                                                                                                                                                                           Myh is divided into different subtypes, and Myh1 is the signature gene of fast-twitch muscle fibers [26], while Myh7 is important for slow-twitch muscle fibers [27]. 			QRT-PCR,统计分析				Myh7
30078552	chr14	92920852	92922852	CHGA	Most islet antigens (Ags), namely insulin (INS) and its precursor preproinsulin (PPI), glutamic acid decarboxylase (GAD65/ GAD2), islet Ag (IA)-2 (PTPRN) (Mallone et al., 2007; Martinuzzi et al., 2008), and zinc transporter 8 (ZnT8/SLC30A8) (Scotto et al., 2012), have been identified based on their targeting by autoantibodies (aAbs). Other Ags such as islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) (Mallone et al., 2007), chromogranin A (CHGA) (Li et al., 2015), and islet amyloid polypeptide (IAPP) (Standifer et al., 2006) have been identified based on studies in the non-obese dia- betic mouse and/or its islet-enriched expression.	human		High+Lowthroughput	Conventional and Neo-antigenic Peptides Presented by β Cells Are Targeted by Circulating Na?ve CD8+ T Cells in Type 1 Diabetic and Healthy Donors	否		Type 1 diabetes (T1D)	CD8+ T cell	E_01_0777	RNA SEQ, immunofluorescence staining, HLA-A2 binding assays	Most islet antigens (Ags), namely insulin (INS) and its precursor preproinsulin (PPI), glutamic acid decarboxylase (GAD65/ GAD2), islet Ag (IA)-2 (PTPRN) (Mallone et al., 2007; Martinuzzi et al., 2008), and zinc transporter 8 (ZnT8/SLC30A8) (Scotto et al., 2012), have been identified based on their targeting by autoantibodies (aAbs). Other Ags such as islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) (Mallone et al., 2007), chromogranin A (CHGA) (Li et al., 2015), and islet amyloid polypeptide (IAPP) (Standifer et al., 2006) have been identified based on studies in the non-obese dia- betic mouse and/or its islet-enriched expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Most islet antigens (Ags), namely insulin (INS) and its precursor preproinsulin (PPI), glutamic acid decarboxylase (GAD65/ GAD2), islet Ag (IA)-2 (PTPRN) (Mallone et al., 2007; Martinuzzi et al., 2008), and zinc transporter 8 (ZnT8/SLC30A8) (Scotto et al., 2012), have been identified based on their targeting by autoantibodies (aAbs). Other Ags such as islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) (Mallone et al., 2007), chromogranin A (CHGA) (Li et al., 2015), and islet amyloid polypeptide (IAPP) (Standifer et al., 2006) have been identified based on studies in the non-obese dia- betic mouse and/or its islet-enriched expression.	Immunohistochemical staining	Most islet antigens (Ags), namely insulin (INS) and its precursor preproinsulin (PPI), glutamic acid decarboxylase (GAD65/ GAD2), islet Ag (IA)-2 (PTPRN) (Mallone et al., 2007; Martinuzzi et al., 2008), and zinc transporter 8 (ZnT8/SLC30A8) (Scotto et al., 2012), have been identified based on their targeting by autoantibodies (aAbs). Other Ags such as islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) (Mallone et al., 2007), chromogranin A (CHGA) (Li et al., 2015), and islet amyloid polypeptide (IAPP) (Standifer et al., 2006) have been identified based on studies in the non-obese dia- betic mouse and/or its islet-enriched expression.	CHGA		RNA-Seq,免疫荧光染色,HLA-A2 Binding Assays	Most islet antigens (Ags), namely insulin (INS) and its precursor preproinsulin (PPI), glutamic acid decarboxylase (GAD65/ GAD2), islet Ag (IA)-2 (PTPRN) (Mallone et al., 2007; Martinuzzi et al., 2008), and zinc transporter 8 (ZnT8/SLC30A8) (Scotto et al., 2012), have been identified based on their targeting by autoantibodies (aAbs). Other Ags such as islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) (Mallone et al., 2007), chromogranin A (CHGA) (Li et al., 2015), and islet amyloid polypeptide (IAPP) (Standifer et al., 2006) have been identified based on studies in the non-obese dia- betic mouse and/or its islet-enriched expression.			
30078552	chr2	219286554	219288554	PTPRN	Most islet antigens (Ags), namely insulin (INS) and its precursor preproinsulin (PPI), glutamic acid decarboxylase (GAD65/ GAD2), islet Ag (IA)-2 (PTPRN) (Mallone et al., 2007; Martinuzzi et al., 2008), and zinc transporter 8 (ZnT8/SLC30A8) (Scotto et al., 2012), have been identified based on their targeting by autoantibodies (aAbs). Other Ags such as islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) (Mallone et al., 2007), chromogranin A (CHGA) (Li et al., 2015), and islet amyloid polypeptide (IAPP) (Standifer et al., 2006) have been identified based on studies in the non-obese dia- betic mouse and/or its islet-enriched expression.	human		High+Lowthroughput	Conventional and Neo-antigenic Peptides Presented by β Cells Are Targeted by Circulating Na?ve CD8+ T Cells in Type 1 Diabetic and Healthy Donors	否		Type 1 diabetes (T1D)	CD8+ T cell	E_01_0777	RNA SEQ, immunofluorescence staining, HLA-A2 binding assays	Most islet antigens (Ags), namely insulin (INS) and its precursor preproinsulin (PPI), glutamic acid decarboxylase (GAD65/ GAD2), islet Ag (IA)-2 (PTPRN) (Mallone et al., 2007; Martinuzzi et al., 2008), and zinc transporter 8 (ZnT8/SLC30A8) (Scotto et al., 2012), have been identified based on their targeting by autoantibodies (aAbs). Other Ags such as islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) (Mallone et al., 2007), chromogranin A (CHGA) (Li et al., 2015), and islet amyloid polypeptide (IAPP) (Standifer et al., 2006) have been identified based on studies in the non-obese dia- betic mouse and/or its islet-enriched expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Most islet antigens (Ags), namely insulin (INS) and its precursor preproinsulin (PPI), glutamic acid decarboxylase (GAD65/ GAD2), islet Ag (IA)-2 (PTPRN) (Mallone et al., 2007; Martinuzzi et al., 2008), and zinc transporter 8 (ZnT8/SLC30A8) (Scotto et al., 2012), have been identified based on their targeting by autoantibodies (aAbs). Other Ags such as islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) (Mallone et al., 2007), chromogranin A (CHGA) (Li et al., 2015), and islet amyloid polypeptide (IAPP) (Standifer et al., 2006) have been identified based on studies in the non-obese dia- betic mouse and/or its islet-enriched expression.		Most islet antigens (Ags), namely insulin (INS) and its precursor preproinsulin (PPI), glutamic acid decarboxylase (GAD65/ GAD2), islet Ag (IA)-2 (PTPRN) (Mallone et al., 2007; Martinuzzi et al., 2008), and zinc transporter 8 (ZnT8/SLC30A8) (Scotto et al., 2012), have been identified based on their targeting by autoantibodies (aAbs). Other Ags such as islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) (Mallone et al., 2007), chromogranin A (CHGA) (Li et al., 2015), and islet amyloid polypeptide (IAPP) (Standifer et al., 2006) have been identified based on studies in the non-obese dia- betic mouse and/or its islet-enriched expression.	Immunohistochemical staining	Most islet antigens (Ags), namely insulin (INS) and its precursor preproinsulin (PPI), glutamic acid decarboxylase (GAD65/ GAD2), islet Ag (IA)-2 (PTPRN) (Mallone et al., 2007; Martinuzzi et al., 2008), and zinc transporter 8 (ZnT8/SLC30A8) (Scotto et al., 2012), have been identified based on their targeting by autoantibodies (aAbs). Other Ags such as islet-specific glucose-6-phosphatase catalytic subunit-related protein (IGRP) (Mallone et al., 2007), chromogranin A (CHGA) (Li et al., 2015), and islet amyloid polypeptide (IAPP) (Standifer et al., 2006) have been identified based on studies in the non-obese dia- betic mouse and/or its islet-enriched expression.			RNA-Seq,免疫荧光染色,HLA-A2 Binding Assays				PTPRN
30077771	chr4	94934152	94936152	Jun	Differential Jun binding near transcription start sites. A) Bar plot showing the proportion of differentially- and commonly-bound Jun sites within 2kb of a TSS whose associated genes are upregulated (left) or downregulated (right) 7 days after sciatic nerve axotomy. 	mouse,human		High+Lowthroughput	The effect of Jun dimerization on neurite outgrowth and motif binding	否		Spinal cord injury	HEK	E_02_0497	Chip qPCR, chipseq, rnaseq, immunofluorescence staining	Differential Jun binding near transcription start sites. A) Bar plot showing the proportion of differentially- and commonly-bound Jun sites within 2kb of a TSS whose associated genes are upregulated (left) or downregulated (right) 7 days after sciatic nerve axotomy. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Differential Jun binding near transcription start sites. A) Bar plot showing the proportion of differentially- and commonly-bound Jun sites within 2kb of a TSS whose associated genes are upregulated (left) or downregulated (right) 7 days after sciatic nerve axotomy. 		Differential Jun binding near transcription start sites. A) Bar plot showing the proportion of differentially- and commonly-bound Jun sites within 2kb of a TSS whose associated genes are upregulated (left) or downregulated (right) 7 days after sciatic nerve axotomy. 	Immunohistochemical staining	Differential Jun binding near transcription start sites. A) Bar plot showing the proportion of differentially- and commonly-bound Jun sites within 2kb of a TSS whose associated genes are upregulated (left) or downregulated (right) 7 days after sciatic nerve axotomy. 			ChIP-qPCR,ChIPseq,RNAseq ,免疫荧光染色				Jun
30076933	chr20	62793633	62795633	MRGBP	This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 	human		High+Lowthroughput	MRGBP promotes AR-mediated transactivation of KLK3 and TMPRSS2 via acetylation of histone H2A.Z in prostate cancer cells	否		prostatic cancer	LNCaP	E_01_0778	QPCR, Western blot, hat assay, statistical analysis	This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 		This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 	Immunohistochemical staining	This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 			qPCR,western blot,HAT assay,统计分析				MRGBP
30076933	chr19	50852155	50854155	KLK3	This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 	human		High+Lowthroughput	MRGBP promotes AR-mediated transactivation of KLK3 and TMPRSS2 via acetylation of histone H2A.Z in prostate cancer cells	否		prostatic cancer	LNCaP	E_01_0778	QPCR, Western blot, hat assay, statistical analysis	This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 		This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 	Immunohistochemical staining	This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 			qPCR,western blot,HAT assay,统计分析				KLK3
30076933	chr21	41461576	41463576	TMPRSS2	This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 	human		High+Lowthroughput	MRGBP promotes AR-mediated transactivation of KLK3 and TMPRSS2 via acetylation of histone H2A.Z in prostate cancer cells	否		prostatic cancer	LNCaP	E_01_0778	QPCR, Western blot, hat assay, statistical analysis	This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 	Immunohistochemical staining	This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 	TMPRSS2		qPCR,western blot,HAT assay,统计分析	This study showed that MRG domain binding protein (MRGBP) accelerated AR-mediated transactivation.                                                                                                                                                                                                                                                          MRGBP increased the expression of certain AR target genes, including KLK3 and TMPRSS2, and it associated with AR binding regions of these genes during androgen treatment. 			
30076409	chr19	15232383	15234383	BRD4	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.	human		High+Lowthroughput	RNAs interact with BRD4 to promote enhanced chromatin engagement and transcription activation	否		colorectal cancer 	SW480 cell	E_01_0779	ChIP-qPCR, qRT-PCR,UV-RIP,SPR,ChIP-Seq,EMSA,western blot	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.	Immunohistochemical staining	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.	BRD4		ChIP-qPCR, qRT-PCR,UV-RIP,SPR,ChIP-Seq,EMSA,western blot	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.			
30076409	chr1	91946544	91948544	BRDT	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.	human		High+Lowthroughput	RNAs interact with BRD4 to promote enhanced chromatin engagement and transcription activation	否		colorectal cancer 	SW480 cell	E_01_0779	ChIP-qPCR, qRT-PCR,UV-RIP,SPR,ChIP-Seq,EMSA,western blot	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.		Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.	Immunohistochemical staining	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.			ChIP-qPCR, qRT-PCR,UV-RIP,SPR,ChIP-Seq,EMSA,western blot				BRDT
30076409	chr16	50310540	50312540	BRD7	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.	human		High+Lowthroughput	RNAs interact with BRD4 to promote enhanced chromatin engagement and transcription activation	否		colorectal cancer 	SW480 cell	E_01_0779	ChIP-qPCR, qRT-PCR,UV-RIP,SPR,ChIP-Seq,EMSA,western blot	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.		Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.	Immunohistochemical staining	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.			ChIP-qPCR, qRT-PCR,UV-RIP,SPR,ChIP-Seq,EMSA,western blot				BRD7
30076409	chr6	32965474	32967474	BRD2	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.	human		High+Lowthroughput	RNAs interact with BRD4 to promote enhanced chromatin engagement and transcription activation	否		colorectal cancer 	SW480 cell	E_01_0779	ChIP-qPCR, qRT-PCR,UV-RIP,SPR,ChIP-Seq,EMSA,western blot	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.		Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.	Immunohistochemical staining	Bromodomain and extra-terminal motif (BET) protein BRD4 binds to acetylated histones at enhancers and promoters through its bromodomains (BDs) to regulate transcriptional elongation.                                                                                                      Through biochemical and biophysical characterizations, we show that BRD4 BDs function cooperatively as docking sites for eRNAs and that the BDs of BRD2, BRD3, BRDT, BRG1, and BRD7 directly interact with eRNAs.			ChIP-qPCR, qRT-PCR,UV-RIP,SPR,ChIP-Seq,EMSA,western blot				BRD2
30076309	chr14	100235442	100237442	YY1	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	human,mouse		High+Lowthroughput	Regulation of miR-181a expression in T cell aging	否		Chicken pox	T cell	E_02_0498	Chip PCR, RNA SEQ, ATAC SEQ, statistical analysis, Western blot	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.		The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	Immunohistochemical staining	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.			ChIP-PCR,RNA-seq,ATAC-seq,统计分析,western blot				YY1
30076309	chr12	89344565	89346565	DUSP6	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	human,mouse		High+Lowthroughput	Regulation of miR-181a expression in T cell aging	否		Chicken pox	T cell	E_02_0498	Chip PCR, RNA SEQ, ATAC SEQ, statistical analysis, Western blot	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.		The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	Immunohistochemical staining	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.			ChIP-PCR,RNA-seq,ATAC-seq,统计分析,western blot				DUSP6
30076309	chr1	113811307	113813307	PTPN22	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	human,mouse		High+Lowthroughput	Regulation of miR-181a expression in T cell aging	否		Chicken pox	T cell	E_02_0498	Chip PCR, RNA SEQ, ATAC SEQ, statistical analysis, Western blot	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.		The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	Immunohistochemical staining	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.			ChIP-PCR,RNA-seq,ATAC-seq,统计分析,western blot				PTPN22
30076309	chr10	110495467	110497467	DUSP5	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	human,mouse		High+Lowthroughput	Regulation of miR-181a expression in T cell aging	否		Chicken pox	T cell	E_02_0498	Chip PCR, RNA SEQ, ATAC SEQ, statistical analysis, Western blot	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.		The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	Immunohistochemical staining	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.			ChIP-PCR,RNA-seq,ATAC-seq,统计分析,western blot				DUSP5
30076309	chr10	87859888	87861888	PTEN	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	human,mouse		High+Lowthroughput	Regulation of miR-181a expression in T cell aging	否		Chicken pox	T cell	E_02_0498	Chip PCR, RNA SEQ, ATAC SEQ, statistical analysis, Western blot	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.		The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.	Immunohistochemical staining	The decline in miR-181a expression correlates with reduced transcription of YY1 in older individuals.                                                                                                                                                                                                                               Functionally, it is an intrinsic regulator of the TCR activation threshold by controlling the expression of the cytoplasmic DUSP6 and other negative feedback pathways including PTPN22, SHP2, DUSP5, and SIRT129 31. In addition, a reduced expression of PTEN and associated effects on the AKT-mTORC1 pathways have been described in one, although not confirmed in a second miR-181a/b1-deficient mouse32,33.			ChIP-PCR,RNA-seq,ATAC-seq,统计分析,western blot				PTEN
30076153	chr11	64724349	64726349	RASGRP2	rASGrp2 activated rAp-1, subsequently affecting nuclear factor kappa-light-chain-enhancer of activated B cells pathway and actin dynamics in FLS. 	mouse	Synovial tissue	High+Lowthroughput	Ectopic RASGRP2 (CalDAG-GEFI) expression in rheumatoid synovium contributes to the development of destructive arthritis	否		Rheumatoid arthritis (RA)	Jurkat cell	E_02_0499	Real time QRT PCR, Western blot, immunofluorescence staining, immunohistochemistry	rASGrp2 activated rAp-1, subsequently affecting nuclear factor kappa-light-chain-enhancer of activated B cells pathway and actin dynamics in FLS. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	rASGrp2 activated rAp-1, subsequently affecting nuclear factor kappa-light-chain-enhancer of activated B cells pathway and actin dynamics in FLS. 		rASGrp2 activated rAp-1, subsequently affecting nuclear factor kappa-light-chain-enhancer of activated B cells pathway and actin dynamics in FLS. 	Immunohistochemical staining	rASGrp2 activated rAp-1, subsequently affecting nuclear factor kappa-light-chain-enhancer of activated B cells pathway and actin dynamics in FLS. 			real-time qRT-PCR,western blot,免疫荧光染色,免疫组化				RASGRP2
30072894	chr1	156460893	156462893	MEF2D	In conclusion, rhynchophylline inhibits MPP+-triggered neurotoxicity by stimulating MEF2D via activating PI3-K/Akt/GSK3β cascade.	human		High+Lowthroughput	Neuroprotection Against MPP(+)-Induced Cytotoxicity Through the Activation of PI3-K/Akt/GSK3β/MEF2D Signaling Pathway by Rhynchophylline, the Major Tetracyclic Oxindole Alkaloid Isolated From Uncaria rhynchophylla	是		Neurodegenerative diseases Parkinson's disease (PD)	PC12 cell	E_01_0780	Western blot, MTT assay, statistical analysis	In conclusion, rhynchophylline inhibits MPP+-triggered neurotoxicity by stimulating MEF2D via activating PI3-K/Akt/GSK3β cascade.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In conclusion, rhynchophylline inhibits MPP+-triggered neurotoxicity by stimulating MEF2D via activating PI3-K/Akt/GSK3β cascade.		In conclusion, rhynchophylline inhibits MPP+-triggered neurotoxicity by stimulating MEF2D via activating PI3-K/Akt/GSK3β cascade.	Immunohistochemical staining	In conclusion, rhynchophylline inhibits MPP+-triggered neurotoxicity by stimulating MEF2D via activating PI3-K/Akt/GSK3β cascade.			western blot,MTT法,统计分析				MEF2D
30072891	chr1	207031208	207033208	PFKFB2	In addition, the mRNA expression levels of peroxisome proliferators-activated receptor γ/α (PPARγ/α), CCAAT/enhancer binding proteinα (C/EBPα), Nuclear respiratory factor 1/2 (NRF1/2), Uncoupling protein 2 (UCP2), and phosphofructokinase 2/fructose-2, 6-bisphosphatase 2 (PFKFB2) were detected by RT-PCR.	human		High+Lowthroughput	Salvianolic Acid B Improves Mitochondrial Function in 3T3-L1 Adipocytes Through a Pathway Involving PPARγ Coactivator-1α (PGC-1α)	否		Obesity, diabetes	3T3‑L1 adipocytes	E_01_0781	Real time PCR, immunofluorescence staining	In addition, the mRNA expression levels of peroxisome proliferators-activated receptor γ/α (PPARγ/α), CCAAT/enhancer binding proteinα (C/EBPα), Nuclear respiratory factor 1/2 (NRF1/2), Uncoupling protein 2 (UCP2), and phosphofructokinase 2/fructose-2, 6-bisphosphatase 2 (PFKFB2) were detected by RT-PCR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, the mRNA expression levels of peroxisome proliferators-activated receptor γ/α (PPARγ/α), CCAAT/enhancer binding proteinα (C/EBPα), Nuclear respiratory factor 1/2 (NRF1/2), Uncoupling protein 2 (UCP2), and phosphofructokinase 2/fructose-2, 6-bisphosphatase 2 (PFKFB2) were detected by RT-PCR.		In addition, the mRNA expression levels of peroxisome proliferators-activated receptor γ/α (PPARγ/α), CCAAT/enhancer binding proteinα (C/EBPα), Nuclear respiratory factor 1/2 (NRF1/2), Uncoupling protein 2 (UCP2), and phosphofructokinase 2/fructose-2, 6-bisphosphatase 2 (PFKFB2) were detected by RT-PCR.	Immunohistochemical staining	In addition, the mRNA expression levels of peroxisome proliferators-activated receptor γ/α (PPARγ/α), CCAAT/enhancer binding proteinα (C/EBPα), Nuclear respiratory factor 1/2 (NRF1/2), Uncoupling protein 2 (UCP2), and phosphofructokinase 2/fructose-2, 6-bisphosphatase 2 (PFKFB2) were detected by RT-PCR.			real-time PCR,免疫荧光染色				PFKFB2
30071900	chr7	148804109	148806109	EZH2	Enhancer of zeste homologue 2 (EZH2), which primarily acts as a histone methyltransferase, is essential for proliferation.                                                                                                                                                                                                                 Post-translational modifications (PTMs) of PCNA facilitate these protein interactions and are essential for the high processivity and accuracy of DNA synthesis.	human		High+Lowthroughput	EZH2 promotes DNA replication by stabilizing interaction of POLδ and PCNA via methylation-mediated PCNA trimerization	否			293T cell	E_01_0782	Western blot, flow cytometry analysis, RNA SEQ, 5-ethynyl-2 ′ - deoxyuridine (EDU) staining, immunofluorescence staining, statistical analysis	Enhancer of zeste homologue 2 (EZH2), which primarily acts as a histone methyltransferase, is essential for proliferation.                                                                                                                                                                                                                 Post-translational modifications (PTMs) of PCNA facilitate these protein interactions and are essential for the high processivity and accuracy of DNA synthesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homologue 2 (EZH2), which primarily acts as a histone methyltransferase, is essential for proliferation.                                                                                                                                                                                                                 Post-translational modifications (PTMs) of PCNA facilitate these protein interactions and are essential for the high processivity and accuracy of DNA synthesis.	Immunohistochemical staining	Enhancer of zeste homologue 2 (EZH2), which primarily acts as a histone methyltransferase, is essential for proliferation.                                                                                                                                                                                                                 Post-translational modifications (PTMs) of PCNA facilitate these protein interactions and are essential for the high processivity and accuracy of DNA synthesis.	EZH2		western blot,流式细胞术分析,RNA-Seq,5-Ethynyl-2′-deoxyuridine (EdU) staining,免疫荧光染色,统计分析	Enhancer of zeste homologue 2 (EZH2), which primarily acts as a histone methyltransferase, is essential for proliferation.                                                                                                                                                                                                                 Post-translational modifications (PTMs) of PCNA facilitate these protein interactions and are essential for the high processivity and accuracy of DNA synthesis.			
30071596	chr12	6531860	6533860	GAPDH	Another antibody was used to detect GAPDH to confirm equivalent protein loading.	mouse,human		High+Lowthroughput	Model Senescent Microglia Induce Disease Related Changes in α-Synuclein Expression and Activity	否		Tumour, Alzheimer's disease (AD)	C8-B4 cell	E_02_0500	RT-PCR, Western blot, statistical analysis	Another antibody was used to detect GAPDH to confirm equivalent protein loading.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Another antibody was used to detect GAPDH to confirm equivalent protein loading.		Another antibody was used to detect GAPDH to confirm equivalent protein loading.	Immunohistochemical staining	Another antibody was used to detect GAPDH to confirm equivalent protein loading.			RT-PCR,western blot,统计分析				GAPDH
30066891	chr7	148804782	148806782	EZH2	Enhancer of zeste homolog 2 (EZH2) is the core enzymatic subunit of polycomb repressor complex 2 and is responsible for the trimethylation of histone 3 on lysine 27 (H3K27me3).                                                                                                                      The central factors for regulating autophagy are adenosine monophosphate (AMP) kinase (AMPK) and mammalian target of rapamycin (mTOR).	human,mouse		High+Lowthroughput	miR?92b promotes autophagy and suppresses viability and invasion in breast cancer by targeting EZH2	否		mammary cancer	COS7 cells	E_02_0501		Enhancer of zeste homolog 2 (EZH2) is the core enzymatic subunit of polycomb repressor complex 2 and is responsible for the trimethylation of histone 3 on lysine 27 (H3K27me3).                                                                                                                      The central factors for regulating autophagy are adenosine monophosphate (AMP) kinase (AMPK) and mammalian target of rapamycin (mTOR).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of zeste homolog 2 (EZH2) is the core enzymatic subunit of polycomb repressor complex 2 and is responsible for the trimethylation of histone 3 on lysine 27 (H3K27me3).                                                                                                                      The central factors for regulating autophagy are adenosine monophosphate (AMP) kinase (AMPK) and mammalian target of rapamycin (mTOR).		Enhancer of zeste homolog 2 (EZH2) is the core enzymatic subunit of polycomb repressor complex 2 and is responsible for the trimethylation of histone 3 on lysine 27 (H3K27me3).                                                                                                                      The central factors for regulating autophagy are adenosine monophosphate (AMP) kinase (AMPK) and mammalian target of rapamycin (mTOR).	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2) is the core enzymatic subunit of polycomb repressor complex 2 and is responsible for the trimethylation of histone 3 on lysine 27 (H3K27me3).                                                                                                                      The central factors for regulating autophagy are adenosine monophosphate (AMP) kinase (AMPK) and mammalian target of rapamycin (mTOR).			GFP-LC3 analyses,western blot,RT-qPCR,统计分析				EZH2
30061944	chr7	148804369	148806369	EZH2	Downregulation of EZH2 expression enhanced the anticancer effect of methyl jasmonate on human colorectal cancer cells through suppression of the Wnt/β-catenin pathway.	human		High+Lowthroughput	EZH2 inhibition promotes methyl jasmonate-induced apoptosis of human colorectal cancer through the Wnt/β-catenin pathway	否		Colorectal cancer, leukemia	T24 cell	E_01_0783	Western blot, statistical analysis, flow cytometry	Downregulation of EZH2 expression enhanced the anticancer effect of methyl jasmonate on human colorectal cancer cells through suppression of the Wnt/β-catenin pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Downregulation of EZH2 expression enhanced the anticancer effect of methyl jasmonate on human colorectal cancer cells through suppression of the Wnt/β-catenin pathway.	Immunohistochemical staining	Downregulation of EZH2 expression enhanced the anticancer effect of methyl jasmonate on human colorectal cancer cells through suppression of the Wnt/β-catenin pathway.	EZH2		western blot,统计分析,流式细胞术	Downregulation of EZH2 expression enhanced the anticancer effect of methyl jasmonate on human colorectal cancer cells through suppression of the Wnt/β-catenin pathway.			
30061199	chr7	34815866	34817866	Cebpa	Extending these findings, pan-hematopoietic murine Cebpa enhancer deletion using Mx1-Cre leads to expanded CLP, fewer preproB cells, markedly reduced proB and preB cells, and reduced mature B cells, without affecting T cell numbers. In contrast, enhancer deletion at the proB stage using Mb1-Cre does not impair B cell maturation.                                                                                                                                                                                            Introduction The C/EBPα basic region-leucine zipper transcription factor (TF) regulates myeloid development and transformation (1). Cebpa / mice manifest neonatal lethality due to hypoglycemia, with marked neutropenia but no reduction in splenic B220+ B cells or thymic CD4+ or CD8+ T cells (2).	mouse,human		High+Lowthroughput	Progression from the Common Lymphoid Progenitor to B/Myeloid PreproB and ProB Precursors during B Lymphopoiesis Requires C/EBPα	否				E_02_0502	Flow cytometry, statistical analysis, PCR	Extending these findings, pan-hematopoietic murine Cebpa enhancer deletion using Mx1-Cre leads to expanded CLP, fewer preproB cells, markedly reduced proB and preB cells, and reduced mature B cells, without affecting T cell numbers. In contrast, enhancer deletion at the proB stage using Mb1-Cre does not impair B cell maturation.                                                                                                                                                                                            Introduction The C/EBPα basic region-leucine zipper transcription factor (TF) regulates myeloid development and transformation (1). Cebpa / mice manifest neonatal lethality due to hypoglycemia, with marked neutropenia but no reduction in splenic B220+ B cells or thymic CD4+ or CD8+ T cells (2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Extending these findings, pan-hematopoietic murine Cebpa enhancer deletion using Mx1-Cre leads to expanded CLP, fewer preproB cells, markedly reduced proB and preB cells, and reduced mature B cells, without affecting T cell numbers. In contrast, enhancer deletion at the proB stage using Mb1-Cre does not impair B cell maturation.                                                                                                                                                                                            Introduction The C/EBPα basic region-leucine zipper transcription factor (TF) regulates myeloid development and transformation (1). Cebpa / mice manifest neonatal lethality due to hypoglycemia, with marked neutropenia but no reduction in splenic B220+ B cells or thymic CD4+ or CD8+ T cells (2).		Extending these findings, pan-hematopoietic murine Cebpa enhancer deletion using Mx1-Cre leads to expanded CLP, fewer preproB cells, markedly reduced proB and preB cells, and reduced mature B cells, without affecting T cell numbers. In contrast, enhancer deletion at the proB stage using Mb1-Cre does not impair B cell maturation.                                                                                                                                                                                            Introduction The C/EBPα basic region-leucine zipper transcription factor (TF) regulates myeloid development and transformation (1). Cebpa / mice manifest neonatal lethality due to hypoglycemia, with marked neutropenia but no reduction in splenic B220+ B cells or thymic CD4+ or CD8+ T cells (2).	Immunohistochemical staining	Extending these findings, pan-hematopoietic murine Cebpa enhancer deletion using Mx1-Cre leads to expanded CLP, fewer preproB cells, markedly reduced proB and preB cells, and reduced mature B cells, without affecting T cell numbers. In contrast, enhancer deletion at the proB stage using Mb1-Cre does not impair B cell maturation.                                                                                                                                                                                            Introduction The C/EBPα basic region-leucine zipper transcription factor (TF) regulates myeloid development and transformation (1). Cebpa / mice manifest neonatal lethality due to hypoglycemia, with marked neutropenia but no reduction in splenic B220+ B cells or thymic CD4+ or CD8+ T cells (2).			流式细胞术,统计分析,PCR				Cebpa
30061199	chr3	133743503	133745503	TF	Extending these findings, pan-hematopoietic murine Cebpa enhancer deletion using Mx1-Cre leads to expanded CLP, fewer preproB cells, markedly reduced proB and preB cells, and reduced mature B cells, without affecting T cell numbers. In contrast, enhancer deletion at the proB stage using Mb1-Cre does not impair B cell maturation.                                                                                                                                                                                            Introduction The C/EBPα basic region-leucine zipper transcription factor (TF) regulates myeloid development and transformation (1). Cebpa / mice manifest neonatal lethality due to hypoglycemia, with marked neutropenia but no reduction in splenic B220+ B cells or thymic CD4+ or CD8+ T cells (2).	mouse,human		High+Lowthroughput	Progression from the Common Lymphoid Progenitor to B/Myeloid PreproB and ProB Precursors during B Lymphopoiesis Requires C/EBPα	否				E_02_0502	Flow cytometry, statistical analysis, PCR	Extending these findings, pan-hematopoietic murine Cebpa enhancer deletion using Mx1-Cre leads to expanded CLP, fewer preproB cells, markedly reduced proB and preB cells, and reduced mature B cells, without affecting T cell numbers. In contrast, enhancer deletion at the proB stage using Mb1-Cre does not impair B cell maturation.                                                                                                                                                                                            Introduction The C/EBPα basic region-leucine zipper transcription factor (TF) regulates myeloid development and transformation (1). Cebpa / mice manifest neonatal lethality due to hypoglycemia, with marked neutropenia but no reduction in splenic B220+ B cells or thymic CD4+ or CD8+ T cells (2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Extending these findings, pan-hematopoietic murine Cebpa enhancer deletion using Mx1-Cre leads to expanded CLP, fewer preproB cells, markedly reduced proB and preB cells, and reduced mature B cells, without affecting T cell numbers. In contrast, enhancer deletion at the proB stage using Mb1-Cre does not impair B cell maturation.                                                                                                                                                                                            Introduction The C/EBPα basic region-leucine zipper transcription factor (TF) regulates myeloid development and transformation (1). Cebpa / mice manifest neonatal lethality due to hypoglycemia, with marked neutropenia but no reduction in splenic B220+ B cells or thymic CD4+ or CD8+ T cells (2).		Extending these findings, pan-hematopoietic murine Cebpa enhancer deletion using Mx1-Cre leads to expanded CLP, fewer preproB cells, markedly reduced proB and preB cells, and reduced mature B cells, without affecting T cell numbers. In contrast, enhancer deletion at the proB stage using Mb1-Cre does not impair B cell maturation.                                                                                                                                                                                            Introduction The C/EBPα basic region-leucine zipper transcription factor (TF) regulates myeloid development and transformation (1). Cebpa / mice manifest neonatal lethality due to hypoglycemia, with marked neutropenia but no reduction in splenic B220+ B cells or thymic CD4+ or CD8+ T cells (2).	Immunohistochemical staining	Extending these findings, pan-hematopoietic murine Cebpa enhancer deletion using Mx1-Cre leads to expanded CLP, fewer preproB cells, markedly reduced proB and preB cells, and reduced mature B cells, without affecting T cell numbers. In contrast, enhancer deletion at the proB stage using Mb1-Cre does not impair B cell maturation.                                                                                                                                                                                            Introduction The C/EBPα basic region-leucine zipper transcription factor (TF) regulates myeloid development and transformation (1). Cebpa / mice manifest neonatal lethality due to hypoglycemia, with marked neutropenia but no reduction in splenic B220+ B cells or thymic CD4+ or CD8+ T cells (2).			流式细胞术,统计分析,PCR				TF
30059522	chr8	91154296	91156296	CPP	As such, these findings introduce E6446 as a novel transfection enhancer and may be of practical relevance to researchers seeking to improve the mRNA transfection efficiency of their preferred CPP. 	human	Epithelial tissues	High+Lowthroughput	mRNA transfection by a Xentry-protamine cell-penetrating peptide is enhanced by TLR antagonist E6446	否		Cystic fibrosis	epithelial cell	E_01_0784	Western blot, immunofluorescence staining	As such, these findings introduce E6446 as a novel transfection enhancer and may be of practical relevance to researchers seeking to improve the mRNA transfection efficiency of their preferred CPP. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	As such, these findings introduce E6446 as a novel transfection enhancer and may be of practical relevance to researchers seeking to improve the mRNA transfection efficiency of their preferred CPP. 		As such, these findings introduce E6446 as a novel transfection enhancer and may be of practical relevance to researchers seeking to improve the mRNA transfection efficiency of their preferred CPP. 	Immunohistochemical staining	As such, these findings introduce E6446 as a novel transfection enhancer and may be of practical relevance to researchers seeking to improve the mRNA transfection efficiency of their preferred CPP. 			western blot,免疫荧光染色				CPP
30058478	chr9	107482373	107484373	KLF4	By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.	human,mouse		High+Lowthroughput	Analysis of KLF4 regulated genes in cancer cells reveals a role of DNA methylation in promoter- enhancer interactions	否		Malignant brain tumors	glioblastoma multiforme	E_02_0503	Statistical analysis of quantitative mass spectrometry, quantitative real-time PCR, Western blot, chromatin immunoprecipitation PCR (chip) - PCR, statistical analysis	By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.		By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.	Immunohistochemical staining	By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.			定量质谱统计分析,Quantitative real-time PCR,western blot,Chromatin immunoprecipitation PCR (ChIP)-PCR,统计分析				KLF4
30058478	chr8	11484323	11486323	BLK	By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.	human,mouse		High+Lowthroughput	Analysis of KLF4 regulated genes in cancer cells reveals a role of DNA methylation in promoter- enhancer interactions	否		Malignant brain tumors	glioblastoma multiforme	E_02_0503	Statistical analysis of quantitative mass spectrometry, quantitative real-time PCR, Western blot, chromatin immunoprecipitation PCR (chip) - PCR, statistical analysis	By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.		By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.	Immunohistochemical staining	By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.			定量质谱统计分析,Quantitative real-time PCR,western blot,Chromatin immunoprecipitation PCR (ChIP)-PCR,统计分析				BLK
30058478	chr13	75618100	75620100	LMO7	By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.	human,mouse		High+Lowthroughput	Analysis of KLF4 regulated genes in cancer cells reveals a role of DNA methylation in promoter- enhancer interactions	否		Malignant brain tumors	glioblastoma multiforme	E_02_0503	Statistical analysis of quantitative mass spectrometry, quantitative real-time PCR, Western blot, chromatin immunoprecipitation PCR (chip) - PCR, statistical analysis	By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.		By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.	Immunohistochemical staining	By chromosome conformation capture (3C) analysis, we demonstrated that KLF4 bound to methylated CpGs at the enhancer regions of the B-cell lymphocyte kinase (BLK) and Lim domain only protein 7 (LMO7) genes, and activated their expression via 3D chromatin loop formation with their promoter regions.			定量质谱统计分析,Quantitative real-time PCR,western blot,Chromatin immunoprecipitation PCR (ChIP)-PCR,统计分析				LMO7
30057145	chr1	212683365	212685365	BATF3	RNAi screening of ATLL lines revealed that their proliferation depends on BATF3 and IRF4, which cooperatively drive ATLL-specific gene expression.	human,mouse		High+Lowthroughput	Targeting the HTLV-I-Regulated BATF3/IRF4 Transcriptional Network in Adult T Cell Leukemia/Lymphoma	否		Adult T cell leukemia / lymphoma (ATLL)	Adult T-Cell Leukemia/Lymphoma	E_02_0504	Q-RT-PCR, chip SEQ, crispr-cas9 screening, immunoblot analysis, Western blot	RNAi screening of ATLL lines revealed that their proliferation depends on BATF3 and IRF4, which cooperatively drive ATLL-specific gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RNAi screening of ATLL lines revealed that their proliferation depends on BATF3 and IRF4, which cooperatively drive ATLL-specific gene expression.		RNAi screening of ATLL lines revealed that their proliferation depends on BATF3 and IRF4, which cooperatively drive ATLL-specific gene expression.	Immunohistochemical staining	RNAi screening of ATLL lines revealed that their proliferation depends on BATF3 and IRF4, which cooperatively drive ATLL-specific gene expression.			Q-RT-PCR,ChIP-seq,CRISPR-Cas9筛析,Immunoblot Analysis,western blot				BATF3
30057145	chr8	127732833	127734833	MYC	RNAi screening of ATLL lines revealed that their proliferation depends on BATF3 and IRF4, which cooperatively drive ATLL-specific gene expression.	human,mouse		High+Lowthroughput	Targeting the HTLV-I-Regulated BATF3/IRF4 Transcriptional Network in Adult T Cell Leukemia/Lymphoma	否		Adult T cell leukemia / lymphoma (ATLL)	Adult T-Cell Leukemia/Lymphoma	E_02_0504	Q-RT-PCR, chip SEQ, crispr-cas9 screening, immunoblot analysis, Western blot	RNAi screening of ATLL lines revealed that their proliferation depends on BATF3 and IRF4, which cooperatively drive ATLL-specific gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RNAi screening of ATLL lines revealed that their proliferation depends on BATF3 and IRF4, which cooperatively drive ATLL-specific gene expression.		RNAi screening of ATLL lines revealed that their proliferation depends on BATF3 and IRF4, which cooperatively drive ATLL-specific gene expression.	Immunohistochemical staining	RNAi screening of ATLL lines revealed that their proliferation depends on BATF3 and IRF4, which cooperatively drive ATLL-specific gene expression.			Q-RT-PCR,ChIP-seq,CRISPR-Cas9筛析,Immunoblot Analysis,western blot				MYC
30057115	chr3	133743395	133745395	TF	The cistromes include functional enhancer sites, where TF binding leads to regulation of gene transcription over large genomic distances (Levine et al., 2014). 	human,mouse		High+Lowthroughput	Diet-Induced Circadian Enhancer Remodeling Synchronizes Opposing Hepatic Lipid Metabolic Processes	否		Obesity (DIO), type 2 diabetes, cardiovascular disease, hypertension, cancer		E_02_0505	GRO-seq,Western Blot,ChIP-seq 	The cistromes include functional enhancer sites, where TF binding leads to regulation of gene transcription over large genomic distances (Levine et al., 2014). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The cistromes include functional enhancer sites, where TF binding leads to regulation of gene transcription over large genomic distances (Levine et al., 2014). 		The cistromes include functional enhancer sites, where TF binding leads to regulation of gene transcription over large genomic distances (Levine et al., 2014). 	Immunohistochemical staining	The cistromes include functional enhancer sites, where TF binding leads to regulation of gene transcription over large genomic distances (Levine et al., 2014). 			GRO-seq,Western Blot,ChIP-seq 				TF
30055251	chr10	96186235	96188235	BLNK	Functional studies involving BLNK were first car- ried out in chicken BLNK-deficient DT40 cells, which exhibited the abolishment of phospholipase C-γ2 (PLC-γ2) tyrosine phosphorylation, a calcium mobilization defect, and impaired activation of c-Jun N- terminal kinase (JNK) [4].                                                                                                                                                                                                                                                                                                                                                                                                                  After SYK phosphorylates several critical tyrosines (Y72, Y84, Y96, Y178, and Y189), BLNK provides docking sites for intracellular sig- naling molecules including guanine nucleotide exchange factors (VAV), non-catalytic region of tyrosine kinase (NCK), Bruton's tyrosine kinase (BTK), and phospholipase Cγ (PLCγ) [1 3].	mouse		High+Lowthroughput	Identification and functional analysis of grouper (Epinephelus coioides) B-cell linker protein BLNK	否			HEK293T	E_02_0506	Western blot, immunofluorescence staining	Functional studies involving BLNK were first car- ried out in chicken BLNK-deficient DT40 cells, which exhibited the abolishment of phospholipase C-γ2 (PLC-γ2) tyrosine phosphorylation, a calcium mobilization defect, and impaired activation of c-Jun N- terminal kinase (JNK) [4].                                                                                                                                                                                                                                                                                                                                                                                                                  After SYK phosphorylates several critical tyrosines (Y72, Y84, Y96, Y178, and Y189), BLNK provides docking sites for intracellular sig- naling molecules including guanine nucleotide exchange factors (VAV), non-catalytic region of tyrosine kinase (NCK), Bruton's tyrosine kinase (BTK), and phospholipase Cγ (PLCγ) [1 3].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Functional studies involving BLNK were first car- ried out in chicken BLNK-deficient DT40 cells, which exhibited the abolishment of phospholipase C-γ2 (PLC-γ2) tyrosine phosphorylation, a calcium mobilization defect, and impaired activation of c-Jun N- terminal kinase (JNK) [4].                                                                                                                                                                                                                                                                                                                                                                                                                  After SYK phosphorylates several critical tyrosines (Y72, Y84, Y96, Y178, and Y189), BLNK provides docking sites for intracellular sig- naling molecules including guanine nucleotide exchange factors (VAV), non-catalytic region of tyrosine kinase (NCK), Bruton's tyrosine kinase (BTK), and phospholipase Cγ (PLCγ) [1 3].		Functional studies involving BLNK were first car- ried out in chicken BLNK-deficient DT40 cells, which exhibited the abolishment of phospholipase C-γ2 (PLC-γ2) tyrosine phosphorylation, a calcium mobilization defect, and impaired activation of c-Jun N- terminal kinase (JNK) [4].                                                                                                                                                                                                                                                                                                                                                                                                                  After SYK phosphorylates several critical tyrosines (Y72, Y84, Y96, Y178, and Y189), BLNK provides docking sites for intracellular sig- naling molecules including guanine nucleotide exchange factors (VAV), non-catalytic region of tyrosine kinase (NCK), Bruton's tyrosine kinase (BTK), and phospholipase Cγ (PLCγ) [1 3].	Immunohistochemical staining	Functional studies involving BLNK were first car- ried out in chicken BLNK-deficient DT40 cells, which exhibited the abolishment of phospholipase C-γ2 (PLC-γ2) tyrosine phosphorylation, a calcium mobilization defect, and impaired activation of c-Jun N- terminal kinase (JNK) [4].                                                                                                                                                                                                                                                                                                                                                                                                                  After SYK phosphorylates several critical tyrosines (Y72, Y84, Y96, Y178, and Y189), BLNK provides docking sites for intracellular sig- naling molecules including guanine nucleotide exchange factors (VAV), non-catalytic region of tyrosine kinase (NCK), Bruton's tyrosine kinase (BTK), and phospholipase Cγ (PLCγ) [1 3].			Western blot,免疫荧光染色				BLNK
30054476	chr10	128093460	128095460	MKI67	MGMT expression can be silenced by the methylation of a promoter/enhancer (P/E) region, which contains a promoter and a 59 bp cis-acting enhancer element that spans the first exon intron boundary of MGMT gene4. 	human		High+Lowthroughput	A novel enhancer regulates MGMT expression and promotes temozolomide resistance in glioblastoma	否		Glioblastoma		E_01_0785	Western blot, real-time PCR, RNA SEQ, MS-PCR, chip SEQ, statistical analysis	MGMT expression can be silenced by the methylation of a promoter/enhancer (P/E) region, which contains a promoter and a 59 bp cis-acting enhancer element that spans the first exon intron boundary of MGMT gene4. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MGMT expression can be silenced by the methylation of a promoter/enhancer (P/E) region, which contains a promoter and a 59 bp cis-acting enhancer element that spans the first exon intron boundary of MGMT gene4. 		MGMT expression can be silenced by the methylation of a promoter/enhancer (P/E) region, which contains a promoter and a 59 bp cis-acting enhancer element that spans the first exon intron boundary of MGMT gene4. 	Immunohistochemical staining	MGMT expression can be silenced by the methylation of a promoter/enhancer (P/E) region, which contains a promoter and a 59 bp cis-acting enhancer element that spans the first exon intron boundary of MGMT gene4. 			Western blot,real-time PCR,RNA-seq,MS-PCR,ChIP-seq,统计分析				MKI67
30054476	chr10	129464679	129466679	MGMT	MGMT expression can be silenced by the methylation of a promoter/enhancer (P/E) region, which contains a promoter and a 59 bp cis-acting enhancer element that spans the first exon intron boundary of MGMT gene4. 	human		High+Lowthroughput	A novel enhancer regulates MGMT expression and promotes temozolomide resistance in glioblastoma	否		Glioblastoma		E_01_0785	Western blot, real-time PCR, RNA SEQ, MS-PCR, chip SEQ, statistical analysis	MGMT expression can be silenced by the methylation of a promoter/enhancer (P/E) region, which contains a promoter and a 59 bp cis-acting enhancer element that spans the first exon intron boundary of MGMT gene4. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MGMT expression can be silenced by the methylation of a promoter/enhancer (P/E) region, which contains a promoter and a 59 bp cis-acting enhancer element that spans the first exon intron boundary of MGMT gene4. 		MGMT expression can be silenced by the methylation of a promoter/enhancer (P/E) region, which contains a promoter and a 59 bp cis-acting enhancer element that spans the first exon intron boundary of MGMT gene4. 	Immunohistochemical staining	MGMT expression can be silenced by the methylation of a promoter/enhancer (P/E) region, which contains a promoter and a 59 bp cis-acting enhancer element that spans the first exon intron boundary of MGMT gene4. 			Western blot,real-time PCR,RNA-seq,MS-PCR,ChIP-seq,统计分析				MGMT
30053869	chr3	41192055	41194055	CTNNB1	Results In BCA, the expression of TLE1 was confined to luminal cells of glandular structures, in contrast to the expression of β-catenin in abluminal cells.                                                                                                                   The BCAC cases had CTNNB1 mutation (2/4) and the laser-captured microdissection allowed the separate collection of infiltrative and non-infiltrative areas to detect the same mutation.          	human		High+Lowthroughput	Difference in transducin-like enhancer of split 1 protein expression between basal cell adenomas and basal cell adenocarcinomas - an immunohistochemical study			Basal cell adenoma (BCA), basal cell adenocarcinoma (BCAC)	acinar cell	E_01_0786	Immunohistochemistry and analysis,PCR 	Results In BCA, the expression of TLE1 was confined to luminal cells of glandular structures, in contrast to the expression of β-catenin in abluminal cells.                                                                                                                   The BCAC cases had CTNNB1 mutation (2/4) and the laser-captured microdissection allowed the separate collection of infiltrative and non-infiltrative areas to detect the same mutation.          	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Results In BCA, the expression of TLE1 was confined to luminal cells of glandular structures, in contrast to the expression of β-catenin in abluminal cells.                                                                                                                   The BCAC cases had CTNNB1 mutation (2/4) and the laser-captured microdissection allowed the separate collection of infiltrative and non-infiltrative areas to detect the same mutation.          	Immunohistochemical staining	Results In BCA, the expression of TLE1 was confined to luminal cells of glandular structures, in contrast to the expression of β-catenin in abluminal cells.                                                                                                                   The BCAC cases had CTNNB1 mutation (2/4) and the laser-captured microdissection allowed the separate collection of infiltrative and non-infiltrative areas to detect the same mutation.          	CTNNB1		Immunohistochemistry and analysis,PCR 	Results In BCA, the expression of TLE1 was confined to luminal cells of glandular structures, in contrast to the expression of β-catenin in abluminal cells.                                                                                                                   The BCAC cases had CTNNB1 mutation (2/4) and the laser-captured microdissection allowed the separate collection of infiltrative and non-infiltrative areas to detect the same mutation.          			
30053869	chr9	81581162	81583162	TLE1	Results In BCA, the expression of TLE1 was confined to luminal cells of glandular structures, in contrast to the expression of β-catenin in abluminal cells.                                                                                                                   The BCAC cases had CTNNB1 mutation (2/4) and the laser-captured microdissection allowed the separate collection of infiltrative and non-infiltrative areas to detect the same mutation.          	human		High+Lowthroughput	Difference in transducin-like enhancer of split 1 protein expression between basal cell adenomas and basal cell adenocarcinomas - an immunohistochemical study			Basal cell adenoma (BCA), basal cell adenocarcinoma (BCAC)	acinar cell	E_01_0786	Immunohistochemistry and analysis,PCR 	Results In BCA, the expression of TLE1 was confined to luminal cells of glandular structures, in contrast to the expression of β-catenin in abluminal cells.                                                                                                                   The BCAC cases had CTNNB1 mutation (2/4) and the laser-captured microdissection allowed the separate collection of infiltrative and non-infiltrative areas to detect the same mutation.          	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Results In BCA, the expression of TLE1 was confined to luminal cells of glandular structures, in contrast to the expression of β-catenin in abluminal cells.                                                                                                                   The BCAC cases had CTNNB1 mutation (2/4) and the laser-captured microdissection allowed the separate collection of infiltrative and non-infiltrative areas to detect the same mutation.          	Immunohistochemical staining	Results In BCA, the expression of TLE1 was confined to luminal cells of glandular structures, in contrast to the expression of β-catenin in abluminal cells.                                                                                                                   The BCAC cases had CTNNB1 mutation (2/4) and the laser-captured microdissection allowed the separate collection of infiltrative and non-infiltrative areas to detect the same mutation.          	TLE1		Immunohistochemistry and analysis,PCR 	Results In BCA, the expression of TLE1 was confined to luminal cells of glandular structures, in contrast to the expression of β-catenin in abluminal cells.                                                                                                                   The BCAC cases had CTNNB1 mutation (2/4) and the laser-captured microdissection allowed the separate collection of infiltrative and non-infiltrative areas to detect the same mutation.          			
30051352	chrX	53079604	53081604	TSPYL2	Testis-specific protein, Y-encoded-like 2 (TSPYL2) is an X-linked gene in the locus for several neurodevelopmental disorders.                                                                                                                                                                                               To identify other genes regulated by TSPYL2, here, we showed that Tspyl2 knockout mice had an increased level of H3K27 trimethylation (H3K27me3) in the hippocampus, and TSPYL2 interacted with the H3K27 methyltransferase enhancer of zeste 2 (EZH2).                                                                                                                                                                                                                                                                                                                                          Our group has shown that TSPYL2 directly regulates the transcription of genes for NMDA receptor subunits 2A (Grin2a) and 2B (Grin2b) in mice [9].	mouse,human		High+Lowthroughput	TSPYL2 Regulates the Expression of EZH2 Target Genes in Neurons	否		Neuroblastoma		E_02_0507	Western blot, immunocytochemistry, hybridization to peptide arrays, chip SEQ, RT qPCR, chip PCR, statistical analysis	Testis-specific protein, Y-encoded-like 2 (TSPYL2) is an X-linked gene in the locus for several neurodevelopmental disorders.                                                                                                                                                                                               To identify other genes regulated by TSPYL2, here, we showed that Tspyl2 knockout mice had an increased level of H3K27 trimethylation (H3K27me3) in the hippocampus, and TSPYL2 interacted with the H3K27 methyltransferase enhancer of zeste 2 (EZH2).                                                                                                                                                                                                                                                                                                                                          Our group has shown that TSPYL2 directly regulates the transcription of genes for NMDA receptor subunits 2A (Grin2a) and 2B (Grin2b) in mice [9].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Testis-specific protein, Y-encoded-like 2 (TSPYL2) is an X-linked gene in the locus for several neurodevelopmental disorders.                                                                                                                                                                                               To identify other genes regulated by TSPYL2, here, we showed that Tspyl2 knockout mice had an increased level of H3K27 trimethylation (H3K27me3) in the hippocampus, and TSPYL2 interacted with the H3K27 methyltransferase enhancer of zeste 2 (EZH2).                                                                                                                                                                                                                                                                                                                                          Our group has shown that TSPYL2 directly regulates the transcription of genes for NMDA receptor subunits 2A (Grin2a) and 2B (Grin2b) in mice [9].		Testis-specific protein, Y-encoded-like 2 (TSPYL2) is an X-linked gene in the locus for several neurodevelopmental disorders.                                                                                                                                                                                               To identify other genes regulated by TSPYL2, here, we showed that Tspyl2 knockout mice had an increased level of H3K27 trimethylation (H3K27me3) in the hippocampus, and TSPYL2 interacted with the H3K27 methyltransferase enhancer of zeste 2 (EZH2).                                                                                                                                                                                                                                                                                                                                          Our group has shown that TSPYL2 directly regulates the transcription of genes for NMDA receptor subunits 2A (Grin2a) and 2B (Grin2b) in mice [9].	Immunohistochemical staining	Testis-specific protein, Y-encoded-like 2 (TSPYL2) is an X-linked gene in the locus for several neurodevelopmental disorders.                                                                                                                                                                                               To identify other genes regulated by TSPYL2, here, we showed that Tspyl2 knockout mice had an increased level of H3K27 trimethylation (H3K27me3) in the hippocampus, and TSPYL2 interacted with the H3K27 methyltransferase enhancer of zeste 2 (EZH2).                                                                                                                                                                                                                                                                                                                                          Our group has shown that TSPYL2 directly regulates the transcription of genes for NMDA receptor subunits 2A (Grin2a) and 2B (Grin2b) in mice [9].			Western Blot,Immunocytochemistry,Hybridization to Peptide Arrays,ChIP-seq,RT-qPCR,ChIP-PCR,统计分析				TSPYL2
30051352	chr7	148804504	148806504	EZH2	Testis-specific protein, Y-encoded-like 2 (TSPYL2) is an X-linked gene in the locus for several neurodevelopmental disorders.                                                                                                                                                                                               To identify other genes regulated by TSPYL2, here, we showed that Tspyl2 knockout mice had an increased level of H3K27 trimethylation (H3K27me3) in the hippocampus, and TSPYL2 interacted with the H3K27 methyltransferase enhancer of zeste 2 (EZH2).                                                                                                                                                                                                                                                                                                                                          Our group has shown that TSPYL2 directly regulates the transcription of genes for NMDA receptor subunits 2A (Grin2a) and 2B (Grin2b) in mice [9].	mouse,human		High+Lowthroughput	TSPYL2 Regulates the Expression of EZH2 Target Genes in Neurons	否		Neuroblastoma		E_02_0507	Western blot, immunocytochemistry, hybridization to peptide arrays, chip SEQ, RT qPCR, chip PCR, statistical analysis	Testis-specific protein, Y-encoded-like 2 (TSPYL2) is an X-linked gene in the locus for several neurodevelopmental disorders.                                                                                                                                                                                               To identify other genes regulated by TSPYL2, here, we showed that Tspyl2 knockout mice had an increased level of H3K27 trimethylation (H3K27me3) in the hippocampus, and TSPYL2 interacted with the H3K27 methyltransferase enhancer of zeste 2 (EZH2).                                                                                                                                                                                                                                                                                                                                          Our group has shown that TSPYL2 directly regulates the transcription of genes for NMDA receptor subunits 2A (Grin2a) and 2B (Grin2b) in mice [9].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Testis-specific protein, Y-encoded-like 2 (TSPYL2) is an X-linked gene in the locus for several neurodevelopmental disorders.                                                                                                                                                                                               To identify other genes regulated by TSPYL2, here, we showed that Tspyl2 knockout mice had an increased level of H3K27 trimethylation (H3K27me3) in the hippocampus, and TSPYL2 interacted with the H3K27 methyltransferase enhancer of zeste 2 (EZH2).                                                                                                                                                                                                                                                                                                                                          Our group has shown that TSPYL2 directly regulates the transcription of genes for NMDA receptor subunits 2A (Grin2a) and 2B (Grin2b) in mice [9].		Testis-specific protein, Y-encoded-like 2 (TSPYL2) is an X-linked gene in the locus for several neurodevelopmental disorders.                                                                                                                                                                                               To identify other genes regulated by TSPYL2, here, we showed that Tspyl2 knockout mice had an increased level of H3K27 trimethylation (H3K27me3) in the hippocampus, and TSPYL2 interacted with the H3K27 methyltransferase enhancer of zeste 2 (EZH2).                                                                                                                                                                                                                                                                                                                                          Our group has shown that TSPYL2 directly regulates the transcription of genes for NMDA receptor subunits 2A (Grin2a) and 2B (Grin2b) in mice [9].	Immunohistochemical staining	Testis-specific protein, Y-encoded-like 2 (TSPYL2) is an X-linked gene in the locus for several neurodevelopmental disorders.                                                                                                                                                                                               To identify other genes regulated by TSPYL2, here, we showed that Tspyl2 knockout mice had an increased level of H3K27 trimethylation (H3K27me3) in the hippocampus, and TSPYL2 interacted with the H3K27 methyltransferase enhancer of zeste 2 (EZH2).                                                                                                                                                                                                                                                                                                                                          Our group has shown that TSPYL2 directly regulates the transcription of genes for NMDA receptor subunits 2A (Grin2a) and 2B (Grin2b) in mice [9].			Western Blot,Immunocytochemistry,Hybridization to Peptide Arrays,ChIP-seq,RT-qPCR,ChIP-PCR,统计分析				EZH2
30048163	chr7	148804302	148806302	EZH2	Results: Initially, lower expressions of HOTAIR and EZH2 in the normal human mammary epithelial cells, while higher expressions in the breast cancer cells of MCF-7, MDA-MB-231, and SKBR-3 were detected.	human		High+Lowthroughput	Downregulation of Long Noncoding RNA HOTAIR and EZH2 Induces Apoptosis and Inhibits Proliferation, Invasion, and Migration of Human Breast Cancer Cells	否		mammary cancer	MCF7 cell	E_01_0787	MTT assay, RT qPCR, flow cytometry, statistical analysis	Results: Initially, lower expressions of HOTAIR and EZH2 in the normal human mammary epithelial cells, while higher expressions in the breast cancer cells of MCF-7, MDA-MB-231, and SKBR-3 were detected.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Results: Initially, lower expressions of HOTAIR and EZH2 in the normal human mammary epithelial cells, while higher expressions in the breast cancer cells of MCF-7, MDA-MB-231, and SKBR-3 were detected.	Immunohistochemical staining	Results: Initially, lower expressions of HOTAIR and EZH2 in the normal human mammary epithelial cells, while higher expressions in the breast cancer cells of MCF-7, MDA-MB-231, and SKBR-3 were detected.	EZH2		MTT assay, RT-qPCR,流式细胞术,统计分析	Results: Initially, lower expressions of HOTAIR and EZH2 in the normal human mammary epithelial cells, while higher expressions in the breast cancer cells of MCF-7, MDA-MB-231, and SKBR-3 were detected.			
30048163	chr12	53959147	53961147	HOTAIR	Results: Initially, lower expressions of HOTAIR and EZH2 in the normal human mammary epithelial cells, while higher expressions in the breast cancer cells of MCF-7, MDA-MB-231, and SKBR-3 were detected.	human		High+Lowthroughput	Downregulation of Long Noncoding RNA HOTAIR and EZH2 Induces Apoptosis and Inhibits Proliferation, Invasion, and Migration of Human Breast Cancer Cells	否		mammary cancer	MCF7 cell	E_01_0787	MTT assay, RT qPCR, flow cytometry, statistical analysis	Results: Initially, lower expressions of HOTAIR and EZH2 in the normal human mammary epithelial cells, while higher expressions in the breast cancer cells of MCF-7, MDA-MB-231, and SKBR-3 were detected.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Results: Initially, lower expressions of HOTAIR and EZH2 in the normal human mammary epithelial cells, while higher expressions in the breast cancer cells of MCF-7, MDA-MB-231, and SKBR-3 were detected.	Immunohistochemical staining	Results: Initially, lower expressions of HOTAIR and EZH2 in the normal human mammary epithelial cells, while higher expressions in the breast cancer cells of MCF-7, MDA-MB-231, and SKBR-3 were detected.	HOTAIR		MTT assay, RT-qPCR,流式细胞术,统计分析	Results: Initially, lower expressions of HOTAIR and EZH2 in the normal human mammary epithelial cells, while higher expressions in the breast cancer cells of MCF-7, MDA-MB-231, and SKBR-3 were detected.			
30046953	chr8	94246601	94248601	GEM	Our results showed that most of the bulk impurities had been removed, and PA-GRFT could capture PRRSV onto GEM particles.	mouse		High+Lowthroughput	Surface-displayed porcine reproductive and respiratory syndrome virus from cell culture onto gram-positive enhancer matrix particles	否		Respiratory syndrome	MARC-145 cell	E_02_0508	SDS-PAGE,western blot	Our results showed that most of the bulk impurities had been removed, and PA-GRFT could capture PRRSV onto GEM particles.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results showed that most of the bulk impurities had been removed, and PA-GRFT could capture PRRSV onto GEM particles.		Our results showed that most of the bulk impurities had been removed, and PA-GRFT could capture PRRSV onto GEM particles.	Immunohistochemical staining	Our results showed that most of the bulk impurities had been removed, and PA-GRFT could capture PRRSV onto GEM particles.			SDS-PAGE,western blot				GEM
30045748	chr13	55970191	55972191	Pitx1	Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].	human,mouse		High+Lowthroughput	Functional characterization of enhancer evolution in the primate lineage	是			HepG2 cell	E_02_0509	Starr SEQ, chip SEQ, PCR, gene knockdown	Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].		Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].	Immunohistochemical staining	Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].			STARR-seq,ChIP-seq,PCR,基因敲降				Pitx1
30045748	chr2	135836881	135838881	MCM6	Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].	human,mouse		High+Lowthroughput	Functional characterization of enhancer evolution in the primate lineage	是			HepG2 cell	E_02_0509	Starr SEQ, chip SEQ, PCR, gene knockdown	Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].		Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].	Immunohistochemical staining	Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].			STARR-seq,ChIP-seq,PCR,基因敲降				MCM6
30044535	chr2	135836643	135838643	MCM6	Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].	human,mouse	Marrow adipose tissue	High+Lowthroughput	A Lox/CHOP-10 crosstalk governs osteogenic and adipogenic cell fate by MSCs	否		Obesity, osteoporosis	stromal cell of bone marrow	E_02_0510	Western blot,Q‐PCR	Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].		Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].	Immunohistochemical staining	Examples of the former include fruitful investigations of how specific enhancers underlie phenotypic changes, e.g. cis-regulatory changes of the yellow locus affecting Drosophila pigmentation [10, 11], recurrent deletions of a Pitx1 enhancer resulting in the loss of pelvic armor in stickleback [12], and recurrent SNPs in the intron of MCM6, resulting in lactase persistence in humans [13, 14].			Western blot,Q‐PCR				MCM6
30043530	chr6	16296402	16298402	ATXN1	Spinocerebellar ataxia type 1 (SCA1) is a fatal, dominantly inherited neurodegenerative disease caused by the expansion of CAG repeats in the Ataxin-1 (ATXN1) gene.	human,mouse		High+Lowthroughput	Astroglia contribute to the pathogenesis of spinocerebellar ataxia Type 1 (SCA1) in a biphasic, stage-of-disease specific manner	否		Spinocerebellar ataxia type 1 (SCA1), amyotrophic lateral sclerosis (ALS), Huntington's disease (hd), Parkinson's disease, multiple system atrophy (MSA)	Astrocyte	E_02_0511	Rotarod analysis, quantitative analysis of immunofluorescent staining, Western blot, RT qPCR, statistical analysis	Spinocerebellar ataxia type 1 (SCA1) is a fatal, dominantly inherited neurodegenerative disease caused by the expansion of CAG repeats in the Ataxin-1 (ATXN1) gene.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Spinocerebellar ataxia type 1 (SCA1) is a fatal, dominantly inherited neurodegenerative disease caused by the expansion of CAG repeats in the Ataxin-1 (ATXN1) gene.		Spinocerebellar ataxia type 1 (SCA1) is a fatal, dominantly inherited neurodegenerative disease caused by the expansion of CAG repeats in the Ataxin-1 (ATXN1) gene.	Immunohistochemical staining	Spinocerebellar ataxia type 1 (SCA1) is a fatal, dominantly inherited neurodegenerative disease caused by the expansion of CAG repeats in the Ataxin-1 (ATXN1) gene.			Rotarod analysis,Quantitative Analysis of immunofluorescent staining,Western blot,RT-qPCR,统计分析				ATXN1
30042166	chr18	58668913	58670913	MALT1	Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.	human	Glioma tissues	High+Lowthroughput	LncRNA SNHG3 enhances the malignant progress of glioma through silencing KLF2 and p21	否		OSCC, colorectal, hepatocellular carcinoma	SHG-44 cell	E_01_0788	QRT PCR, Western blot, chromatin immunoprecipitation, RNA immunoprecipitation (RIP), statistical analysis, flow cytometry	Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.		Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.	Immunohistochemical staining	Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.			qRT-PCR,Western blot,Chromatin immunoprecipitation,RNA immunoprecipitation (RIP),统计分析,流式细胞术				MALT1
30042166	chr16	54842637	54844637	CRNDE	Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.	human	Glioma tissues	High+Lowthroughput	LncRNA SNHG3 enhances the malignant progress of glioma through silencing KLF2 and p21	否		OSCC, colorectal, hepatocellular carcinoma	SHG-44 cell	E_01_0788	QRT PCR, Western blot, chromatin immunoprecipitation, RNA immunoprecipitation (RIP), statistical analysis, flow cytometry	Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.		Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.	Immunohistochemical staining	Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.			qRT-PCR,Western blot,Chromatin immunoprecipitation,RNA immunoprecipitation (RIP),统计分析,流式细胞术				CRNDE
30042166	chr19	16321697	16323697	KLF2	Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.	human	Glioma tissues	High+Lowthroughput	LncRNA SNHG3 enhances the malignant progress of glioma through silencing KLF2 and p21	否		OSCC, colorectal, hepatocellular carcinoma	SHG-44 cell	E_01_0788	QRT PCR, Western blot, chromatin immunoprecipitation, RNA immunoprecipitation (RIP), statistical analysis, flow cytometry	Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.	Immunohistochemical staining	Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.	KLF2		qRT-PCR,Western blot,Chromatin immunoprecipitation,RNA immunoprecipitation (RIP),统计分析,流式细胞术	Besides, it was also found out that KLF2 and p21 were down-regulated in glioma tissues.			
30042132	chr3	181708868	181710868	SOX2	Epigenome silencing of these repeat sites does not affect gene expression in unrelated cells, can prevent the induction of gene expression by EWS-FLI1, and, in the case of a GGAA repeat that controls SOX2 expression from a distance of 470 kb, is sufficient to impair the growth of Ewing sarcoma xenografts.                                                                                                                                                                                                                             Ewing sarcoma, the second most common pediatric bone cancer, is characterized by specific chromosomal translocations that generate fusions between the EWSR1 gene and members of the ETS family of transcription factors, most commonly FLI1 (Delattre et al. 1992).	human		High+Lowthroughput	Epigenome editing of microsatellite repeats defines tumor-specific enhancer functions and dependencies	否		Ewing sarcoma	SK-N-MC cell	E_01_0789	RT qPCR, Western blot, chip SEQ, chip qPCR, NRO RT qPCR, NRO SEQ, statistical analysis	Epigenome silencing of these repeat sites does not affect gene expression in unrelated cells, can prevent the induction of gene expression by EWS-FLI1, and, in the case of a GGAA repeat that controls SOX2 expression from a distance of 470 kb, is sufficient to impair the growth of Ewing sarcoma xenografts.                                                                                                                                                                                                                             Ewing sarcoma, the second most common pediatric bone cancer, is characterized by specific chromosomal translocations that generate fusions between the EWSR1 gene and members of the ETS family of transcription factors, most commonly FLI1 (Delattre et al. 1992).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Epigenome silencing of these repeat sites does not affect gene expression in unrelated cells, can prevent the induction of gene expression by EWS-FLI1, and, in the case of a GGAA repeat that controls SOX2 expression from a distance of 470 kb, is sufficient to impair the growth of Ewing sarcoma xenografts.                                                                                                                                                                                                                             Ewing sarcoma, the second most common pediatric bone cancer, is characterized by specific chromosomal translocations that generate fusions between the EWSR1 gene and members of the ETS family of transcription factors, most commonly FLI1 (Delattre et al. 1992).	Immunohistochemical staining	Epigenome silencing of these repeat sites does not affect gene expression in unrelated cells, can prevent the induction of gene expression by EWS-FLI1, and, in the case of a GGAA repeat that controls SOX2 expression from a distance of 470 kb, is sufficient to impair the growth of Ewing sarcoma xenografts.                                                                                                                                                                                                                             Ewing sarcoma, the second most common pediatric bone cancer, is characterized by specific chromosomal translocations that generate fusions between the EWSR1 gene and members of the ETS family of transcription factors, most commonly FLI1 (Delattre et al. 1992).	SOX2		RT-qPCR,Western blot,ChIP-seq,ChIP-qPCR,NRO-RT-qPCR,NRO-seq,统计分析	Epigenome silencing of these repeat sites does not affect gene expression in unrelated cells, can prevent the induction of gene expression by EWS-FLI1, and, in the case of a GGAA repeat that controls SOX2 expression from a distance of 470 kb, is sufficient to impair the growth of Ewing sarcoma xenografts.                                                                                                                                                                                                                             Ewing sarcoma, the second most common pediatric bone cancer, is characterized by specific chromosomal translocations that generate fusions between the EWSR1 gene and members of the ETS family of transcription factors, most commonly FLI1 (Delattre et al. 1992).			
30042132	chr22	29265492	29267492	EWSR1	Epigenome silencing of these repeat sites does not affect gene expression in unrelated cells, can prevent the induction of gene expression by EWS-FLI1, and, in the case of a GGAA repeat that controls SOX2 expression from a distance of 470 kb, is sufficient to impair the growth of Ewing sarcoma xenografts.                                                                                                                                                                                                                             Ewing sarcoma, the second most common pediatric bone cancer, is characterized by specific chromosomal translocations that generate fusions between the EWSR1 gene and members of the ETS family of transcription factors, most commonly FLI1 (Delattre et al. 1992).	human		High+Lowthroughput	Epigenome editing of microsatellite repeats defines tumor-specific enhancer functions and dependencies	否		Ewing sarcoma	SK-N-MC cell	E_01_0789	RT qPCR, Western blot, chip SEQ, chip qPCR, NRO RT qPCR, NRO SEQ, statistical analysis	Epigenome silencing of these repeat sites does not affect gene expression in unrelated cells, can prevent the induction of gene expression by EWS-FLI1, and, in the case of a GGAA repeat that controls SOX2 expression from a distance of 470 kb, is sufficient to impair the growth of Ewing sarcoma xenografts.                                                                                                                                                                                                                             Ewing sarcoma, the second most common pediatric bone cancer, is characterized by specific chromosomal translocations that generate fusions between the EWSR1 gene and members of the ETS family of transcription factors, most commonly FLI1 (Delattre et al. 1992).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Epigenome silencing of these repeat sites does not affect gene expression in unrelated cells, can prevent the induction of gene expression by EWS-FLI1, and, in the case of a GGAA repeat that controls SOX2 expression from a distance of 470 kb, is sufficient to impair the growth of Ewing sarcoma xenografts.                                                                                                                                                                                                                             Ewing sarcoma, the second most common pediatric bone cancer, is characterized by specific chromosomal translocations that generate fusions between the EWSR1 gene and members of the ETS family of transcription factors, most commonly FLI1 (Delattre et al. 1992).	Immunohistochemical staining	Epigenome silencing of these repeat sites does not affect gene expression in unrelated cells, can prevent the induction of gene expression by EWS-FLI1, and, in the case of a GGAA repeat that controls SOX2 expression from a distance of 470 kb, is sufficient to impair the growth of Ewing sarcoma xenografts.                                                                                                                                                                                                                             Ewing sarcoma, the second most common pediatric bone cancer, is characterized by specific chromosomal translocations that generate fusions between the EWSR1 gene and members of the ETS family of transcription factors, most commonly FLI1 (Delattre et al. 1992).	EWSR1		RT-qPCR,Western blot,ChIP-seq,ChIP-qPCR,NRO-RT-qPCR,NRO-seq,统计分析	Epigenome silencing of these repeat sites does not affect gene expression in unrelated cells, can prevent the induction of gene expression by EWS-FLI1, and, in the case of a GGAA repeat that controls SOX2 expression from a distance of 470 kb, is sufficient to impair the growth of Ewing sarcoma xenografts.                                                                                                                                                                                                                             Ewing sarcoma, the second most common pediatric bone cancer, is characterized by specific chromosomal translocations that generate fusions between the EWSR1 gene and members of the ETS family of transcription factors, most commonly FLI1 (Delattre et al. 1992).			
30038553	chr18	59216984	59218984	GRP	GRP, glucose-regulated protein 78 kDa.	mouse		High+Lowthroughput	Tauroursodeoxycholic Acid Alleviates H(2)O(2)-Induced Oxidative Stress and Apoptosis via Suppressing Endoplasmic Reticulum Stress in Neonatal Rat Cardiomyocytes	否		Acute myocardial infarction (MI)	cardiac muscle cell (sensu Arthopoda)	E_02_0512	Enzyme linked immunosorbent assay, Western blot, flow cytometry, statistical analysis	GRP, glucose-regulated protein 78 kDa.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	GRP, glucose-regulated protein 78 kDa.		GRP, glucose-regulated protein 78 kDa.	Immunohistochemical staining	GRP, glucose-regulated protein 78 kDa.			Enzyme-Linked Immunosorbent Assay,Western Blot,流式细胞术,统计分析				GRP
30038060	chr4	25645137	25647137	SLC34A2	Here, we indicated that SLC34A2 expression was markedly increased in SW480 and HT29 cell line cells compared with that in normal colorectal epithelial cell line cells.                                                                                                                  We demonstrated that SLC34A2 induced EZH2 expression and activated its promoter activity.	human		High+Lowthroughput	The SLC34A2-ROS-HIF-1-induced up-regulation of EZH2 expression promotes proliferation and chemo-resistance to apoptosis in colorectal cancer	否		Colorectal, ovarian, breast, gastric, lung	HT29 cell	E_01_0790	Quantitative real-time RT-PCR, Western blot, MTT assay, TUNEL assay, FACS analysis, statistical analysis, gene knockdown	Here, we indicated that SLC34A2 expression was markedly increased in SW480 and HT29 cell line cells compared with that in normal colorectal epithelial cell line cells.                                                                                                                  We demonstrated that SLC34A2 induced EZH2 expression and activated its promoter activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we indicated that SLC34A2 expression was markedly increased in SW480 and HT29 cell line cells compared with that in normal colorectal epithelial cell line cells.                                                                                                                  We demonstrated that SLC34A2 induced EZH2 expression and activated its promoter activity.		Here, we indicated that SLC34A2 expression was markedly increased in SW480 and HT29 cell line cells compared with that in normal colorectal epithelial cell line cells.                                                                                                                  We demonstrated that SLC34A2 induced EZH2 expression and activated its promoter activity.	Immunohistochemical staining	Here, we indicated that SLC34A2 expression was markedly increased in SW480 and HT29 cell line cells compared with that in normal colorectal epithelial cell line cells.                                                                                                                  We demonstrated that SLC34A2 induced EZH2 expression and activated its promoter activity.			Quantitative real-time RT-PCR,Western blot,MTT assay,TUNEL assay,FACS分析,统计分析,基因敲降				SLC34A2
30038060	chr7	148804576	148806576	EZH2	Here, we indicated that SLC34A2 expression was markedly increased in SW480 and HT29 cell line cells compared with that in normal colorectal epithelial cell line cells.                                                                                                                  We demonstrated that SLC34A2 induced EZH2 expression and activated its promoter activity.	human		High+Lowthroughput	The SLC34A2-ROS-HIF-1-induced up-regulation of EZH2 expression promotes proliferation and chemo-resistance to apoptosis in colorectal cancer	否		Colorectal, ovarian, breast, gastric, lung	HT29 cell	E_01_0790	Quantitative real-time RT-PCR, Western blot, MTT assay, TUNEL assay, FACS analysis, statistical analysis, gene knockdown	Here, we indicated that SLC34A2 expression was markedly increased in SW480 and HT29 cell line cells compared with that in normal colorectal epithelial cell line cells.                                                                                                                  We demonstrated that SLC34A2 induced EZH2 expression and activated its promoter activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we indicated that SLC34A2 expression was markedly increased in SW480 and HT29 cell line cells compared with that in normal colorectal epithelial cell line cells.                                                                                                                  We demonstrated that SLC34A2 induced EZH2 expression and activated its promoter activity.	Immunohistochemical staining	Here, we indicated that SLC34A2 expression was markedly increased in SW480 and HT29 cell line cells compared with that in normal colorectal epithelial cell line cells.                                                                                                                  We demonstrated that SLC34A2 induced EZH2 expression and activated its promoter activity.	EZH2		Quantitative real-time RT-PCR,Western blot,MTT assay,TUNEL assay,FACS分析,统计分析,基因敲降	Here, we indicated that SLC34A2 expression was markedly increased in SW480 and HT29 cell line cells compared with that in normal colorectal epithelial cell line cells.                                                                                                                  We demonstrated that SLC34A2 induced EZH2 expression and activated its promoter activity.			
30037979	chr17	10626067	10628067	MYH3	MUNC is required for optimal myogenic differentiation, induces specific myogenic transcripts in trans (MYOD, MYOGENIN, and MYH3), and has a functional human homolog.	human		High+Lowthroughput	MUNC, an Enhancer RNA Upstream from the MYOD Gene, Induces a Subgroup of Myogenic Transcripts in trans Independently of MyoD	否			C2C12 cell	E_01_0791	qRT-PCR,Western blot,Southern blot,Immunofluorescence assay,RNA-Seq	MUNC is required for optimal myogenic differentiation, induces specific myogenic transcripts in trans (MYOD, MYOGENIN, and MYH3), and has a functional human homolog.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MUNC is required for optimal myogenic differentiation, induces specific myogenic transcripts in trans (MYOD, MYOGENIN, and MYH3), and has a functional human homolog.		MUNC is required for optimal myogenic differentiation, induces specific myogenic transcripts in trans (MYOD, MYOGENIN, and MYH3), and has a functional human homolog.	Immunohistochemical staining	MUNC is required for optimal myogenic differentiation, induces specific myogenic transcripts in trans (MYOD, MYOGENIN, and MYH3), and has a functional human homolog.			qRT-PCR,Western blot,Southern blot,Immunofluorescence assay,RNA-Seq				MYH3
30037904	chrX	71530600	71532600	OGT	Here, we demonstrate the existence of a homeostatic mechanism involving mutual regulation of the O-GlcNAc cycling enzymes O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) at the transcriptional level.	mouse,human		High+Lowthroughput	Transcriptional regulation of O-GlcNAc homeostasis is disrupted in pancreatic cancer	否		Cancer, diabetes, cardiovascular, neurodegenerative disease, pancreatic cancer	PDAC cell	E_02_0513	RT–qPCR,ChIP-seq,western blot	Here, we demonstrate the existence of a homeostatic mechanism involving mutual regulation of the O-GlcNAc cycling enzymes O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) at the transcriptional level.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we demonstrate the existence of a homeostatic mechanism involving mutual regulation of the O-GlcNAc cycling enzymes O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) at the transcriptional level.		Here, we demonstrate the existence of a homeostatic mechanism involving mutual regulation of the O-GlcNAc cycling enzymes O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) at the transcriptional level.	Immunohistochemical staining	Here, we demonstrate the existence of a homeostatic mechanism involving mutual regulation of the O-GlcNAc cycling enzymes O-GlcNAc transferase (OGT) and O-GlcNAcase (OGA) at the transcriptional level.			RT–qPCR,ChIP-seq,western blot				OGT
30037417	chr4	186066455	186068455	TLR3	Poly I:C is a synthetic analog of double-stranded RNA which is present in some viruses and is a TLR3 agonist.	mouse		High+Lowthroughput	Comparison of immunogenicity, efficacy and transcriptome changes of inactivated rabies virus vaccine with different adjuvants	否		rabies	BHK-21 cell	E_02_0514	ELISA, RFFIT, RT qPCR, statistical analysis	Poly I:C is a synthetic analog of double-stranded RNA which is present in some viruses and is a TLR3 agonist.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Poly I:C is a synthetic analog of double-stranded RNA which is present in some viruses and is a TLR3 agonist.		Poly I:C is a synthetic analog of double-stranded RNA which is present in some viruses and is a TLR3 agonist.	Immunohistochemical staining	Poly I:C is a synthetic analog of double-stranded RNA which is present in some viruses and is a TLR3 agonist.			ELISA,RFFIT,RT-qPCR,统计分析				TLR3
30036660	chr1	161763256	161765256	ATF6	This study first showed that inhibition of activating transcription factor 6 (ATF6) by apelin-13 could reduce endoplasmic reticulum (ER)-stress-mediated apoptosis and blood-brain-barrier (BBB) disruption after SAH.	human		High+Lowthroughput	Apelin-13 Alleviates Early Brain Injury after Subarachnoid Hemorrhage via Suppression of Endoplasmic Reticulum Stress-mediated Apoptosis and Blood-Brain Barrier Disruption: Possible Involvement of ATF6/CHOP Pathway	否		Subarachnoid hemorrhage	neuronal cell	E_01_0792	RT-PCR, immunofluorescence staining, Western blot	This study first showed that inhibition of activating transcription factor 6 (ATF6) by apelin-13 could reduce endoplasmic reticulum (ER)-stress-mediated apoptosis and blood-brain-barrier (BBB) disruption after SAH.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			This study first showed that inhibition of activating transcription factor 6 (ATF6) by apelin-13 could reduce endoplasmic reticulum (ER)-stress-mediated apoptosis and blood-brain-barrier (BBB) disruption after SAH.	Immunohistochemical staining	This study first showed that inhibition of activating transcription factor 6 (ATF6) by apelin-13 could reduce endoplasmic reticulum (ER)-stress-mediated apoptosis and blood-brain-barrier (BBB) disruption after SAH.	ATF6		RT-PCR, 免疫荧光染色,western blot	This study first showed that inhibition of activating transcription factor 6 (ATF6) by apelin-13 could reduce endoplasmic reticulum (ER)-stress-mediated apoptosis and blood-brain-barrier (BBB) disruption after SAH.			
30035248	chr8	11673642	11675642	GATA4	GATA4 is a zinc finger transcription factor that is a pioneer factor in various tissues and regulates tissue specific gene regulation.                                                                                                                                                                                To determine if Runx2 is a direct target of GATA4, chromatin immunoprecipitation (ChIP) was performed, and it demonstrated that GATA4 is recruited to the two Runx2 promoters and an enhancer region.            	mouse,human	Skeletal tissues	High+Lowthroughput	GATA4 Directly Regulates Runx2 Expression and Osteoblast Differentiation	否			cementoblast	E_02_0515	Immunohistochemistry, RNA in situ (rnascope), quantitative PCR, statistical analysis	GATA4 is a zinc finger transcription factor that is a pioneer factor in various tissues and regulates tissue specific gene regulation.                                                                                                                                                                                To determine if Runx2 is a direct target of GATA4, chromatin immunoprecipitation (ChIP) was performed, and it demonstrated that GATA4 is recruited to the two Runx2 promoters and an enhancer region.            	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	GATA4 is a zinc finger transcription factor that is a pioneer factor in various tissues and regulates tissue specific gene regulation.                                                                                                                                                                                To determine if Runx2 is a direct target of GATA4, chromatin immunoprecipitation (ChIP) was performed, and it demonstrated that GATA4 is recruited to the two Runx2 promoters and an enhancer region.            		GATA4 is a zinc finger transcription factor that is a pioneer factor in various tissues and regulates tissue specific gene regulation.                                                                                                                                                                                To determine if Runx2 is a direct target of GATA4, chromatin immunoprecipitation (ChIP) was performed, and it demonstrated that GATA4 is recruited to the two Runx2 promoters and an enhancer region.            	Immunohistochemical staining	GATA4 is a zinc finger transcription factor that is a pioneer factor in various tissues and regulates tissue specific gene regulation.                                                                                                                                                                                To determine if Runx2 is a direct target of GATA4, chromatin immunoprecipitation (ChIP) was performed, and it demonstrated that GATA4 is recruited to the two Runx2 promoters and an enhancer region.            			Immunohistochemistry,RNA in situ (RNAscope),Quantitative PCR,统计分析				GATA4
30035248	chr17	44804035	44806035	Runx2	GATA4 is a zinc finger transcription factor that is a pioneer factor in various tissues and regulates tissue specific gene regulation.                                                                                                                                                                                To determine if Runx2 is a direct target of GATA4, chromatin immunoprecipitation (ChIP) was performed, and it demonstrated that GATA4 is recruited to the two Runx2 promoters and an enhancer region.            	mouse,human	Skeletal tissues	High+Lowthroughput	GATA4 Directly Regulates Runx2 Expression and Osteoblast Differentiation	否			cementoblast	E_02_0515	Immunohistochemistry, RNA in situ (rnascope), quantitative PCR, statistical analysis	GATA4 is a zinc finger transcription factor that is a pioneer factor in various tissues and regulates tissue specific gene regulation.                                                                                                                                                                                To determine if Runx2 is a direct target of GATA4, chromatin immunoprecipitation (ChIP) was performed, and it demonstrated that GATA4 is recruited to the two Runx2 promoters and an enhancer region.            	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	GATA4 is a zinc finger transcription factor that is a pioneer factor in various tissues and regulates tissue specific gene regulation.                                                                                                                                                                                To determine if Runx2 is a direct target of GATA4, chromatin immunoprecipitation (ChIP) was performed, and it demonstrated that GATA4 is recruited to the two Runx2 promoters and an enhancer region.            		GATA4 is a zinc finger transcription factor that is a pioneer factor in various tissues and regulates tissue specific gene regulation.                                                                                                                                                                                To determine if Runx2 is a direct target of GATA4, chromatin immunoprecipitation (ChIP) was performed, and it demonstrated that GATA4 is recruited to the two Runx2 promoters and an enhancer region.            	Immunohistochemical staining	GATA4 is a zinc finger transcription factor that is a pioneer factor in various tissues and regulates tissue specific gene regulation.                                                                                                                                                                                To determine if Runx2 is a direct target of GATA4, chromatin immunoprecipitation (ChIP) was performed, and it demonstrated that GATA4 is recruited to the two Runx2 promoters and an enhancer region.            			Immunohistochemistry,RNA in situ (RNAscope),Quantitative PCR,统计分析				Runx2
30033370	chr8	127732613	127734613	MYC	Tandem duplication hotspots also occur near MYC, in lncRNAs associated with post-translational MYC regulation. Classes of structural variations were linked to distinct DNA repair deficiencies, suggesting their etiology, including associations of CDK12 mutation with tandem duplications, TP53 inactivation with inverted rearrangements and chromothripsis, and BRCA2 inactivation with deletions. Together, these observations provide a comprehensive view of how structural variations affect critical regulators in metastatic prostate cancer.	human		High+Lowthroughput	Genomic Hallmarks and Structural Variation in Metastatic Prostate Cancer	否		prostatic cancer	neoplastic cell	E_01_0793	RNA sequencing, statistical analysis	Tandem duplication hotspots also occur near MYC, in lncRNAs associated with post-translational MYC regulation. Classes of structural variations were linked to distinct DNA repair deficiencies, suggesting their etiology, including associations of CDK12 mutation with tandem duplications, TP53 inactivation with inverted rearrangements and chromothripsis, and BRCA2 inactivation with deletions. Together, these observations provide a comprehensive view of how structural variations affect critical regulators in metastatic prostate cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Tandem duplication hotspots also occur near MYC, in lncRNAs associated with post-translational MYC regulation. Classes of structural variations were linked to distinct DNA repair deficiencies, suggesting their etiology, including associations of CDK12 mutation with tandem duplications, TP53 inactivation with inverted rearrangements and chromothripsis, and BRCA2 inactivation with deletions. Together, these observations provide a comprehensive view of how structural variations affect critical regulators in metastatic prostate cancer.	Immunohistochemical staining	Tandem duplication hotspots also occur near MYC, in lncRNAs associated with post-translational MYC regulation. Classes of structural variations were linked to distinct DNA repair deficiencies, suggesting their etiology, including associations of CDK12 mutation with tandem duplications, TP53 inactivation with inverted rearrangements and chromothripsis, and BRCA2 inactivation with deletions. Together, these observations provide a comprehensive view of how structural variations affect critical regulators in metastatic prostate cancer.	MYC		RNA Sequencing,统计分析	Tandem duplication hotspots also occur near MYC, in lncRNAs associated with post-translational MYC regulation. Classes of structural variations were linked to distinct DNA repair deficiencies, suggesting their etiology, including associations of CDK12 mutation with tandem duplications, TP53 inactivation with inverted rearrangements and chromothripsis, and BRCA2 inactivation with deletions. Together, these observations provide a comprehensive view of how structural variations affect critical regulators in metastatic prostate cancer.			
30033370	chr13	32312135	32314135	BRCA2	Tandem duplication hotspots also occur near MYC, in lncRNAs associated with post-translational MYC regulation. Classes of structural variations were linked to distinct DNA repair deficiencies, suggesting their etiology, including associations of CDK12 mutation with tandem duplications, TP53 inactivation with inverted rearrangements and chromothripsis, and BRCA2 inactivation with deletions. Together, these observations provide a comprehensive view of how structural variations affect critical regulators in metastatic prostate cancer.	human		High+Lowthroughput	Genomic Hallmarks and Structural Variation in Metastatic Prostate Cancer	否		prostatic cancer	neoplastic cell	E_01_0793	RNA sequencing, statistical analysis	Tandem duplication hotspots also occur near MYC, in lncRNAs associated with post-translational MYC regulation. Classes of structural variations were linked to distinct DNA repair deficiencies, suggesting their etiology, including associations of CDK12 mutation with tandem duplications, TP53 inactivation with inverted rearrangements and chromothripsis, and BRCA2 inactivation with deletions. Together, these observations provide a comprehensive view of how structural variations affect critical regulators in metastatic prostate cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Tandem duplication hotspots also occur near MYC, in lncRNAs associated with post-translational MYC regulation. Classes of structural variations were linked to distinct DNA repair deficiencies, suggesting their etiology, including associations of CDK12 mutation with tandem duplications, TP53 inactivation with inverted rearrangements and chromothripsis, and BRCA2 inactivation with deletions. Together, these observations provide a comprehensive view of how structural variations affect critical regulators in metastatic prostate cancer.	Immunohistochemical staining	Tandem duplication hotspots also occur near MYC, in lncRNAs associated with post-translational MYC regulation. Classes of structural variations were linked to distinct DNA repair deficiencies, suggesting their etiology, including associations of CDK12 mutation with tandem duplications, TP53 inactivation with inverted rearrangements and chromothripsis, and BRCA2 inactivation with deletions. Together, these observations provide a comprehensive view of how structural variations affect critical regulators in metastatic prostate cancer.	BRCA2		RNA Sequencing,统计分析	Tandem duplication hotspots also occur near MYC, in lncRNAs associated with post-translational MYC regulation. Classes of structural variations were linked to distinct DNA repair deficiencies, suggesting their etiology, including associations of CDK12 mutation with tandem duplications, TP53 inactivation with inverted rearrangements and chromothripsis, and BRCA2 inactivation with deletions. Together, these observations provide a comprehensive view of how structural variations affect critical regulators in metastatic prostate cancer.			
30033362	chr19	41447287	41449287	PCAT19	We showed that rs11672691 maps to the promoter of a short isoform of long noncoding RNA PCAT19 (PCAT19-short), which is in the third intron of the long isoform (PCAT19-long).	human		High+Lowthroughput	Risk SNP-Mediated Promoter-Enhancer Switching Drives Prostate Cancer through lncRNA PCAT19	是	rs11672691,rs887391,rs35148638,rs78943174 	prostatic cancer	LNCaP	E_01_0794	RNA pull-down (chirp) assay, RT qPCR, Western blot, RNA SEQ, eQTL analysis, crispri assay, statistical analysis	We showed that rs11672691 maps to the promoter of a short isoform of long noncoding RNA PCAT19 (PCAT19-short), which is in the third intron of the long isoform (PCAT19-long).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We showed that rs11672691 maps to the promoter of a short isoform of long noncoding RNA PCAT19 (PCAT19-short), which is in the third intron of the long isoform (PCAT19-long).		We showed that rs11672691 maps to the promoter of a short isoform of long noncoding RNA PCAT19 (PCAT19-short), which is in the third intron of the long isoform (PCAT19-long).	Immunohistochemical staining	We showed that rs11672691 maps to the promoter of a short isoform of long noncoding RNA PCAT19 (PCAT19-short), which is in the third intron of the long isoform (PCAT19-long).			RNA pull-down (ChIRP) assay,RT-qPCR,Western blot,RNA-seq,eQTL分析,CRISPRi assay,统计分析				PCAT19
30033361	chr19	41446587	41448587	PCAT19	We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.	human		High+Lowthroughput	Biology and Clinical Implications of the 19q13 Aggressive Prostate Cancer Susceptibility Locus	是	rs11672691	Aggressive prostate cancer (PCA)	RWPE1 cell	E_01_0795	STARR-seq,eQTL analysis,Quantitative RT-PCR,Chromatin immunoprecipitation (ChIP),Western Blot,RNA-Seq 	We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.		We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.	Immunohistochemical staining	We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.			STARR-seq,eQTL analysis,Quantitative RT-PCR,Chromatin immunoprecipitation (ChIP),Western Blot,RNA-Seq 				PCAT19
30033361	chr19	41546520	41548520	CEACAM21	We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.	human		High+Lowthroughput	Biology and Clinical Implications of the 19q13 Aggressive Prostate Cancer Susceptibility Locus	是	rs11672691	Aggressive prostate cancer (PCA)	RWPE1 cell	E_01_0795	STARR-seq,eQTL analysis,Quantitative RT-PCR,Chromatin immunoprecipitation (ChIP),Western Blot,RNA-Seq 	We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.		We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.	Immunohistochemical staining	We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.			STARR-seq,eQTL analysis,Quantitative RT-PCR,Chromatin immunoprecipitation (ChIP),Western Blot,RNA-Seq 				CEACAM21
30033361	chr7	27097791	27099791	HOXA2	We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.	human		High+Lowthroughput	Biology and Clinical Implications of the 19q13 Aggressive Prostate Cancer Susceptibility Locus	是	rs11672691	Aggressive prostate cancer (PCA)	RWPE1 cell	E_01_0795	STARR-seq,eQTL analysis,Quantitative RT-PCR,Chromatin immunoprecipitation (ChIP),Western Blot,RNA-Seq 	We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.	Immunohistochemical staining	We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.	HOXA2		STARR-seq,eQTL analysis,Quantitative RT-PCR,Chromatin immunoprecipitation (ChIP),Western Blot,RNA-Seq 	We found an association of the aggressive PCa-associated allele G of rs11672691 with elevated mRNA levels of two biologically plausible candidate genes PCAT19 and CEACAM21, implicating in PCa cell growth and tumor progression. Mechanistically, rs11672691 resides in an enhancer element and alters the binding site of HOXA2, a novel oncogenic transcription factor with prognostic potential in PCa.			
30033119	chr8	38291071	38304326	TF	Enhancer function requires transcription factor (TF) binding and correlates with histone modifications.                                                                                                                                                                                                                                                    Although active enhancers associate with TFs, only a minority of regions marked by NANOG, OCT4, H3K27ac, and H3K4me1 function as enhancers, with activity markedly changing under naive versus primed culture conditions. 	human		Low+High throughput	Functional Dissection of the Enhancer Repertoire in Human Embryonic Stem Cells	否	--	--	Embryonic stem cell	E_02_0516	ChIP-STARR-seq	Visual inspection of selected genomic regions illustrates the broad spectrum of enhancer activity measured by ChIP-STARR-seq. For instance, ChIP-seq for NANOG indicates two strong binding sites up- and downstream of SOX2, but only the downstream binding site resulted in ChIP-STARR-seq RNA in excess of plasmid abundance.	Super-Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,qRT-PCR	Luciferase assays confirmed spatially restricted Enhancer activity of DNA in the neighborhood of the central active region of the FGFR1 SE.	BFGFR,CD331,CEK,ECCL,FGFBR,FGFR-1,FLG,FLT-2,FLT2,HBGFR,HH2,HRTFDS,KAL2,N-SAM,OGD,bFGF-R-1	Although transposable elements associate with putative enhancers, only some exhibit activity.	Luciferase Reporter Assay,CRISPR/Cas9	Luciferase assays confirmed spatially restricted Enhancer activity of DNA in the neighborhood of the central active region of the FGFR1 SE	POU5F1 	OCT3,OCT4,OTF-3,OTF3,OTF4,Oct-3,Oct-4,ANOP3,MCOPS3,NANOG	ChIP-qPCR	To investigate the functional potential of enhancers in ESCs, we first focused on primed H9 ESCs (Figures S1A and S1B) and performed ChIP for NANOG, OCT4, H3K4me1 and H3K27ac.ChIP-qPCR and ChIP-seq were similar to previous results (Figures S1C and 1D).Applying this threshold to regions bound by NANOG, OCT4, H3K4me1, H3K27ac, or combinations of these factors indicates that only a minority of ChIP-seq peaks showed enhancer activity (Figure 2D and S3C), with regions bound by OCT4 having the highest proportion of high activity enhancers.	--	--	FGFR1
30033119	chr8	38291071	38304326	NANOG	Enhancer function requires transcription factor (TF) binding and correlates with histone modifications.                                                                                                                                                                                                                                                    Although active enhancers associate with TFs, only a minority of regions marked by NANOG, OCT4, H3K27ac, and H3K4me1 function as enhancers, with activity markedly changing under naive versus primed culture conditions. 	human		Low+High throughput	Functional Dissection of the Enhancer Repertoire in Human Embryonic Stem Cells	否	--	--	Embryonic stem cell	E_02_0516	ChIP-STARR-seq	Visual inspection of selected genomic regions illustrates the broad spectrum of enhancer activity measured by ChIP-STARR-seq. For instance, ChIP-seq for NANOG indicates two strong binding sites up- and downstream of SOX2, but only the downstream binding site resulted in ChIP-STARR-seq RNA in excess of plasmid abundance.	Super-Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,qRT-PCR	Luciferase assays confirmed spatially restricted Enhancer activity of DNA in the neighborhood of the central active region of the FGFR1 SE.	BFGFR,CD331,CEK,ECCL,FGFBR,FGFR-1,FLG,FLT-2,FLT2,HBGFR,HH2,HRTFDS,KAL2,N-SAM,OGD,bFGF-R-1	Although transposable elements associate with putative enhancers, only some exhibit activity.	Luciferase Reporter Assay,CRISPR/Cas9	Luciferase assays confirmed spatially restricted Enhancer activity of DNA in the neighborhood of the central active region of the FGFR1 SE	POU5F1 	OCT3,OCT4,OTF-3,OTF3,OTF4,Oct-3,Oct-4,ANOP3,MCOPS3,NANOG	ChIP-qPCR	To investigate the functional potential of enhancers in ESCs, we first focused on primed H9 ESCs (Figures S1A and S1B) and performed ChIP for NANOG, OCT4, H3K4me1 and H3K27ac.ChIP-qPCR and ChIP-seq were similar to previous results (Figures S1C and 1D).Applying this threshold to regions bound by NANOG, OCT4, H3K4me1, H3K27ac, or combinations of these factors indicates that only a minority of ChIP-seq peaks showed enhancer activity (Figure 2D and S3C), with regions bound by OCT4 having the highest proportion of high activity enhancers.	--	--	FGFR1
30031062	chr8	66917733	66919733	SNHG6	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].	human,mouse		High+Lowthroughput	Long noncoding RNA SNHG6 regulates p21 expression via activation of the JNK pathway and regulation of EZH2 in gastric cancer cells	否		gastric cancer	GC cell	E_02_0517	QRT PCR, immunohistochemical staining, Western blot, rna-fish, statistical analysis	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].		Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].	Immunohistochemical staining	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].			qRT-PCR,Immunohistochemical staining,western blot,RNA-FISH,统计分析				SNHG6
30031062	chr7	148803913	148805913	EZH2	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].	human,mouse		High+Lowthroughput	Long noncoding RNA SNHG6 regulates p21 expression via activation of the JNK pathway and regulation of EZH2 in gastric cancer cells	否		gastric cancer	GC cell	E_02_0517	QRT PCR, immunohistochemical staining, Western blot, rna-fish, statistical analysis	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].		Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].	Immunohistochemical staining	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].			qRT-PCR,Immunohistochemical staining,western blot,RNA-FISH,统计分析				EZH2
30031062	chr11	1992846	1994846	H19	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].	human,mouse		High+Lowthroughput	Long noncoding RNA SNHG6 regulates p21 expression via activation of the JNK pathway and regulation of EZH2 in gastric cancer cells	否		gastric cancer	GC cell	E_02_0517	QRT PCR, immunohistochemical staining, Western blot, rna-fish, statistical analysis	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].		Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].	Immunohistochemical staining	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].			qRT-PCR,Immunohistochemical staining,western blot,RNA-FISH,统计分析				H19
30031062	chrX	73818034	73820034	XIST	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].	human,mouse		High+Lowthroughput	Long noncoding RNA SNHG6 regulates p21 expression via activation of the JNK pathway and regulation of EZH2 in gastric cancer cells	否		gastric cancer	GC cell	E_02_0517	QRT PCR, immunohistochemical staining, Western blot, rna-fish, statistical analysis	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].		Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].	Immunohistochemical staining	Small nucleolar RNA host gene 6 (SNHG6) plays a role in the progression of human cancers.                                                                                                                                                                                                                                                             Furthermore, the activation of the c-Jun N-terminal kinase (JNK) pathway and the decrease in Enhancer of Zeste Homolog 2 (EZH2) expression levels represented two mutually independent mechanisms by which SNHG6 knockdown resulted in the upregulation of p21.                                                                                                                                                                                                                                                                                                                                                                   H19 and XIST, the first two non-coding RNAs (ncRNAs), are found to lack large open reading frames and the capability to produce identifiable protein products [4-6].			qRT-PCR,Immunohistochemical staining,western blot,RNA-FISH,统计分析				XIST
30031040	chr10	88950934	88952934	FAS	PFBS treatments significantly increased the protein and mRNA levels of the master transcription factors in adipocyte differentiation; CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ), along with acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), the key proteins in lipogenesis.                                                                                                                                                                                   Previously, PFASs, particularly PFOS and perfluorooctanoic acid (PFOA), were reported to promote adipogenesis in 3T3-L1 adipocytes with increased expression of adipogenic genes, including CCAAT/enhancer-binding protein alpha (C/EBPα), peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid binding protein 4 (FABP4) and lipoprotein lipase (LPL) (Watkins et al. 2015, Yamamoto et al.	human,mouse		High+Lowthroughput	Perfluorobutanesulfonic acid (PFBS) potentiates adipogenesis of 3T3-L1 adipocytes	否			3T3‑L1 adipocytes	E_02_0518	Q-PCR, MTT assay, immunoblotting, Western blot	PFBS treatments significantly increased the protein and mRNA levels of the master transcription factors in adipocyte differentiation; CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ), along with acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), the key proteins in lipogenesis.                                                                                                                                                                                   Previously, PFASs, particularly PFOS and perfluorooctanoic acid (PFOA), were reported to promote adipogenesis in 3T3-L1 adipocytes with increased expression of adipogenic genes, including CCAAT/enhancer-binding protein alpha (C/EBPα), peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid binding protein 4 (FABP4) and lipoprotein lipase (LPL) (Watkins et al. 2015, Yamamoto et al.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	PFBS treatments significantly increased the protein and mRNA levels of the master transcription factors in adipocyte differentiation; CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ), along with acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), the key proteins in lipogenesis.                                                                                                                                                                                   Previously, PFASs, particularly PFOS and perfluorooctanoic acid (PFOA), were reported to promote adipogenesis in 3T3-L1 adipocytes with increased expression of adipogenic genes, including CCAAT/enhancer-binding protein alpha (C/EBPα), peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid binding protein 4 (FABP4) and lipoprotein lipase (LPL) (Watkins et al. 2015, Yamamoto et al.		PFBS treatments significantly increased the protein and mRNA levels of the master transcription factors in adipocyte differentiation; CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ), along with acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), the key proteins in lipogenesis.                                                                                                                                                                                   Previously, PFASs, particularly PFOS and perfluorooctanoic acid (PFOA), were reported to promote adipogenesis in 3T3-L1 adipocytes with increased expression of adipogenic genes, including CCAAT/enhancer-binding protein alpha (C/EBPα), peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid binding protein 4 (FABP4) and lipoprotein lipase (LPL) (Watkins et al. 2015, Yamamoto et al.	Immunohistochemical staining	PFBS treatments significantly increased the protein and mRNA levels of the master transcription factors in adipocyte differentiation; CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ), along with acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), the key proteins in lipogenesis.                                                                                                                                                                                   Previously, PFASs, particularly PFOS and perfluorooctanoic acid (PFOA), were reported to promote adipogenesis in 3T3-L1 adipocytes with increased expression of adipogenic genes, including CCAAT/enhancer-binding protein alpha (C/EBPα), peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid binding protein 4 (FABP4) and lipoprotein lipase (LPL) (Watkins et al. 2015, Yamamoto et al.			q-PCR,MTT法,Immunoblotting,western blot				FAS
30031040	chr8	81475913	81477913	FABP4	PFBS treatments significantly increased the protein and mRNA levels of the master transcription factors in adipocyte differentiation; CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ), along with acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), the key proteins in lipogenesis.                                                                                                                                                                                   Previously, PFASs, particularly PFOS and perfluorooctanoic acid (PFOA), were reported to promote adipogenesis in 3T3-L1 adipocytes with increased expression of adipogenic genes, including CCAAT/enhancer-binding protein alpha (C/EBPα), peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid binding protein 4 (FABP4) and lipoprotein lipase (LPL) (Watkins et al. 2015, Yamamoto et al.	human,mouse		High+Lowthroughput	Perfluorobutanesulfonic acid (PFBS) potentiates adipogenesis of 3T3-L1 adipocytes	否			3T3‑L1 adipocytes	E_02_0518	Q-PCR, MTT assay, immunoblotting, Western blot	PFBS treatments significantly increased the protein and mRNA levels of the master transcription factors in adipocyte differentiation; CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ), along with acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), the key proteins in lipogenesis.                                                                                                                                                                                   Previously, PFASs, particularly PFOS and perfluorooctanoic acid (PFOA), were reported to promote adipogenesis in 3T3-L1 adipocytes with increased expression of adipogenic genes, including CCAAT/enhancer-binding protein alpha (C/EBPα), peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid binding protein 4 (FABP4) and lipoprotein lipase (LPL) (Watkins et al. 2015, Yamamoto et al.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	PFBS treatments significantly increased the protein and mRNA levels of the master transcription factors in adipocyte differentiation; CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ), along with acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), the key proteins in lipogenesis.                                                                                                                                                                                   Previously, PFASs, particularly PFOS and perfluorooctanoic acid (PFOA), were reported to promote adipogenesis in 3T3-L1 adipocytes with increased expression of adipogenic genes, including CCAAT/enhancer-binding protein alpha (C/EBPα), peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid binding protein 4 (FABP4) and lipoprotein lipase (LPL) (Watkins et al. 2015, Yamamoto et al.		PFBS treatments significantly increased the protein and mRNA levels of the master transcription factors in adipocyte differentiation; CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ), along with acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), the key proteins in lipogenesis.                                                                                                                                                                                   Previously, PFASs, particularly PFOS and perfluorooctanoic acid (PFOA), were reported to promote adipogenesis in 3T3-L1 adipocytes with increased expression of adipogenic genes, including CCAAT/enhancer-binding protein alpha (C/EBPα), peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid binding protein 4 (FABP4) and lipoprotein lipase (LPL) (Watkins et al. 2015, Yamamoto et al.	Immunohistochemical staining	PFBS treatments significantly increased the protein and mRNA levels of the master transcription factors in adipocyte differentiation; CCAAT/enhancer-binding protein α (C/EBPα) and peroxisome proliferator-activated receptor gamma (PPARγ), along with acetyl-CoA carboxylase (ACC) and fatty acid synthase (FAS), the key proteins in lipogenesis.                                                                                                                                                                                   Previously, PFASs, particularly PFOS and perfluorooctanoic acid (PFOA), were reported to promote adipogenesis in 3T3-L1 adipocytes with increased expression of adipogenic genes, including CCAAT/enhancer-binding protein alpha (C/EBPα), peroxisome proliferator-activated receptor gamma (PPARγ), fatty acid binding protein 4 (FABP4) and lipoprotein lipase (LPL) (Watkins et al. 2015, Yamamoto et al.			q-PCR,MTT法,Immunoblotting,western blot				FABP4
30030400	chr7	148804570	148806570	EZH2	Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.	mouse		High+Lowthroughput	EZH2 Methyltransferase Activity Controls Pten Expression and mTOR Signaling during Fear Memory Reconsolidation	否				E_02_0519	ELISA, real-time PCR, Wesern blot, statistical analysis	Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.		Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.	Immunohistochemical staining	Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.			ELISA,real-time PCR,wesern blot,统计分析				EZH2
30030400	chr10	87859745	87861745	PTEN	Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.	mouse		High+Lowthroughput	EZH2 Methyltransferase Activity Controls Pten Expression and mTOR Signaling during Fear Memory Reconsolidation	否				E_02_0519	ELISA, real-time PCR, Wesern blot, statistical analysis	Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.		Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.	Immunohistochemical staining	Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.			ELISA,real-time PCR,wesern blot,统计分析				PTEN
30030400	chr16	2535290	2537290	PDPK1	Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.	mouse		High+Lowthroughput	EZH2 Methyltransferase Activity Controls Pten Expression and mTOR Signaling during Fear Memory Reconsolidation	否				E_02_0519	ELISA, real-time PCR, Wesern blot, statistical analysis	Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.		Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.	Immunohistochemical staining	Here, we found that in male rats retrieval of a contextual fear memory transiently increased Enhancer of Zeste Homolog 2 (EZH2) levels along with increased histone H3 lysine 27 trimethylation (H3K27me3) levels, which correlated with decreased levels of phosphatase and tensin homolog (PTEN), a potent inhibitor of AKT mTOR-dependent signaling in the hippocampus. Further experiments found increased H3K27me3 levels and DNA methylation across the Pten promoter and coding regions, indicating transcriptional silencing of the Pten gene.                                                                                                                                                                                                                                   In this pathway, PI3K phosphorylates phosphatidylinositol(3,4,5)-trisphosphate (PIP3), which regulates the phosphorylation of AKT through PDPK1.			ELISA,real-time PCR,wesern blot,统计分析				PDPK1
30029004	chr1	50020990	50022990	ELAVL4	Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).	human,mouse		High+Lowthroughput	HuD Is a Neural Translation Enhancer Acting on mTORC1-Responsive Genes and Counteracted by the Y3 Small Non-coding RNA	否		Neuroblastoma, amyotrophic lateral sclerosis (ALS)	NSC-34 cell	E_02_0520	RT qPCR, immunofluorescence staining, RNA SEQ, pol SEQ, northern, Western blot, statistical analysis	Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).		Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).	Immunohistochemical staining	Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).			RT-qPCR,免疫荧光染色,RNA-Seq,POL-Seq,Northern,western blot,统计分析				ELAVL4
30029004	chr9	23687095	23689095	ELAVL2	Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).	human,mouse		High+Lowthroughput	HuD Is a Neural Translation Enhancer Acting on mTORC1-Responsive Genes and Counteracted by the Y3 Small Non-coding RNA	否		Neuroblastoma, amyotrophic lateral sclerosis (ALS)	NSC-34 cell	E_02_0520	RT qPCR, immunofluorescence staining, RNA SEQ, pol SEQ, northern, Western blot, statistical analysis	Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).		Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).	Immunohistochemical staining	Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).			RT-qPCR,免疫荧光染色,RNA-Seq,POL-Seq,Northern,western blot,统计分析				ELAVL2
30029004	chr19	7956135	7958135	ELAVL1	Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).	human,mouse		High+Lowthroughput	HuD Is a Neural Translation Enhancer Acting on mTORC1-Responsive Genes and Counteracted by the Y3 Small Non-coding RNA	否		Neuroblastoma, amyotrophic lateral sclerosis (ALS)	NSC-34 cell	E_02_0520	RT qPCR, immunofluorescence staining, RNA SEQ, pol SEQ, northern, Western blot, statistical analysis	Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).		Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).	Immunohistochemical staining	Object name is fx1.jpg Go to: Introduction The intensively studied RNA-binding protein (RBP) human antigen D (HuD)/embryonic lethal, abnormal vision like 4 (ELAVL4) is predominantly expressed in differentiated neurons, as are the other neuronal members (nELAV) of the ELAV family, HuB (ELAVL2) and HuC (ELAVL3). In contrast, HuR (ELAVL1) is ubiquitously expressed (Pascale et al., 2008).			RT-qPCR,免疫荧光染色,RNA-Seq,POL-Seq,Northern,western blot,统计分析				ELAVL1
30026867	chr16	4253924	4255924	TFAP4	It has been reported that the transcription factor activating enhancer-binding protein 4 (TFAP4) is upregulated and associated with an aggressive phenotype in several cancers.                                                                                                                                        Mechanistically, we demonstrated that TFAP4 played an important role in activating Wnt/β-catenin signaling by directly binding to the promoters of DVL1 (dishevelled segment polarity protein 1) and LEF1 (lymphoid enhancer binding factor 1). 	human		High+Lowthroughput	Transcription factor AP-4 promotes tumorigenic capability and activates the Wnt/β-catenin pathway in hepatocellular carcinoma	否		Hepatocellular carcinoma	HCC cell	E_01_0796	Western blot, immunohistochemistry, chip qPCR, flow cytometry, statistical analysis	It has been reported that the transcription factor activating enhancer-binding protein 4 (TFAP4) is upregulated and associated with an aggressive phenotype in several cancers.                                                                                                                                        Mechanistically, we demonstrated that TFAP4 played an important role in activating Wnt/β-catenin signaling by directly binding to the promoters of DVL1 (dishevelled segment polarity protein 1) and LEF1 (lymphoid enhancer binding factor 1). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			It has been reported that the transcription factor activating enhancer-binding protein 4 (TFAP4) is upregulated and associated with an aggressive phenotype in several cancers.                                                                                                                                        Mechanistically, we demonstrated that TFAP4 played an important role in activating Wnt/β-catenin signaling by directly binding to the promoters of DVL1 (dishevelled segment polarity protein 1) and LEF1 (lymphoid enhancer binding factor 1). 	Immunohistochemical staining	It has been reported that the transcription factor activating enhancer-binding protein 4 (TFAP4) is upregulated and associated with an aggressive phenotype in several cancers.                                                                                                                                        Mechanistically, we demonstrated that TFAP4 played an important role in activating Wnt/β-catenin signaling by directly binding to the promoters of DVL1 (dishevelled segment polarity protein 1) and LEF1 (lymphoid enhancer binding factor 1). 	TFAP4		western blot,Immunohistochemistry,ChIP-qPCR,流式细胞术,统计分析	It has been reported that the transcription factor activating enhancer-binding protein 4 (TFAP4) is upregulated and associated with an aggressive phenotype in several cancers.                                                                                                                                        Mechanistically, we demonstrated that TFAP4 played an important role in activating Wnt/β-catenin signaling by directly binding to the promoters of DVL1 (dishevelled segment polarity protein 1) and LEF1 (lymphoid enhancer binding factor 1). 			
30026867	chr4	108044809	108046809	LEF1	It has been reported that the transcription factor activating enhancer-binding protein 4 (TFAP4) is upregulated and associated with an aggressive phenotype in several cancers.                                                                                                                                        Mechanistically, we demonstrated that TFAP4 played an important role in activating Wnt/β-catenin signaling by directly binding to the promoters of DVL1 (dishevelled segment polarity protein 1) and LEF1 (lymphoid enhancer binding factor 1). 	human		High+Lowthroughput	Transcription factor AP-4 promotes tumorigenic capability and activates the Wnt/β-catenin pathway in hepatocellular carcinoma	否		Hepatocellular carcinoma	HCC cell	E_01_0796	Western blot, immunohistochemistry, chip qPCR, flow cytometry, statistical analysis	It has been reported that the transcription factor activating enhancer-binding protein 4 (TFAP4) is upregulated and associated with an aggressive phenotype in several cancers.                                                                                                                                        Mechanistically, we demonstrated that TFAP4 played an important role in activating Wnt/β-catenin signaling by directly binding to the promoters of DVL1 (dishevelled segment polarity protein 1) and LEF1 (lymphoid enhancer binding factor 1). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			It has been reported that the transcription factor activating enhancer-binding protein 4 (TFAP4) is upregulated and associated with an aggressive phenotype in several cancers.                                                                                                                                        Mechanistically, we demonstrated that TFAP4 played an important role in activating Wnt/β-catenin signaling by directly binding to the promoters of DVL1 (dishevelled segment polarity protein 1) and LEF1 (lymphoid enhancer binding factor 1). 	Immunohistochemical staining	It has been reported that the transcription factor activating enhancer-binding protein 4 (TFAP4) is upregulated and associated with an aggressive phenotype in several cancers.                                                                                                                                        Mechanistically, we demonstrated that TFAP4 played an important role in activating Wnt/β-catenin signaling by directly binding to the promoters of DVL1 (dishevelled segment polarity protein 1) and LEF1 (lymphoid enhancer binding factor 1). 	LEF1		western blot,Immunohistochemistry,ChIP-qPCR,流式细胞术,统计分析	It has been reported that the transcription factor activating enhancer-binding protein 4 (TFAP4) is upregulated and associated with an aggressive phenotype in several cancers.                                                                                                                                        Mechanistically, we demonstrated that TFAP4 played an important role in activating Wnt/β-catenin signaling by directly binding to the promoters of DVL1 (dishevelled segment polarity protein 1) and LEF1 (lymphoid enhancer binding factor 1). 			
30026326	chr12	50760530	50762530	ATF1	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	human		High+Lowthroughput	A Rare Missense Variant in TCF7L2 Associates with Colorectal Cancer Risk by Interacting with a GWAS-Identified Regulatory Variant in the MYC Enhancer	是	rs111169571,rs138649767,rs6983267	Colorectal cancer (CRC)		E_01_0797	ATF1 ChIP-seq,PCR	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	Immunohistochemical staining	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	ATF1		ATF1 ChIP-seq,PCR	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           			
30026326	chr10	112947225	112949225	TCF7L2	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	human		High+Lowthroughput	A Rare Missense Variant in TCF7L2 Associates with Colorectal Cancer Risk by Interacting with a GWAS-Identified Regulatory Variant in the MYC Enhancer	是	rs111169571,rs138649767,rs6983267	Colorectal cancer (CRC)		E_01_0797	ATF1 ChIP-seq,PCR	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	Immunohistochemical staining	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	TCF7L2		ATF1 ChIP-seq,PCR	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           			
30026326	chr1	114702192	114704192	NRAS	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	human		High+Lowthroughput	A Rare Missense Variant in TCF7L2 Associates with Colorectal Cancer Risk by Interacting with a GWAS-Identified Regulatory Variant in the MYC Enhancer	是	rs111169571,rs138649767,rs6983267	Colorectal cancer (CRC)		E_01_0797	ATF1 ChIP-seq,PCR	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           		We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	Immunohistochemical staining	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           			ATF1 ChIP-seq,PCR				NRAS
30026326	chr8	127732598	127734598	MYC	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	human		High+Lowthroughput	A Rare Missense Variant in TCF7L2 Associates with Colorectal Cancer Risk by Interacting with a GWAS-Identified Regulatory Variant in the MYC Enhancer	是	rs111169571,rs138649767,rs6983267	Colorectal cancer (CRC)		E_01_0797	ATF1 ChIP-seq,PCR	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	Immunohistochemical staining	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	MYC		ATF1 ChIP-seq,PCR	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           			
30026326	chr7	140716665	140718665	BRAF	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	human		High+Lowthroughput	A Rare Missense Variant in TCF7L2 Associates with Colorectal Cancer Risk by Interacting with a GWAS-Identified Regulatory Variant in the MYC Enhancer	是	rs111169571,rs138649767,rs6983267	Colorectal cancer (CRC)		E_01_0797	ATF1 ChIP-seq,PCR	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	Immunohistochemical staining	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           	BRAF		ATF1 ChIP-seq,PCR	We found a significant interaction between the TCF7L2 missense48 variant rs138649767 and a previous GWAS-identified regulatory variant rs6983267 in the49 MYC enhancer (Pinteraction = 0.0002).                                  Functional analysis of this variant revealed that50 TCF7L2 with rs138649767-A allele harbored the ability to activate the MYC enhancer with51 rs6983267-G allele and enhance CRC cell proliferation.                                            Further ChIP-seq and gene co-expression analyses showed that54 oncogenes NRAS and BRAF were activated by ATF1 in CRC.                                                           			
30026272	chr9	32544664	32546664	Ets1	Approach and Results We screened various combinations of transcription factors, including Myocd, Mef2C, Mef2B, Mkl1, Gata4, Gata5, Gata6, Ets1, and their corresponding carboxyterminal fusions to the transactivation domain of MyoD indicated by *-, for their effects on reprogramming mouse embryonic fibroblasts (MEFs) and human adult dermal fibroblasts (hFBs) to the smooth muscle cell fate as determined by the expression of specific markers.	mouse,human		High+Lowthroughput	Direct Reprogramming of Fibroblasts Into Smooth Muscle-Like Cells With Defined Transcription Factors-Brief Report	否		inflammation	smooth muscle cell	E_02_0521	QRT PCR, immunofluorescence staining, statistical analysis	Approach and Results We screened various combinations of transcription factors, including Myocd, Mef2C, Mef2B, Mkl1, Gata4, Gata5, Gata6, Ets1, and their corresponding carboxyterminal fusions to the transactivation domain of MyoD indicated by *-, for their effects on reprogramming mouse embryonic fibroblasts (MEFs) and human adult dermal fibroblasts (hFBs) to the smooth muscle cell fate as determined by the expression of specific markers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Approach and Results We screened various combinations of transcription factors, including Myocd, Mef2C, Mef2B, Mkl1, Gata4, Gata5, Gata6, Ets1, and their corresponding carboxyterminal fusions to the transactivation domain of MyoD indicated by *-, for their effects on reprogramming mouse embryonic fibroblasts (MEFs) and human adult dermal fibroblasts (hFBs) to the smooth muscle cell fate as determined by the expression of specific markers.		Approach and Results We screened various combinations of transcription factors, including Myocd, Mef2C, Mef2B, Mkl1, Gata4, Gata5, Gata6, Ets1, and their corresponding carboxyterminal fusions to the transactivation domain of MyoD indicated by *-, for their effects on reprogramming mouse embryonic fibroblasts (MEFs) and human adult dermal fibroblasts (hFBs) to the smooth muscle cell fate as determined by the expression of specific markers.	Immunohistochemical staining	Approach and Results We screened various combinations of transcription factors, including Myocd, Mef2C, Mef2B, Mkl1, Gata4, Gata5, Gata6, Ets1, and their corresponding carboxyterminal fusions to the transactivation domain of MyoD indicated by *-, for their effects on reprogramming mouse embryonic fibroblasts (MEFs) and human adult dermal fibroblasts (hFBs) to the smooth muscle cell fate as determined by the expression of specific markers.			qRT-PCR,免疫荧光染色,统计分析				Ets1
30026272	chr14	63433722	63435722	Gata4	Approach and Results We screened various combinations of transcription factors, including Myocd, Mef2C, Mef2B, Mkl1, Gata4, Gata5, Gata6, Ets1, and their corresponding carboxyterminal fusions to the transactivation domain of MyoD indicated by *-, for their effects on reprogramming mouse embryonic fibroblasts (MEFs) and human adult dermal fibroblasts (hFBs) to the smooth muscle cell fate as determined by the expression of specific markers.	mouse,human		High+Lowthroughput	Direct Reprogramming of Fibroblasts Into Smooth Muscle-Like Cells With Defined Transcription Factors-Brief Report	否		inflammation	smooth muscle cell	E_02_0521	QRT PCR, immunofluorescence staining, statistical analysis	Approach and Results We screened various combinations of transcription factors, including Myocd, Mef2C, Mef2B, Mkl1, Gata4, Gata5, Gata6, Ets1, and their corresponding carboxyterminal fusions to the transactivation domain of MyoD indicated by *-, for their effects on reprogramming mouse embryonic fibroblasts (MEFs) and human adult dermal fibroblasts (hFBs) to the smooth muscle cell fate as determined by the expression of specific markers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Approach and Results We screened various combinations of transcription factors, including Myocd, Mef2C, Mef2B, Mkl1, Gata4, Gata5, Gata6, Ets1, and their corresponding carboxyterminal fusions to the transactivation domain of MyoD indicated by *-, for their effects on reprogramming mouse embryonic fibroblasts (MEFs) and human adult dermal fibroblasts (hFBs) to the smooth muscle cell fate as determined by the expression of specific markers.		Approach and Results We screened various combinations of transcription factors, including Myocd, Mef2C, Mef2B, Mkl1, Gata4, Gata5, Gata6, Ets1, and their corresponding carboxyterminal fusions to the transactivation domain of MyoD indicated by *-, for their effects on reprogramming mouse embryonic fibroblasts (MEFs) and human adult dermal fibroblasts (hFBs) to the smooth muscle cell fate as determined by the expression of specific markers.	Immunohistochemical staining	Approach and Results We screened various combinations of transcription factors, including Myocd, Mef2C, Mef2B, Mkl1, Gata4, Gata5, Gata6, Ets1, and their corresponding carboxyterminal fusions to the transactivation domain of MyoD indicated by *-, for their effects on reprogramming mouse embryonic fibroblasts (MEFs) and human adult dermal fibroblasts (hFBs) to the smooth muscle cell fate as determined by the expression of specific markers.			qRT-PCR,免疫荧光染色,统计分析				Gata4
30022673	chr4	109910279	109912279	EGF	The immortalised cells were routinely propagated in Opti-MEM, supplemented with 4% v/v fetal bovine serum (FBS), 2mM L-glutamine, 2mM GlutaMAX, 10mM 4-(2-hydroxyethyl)-1-piperazineethanesul- phonic acid (HEPES), 20ng/ml Epidermal Growth Factor (EGF), 10 g/ml insulin, and 150nM hydrocor- tisone, and were incubated at 32 C, 6% v/v CO 2 in a humidified atmosphere.	human		High+Lowthroughput	Characterisation of a canine epithelial cell line for modelling the intestinal barrier	否		Colorectal Adenocarcinoma 	Caco-2 cell	E_01_0798	NF -  B assay, flow cytometry, statistical analysis, immunofluorescence staining	The immortalised cells were routinely propagated in Opti-MEM, supplemented with 4% v/v fetal bovine serum (FBS), 2mM L-glutamine, 2mM GlutaMAX, 10mM 4-(2-hydroxyethyl)-1-piperazineethanesul- phonic acid (HEPES), 20ng/ml Epidermal Growth Factor (EGF), 10 g/ml insulin, and 150nM hydrocor- tisone, and were incubated at 32 C, 6% v/v CO 2 in a humidified atmosphere.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The immortalised cells were routinely propagated in Opti-MEM, supplemented with 4% v/v fetal bovine serum (FBS), 2mM L-glutamine, 2mM GlutaMAX, 10mM 4-(2-hydroxyethyl)-1-piperazineethanesul- phonic acid (HEPES), 20ng/ml Epidermal Growth Factor (EGF), 10 g/ml insulin, and 150nM hydrocor- tisone, and were incubated at 32 C, 6% v/v CO 2 in a humidified atmosphere.	Immunohistochemical staining	The immortalised cells were routinely propagated in Opti-MEM, supplemented with 4% v/v fetal bovine serum (FBS), 2mM L-glutamine, 2mM GlutaMAX, 10mM 4-(2-hydroxyethyl)-1-piperazineethanesul- phonic acid (HEPES), 20ng/ml Epidermal Growth Factor (EGF), 10 g/ml insulin, and 150nM hydrocor- tisone, and were incubated at 32 C, 6% v/v CO 2 in a humidified atmosphere.	EGF		NF-B assay,流式细胞术,统计分析,免疫荧光染色	The immortalised cells were routinely propagated in Opti-MEM, supplemented with 4% v/v fetal bovine serum (FBS), 2mM L-glutamine, 2mM GlutaMAX, 10mM 4-(2-hydroxyethyl)-1-piperazineethanesul- phonic acid (HEPES), 20ng/ml Epidermal Growth Factor (EGF), 10 g/ml insulin, and 150nM hydrocor- tisone, and were incubated at 32 C, 6% v/v CO 2 in a humidified atmosphere.			
30021904	chr4	26160604	26162604	RBPJ	We demonstrate that EBNA2 can activate IRF4 and miR-155HG expression through specific upstream enhancers that are dependent on the Notch signaling transcription factor RBPJ, a known binding partner of EBNA2.	human,mouse,Epstein,Barr,virus,(EBV)		High+Lowthroughput	Enhancer Control of MicroRNA miR-155 Expression in Epstein-Barr Virus-Infected B Cells	否		Malignancy	B cell	E_02_0522	SDS-PAGE and Western blotting,ChIP-QPCR,RT-QPCR,western blot	We demonstrate that EBNA2 can activate IRF4 and miR-155HG expression through specific upstream enhancers that are dependent on the Notch signaling transcription factor RBPJ, a known binding partner of EBNA2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We demonstrate that EBNA2 can activate IRF4 and miR-155HG expression through specific upstream enhancers that are dependent on the Notch signaling transcription factor RBPJ, a known binding partner of EBNA2.		We demonstrate that EBNA2 can activate IRF4 and miR-155HG expression through specific upstream enhancers that are dependent on the Notch signaling transcription factor RBPJ, a known binding partner of EBNA2.	Immunohistochemical staining	We demonstrate that EBNA2 can activate IRF4 and miR-155HG expression through specific upstream enhancers that are dependent on the Notch signaling transcription factor RBPJ, a known binding partner of EBNA2.			SDS-PAGE and Western blotting,ChIP-QPCR,RT-QPCR,western blot				RBPJ
30021842	chr17	72118219	72120219	SOX9	SOX9 controls cell lineage fate and differentiation in major biological processes.                                                                                                                                                                                                                                                                                                                                                                                                                                           By profiling the whole transcriptome and the whole epigenome of wild-type and Sox9-deficient mouse embryo limb buds, we uncover multiple structural and regulatory genes, including Fam101a, Myh14, Sema3c and Sema3d, as specific markers of precartilaginous condensation, and we provide evidence of their direct transactivation by SOX9.	mouse		High+Lowthroughput	SOX9 is dispensable for the initiation of epigenetic remodeling and the activation of marker genes at the onset of chondrogenesis	否		Osteoarthritis	chondroblast	E_02_0523	RNA-seq,qRT-PCR,ChIP-seq	SOX9 controls cell lineage fate and differentiation in major biological processes.                                                                                                                                                                                                                                                                                                                                                                                                                                           By profiling the whole transcriptome and the whole epigenome of wild-type and Sox9-deficient mouse embryo limb buds, we uncover multiple structural and regulatory genes, including Fam101a, Myh14, Sema3c and Sema3d, as specific markers of precartilaginous condensation, and we provide evidence of their direct transactivation by SOX9.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SOX9 controls cell lineage fate and differentiation in major biological processes.                                                                                                                                                                                                                                                                                                                                                                                                                                           By profiling the whole transcriptome and the whole epigenome of wild-type and Sox9-deficient mouse embryo limb buds, we uncover multiple structural and regulatory genes, including Fam101a, Myh14, Sema3c and Sema3d, as specific markers of precartilaginous condensation, and we provide evidence of their direct transactivation by SOX9.		SOX9 controls cell lineage fate and differentiation in major biological processes.                                                                                                                                                                                                                                                                                                                                                                                                                                           By profiling the whole transcriptome and the whole epigenome of wild-type and Sox9-deficient mouse embryo limb buds, we uncover multiple structural and regulatory genes, including Fam101a, Myh14, Sema3c and Sema3d, as specific markers of precartilaginous condensation, and we provide evidence of their direct transactivation by SOX9.	Immunohistochemical staining	SOX9 controls cell lineage fate and differentiation in major biological processes.                                                                                                                                                                                                                                                                                                                                                                                                                                           By profiling the whole transcriptome and the whole epigenome of wild-type and Sox9-deficient mouse embryo limb buds, we uncover multiple structural and regulatory genes, including Fam101a, Myh14, Sema3c and Sema3d, as specific markers of precartilaginous condensation, and we provide evidence of their direct transactivation by SOX9.			RNA-seq,qRT-PCR,ChIP-seq				SOX9
30021842	chr7	44252476	44254476	Myh14	SOX9 controls cell lineage fate and differentiation in major biological processes.                                                                                                                                                                                                                                                                                                                                                                                                                                           By profiling the whole transcriptome and the whole epigenome of wild-type and Sox9-deficient mouse embryo limb buds, we uncover multiple structural and regulatory genes, including Fam101a, Myh14, Sema3c and Sema3d, as specific markers of precartilaginous condensation, and we provide evidence of their direct transactivation by SOX9.	mouse		High+Lowthroughput	SOX9 is dispensable for the initiation of epigenetic remodeling and the activation of marker genes at the onset of chondrogenesis	否		Osteoarthritis	chondroblast	E_02_0523	RNA-seq,qRT-PCR,ChIP-seq	SOX9 controls cell lineage fate and differentiation in major biological processes.                                                                                                                                                                                                                                                                                                                                                                                                                                           By profiling the whole transcriptome and the whole epigenome of wild-type and Sox9-deficient mouse embryo limb buds, we uncover multiple structural and regulatory genes, including Fam101a, Myh14, Sema3c and Sema3d, as specific markers of precartilaginous condensation, and we provide evidence of their direct transactivation by SOX9.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SOX9 controls cell lineage fate and differentiation in major biological processes.                                                                                                                                                                                                                                                                                                                                                                                                                                           By profiling the whole transcriptome and the whole epigenome of wild-type and Sox9-deficient mouse embryo limb buds, we uncover multiple structural and regulatory genes, including Fam101a, Myh14, Sema3c and Sema3d, as specific markers of precartilaginous condensation, and we provide evidence of their direct transactivation by SOX9.		SOX9 controls cell lineage fate and differentiation in major biological processes.                                                                                                                                                                                                                                                                                                                                                                                                                                           By profiling the whole transcriptome and the whole epigenome of wild-type and Sox9-deficient mouse embryo limb buds, we uncover multiple structural and regulatory genes, including Fam101a, Myh14, Sema3c and Sema3d, as specific markers of precartilaginous condensation, and we provide evidence of their direct transactivation by SOX9.	Immunohistochemical staining	SOX9 controls cell lineage fate and differentiation in major biological processes.                                                                                                                                                                                                                                                                                                                                                                                                                                           By profiling the whole transcriptome and the whole epigenome of wild-type and Sox9-deficient mouse embryo limb buds, we uncover multiple structural and regulatory genes, including Fam101a, Myh14, Sema3c and Sema3d, as specific markers of precartilaginous condensation, and we provide evidence of their direct transactivation by SOX9.			RNA-seq,qRT-PCR,ChIP-seq				Myh14
30021349	chr7	27195996	27197996	HOTTIP	Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	human		High+Lowthroughput	Long non-coding RNA HOTTIP is upregulated in renal cell carcinoma and regulates cell growth and apoptosis by epigenetically silencing of LATS2	否		Renal cell carcinoma (RCC)	OS-RC2 cell	E_01_0799	RT qPCR, chromatin immunoprecipitation (chip) analysis, Western blot, statistical analysis, immunoblotting analysis	Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.		Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	Immunohistochemical staining	Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.			RT-qPCR,Chromatin immunoprecipitation (ChIP) analysi,western blot,统计分析,Immunoblotting analysis				HOTTIP
30021349	chr7	148804343	148806343	EZH2	Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	human		High+Lowthroughput	Long non-coding RNA HOTTIP is upregulated in renal cell carcinoma and regulates cell growth and apoptosis by epigenetically silencing of LATS2	否		Renal cell carcinoma (RCC)	OS-RC2 cell	E_01_0799	RT qPCR, chromatin immunoprecipitation (chip) analysis, Western blot, statistical analysis, immunoblotting analysis	Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	Immunohistochemical staining	Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	EZH2		RT-qPCR,Chromatin immunoprecipitation (ChIP) analysi,western blot,统计分析,Immunoblotting analysis	Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.			
30021349	chr13	20970300	20972300	LATS2	Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	human		High+Lowthroughput	Long non-coding RNA HOTTIP is upregulated in renal cell carcinoma and regulates cell growth and apoptosis by epigenetically silencing of LATS2	否		Renal cell carcinoma (RCC)	OS-RC2 cell	E_01_0799	RT qPCR, chromatin immunoprecipitation (chip) analysis, Western blot, statistical analysis, immunoblotting analysis	Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.		Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.	Immunohistochemical staining	Specifically, HOTTIP is upregulated and exerts oncogenic properties in some cancers.                                                                                                                                                                                                                                                                                                                                                       The mechanistic investigations showed that HOTTIP could bind to enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1), thereby repressing LATS2 expression.			RT-qPCR,Chromatin immunoprecipitation (ChIP) analysi,western blot,统计分析,Immunoblotting analysis				LATS2
30018722	chr9	104777916	104779916	ABCA1	Furthermore, dramatically increased the expression of Fc receptors (FcR) on peripheral blood mononuclear macrophages, suggesting that the mechanism of phagocytosis of ox-LDL by mononuclear macrophages may rely more on FcR than the cluster of differentiation 36 (CD36) scavenger receptor with P210-Ab. Both in vitro and in vivo, P210-Ab triggered the promoter of ATP-binding cassette transporter A1 (ABCA1) to increase peroxisome proliferator-activated receptor alpha (α) activity and inhibit the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway.	mouse,human		High+Lowthroughput	Apolipoprotein B-100 peptide 210 antibody inhibits atherosclerosis by regulation of macrophages that phagocytize oxidized lipid	否		atherosclerosis	macrophage	E_02_0524	ELISA, Western blot, immunohistochemistry, flow cytometry, immunofluorescence staining, oil-red-O staining, statistical analysis	Furthermore, dramatically increased the expression of Fc receptors (FcR) on peripheral blood mononuclear macrophages, suggesting that the mechanism of phagocytosis of ox-LDL by mononuclear macrophages may rely more on FcR than the cluster of differentiation 36 (CD36) scavenger receptor with P210-Ab. Both in vitro and in vivo, P210-Ab triggered the promoter of ATP-binding cassette transporter A1 (ABCA1) to increase peroxisome proliferator-activated receptor alpha (α) activity and inhibit the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, dramatically increased the expression of Fc receptors (FcR) on peripheral blood mononuclear macrophages, suggesting that the mechanism of phagocytosis of ox-LDL by mononuclear macrophages may rely more on FcR than the cluster of differentiation 36 (CD36) scavenger receptor with P210-Ab. Both in vitro and in vivo, P210-Ab triggered the promoter of ATP-binding cassette transporter A1 (ABCA1) to increase peroxisome proliferator-activated receptor alpha (α) activity and inhibit the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway.		Furthermore, dramatically increased the expression of Fc receptors (FcR) on peripheral blood mononuclear macrophages, suggesting that the mechanism of phagocytosis of ox-LDL by mononuclear macrophages may rely more on FcR than the cluster of differentiation 36 (CD36) scavenger receptor with P210-Ab. Both in vitro and in vivo, P210-Ab triggered the promoter of ATP-binding cassette transporter A1 (ABCA1) to increase peroxisome proliferator-activated receptor alpha (α) activity and inhibit the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway.	Immunohistochemical staining	Furthermore, dramatically increased the expression of Fc receptors (FcR) on peripheral blood mononuclear macrophages, suggesting that the mechanism of phagocytosis of ox-LDL by mononuclear macrophages may rely more on FcR than the cluster of differentiation 36 (CD36) scavenger receptor with P210-Ab. Both in vitro and in vivo, P210-Ab triggered the promoter of ATP-binding cassette transporter A1 (ABCA1) to increase peroxisome proliferator-activated receptor alpha (α) activity and inhibit the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway.			ELISA,Western blot,Immunohistochemistry,流式细胞术,免疫荧光染色,Oil-red-O staining,统计分析				ABCA1
30017589	chr13	30108722	30109111	GRHL2	Here, we show the transcription factor GRHL2 is necessary and sufficient to activate an epithelial subset of enhancers as naïve embryonic stem cells (ESCs) transition into formative epiblast-like cells (EpiLCs).	mouse		Low+High throughput	GRHL2-Dependent Enhancer Switching Maintains a Pluripotent Stem Cell Transcriptional Subnetwork after Exit from Naive Pluripotency	否	--	--	stem cell	E_02_0525	ChIP-seq	Our findings were corroborated by H3K4me1 and H3K27ac ChIP-seq data from an alternative na?ve-to-formative differentiation system. As a control, we found little change in these marks at SMC1 sites common to both states. These results indicate that GRHL2 binding correlates with full enhancer activation, suggesting a role for GRHL2 not only in regulation of cohesin binding, but also in regulation of other crucial steps in enhancer activation.Together, these results suggest that our SMC1 ChIP-seq data reflect changing enhancer activity and that cohesin binding at enhancers is highly dynamic during the ESC to EpiLC transition.	Enhancer	CRISPR/Cas9	ChIP-seq,qRT-PCR	We then assessed the effects of each Enhancer deletion on Dsp expression in ES cells and EpiLCs by qRT-PCR.Indeed, we found that deletion of one or both KLF4-bound enhancers led to a significant reduction in Dsp expression in ESCs but had no effect in EpiLCs(Figure 6B). Conversely, deletion of the GRHL2-bound enhancer resulted in significantly reduced Dsp expression in the EpiLC state but had no effect in ESCs (Figure 6B). We observed similar state-specific reductions in target gene expression with deletions of the KLF4-bound and GRHL2-bound enhancers at the Cdh1 and Jam1 loci (Figure 6C and D, S6A and B).	2300002E22Rik,5730453H04Rik,AA407887,AA407888,AW109828,DP,rul	GRHL2 therefore control over a subset of the naive network via Enhancer switching to maintain expression of epithelial genes upon exit from naive pluripotency	ChIP-seq	Together,these results suggest that our SMC1 ChIP-seq data reflect changing Enhancer activity and that cohesin binding at Enhancers is highly dynamic during the ESC to EpiLC transition.	Grhl2	0610015A08Rik,BOM,Tcfcp2l3,clft3	ChIP-seq,ATAC-seq	Given the strong association between GRHL2 binding and various events in enhancer activation, we asked whether GRHL2 binding is necessary for each of these events. To address this question, we assessed levels of each active enhancer mark in wildtype and GHRL2 KO EpiLCs by performing ATAC-seq and ChIP-seq for H3K4me1, H3K27ac, and SMC1. There was a strong reduction in all active enhancer marks (chromatin accessibility, H3K4me1, H3K27ac, and SMC1 levels) at GRHL2 sites in GRHL2 KO EpiLCs, suggesting a near complete block in enhancer activation in the absence of GRHL2. Together, these results indicate an absolute requirement for GRHL2 for enhancer activation specifically at its target sites.	--	--	Dsp
30017589	chr13	30108722	30109111	KLF2	Here, we show the transcription factor GRHL2 is necessary and sufficient to activate an epithelial subset of enhancers as naïve embryonic stem cells (ESCs) transition into formative epiblast-like cells (EpiLCs).	mouse		Low+High throughput	GRHL2-Dependent Enhancer Switching Maintains a Pluripotent Stem Cell Transcriptional Subnetwork after Exit from Naive Pluripotency	否	--	--	stem cell	E_02_0525	ChIP-seq	Our findings were corroborated by H3K4me1 and H3K27ac ChIP-seq data from an alternative na?ve-to-formative differentiation system. As a control, we found little change in these marks at SMC1 sites common to both states. These results indicate that GRHL2 binding correlates with full enhancer activation, suggesting a role for GRHL2 not only in regulation of cohesin binding, but also in regulation of other crucial steps in enhancer activation.Together, these results suggest that our SMC1 ChIP-seq data reflect changing enhancer activity and that cohesin binding at enhancers is highly dynamic during the ESC to EpiLC transition.	Enhancer	CRISPR/Cas9	ChIP-seq,qRT-PCR	We then assessed the effects of each Enhancer deletion on Dsp expression in ES cells and EpiLCs by qRT-PCR.Indeed, we found that deletion of one or both KLF4-bound enhancers led to a significant reduction in Dsp expression in ESCs but had no effect in EpiLCs(Figure 6B). Conversely, deletion of the GRHL2-bound enhancer resulted in significantly reduced Dsp expression in the EpiLC state but had no effect in ESCs (Figure 6B). We observed similar state-specific reductions in target gene expression with deletions of the KLF4-bound and GRHL2-bound enhancers at the Cdh1 and Jam1 loci (Figure 6C and D, S6A and B).	2300002E22Rik,5730453H04Rik,AA407887,AA407888,AW109828,DP,rul	GRHL2 therefore control over a subset of the naive network via Enhancer switching to maintain expression of epithelial genes upon exit from naive pluripotency	ChIP-seq	Together,these results suggest that our SMC1 ChIP-seq data reflect changing Enhancer activity and that cohesin binding at Enhancers is highly dynamic during the ESC to EpiLC transition.	Grhl2	0610015A08Rik,BOM,Tcfcp2l3,clft3	ChIP-seq,ATAC-seq	Given the strong association between GRHL2 binding and various events in enhancer activation, we asked whether GRHL2 binding is necessary for each of these events. To address this question, we assessed levels of each active enhancer mark in wildtype and GHRL2 KO EpiLCs by performing ATAC-seq and ChIP-seq for H3K4me1, H3K27ac, and SMC1. There was a strong reduction in all active enhancer marks (chromatin accessibility, H3K4me1, H3K27ac, and SMC1 levels) at GRHL2 sites in GRHL2 KO EpiLCs, suggesting a near complete block in enhancer activation in the absence of GRHL2. Together, these results indicate an absolute requirement for GRHL2 for enhancer activation specifically at its target sites.	--	--	Dsp
30017589	chr13	30108722	30109111	KLF4	Here, we show the transcription factor GRHL2 is necessary and sufficient to activate an epithelial subset of enhancers as naïve embryonic stem cells (ESCs) transition into formative epiblast-like cells (EpiLCs).	mouse		Low+High throughput	GRHL2-Dependent Enhancer Switching Maintains a Pluripotent Stem Cell Transcriptional Subnetwork after Exit from Naive Pluripotency	否	--	--	stem cell	E_02_0525	ChIP-seq	Our findings were corroborated by H3K4me1 and H3K27ac ChIP-seq data from an alternative na?ve-to-formative differentiation system. As a control, we found little change in these marks at SMC1 sites common to both states. These results indicate that GRHL2 binding correlates with full enhancer activation, suggesting a role for GRHL2 not only in regulation of cohesin binding, but also in regulation of other crucial steps in enhancer activation.Together, these results suggest that our SMC1 ChIP-seq data reflect changing enhancer activity and that cohesin binding at enhancers is highly dynamic during the ESC to EpiLC transition.	Enhancer	CRISPR/Cas9	ChIP-seq,qRT-PCR	We then assessed the effects of each Enhancer deletion on Dsp expression in ES cells and EpiLCs by qRT-PCR.Indeed, we found that deletion of one or both KLF4-bound enhancers led to a significant reduction in Dsp expression in ESCs but had no effect in EpiLCs(Figure 6B). Conversely, deletion of the GRHL2-bound enhancer resulted in significantly reduced Dsp expression in the EpiLC state but had no effect in ESCs (Figure 6B). We observed similar state-specific reductions in target gene expression with deletions of the KLF4-bound and GRHL2-bound enhancers at the Cdh1 and Jam1 loci (Figure 6C and D, S6A and B).	2300002E22Rik,5730453H04Rik,AA407887,AA407888,AW109828,DP,rul	GRHL2 therefore control over a subset of the naive network via Enhancer switching to maintain expression of epithelial genes upon exit from naive pluripotency	ChIP-seq	Together,these results suggest that our SMC1 ChIP-seq data reflect changing Enhancer activity and that cohesin binding at Enhancers is highly dynamic during the ESC to EpiLC transition.	Grhl2	0610015A08Rik,BOM,Tcfcp2l3,clft3	ChIP-seq,ATAC-seq	Given the strong association between GRHL2 binding and various events in enhancer activation, we asked whether GRHL2 binding is necessary for each of these events. To address this question, we assessed levels of each active enhancer mark in wildtype and GHRL2 KO EpiLCs by performing ATAC-seq and ChIP-seq for H3K4me1, H3K27ac, and SMC1. There was a strong reduction in all active enhancer marks (chromatin accessibility, H3K4me1, H3K27ac, and SMC1 levels) at GRHL2 sites in GRHL2 KO EpiLCs, suggesting a near complete block in enhancer activation in the absence of GRHL2. Together, these results indicate an absolute requirement for GRHL2 for enhancer activation specifically at its target sites.	--	--	Dsp
30017589	chr13	30108722	30109111	LIF	Here, we show the transcription factor GRHL2 is necessary and sufficient to activate an epithelial subset of enhancers as naïve embryonic stem cells (ESCs) transition into formative epiblast-like cells (EpiLCs).	mouse		Low+High throughput	GRHL2-Dependent Enhancer Switching Maintains a Pluripotent Stem Cell Transcriptional Subnetwork after Exit from Naive Pluripotency	否	--	--	stem cell	E_02_0525	ChIP-seq	Our findings were corroborated by H3K4me1 and H3K27ac ChIP-seq data from an alternative na?ve-to-formative differentiation system. As a control, we found little change in these marks at SMC1 sites common to both states. These results indicate that GRHL2 binding correlates with full enhancer activation, suggesting a role for GRHL2 not only in regulation of cohesin binding, but also in regulation of other crucial steps in enhancer activation.Together, these results suggest that our SMC1 ChIP-seq data reflect changing enhancer activity and that cohesin binding at enhancers is highly dynamic during the ESC to EpiLC transition.	Enhancer	CRISPR/Cas9	ChIP-seq,qRT-PCR	We then assessed the effects of each Enhancer deletion on Dsp expression in ES cells and EpiLCs by qRT-PCR.Indeed, we found that deletion of one or both KLF4-bound enhancers led to a significant reduction in Dsp expression in ESCs but had no effect in EpiLCs(Figure 6B). Conversely, deletion of the GRHL2-bound enhancer resulted in significantly reduced Dsp expression in the EpiLC state but had no effect in ESCs (Figure 6B). We observed similar state-specific reductions in target gene expression with deletions of the KLF4-bound and GRHL2-bound enhancers at the Cdh1 and Jam1 loci (Figure 6C and D, S6A and B).	2300002E22Rik,5730453H04Rik,AA407887,AA407888,AW109828,DP,rul	GRHL2 therefore control over a subset of the naive network via Enhancer switching to maintain expression of epithelial genes upon exit from naive pluripotency	ChIP-seq	Together,these results suggest that our SMC1 ChIP-seq data reflect changing Enhancer activity and that cohesin binding at Enhancers is highly dynamic during the ESC to EpiLC transition.	Grhl2	0610015A08Rik,BOM,Tcfcp2l3,clft3	ChIP-seq,ATAC-seq	Given the strong association between GRHL2 binding and various events in enhancer activation, we asked whether GRHL2 binding is necessary for each of these events. To address this question, we assessed levels of each active enhancer mark in wildtype and GHRL2 KO EpiLCs by performing ATAC-seq and ChIP-seq for H3K4me1, H3K27ac, and SMC1. There was a strong reduction in all active enhancer marks (chromatin accessibility, H3K4me1, H3K27ac, and SMC1 levels) at GRHL2 sites in GRHL2 KO EpiLCs, suggesting a near complete block in enhancer activation in the absence of GRHL2. Together, these results indicate an absolute requirement for GRHL2 for enhancer activation specifically at its target sites.	--	--	Dsp
30016766	chr1	204187679	204189679	KISS1	We also identified KISS-1 metastasis-suppressor (KISS1) was significantly upregulated in TP73-AS1 knockdown cells. Further, we revealed that TP73-AS1 suppressed KISS1 expression through the interaction with Enhancer of zeste homolog 2 (EZH2) and the specific binding to KISS1 gene promoter region.	human		High+Lowthroughput	LncRNA TP73-AS1 Promotes Cell Proliferation and Inhibits Cell Apoptosis in Clear Cell Renal Cell Carcinoma Through Repressing KISS1 Expression and Inactivation of PI3K/Akt/mTOR Signaling Pathway	否		Renal cell carcinoma (RCC)	renal cancer cell	E_01_0800	Real time PCR, flow cytometry, Western blot	We also identified KISS-1 metastasis-suppressor (KISS1) was significantly upregulated in TP73-AS1 knockdown cells. Further, we revealed that TP73-AS1 suppressed KISS1 expression through the interaction with Enhancer of zeste homolog 2 (EZH2) and the specific binding to KISS1 gene promoter region.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We also identified KISS-1 metastasis-suppressor (KISS1) was significantly upregulated in TP73-AS1 knockdown cells. Further, we revealed that TP73-AS1 suppressed KISS1 expression through the interaction with Enhancer of zeste homolog 2 (EZH2) and the specific binding to KISS1 gene promoter region.		We also identified KISS-1 metastasis-suppressor (KISS1) was significantly upregulated in TP73-AS1 knockdown cells. Further, we revealed that TP73-AS1 suppressed KISS1 expression through the interaction with Enhancer of zeste homolog 2 (EZH2) and the specific binding to KISS1 gene promoter region.	Immunohistochemical staining	We also identified KISS-1 metastasis-suppressor (KISS1) was significantly upregulated in TP73-AS1 knockdown cells. Further, we revealed that TP73-AS1 suppressed KISS1 expression through the interaction with Enhancer of zeste homolog 2 (EZH2) and the specific binding to KISS1 gene promoter region.			real-time PCR,流式细胞术,western blot				KISS1
30016766	chr7	148805017	148807017	EZH2	We also identified KISS-1 metastasis-suppressor (KISS1) was significantly upregulated in TP73-AS1 knockdown cells. Further, we revealed that TP73-AS1 suppressed KISS1 expression through the interaction with Enhancer of zeste homolog 2 (EZH2) and the specific binding to KISS1 gene promoter region.	human		High+Lowthroughput	LncRNA TP73-AS1 Promotes Cell Proliferation and Inhibits Cell Apoptosis in Clear Cell Renal Cell Carcinoma Through Repressing KISS1 Expression and Inactivation of PI3K/Akt/mTOR Signaling Pathway	否		Renal cell carcinoma (RCC)	renal cancer cell	E_01_0800	Real time PCR, flow cytometry, Western blot	We also identified KISS-1 metastasis-suppressor (KISS1) was significantly upregulated in TP73-AS1 knockdown cells. Further, we revealed that TP73-AS1 suppressed KISS1 expression through the interaction with Enhancer of zeste homolog 2 (EZH2) and the specific binding to KISS1 gene promoter region.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We also identified KISS-1 metastasis-suppressor (KISS1) was significantly upregulated in TP73-AS1 knockdown cells. Further, we revealed that TP73-AS1 suppressed KISS1 expression through the interaction with Enhancer of zeste homolog 2 (EZH2) and the specific binding to KISS1 gene promoter region.	Immunohistochemical staining	We also identified KISS-1 metastasis-suppressor (KISS1) was significantly upregulated in TP73-AS1 knockdown cells. Further, we revealed that TP73-AS1 suppressed KISS1 expression through the interaction with Enhancer of zeste homolog 2 (EZH2) and the specific binding to KISS1 gene promoter region.	EZH2		real-time PCR,流式细胞术,western blot	We also identified KISS-1 metastasis-suppressor (KISS1) was significantly upregulated in TP73-AS1 knockdown cells. Further, we revealed that TP73-AS1 suppressed KISS1 expression through the interaction with Enhancer of zeste homolog 2 (EZH2) and the specific binding to KISS1 gene promoter region.			
30016502	chr21	34784861	34786861	RUNX1	The AR transcriptional network is tissue-specific and may be mediated in part by distinct AR co-factors including CAAT-enhancer binding protein beta (CEBPB) and runt-related transcription factor 1 (RUNX1).                                                                         Further analysis at a single AR-regulated locus (FK506-binding protein 5, FKPB5) suggests that CEBPB may be a co-activator. 	human		High+Lowthroughput	A novel transcriptional network for the androgen receptor in human epididymis epithelial cells	否		prostatic cancer		E_01_0801	Reverse transcription quantitative PCR, RNA SEQ, chip SEQ, chip qPCR, statistical analysis	The AR transcriptional network is tissue-specific and may be mediated in part by distinct AR co-factors including CAAT-enhancer binding protein beta (CEBPB) and runt-related transcription factor 1 (RUNX1).                                                                         Further analysis at a single AR-regulated locus (FK506-binding protein 5, FKPB5) suggests that CEBPB may be a co-activator. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The AR transcriptional network is tissue-specific and may be mediated in part by distinct AR co-factors including CAAT-enhancer binding protein beta (CEBPB) and runt-related transcription factor 1 (RUNX1).                                                                         Further analysis at a single AR-regulated locus (FK506-binding protein 5, FKPB5) suggests that CEBPB may be a co-activator. 	Immunohistochemical staining	The AR transcriptional network is tissue-specific and may be mediated in part by distinct AR co-factors including CAAT-enhancer binding protein beta (CEBPB) and runt-related transcription factor 1 (RUNX1).                                                                         Further analysis at a single AR-regulated locus (FK506-binding protein 5, FKPB5) suggests that CEBPB may be a co-activator. 	RUNX1		Reverse transcription quantitative PCR,RNA-seq,ChIP-seq,ChIP-qPCR,统计分析	The AR transcriptional network is tissue-specific and may be mediated in part by distinct AR co-factors including CAAT-enhancer binding protein beta (CEBPB) and runt-related transcription factor 1 (RUNX1).                                                                         Further analysis at a single AR-regulated locus (FK506-binding protein 5, FKPB5) suggests that CEBPB may be a co-activator. 			
30016502	chr14	37587026	37589026	FOXA1	The AR transcriptional network is tissue-specific and may be mediated in part by distinct AR co-factors including CAAT-enhancer binding protein beta (CEBPB) and runt-related transcription factor 1 (RUNX1).                                                                         Further analysis at a single AR-regulated locus (FK506-binding protein 5, FKPB5) suggests that CEBPB may be a co-activator. 	human		High+Lowthroughput	A novel transcriptional network for the androgen receptor in human epididymis epithelial cells	否		prostatic cancer		E_01_0801	Reverse transcription quantitative PCR, RNA SEQ, chip SEQ, chip qPCR, statistical analysis	The AR transcriptional network is tissue-specific and may be mediated in part by distinct AR co-factors including CAAT-enhancer binding protein beta (CEBPB) and runt-related transcription factor 1 (RUNX1).                                                                         Further analysis at a single AR-regulated locus (FK506-binding protein 5, FKPB5) suggests that CEBPB may be a co-activator. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The AR transcriptional network is tissue-specific and may be mediated in part by distinct AR co-factors including CAAT-enhancer binding protein beta (CEBPB) and runt-related transcription factor 1 (RUNX1).                                                                         Further analysis at a single AR-regulated locus (FK506-binding protein 5, FKPB5) suggests that CEBPB may be a co-activator. 	Immunohistochemical staining	The AR transcriptional network is tissue-specific and may be mediated in part by distinct AR co-factors including CAAT-enhancer binding protein beta (CEBPB) and runt-related transcription factor 1 (RUNX1).                                                                         Further analysis at a single AR-regulated locus (FK506-binding protein 5, FKPB5) suggests that CEBPB may be a co-activator. 	FOXA1		Reverse transcription quantitative PCR,RNA-seq,ChIP-seq,ChIP-qPCR,统计分析	The AR transcriptional network is tissue-specific and may be mediated in part by distinct AR co-factors including CAAT-enhancer binding protein beta (CEBPB) and runt-related transcription factor 1 (RUNX1).                                                                         Further analysis at a single AR-regulated locus (FK506-binding protein 5, FKPB5) suggests that CEBPB may be a co-activator. 			
30015909	chr2	238235826	238237826	HES6	HES6 is a member of the hairy-enhancer of the split homolog family, which has been implicated in oncogenesis and cancer progression in a variety of human cancers, including prostate and breast cancer.	human		High+Lowthroughput	Overexpression of HES6 has prognostic value and promotes metastasis via the Wnt/β-catenin signaling pathway in colorectal cancer	否		Prostate, breast, colorectal (CRC), lung		E_01_0802	RT-qPCR,Western blot,Immunohistochemistry (IHC),Dual-Luciferase assay	HES6 is a member of the hairy-enhancer of the split homolog family, which has been implicated in oncogenesis and cancer progression in a variety of human cancers, including prostate and breast cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			HES6 is a member of the hairy-enhancer of the split homolog family, which has been implicated in oncogenesis and cancer progression in a variety of human cancers, including prostate and breast cancer.	Immunohistochemical staining	HES6 is a member of the hairy-enhancer of the split homolog family, which has been implicated in oncogenesis and cancer progression in a variety of human cancers, including prostate and breast cancer.	HES6		RT-qPCR,Western blot,Immunohistochemistry (IHC),Dual-Luciferase assay	HES6 is a member of the hairy-enhancer of the split homolog family, which has been implicated in oncogenesis and cancer progression in a variety of human cancers, including prostate and breast cancer.			
30014220	chr16	69184468	69186468	SNTB2	The scaffold protein beta 2 syntrophin (SNTB2) controls signaling events by recruiting distinct membrane and cytoskeletal proteins, and binds to utrophin.                                                                                                                                                                                 In vitro data suppose a function of the syntrophins in stabilizing ATP-binding cassette transporter A1 (ABCA1), a major regulator of serum cholesterol levels [8].	mouse,human	adipose tissue	High+Lowthroughput	The utrophin-beta 2 syntrophin complex regulates adipocyte lipid droplet size independent of adipogenesis	否		inflammation	3T3‑L1 adipocytes	E_02_0526	Western blot, immunofluorescence staining, gene knockdown	The scaffold protein beta 2 syntrophin (SNTB2) controls signaling events by recruiting distinct membrane and cytoskeletal proteins, and binds to utrophin.                                                                                                                                                                                 In vitro data suppose a function of the syntrophins in stabilizing ATP-binding cassette transporter A1 (ABCA1), a major regulator of serum cholesterol levels [8].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The scaffold protein beta 2 syntrophin (SNTB2) controls signaling events by recruiting distinct membrane and cytoskeletal proteins, and binds to utrophin.                                                                                                                                                                                 In vitro data suppose a function of the syntrophins in stabilizing ATP-binding cassette transporter A1 (ABCA1), a major regulator of serum cholesterol levels [8].		The scaffold protein beta 2 syntrophin (SNTB2) controls signaling events by recruiting distinct membrane and cytoskeletal proteins, and binds to utrophin.                                                                                                                                                                                 In vitro data suppose a function of the syntrophins in stabilizing ATP-binding cassette transporter A1 (ABCA1), a major regulator of serum cholesterol levels [8].	Immunohistochemical staining	The scaffold protein beta 2 syntrophin (SNTB2) controls signaling events by recruiting distinct membrane and cytoskeletal proteins, and binds to utrophin.                                                                                                                                                                                 In vitro data suppose a function of the syntrophins in stabilizing ATP-binding cassette transporter A1 (ABCA1), a major regulator of serum cholesterol levels [8].			western blot,免疫荧光染色,基因敲降				SNTB2
30014220	chr9	104778436	104780436	ABCA1	The scaffold protein beta 2 syntrophin (SNTB2) controls signaling events by recruiting distinct membrane and cytoskeletal proteins, and binds to utrophin.                                                                                                                                                                                 In vitro data suppose a function of the syntrophins in stabilizing ATP-binding cassette transporter A1 (ABCA1), a major regulator of serum cholesterol levels [8].	mouse,human	adipose tissue	High+Lowthroughput	The utrophin-beta 2 syntrophin complex regulates adipocyte lipid droplet size independent of adipogenesis	否		inflammation	3T3‑L1 adipocytes	E_02_0526	Western blot, immunofluorescence staining, gene knockdown	The scaffold protein beta 2 syntrophin (SNTB2) controls signaling events by recruiting distinct membrane and cytoskeletal proteins, and binds to utrophin.                                                                                                                                                                                 In vitro data suppose a function of the syntrophins in stabilizing ATP-binding cassette transporter A1 (ABCA1), a major regulator of serum cholesterol levels [8].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The scaffold protein beta 2 syntrophin (SNTB2) controls signaling events by recruiting distinct membrane and cytoskeletal proteins, and binds to utrophin.                                                                                                                                                                                 In vitro data suppose a function of the syntrophins in stabilizing ATP-binding cassette transporter A1 (ABCA1), a major regulator of serum cholesterol levels [8].		The scaffold protein beta 2 syntrophin (SNTB2) controls signaling events by recruiting distinct membrane and cytoskeletal proteins, and binds to utrophin.                                                                                                                                                                                 In vitro data suppose a function of the syntrophins in stabilizing ATP-binding cassette transporter A1 (ABCA1), a major regulator of serum cholesterol levels [8].	Immunohistochemical staining	The scaffold protein beta 2 syntrophin (SNTB2) controls signaling events by recruiting distinct membrane and cytoskeletal proteins, and binds to utrophin.                                                                                                                                                                                 In vitro data suppose a function of the syntrophins in stabilizing ATP-binding cassette transporter A1 (ABCA1), a major regulator of serum cholesterol levels [8].			western blot,免疫荧光染色,基因敲降				ABCA1
30012865	chr11	5279732	5280272	USF1	This site is occupied by transcription factors USF1, USF2, EGR1, MafK, and NF-E2 in the human erythroleukemia cell line K562 and exhibits histone modifications typical for enhancers.	human		Low+High throughput	Identification of a Novel Enhancer/Chromatin Opening Element Associated with High-Level γ-Globin Gene Expression	是	--	Erythrocytic Leukemia	erythrocyte	E_02_0527	ChIP-seq	We generated a synthetic zinc finger DNA-binding domain (ZF) targeting the HBG-4kb HS. The HBG-4kb ZF interacted with the target site in vitro and in the context of cells with high affinity and specificity.	Enhancer	--	PCR	The regions that we analyzed were the HBG-4kb HS,a 327 region located 4 kb upstream (HBG-8kb) or 1 and 2 kb downstream(HBG-3kb and HBG-2kb) of 328 the HBG-4kb HS,the Gγ-(HBG2) and Aγ-(HBG1) globin gene promoter regions.	HBG-T1,TNCY	the HBG-4kb HS site is important for fetal globin production and suggest that it may act by opening chromatin in a directional manner.	CRISPR/Cas9	Expression of the adult β-globin, the embryonic -globin, and the GATA1 genes was not affected by the HBG-4kb ZF. Delivery of the Control ZF did not cause any change in expression of the γ-globin, β-globin, -globin, or GATA1 genes.	USF1,USF2,EGR1,MAFK,NFE2	FCHL,FCHL1,HYPLIP1,MLTF,MLTFI,UEF,bHLHb11,FIP,bHLHb12,AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225,NFE2U,P18,NF-E2,p45	ChIP	Reduced binding of transcription factors with the HBG-4kb HS in K562 cells expressing the HBG-4kb ZF. K562 cells (Untreated) or K562 cells exposed to 500 nM HBG-4kb ZF for 12 h were subjected to ChIP using antibodies specific for EGR1, USF1, USF2, NF-E2 (p45), MafK, or the negative control, IgG.	--	--	HBG2
30012865	chr11	5279732	5280272	USF2	This site is occupied by transcription factors USF1, USF2, EGR1, MafK, and NF-E2 in the human erythroleukemia cell line K562 and exhibits histone modifications typical for enhancers.	human		Low+High throughput	Identification of a Novel Enhancer/Chromatin Opening Element Associated with High-Level γ-Globin Gene Expression	是	--	Erythrocytic Leukemia	erythrocyte	E_02_0527	ChIP-seq	We generated a synthetic zinc finger DNA-binding domain (ZF) targeting the HBG-4kb HS. The HBG-4kb ZF interacted with the target site in vitro and in the context of cells with high affinity and specificity.	Enhancer	--	PCR	The regions that we analyzed were the HBG-4kb HS,a 327 region located 4 kb upstream (HBG-8kb) or 1 and 2 kb downstream(HBG-3kb and HBG-2kb) of 328 the HBG-4kb HS,the Gγ-(HBG2) and Aγ-(HBG1) globin gene promoter regions.	HBG-T1,TNCY	the HBG-4kb HS site is important for fetal globin production and suggest that it may act by opening chromatin in a directional manner.	CRISPR/Cas9	Expression of the adult β-globin, the embryonic -globin, and the GATA1 genes was not affected by the HBG-4kb ZF. Delivery of the Control ZF did not cause any change in expression of the γ-globin, β-globin, -globin, or GATA1 genes.	USF1,USF2,EGR1,MAFK,NFE2	FCHL,FCHL1,HYPLIP1,MLTF,MLTFI,UEF,bHLHb11,FIP,bHLHb12,AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225,NFE2U,P18,NF-E2,p45	ChIP	Reduced binding of transcription factors with the HBG-4kb HS in K562 cells expressing the HBG-4kb ZF. K562 cells (Untreated) or K562 cells exposed to 500 nM HBG-4kb ZF for 12 h were subjected to ChIP using antibodies specific for EGR1, USF1, USF2, NF-E2 (p45), MafK, or the negative control, IgG.	--	--	HBG2
30012865	chr11	5279732	5280272	EGR1	This site is occupied by transcription factors USF1, USF2, EGR1, MafK, and NF-E2 in the human erythroleukemia cell line K562 and exhibits histone modifications typical for enhancers.	human		Low+High throughput	Identification of a Novel Enhancer/Chromatin Opening Element Associated with High-Level γ-Globin Gene Expression	是	--	Erythrocytic Leukemia	erythrocyte	E_02_0527	ChIP-seq	We generated a synthetic zinc finger DNA-binding domain (ZF) targeting the HBG-4kb HS. The HBG-4kb ZF interacted with the target site in vitro and in the context of cells with high affinity and specificity.	Enhancer	--	PCR	The regions that we analyzed were the HBG-4kb HS,a 327 region located 4 kb upstream (HBG-8kb) or 1 and 2 kb downstream(HBG-3kb and HBG-2kb) of 328 the HBG-4kb HS,the Gγ-(HBG2) and Aγ-(HBG1) globin gene promoter regions.	HBG-T1,TNCY	the HBG-4kb HS site is important for fetal globin production and suggest that it may act by opening chromatin in a directional manner.	CRISPR/Cas9	Expression of the adult β-globin, the embryonic -globin, and the GATA1 genes was not affected by the HBG-4kb ZF. Delivery of the Control ZF did not cause any change in expression of the γ-globin, β-globin, -globin, or GATA1 genes.	USF1,USF2,EGR1,MAFK,NFE2	FCHL,FCHL1,HYPLIP1,MLTF,MLTFI,UEF,bHLHb11,FIP,bHLHb12,AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225,NFE2U,P18,NF-E2,p45	ChIP	Reduced binding of transcription factors with the HBG-4kb HS in K562 cells expressing the HBG-4kb ZF. K562 cells (Untreated) or K562 cells exposed to 500 nM HBG-4kb ZF for 12 h were subjected to ChIP using antibodies specific for EGR1, USF1, USF2, NF-E2 (p45), MafK, or the negative control, IgG.	--	--	HBG2
30012153	chr7	96478877	96480877	SEM1	Some other endogenous amyloid aggregates that increase HIV-1 infectivity, including the PAP N-proximal fragment (PAP85 120) and semenogelins (SEM1 and SEM2), have been identified in human semen [7, 8], which may explain the discrepancy between the low infectiousness of HIV in vitro and its observed efficient sexual transmission.	human,immunodeficiency,virus,(HIV)		High+Lowthroughput	Myricetin antagonizes semen-derived enhancer of viral infection (SEVI) formation and influences its infection-enhancing activity	否		HIV	TZM-b1 cell	E_02_0528	MTT assay, WB assay, SPR analysis, flow cytometry, statistical analysis, immunofluorescence staining	Some other endogenous amyloid aggregates that increase HIV-1 infectivity, including the PAP N-proximal fragment (PAP85 120) and semenogelins (SEM1 and SEM2), have been identified in human semen [7, 8], which may explain the discrepancy between the low infectiousness of HIV in vitro and its observed efficient sexual transmission.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Some other endogenous amyloid aggregates that increase HIV-1 infectivity, including the PAP N-proximal fragment (PAP85 120) and semenogelins (SEM1 and SEM2), have been identified in human semen [7, 8], which may explain the discrepancy between the low infectiousness of HIV in vitro and its observed efficient sexual transmission.		Some other endogenous amyloid aggregates that increase HIV-1 infectivity, including the PAP N-proximal fragment (PAP85 120) and semenogelins (SEM1 and SEM2), have been identified in human semen [7, 8], which may explain the discrepancy between the low infectiousness of HIV in vitro and its observed efficient sexual transmission.	Immunohistochemical staining	Some other endogenous amyloid aggregates that increase HIV-1 infectivity, including the PAP N-proximal fragment (PAP85 120) and semenogelins (SEM1 and SEM2), have been identified in human semen [7, 8], which may explain the discrepancy between the low infectiousness of HIV in vitro and its observed efficient sexual transmission.			MTT法,WB assay,,SPR analysis,流式细胞术,统计分析,免疫荧光染色				SEM1
30010625	chr13	27917694	27919694	PDX1	BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. 	human,mouse	Tumor tissues	High+Lowthroughput	The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis	是		Pancreatic ductal adenocarcinoma (PDA)	acinar cell	E_02_0529	Immunohistochemistry,ChIP-seq,RT-PCR,ChIP qPCR	BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. 		BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. 	Immunohistochemical staining	BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. 			Immunohistochemistry,ChIP-seq,RT-PCR,ChIP qPCR				PDX1
30010625	chr17	72118672	72120672	SOX9	BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. 	human,mouse	Tumor tissues	High+Lowthroughput	The BRG1/SOX9 axis is critical for acinar cell-derived pancreatic tumorigenesis	是		Pancreatic ductal adenocarcinoma (PDA)	acinar cell	E_02_0529	Immunohistochemistry,ChIP-seq,RT-PCR,ChIP qPCR	BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. 		BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. 	Immunohistochemical staining	BRG1 bound to regions of the Sox9 promoter to regulate its expression and was critical for recruitment of upstream regulators, including PDX1, to the Sox9 promoter and enhancer in acinar cells. 			Immunohistochemistry,ChIP-seq,RT-PCR,ChIP qPCR				SOX9
30008319	chr4	129406952	129408952	Hdac1	The complex combines two enzymatic activities in the form of class I lysine deacetylation, encoded by the Hdac1 and 2 proteins, with the Swi/Snf-type ATPase and nucleosome remodeling of Chd4.	mouse,human		High+Lowthroughput	The Nucleosome Remodeling and Deacetylation Complex Modulates Chromatin Structure at Sites of Active Transcription to Fine-Tune Gene Expression	否				E_02_0530	Chip SEQ, RNA SEQ, mnase SEQ, mnase qPCR, statistical analysis, Western blot	The complex combines two enzymatic activities in the form of class I lysine deacetylation, encoded by the Hdac1 and 2 proteins, with the Swi/Snf-type ATPase and nucleosome remodeling of Chd4.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The complex combines two enzymatic activities in the form of class I lysine deacetylation, encoded by the Hdac1 and 2 proteins, with the Swi/Snf-type ATPase and nucleosome remodeling of Chd4.		The complex combines two enzymatic activities in the form of class I lysine deacetylation, encoded by the Hdac1 and 2 proteins, with the Swi/Snf-type ATPase and nucleosome remodeling of Chd4.	Immunohistochemical staining	The complex combines two enzymatic activities in the form of class I lysine deacetylation, encoded by the Hdac1 and 2 proteins, with the Swi/Snf-type ATPase and nucleosome remodeling of Chd4.			ChIP-seq,RNA-seq,MNase-seq,MNase qPCR,统计分析,western blot				Hdac1
30008316	chr1	160536893	160537651	INTS13	The control of cell fate is an epigenetic process initiated by transcription factors (TFs) that recognize DNA motifs and recruit activator complexes and transcriptional machineries to chromatin.                                                                                                                               Here we show that INTS13 functions as an independent sub-module and targets enhancers through Early Growth Response (EGR1/2) TFs and their co-factor NAB2.                                                                                                                               Independent depletion of INTS13, EGR1 or NAB2 impairs monocytic differentiation of cell lines and primary human progenitors.	human		Low+High throughput	Targeted Enhancer Activation by a Subunit of the Integrator Complex	否	--	--	HL-60	E_02_0531	ChIP-seq,ChIP-qPCR	Notably, INTS11-gained regions were largely enriched for proximal promoters(62.2%), mirroring the known RNAPII-associated activity of the complex, and displayed robust binding of INTS13 as well. Conversely, INTS13-gained regions were largely found distal from the TSS of protein-coding genes (82.5%) and only partially overlapped with INTS11.	Enhancer	CRISPR/Cas9,3C	qRT-PCR	We performed chromosome conformation capture (3C) on the enhancer of CSF1R to infer the consequences of INTS13 depletion on genome architecture. During differentiation of HL-60 cells, we detected a robust interaction between the intronic enhancer of CSF1R and the proximal promoter, as compared to other regions within the CSF1R gene or with the promoter of neighboring genes.	LY9B,SLAMF5,hCD84,mCD84	--	--	--	INTS13,EGR1,NAB2	ASUN,C12orf11,GCT1,Mat89Bb,NET48,SPATA30,AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225,MADER	Immunoprecipitation,Colony-forming Unit (CFU) Assay	Immunoprecipitation of INTS13 in undifferentiated (CTRL) and differentiated (PMA) HL-60 cells confirms the interaction between INTS13 and NAB2 after PMA treatment.Colony-forming unit (CFU) assay of cord blood derived CD34+ cells infected with shRNAs against NAB2 and EGR1 shows that the number of monocytic/macrophagic colonies is significantly reduced in both NAB2- and EGR1-depleted cells when compared to control.	--	--	CD84
30008316	chr1	160536893	160537651	EGR1	The control of cell fate is an epigenetic process initiated by transcription factors (TFs) that recognize DNA motifs and recruit activator complexes and transcriptional machineries to chromatin.                                                                                                                               Here we show that INTS13 functions as an independent sub-module and targets enhancers through Early Growth Response (EGR1/2) TFs and their co-factor NAB2.                                                                                                                               Independent depletion of INTS13, EGR1 or NAB2 impairs monocytic differentiation of cell lines and primary human progenitors.	human		Low+High throughput	Targeted Enhancer Activation by a Subunit of the Integrator Complex	否	--	--	HL-60	E_02_0531	ChIP-seq,ChIP-qPCR	Notably, INTS11-gained regions were largely enriched for proximal promoters(62.2%), mirroring the known RNAPII-associated activity of the complex, and displayed robust binding of INTS13 as well. Conversely, INTS13-gained regions were largely found distal from the TSS of protein-coding genes (82.5%) and only partially overlapped with INTS11.	Enhancer	CRISPR/Cas9,3C	qRT-PCR	We performed chromosome conformation capture (3C) on the enhancer of CSF1R to infer the consequences of INTS13 depletion on genome architecture. During differentiation of HL-60 cells, we detected a robust interaction between the intronic enhancer of CSF1R and the proximal promoter, as compared to other regions within the CSF1R gene or with the promoter of neighboring genes.	LY9B,SLAMF5,hCD84,mCD84	--	--	--	INTS13,EGR1,NAB2	ASUN,C12orf11,GCT1,Mat89Bb,NET48,SPATA30,AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225,MADER	Immunoprecipitation,Colony-forming Unit (CFU) Assay	Immunoprecipitation of INTS13 in undifferentiated (CTRL) and differentiated (PMA) HL-60 cells confirms the interaction between INTS13 and NAB2 after PMA treatment.Colony-forming unit (CFU) assay of cord blood derived CD34+ cells infected with shRNAs against NAB2 and EGR1 shows that the number of monocytic/macrophagic colonies is significantly reduced in both NAB2- and EGR1-depleted cells when compared to control.	--	--	CD84
30008316	chr1	160536893	160537651	NAB2	The control of cell fate is an epigenetic process initiated by transcription factors (TFs) that recognize DNA motifs and recruit activator complexes and transcriptional machineries to chromatin.                                                                                                                               Here we show that INTS13 functions as an independent sub-module and targets enhancers through Early Growth Response (EGR1/2) TFs and their co-factor NAB2.                                                                                                                               Independent depletion of INTS13, EGR1 or NAB2 impairs monocytic differentiation of cell lines and primary human progenitors.	human		Low+High throughput	Targeted Enhancer Activation by a Subunit of the Integrator Complex	否	--	--	HL-60	E_02_0531	ChIP-seq,ChIP-qPCR	Notably, INTS11-gained regions were largely enriched for proximal promoters(62.2%), mirroring the known RNAPII-associated activity of the complex, and displayed robust binding of INTS13 as well. Conversely, INTS13-gained regions were largely found distal from the TSS of protein-coding genes (82.5%) and only partially overlapped with INTS11.	Enhancer	CRISPR/Cas9,3C	qRT-PCR	We performed chromosome conformation capture (3C) on the enhancer of CSF1R to infer the consequences of INTS13 depletion on genome architecture. During differentiation of HL-60 cells, we detected a robust interaction between the intronic enhancer of CSF1R and the proximal promoter, as compared to other regions within the CSF1R gene or with the promoter of neighboring genes.	LY9B,SLAMF5,hCD84,mCD84	--	--	--	INTS13,EGR1,NAB2	ASUN,C12orf11,GCT1,Mat89Bb,NET48,SPATA30,AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225,MADER	Immunoprecipitation,Colony-forming Unit (CFU) Assay	Immunoprecipitation of INTS13 in undifferentiated (CTRL) and differentiated (PMA) HL-60 cells confirms the interaction between INTS13 and NAB2 after PMA treatment.Colony-forming unit (CFU) assay of cord blood derived CD34+ cells infected with shRNAs against NAB2 and EGR1 shows that the number of monocytic/macrophagic colonies is significantly reduced in both NAB2- and EGR1-depleted cells when compared to control.	--	--	CD84
30006306	chr7	148804160	148806160	EZH2	The gene and protein expression of polycomb repressor13 proteins B cell specific moloney murine leukemia virus integration site 1 (BMI-1) and14 enhancer of zeste homolog 2 (EZH2) was significantly over expressed with enhanced15 trimethylation of H3K27 and ubiquitination of H2AK119.	human,mouse		High+Lowthroughput	Aflatoxin B(1) induced multiple epigenetic modulators in human epithelial cell lines	否		leukemia	HaCaT  cell	E_02_0532	MTT assay, quantitative real-time polymerase chain reaction, Western blot, and statistical analysis	The gene and protein expression of polycomb repressor13 proteins B cell specific moloney murine leukemia virus integration site 1 (BMI-1) and14 enhancer of zeste homolog 2 (EZH2) was significantly over expressed with enhanced15 trimethylation of H3K27 and ubiquitination of H2AK119.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The gene and protein expression of polycomb repressor13 proteins B cell specific moloney murine leukemia virus integration site 1 (BMI-1) and14 enhancer of zeste homolog 2 (EZH2) was significantly over expressed with enhanced15 trimethylation of H3K27 and ubiquitination of H2AK119.		The gene and protein expression of polycomb repressor13 proteins B cell specific moloney murine leukemia virus integration site 1 (BMI-1) and14 enhancer of zeste homolog 2 (EZH2) was significantly over expressed with enhanced15 trimethylation of H3K27 and ubiquitination of H2AK119.	Immunohistochemical staining	The gene and protein expression of polycomb repressor13 proteins B cell specific moloney murine leukemia virus integration site 1 (BMI-1) and14 enhancer of zeste homolog 2 (EZH2) was significantly over expressed with enhanced15 trimethylation of H3K27 and ubiquitination of H2AK119.			MTT法,quantitative real-time polymerase chain reaction,Western blot,统计分析				EZH2
30006149	chr1	116511683	116513683	CD58	Abstract CD58 is expressed on the surface of antigen-presenting cells, including B-cells, and provides co- stimulation to regulatory T-cells (Treg) through CD2 receptor binding.                                                                                                               Using bioinformatics and pull-down assay we found that the protective (C) rs1335532 allele created functional binding site for ASCL2 transcription factor, a target of the Wnt signaling pathway. 	human		High+Lowthroughput	Protective C allele of the single-nucleotide polymorphism rs1335532 is associated with strong binding of Ascl2 transcription factor and elevated CD58 expression in B-cells	是	rs2300747,rs1335532	Multiple sclerosis (MS)	leukocyte	E_01_0803	Pull down assay, real time PCR, Western blot, statistical analysis, gene knockdown	Abstract CD58 is expressed on the surface of antigen-presenting cells, including B-cells, and provides co- stimulation to regulatory T-cells (Treg) through CD2 receptor binding.                                                                                                               Using bioinformatics and pull-down assay we found that the protective (C) rs1335532 allele created functional binding site for ASCL2 transcription factor, a target of the Wnt signaling pathway. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Abstract CD58 is expressed on the surface of antigen-presenting cells, including B-cells, and provides co- stimulation to regulatory T-cells (Treg) through CD2 receptor binding.                                                                                                               Using bioinformatics and pull-down assay we found that the protective (C) rs1335532 allele created functional binding site for ASCL2 transcription factor, a target of the Wnt signaling pathway. 		Abstract CD58 is expressed on the surface of antigen-presenting cells, including B-cells, and provides co- stimulation to regulatory T-cells (Treg) through CD2 receptor binding.                                                                                                               Using bioinformatics and pull-down assay we found that the protective (C) rs1335532 allele created functional binding site for ASCL2 transcription factor, a target of the Wnt signaling pathway. 	Immunohistochemical staining	Abstract CD58 is expressed on the surface of antigen-presenting cells, including B-cells, and provides co- stimulation to regulatory T-cells (Treg) through CD2 receptor binding.                                                                                                               Using bioinformatics and pull-down assay we found that the protective (C) rs1335532 allele created functional binding site for ASCL2 transcription factor, a target of the Wnt signaling pathway. 			Pull-Down Assay,Real-Time PCR,Western Blot,统计分析,基因敲降				CD58
30006149	chr11	2265829	2267829	ASCL2	Abstract CD58 is expressed on the surface of antigen-presenting cells, including B-cells, and provides co- stimulation to regulatory T-cells (Treg) through CD2 receptor binding.                                                                                                               Using bioinformatics and pull-down assay we found that the protective (C) rs1335532 allele created functional binding site for ASCL2 transcription factor, a target of the Wnt signaling pathway. 	human		High+Lowthroughput	Protective C allele of the single-nucleotide polymorphism rs1335532 is associated with strong binding of Ascl2 transcription factor and elevated CD58 expression in B-cells	是	rs2300747,rs1335532	Multiple sclerosis (MS)	leukocyte	E_01_0803	Pull down assay, real time PCR, Western blot, statistical analysis, gene knockdown	Abstract CD58 is expressed on the surface of antigen-presenting cells, including B-cells, and provides co- stimulation to regulatory T-cells (Treg) through CD2 receptor binding.                                                                                                               Using bioinformatics and pull-down assay we found that the protective (C) rs1335532 allele created functional binding site for ASCL2 transcription factor, a target of the Wnt signaling pathway. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Abstract CD58 is expressed on the surface of antigen-presenting cells, including B-cells, and provides co- stimulation to regulatory T-cells (Treg) through CD2 receptor binding.                                                                                                               Using bioinformatics and pull-down assay we found that the protective (C) rs1335532 allele created functional binding site for ASCL2 transcription factor, a target of the Wnt signaling pathway. 	Immunohistochemical staining	Abstract CD58 is expressed on the surface of antigen-presenting cells, including B-cells, and provides co- stimulation to regulatory T-cells (Treg) through CD2 receptor binding.                                                                                                               Using bioinformatics and pull-down assay we found that the protective (C) rs1335532 allele created functional binding site for ASCL2 transcription factor, a target of the Wnt signaling pathway. 	ASCL2		Pull-Down Assay,Real-Time PCR,Western Blot,统计分析,基因敲降	Abstract CD58 is expressed on the surface of antigen-presenting cells, including B-cells, and provides co- stimulation to regulatory T-cells (Treg) through CD2 receptor binding.                                                                                                               Using bioinformatics and pull-down assay we found that the protective (C) rs1335532 allele created functional binding site for ASCL2 transcription factor, a target of the Wnt signaling pathway. 			
30003124	chr12	25202764	25204764	KRAS	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 	human,mouse		High+Lowthroughput	E47 Governs the MYC-CDKN1B/p27(KIP1)-RB Network to Growth Arrest PDA Cells Independent of CDKN2A/p16(INK4A) and Wild-Type p53	否		Pancreatic ductal adenocarcinoma (PDA)		E_02_0533	RNA SEQ, cell cycle PCR array analysis, flow cytometry, statistical analysis	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 		Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 	Immunohistochemical staining	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 			RNA-Seq,Cell-Cycle PCR Array Analysis,流式细胞术,统计分析				KRAS
30003124	chr8	127732050	127734050	MYC	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 	human,mouse		High+Lowthroughput	E47 Governs the MYC-CDKN1B/p27(KIP1)-RB Network to Growth Arrest PDA Cells Independent of CDKN2A/p16(INK4A) and Wild-Type p53	否		Pancreatic ductal adenocarcinoma (PDA)		E_02_0533	RNA SEQ, cell cycle PCR array analysis, flow cytometry, statistical analysis	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 		Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 	Immunohistochemical staining	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 			RNA-Seq,Cell-Cycle PCR Array Analysis,流式细胞术,统计分析				MYC
30003124	chr9	21964876	21966876	CDKN2A	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 	human,mouse		High+Lowthroughput	E47 Governs the MYC-CDKN1B/p27(KIP1)-RB Network to Growth Arrest PDA Cells Independent of CDKN2A/p16(INK4A) and Wild-Type p53	否		Pancreatic ductal adenocarcinoma (PDA)		E_02_0533	RNA SEQ, cell cycle PCR array analysis, flow cytometry, statistical analysis	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 		Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 	Immunohistochemical staining	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 			RNA-Seq,Cell-Cycle PCR Array Analysis,流式细胞术,统计分析				CDKN2A
30003124	chr18	51026057	51028057	SMAD4	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 	human,mouse		High+Lowthroughput	E47 Governs the MYC-CDKN1B/p27(KIP1)-RB Network to Growth Arrest PDA Cells Independent of CDKN2A/p16(INK4A) and Wild-Type p53	否		Pancreatic ductal adenocarcinoma (PDA)		E_02_0533	RNA SEQ, cell cycle PCR array analysis, flow cytometry, statistical analysis	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 		Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 	Immunohistochemical staining	Background & Aims Oncogenic mutations in KRAS, coupled with inactivation of p53, CDKN2A/p16INK4A, and SMAD4, drive progression of pancreatic ductal adenocarcinoma (PDA).Overexpression of MYC and deregulation of retinoblastoma (RB) further promote cell proliferation and make identifying a means to therapeutically alter cell-cycle control pathways in PDA a significant challenge. 			RNA-Seq,Cell-Cycle PCR Array Analysis,流式细胞术,统计分析				SMAD4
30002127	chr19	33297216	33299216	CEBPA	Lack of, aberrant or suboptimal C/EBPα activity can result from genomic mutations in the CEBPA gene,8 transcriptional suppression originating from promoter hypermethylation, or functional inactivation by phosphorylation.	mouse,human		High+Lowthroughput	Inhibition of protein disulfide isomerase induces differentiation of acute myeloid leukemia cells	否		Acute myeloid leukemia	HL-60	E_02_0534	Western blot, real time PCR, statistical analysis	Lack of, aberrant or suboptimal C/EBPα activity can result from genomic mutations in the CEBPA gene,8 transcriptional suppression originating from promoter hypermethylation, or functional inactivation by phosphorylation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Lack of, aberrant or suboptimal C/EBPα activity can result from genomic mutations in the CEBPA gene,8 transcriptional suppression originating from promoter hypermethylation, or functional inactivation by phosphorylation.		Lack of, aberrant or suboptimal C/EBPα activity can result from genomic mutations in the CEBPA gene,8 transcriptional suppression originating from promoter hypermethylation, or functional inactivation by phosphorylation.	Immunohistochemical staining	Lack of, aberrant or suboptimal C/EBPα activity can result from genomic mutations in the CEBPA gene,8 transcriptional suppression originating from promoter hypermethylation, or functional inactivation by phosphorylation.			Western blot,Real-Time PCR,统计分析				CEBPA
30002061	chr21	43049901	43051901	CBS	Since laminar flow-induced CSE suppression is lost in areas of disturbed flow, we wanted to know whether this led to the elevation of H2S and its metabolites.	mouse,human		High+Lowthroughput	Cystathionine γ-Lyase Modulates Flow-Dependent Vascular Remodeling	否		atherosclerosis	endothelial cell	E_02_0535	Immunoblotting, QRT PCR, immunocytochemistry, statistical analysis	Since laminar flow-induced CSE suppression is lost in areas of disturbed flow, we wanted to know whether this led to the elevation of H2S and its metabolites.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Since laminar flow-induced CSE suppression is lost in areas of disturbed flow, we wanted to know whether this led to the elevation of H2S and its metabolites.		Since laminar flow-induced CSE suppression is lost in areas of disturbed flow, we wanted to know whether this led to the elevation of H2S and its metabolites.	Immunohistochemical staining	Since laminar flow-induced CSE suppression is lost in areas of disturbed flow, we wanted to know whether this led to the elevation of H2S and its metabolites.			Immunoblotting,qRT-PCR,Immunocytochemistry,统计分析				CBS
29995890	chr15	90963074	90965074	PRC1	Altogether, our results suggest that Cyclin G, PRC1 and PR-DUB cooperate for developmental stability.	mouse		High+Lowthroughput	Cyclin G and the Polycomb Repressive complexes PRC1 and PR-DUB cooperate for developmental stability	否			Mesothelioma cell	E_02_0536	RNA-seq,RT-qPCR,ChIP-seq,ChIP-qPCR	Altogether, our results suggest that Cyclin G, PRC1 and PR-DUB cooperate for developmental stability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Altogether, our results suggest that Cyclin G, PRC1 and PR-DUB cooperate for developmental stability.		Altogether, our results suggest that Cyclin G, PRC1 and PR-DUB cooperate for developmental stability.	Immunohistochemical staining	Altogether, our results suggest that Cyclin G, PRC1 and PR-DUB cooperate for developmental stability.			RNA-seq,RT-qPCR,ChIP-seq,ChIP-qPCR				PRC1
29992973	chr13	99979122	99981122	ZIC2	ZIC2 mutation is known to cause holoprosencephaly (HPE). 	human,mouse		High+Lowthroughput	A Requirement for Zic2 in the Regulation of Nodal Expression Underlies the Establishment of Left-Sided Identity	是	rs13482392	Holoprosencephaly (HPE), congenital heart		E_02_0537	Microarray analysis,qPCR,In situ hybridisation,Chip-Seq,EMSA assays	ZIC2 mutation is known to cause holoprosencephaly (HPE). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ZIC2 mutation is known to cause holoprosencephaly (HPE). 		ZIC2 mutation is known to cause holoprosencephaly (HPE). 	Immunohistochemical staining	ZIC2 mutation is known to cause holoprosencephaly (HPE). 			Microarray analysis,qPCR,In situ hybridisation,Chip-Seq,EMSA assays				ZIC2
29991769	chr4	108044640	108046640	LEF1	Here, we investigated the relationship between lymphoid enhancer-binding factor 1 (LEF1) and transcriptional co-activator with PDZ-binding motif (TAZ), both of which are transcriptional regulators that mediate canonical Wnt signalling during osteoblast differentiation.                                                                                                                                                                                                                                                                                                                                                                 Moreover, we found that LEF1 and TAZ formed a transcriptional complex with runt-related transcription factor 2 (Runx2) and that inhibition of LEF1 or TAZ by their dominant-negative forms dramatically suppressed the osteoblastogenic activity of Ruxn2. 	human		High+Lowthroughput	Interaction of LEF1 with TAZ is necessary for the osteoblastogenic activity of Wnt3a	否		Osteoporosis	fat cell	E_01_0804	RT qPCR, immunoprecipitation, immunoblotting and co immunoprecipitation, statistical analysis	Here, we investigated the relationship between lymphoid enhancer-binding factor 1 (LEF1) and transcriptional co-activator with PDZ-binding motif (TAZ), both of which are transcriptional regulators that mediate canonical Wnt signalling during osteoblast differentiation.                                                                                                                                                                                                                                                                                                                                                                 Moreover, we found that LEF1 and TAZ formed a transcriptional complex with runt-related transcription factor 2 (Runx2) and that inhibition of LEF1 or TAZ by their dominant-negative forms dramatically suppressed the osteoblastogenic activity of Ruxn2. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we investigated the relationship between lymphoid enhancer-binding factor 1 (LEF1) and transcriptional co-activator with PDZ-binding motif (TAZ), both of which are transcriptional regulators that mediate canonical Wnt signalling during osteoblast differentiation.                                                                                                                                                                                                                                                                                                                                                                 Moreover, we found that LEF1 and TAZ formed a transcriptional complex with runt-related transcription factor 2 (Runx2) and that inhibition of LEF1 or TAZ by their dominant-negative forms dramatically suppressed the osteoblastogenic activity of Ruxn2. 	Immunohistochemical staining	Here, we investigated the relationship between lymphoid enhancer-binding factor 1 (LEF1) and transcriptional co-activator with PDZ-binding motif (TAZ), both of which are transcriptional regulators that mediate canonical Wnt signalling during osteoblast differentiation.                                                                                                                                                                                                                                                                                                                                                                 Moreover, we found that LEF1 and TAZ formed a transcriptional complex with runt-related transcription factor 2 (Runx2) and that inhibition of LEF1 or TAZ by their dominant-negative forms dramatically suppressed the osteoblastogenic activity of Ruxn2. 	LEF1		RT-qPCR,Immunoprecipitation, immunoblotting and co-immunoprecipitation,统计分析	Here, we investigated the relationship between lymphoid enhancer-binding factor 1 (LEF1) and transcriptional co-activator with PDZ-binding motif (TAZ), both of which are transcriptional regulators that mediate canonical Wnt signalling during osteoblast differentiation.                                                                                                                                                                                                                                                                                                                                                                 Moreover, we found that LEF1 and TAZ formed a transcriptional complex with runt-related transcription factor 2 (Runx2) and that inhibition of LEF1 or TAZ by their dominant-negative forms dramatically suppressed the osteoblastogenic activity of Ruxn2. 			
29991769	chr17	44804517	44806517	Runx2	Here, we investigated the relationship between lymphoid enhancer-binding factor 1 (LEF1) and transcriptional co-activator with PDZ-binding motif (TAZ), both of which are transcriptional regulators that mediate canonical Wnt signalling during osteoblast differentiation.                                                                                                                                                                                                                                                                                                                                                                 Moreover, we found that LEF1 and TAZ formed a transcriptional complex with runt-related transcription factor 2 (Runx2) and that inhibition of LEF1 or TAZ by their dominant-negative forms dramatically suppressed the osteoblastogenic activity of Ruxn2. 	human		High+Lowthroughput	Interaction of LEF1 with TAZ is necessary for the osteoblastogenic activity of Wnt3a	否		Osteoporosis	fat cell	E_01_0804	RT qPCR, immunoprecipitation, immunoblotting and co immunoprecipitation, statistical analysis	Here, we investigated the relationship between lymphoid enhancer-binding factor 1 (LEF1) and transcriptional co-activator with PDZ-binding motif (TAZ), both of which are transcriptional regulators that mediate canonical Wnt signalling during osteoblast differentiation.                                                                                                                                                                                                                                                                                                                                                                 Moreover, we found that LEF1 and TAZ formed a transcriptional complex with runt-related transcription factor 2 (Runx2) and that inhibition of LEF1 or TAZ by their dominant-negative forms dramatically suppressed the osteoblastogenic activity of Ruxn2. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we investigated the relationship between lymphoid enhancer-binding factor 1 (LEF1) and transcriptional co-activator with PDZ-binding motif (TAZ), both of which are transcriptional regulators that mediate canonical Wnt signalling during osteoblast differentiation.                                                                                                                                                                                                                                                                                                                                                                 Moreover, we found that LEF1 and TAZ formed a transcriptional complex with runt-related transcription factor 2 (Runx2) and that inhibition of LEF1 or TAZ by their dominant-negative forms dramatically suppressed the osteoblastogenic activity of Ruxn2. 		Here, we investigated the relationship between lymphoid enhancer-binding factor 1 (LEF1) and transcriptional co-activator with PDZ-binding motif (TAZ), both of which are transcriptional regulators that mediate canonical Wnt signalling during osteoblast differentiation.                                                                                                                                                                                                                                                                                                                                                                 Moreover, we found that LEF1 and TAZ formed a transcriptional complex with runt-related transcription factor 2 (Runx2) and that inhibition of LEF1 or TAZ by their dominant-negative forms dramatically suppressed the osteoblastogenic activity of Ruxn2. 	Immunohistochemical staining	Here, we investigated the relationship between lymphoid enhancer-binding factor 1 (LEF1) and transcriptional co-activator with PDZ-binding motif (TAZ), both of which are transcriptional regulators that mediate canonical Wnt signalling during osteoblast differentiation.                                                                                                                                                                                                                                                                                                                                                                 Moreover, we found that LEF1 and TAZ formed a transcriptional complex with runt-related transcription factor 2 (Runx2) and that inhibition of LEF1 or TAZ by their dominant-negative forms dramatically suppressed the osteoblastogenic activity of Ruxn2. 			RT-qPCR,Immunoprecipitation, immunoblotting and co-immunoprecipitation,统计分析				Runx2
29988121	chr16	67559717	67561717	CTCF	Similarly, in population-based assays, individual CTCF sites can be seen con- tacting multiple other CTCF sites. 	human		High+Lowthroughput	Enhancer hubs and loop collisions identified from single-allele topologies	否		cancer	hepatocyte	E_01_0805	MC-4C viewpoint specific PCR, Hi-C sequencing	Similarly, in population-based assays, individual CTCF sites can be seen con- tacting multiple other CTCF sites. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Similarly, in population-based assays, individual CTCF sites can be seen con- tacting multiple other CTCF sites. 	Immunohistochemical staining	Similarly, in population-based assays, individual CTCF sites can be seen con- tacting multiple other CTCF sites. 	CTCF		MC-4C viewpoint-specific PCR,Hi-C测序	Similarly, in population-based assays, individual CTCF sites can be seen con- tacting multiple other CTCF sites. 			
29986647	chr4	88004722	88006722	PKD2	Here, we analyse the spatial organization of a large region spanning the polycystic kidney disease 2 (PKD2) gene, one of the genes responsible of autosomal dominant polycystic kidney disease (ADPKD).                                                                                                                                   Conclusions Finally, through alignment of CCCTC-binding factor (CTCF) sites, we suggest that these novel enhancer elements are brought to the PKD2 promoter by chromatin looping via the recruitment of CTCF.	human		High+Lowthroughput	Novel long-range regulatory mechanisms controlling PKD2 gene expression	否		Polycystic kidney disease (ADPKD), lung cancer	epithelial cell	E_01_0806	PCR,Hi-C	Here, we analyse the spatial organization of a large region spanning the polycystic kidney disease 2 (PKD2) gene, one of the genes responsible of autosomal dominant polycystic kidney disease (ADPKD).                                                                                                                                   Conclusions Finally, through alignment of CCCTC-binding factor (CTCF) sites, we suggest that these novel enhancer elements are brought to the PKD2 promoter by chromatin looping via the recruitment of CTCF.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we analyse the spatial organization of a large region spanning the polycystic kidney disease 2 (PKD2) gene, one of the genes responsible of autosomal dominant polycystic kidney disease (ADPKD).                                                                                                                                   Conclusions Finally, through alignment of CCCTC-binding factor (CTCF) sites, we suggest that these novel enhancer elements are brought to the PKD2 promoter by chromatin looping via the recruitment of CTCF.		Here, we analyse the spatial organization of a large region spanning the polycystic kidney disease 2 (PKD2) gene, one of the genes responsible of autosomal dominant polycystic kidney disease (ADPKD).                                                                                                                                   Conclusions Finally, through alignment of CCCTC-binding factor (CTCF) sites, we suggest that these novel enhancer elements are brought to the PKD2 promoter by chromatin looping via the recruitment of CTCF.	Immunohistochemical staining	Here, we analyse the spatial organization of a large region spanning the polycystic kidney disease 2 (PKD2) gene, one of the genes responsible of autosomal dominant polycystic kidney disease (ADPKD).                                                                                                                                   Conclusions Finally, through alignment of CCCTC-binding factor (CTCF) sites, we suggest that these novel enhancer elements are brought to the PKD2 promoter by chromatin looping via the recruitment of CTCF.			PCR,Hi-C				PKD2
29986647	chr16	67559830	67561830	CTCF	Here, we analyse the spatial organization of a large region spanning the polycystic kidney disease 2 (PKD2) gene, one of the genes responsible of autosomal dominant polycystic kidney disease (ADPKD).                                                                                                                                   Conclusions Finally, through alignment of CCCTC-binding factor (CTCF) sites, we suggest that these novel enhancer elements are brought to the PKD2 promoter by chromatin looping via the recruitment of CTCF.	human		High+Lowthroughput	Novel long-range regulatory mechanisms controlling PKD2 gene expression	否		Polycystic kidney disease (ADPKD), lung cancer	epithelial cell	E_01_0806	PCR,Hi-C	Here, we analyse the spatial organization of a large region spanning the polycystic kidney disease 2 (PKD2) gene, one of the genes responsible of autosomal dominant polycystic kidney disease (ADPKD).                                                                                                                                   Conclusions Finally, through alignment of CCCTC-binding factor (CTCF) sites, we suggest that these novel enhancer elements are brought to the PKD2 promoter by chromatin looping via the recruitment of CTCF.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Here, we analyse the spatial organization of a large region spanning the polycystic kidney disease 2 (PKD2) gene, one of the genes responsible of autosomal dominant polycystic kidney disease (ADPKD).                                                                                                                                   Conclusions Finally, through alignment of CCCTC-binding factor (CTCF) sites, we suggest that these novel enhancer elements are brought to the PKD2 promoter by chromatin looping via the recruitment of CTCF.	Immunohistochemical staining	Here, we analyse the spatial organization of a large region spanning the polycystic kidney disease 2 (PKD2) gene, one of the genes responsible of autosomal dominant polycystic kidney disease (ADPKD).                                                                                                                                   Conclusions Finally, through alignment of CCCTC-binding factor (CTCF) sites, we suggest that these novel enhancer elements are brought to the PKD2 promoter by chromatin looping via the recruitment of CTCF.	CTCF		PCR,Hi-C	Here, we analyse the spatial organization of a large region spanning the polycystic kidney disease 2 (PKD2) gene, one of the genes responsible of autosomal dominant polycystic kidney disease (ADPKD).                                                                                                                                   Conclusions Finally, through alignment of CCCTC-binding factor (CTCF) sites, we suggest that these novel enhancer elements are brought to the PKD2 promoter by chromatin looping via the recruitment of CTCF.			
29985393	chr1	116751815	116753815	CD2	Go to: Results Characteristics of thymic iNKT cell subsets We analyzed thymic iNKT cells from BALB/c mice in which the human CD2 gene was knocked-in into the IL-4 locus (KN2), thereby allowing for the identification by flow cytometry of IL-4-secreting iNKT2 cells directly ex vivo.                                                                                                                                                                                                                                                                                        Development of iNKT cells diverges from that of conventional T cells primarily at the double-positive CD4+ CD8+ (DP) stage and requires TCR recognition of CD1d on DP cells, involving homotypic interactions across a DP DP synapse where second signals are initiated by the engagement of homophilic receptors of the signaling lymphocytic-activation molecule (SLAM) family, Slamf1 (SLAM) and Slamf6 (Ly108). 	human,mouse		High+Lowthroughput	TCR signal strength controls thymic differentiation of iNKT cell subsets	否				E_02_0538	RNA SEQ, RNA SEQ, statistical analysis, flow cytometry	Go to: Results Characteristics of thymic iNKT cell subsets We analyzed thymic iNKT cells from BALB/c mice in which the human CD2 gene was knocked-in into the IL-4 locus (KN2), thereby allowing for the identification by flow cytometry of IL-4-secreting iNKT2 cells directly ex vivo.                                                                                                                                                                                                                                                                                        Development of iNKT cells diverges from that of conventional T cells primarily at the double-positive CD4+ CD8+ (DP) stage and requires TCR recognition of CD1d on DP cells, involving homotypic interactions across a DP DP synapse where second signals are initiated by the engagement of homophilic receptors of the signaling lymphocytic-activation molecule (SLAM) family, Slamf1 (SLAM) and Slamf6 (Ly108). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Go to: Results Characteristics of thymic iNKT cell subsets We analyzed thymic iNKT cells from BALB/c mice in which the human CD2 gene was knocked-in into the IL-4 locus (KN2), thereby allowing for the identification by flow cytometry of IL-4-secreting iNKT2 cells directly ex vivo.                                                                                                                                                                                                                                                                                        Development of iNKT cells diverges from that of conventional T cells primarily at the double-positive CD4+ CD8+ (DP) stage and requires TCR recognition of CD1d on DP cells, involving homotypic interactions across a DP DP synapse where second signals are initiated by the engagement of homophilic receptors of the signaling lymphocytic-activation molecule (SLAM) family, Slamf1 (SLAM) and Slamf6 (Ly108). 		Go to: Results Characteristics of thymic iNKT cell subsets We analyzed thymic iNKT cells from BALB/c mice in which the human CD2 gene was knocked-in into the IL-4 locus (KN2), thereby allowing for the identification by flow cytometry of IL-4-secreting iNKT2 cells directly ex vivo.                                                                                                                                                                                                                                                                                        Development of iNKT cells diverges from that of conventional T cells primarily at the double-positive CD4+ CD8+ (DP) stage and requires TCR recognition of CD1d on DP cells, involving homotypic interactions across a DP DP synapse where second signals are initiated by the engagement of homophilic receptors of the signaling lymphocytic-activation molecule (SLAM) family, Slamf1 (SLAM) and Slamf6 (Ly108). 	Immunohistochemical staining	Go to: Results Characteristics of thymic iNKT cell subsets We analyzed thymic iNKT cells from BALB/c mice in which the human CD2 gene was knocked-in into the IL-4 locus (KN2), thereby allowing for the identification by flow cytometry of IL-4-secreting iNKT2 cells directly ex vivo.                                                                                                                                                                                                                                                                                        Development of iNKT cells diverges from that of conventional T cells primarily at the double-positive CD4+ CD8+ (DP) stage and requires TCR recognition of CD1d on DP cells, involving homotypic interactions across a DP DP synapse where second signals are initiated by the engagement of homophilic receptors of the signaling lymphocytic-activation molecule (SLAM) family, Slamf1 (SLAM) and Slamf6 (Ly108). 			RNA-Seq,RNA-Seq,统计分析,流式细胞术				CD2
29983891	chr11	1072345	1074345	MUC2	Tissue organization and expression of mucin 2 (MUC2) and lysozyme (LYZ) demonstrated histologic faithfulness of organoids to healthy and diseased colonic epithelium. 	human		High+Lowthroughput	Cancer-predicting transcriptomic and epigenetic signatures revealed for ulcerative colitis in patient-derived epithelial organoids	否		Ulcerative colitis (UC)	goblet cell	E_01_0807	Immunohistochemistry, RNA SEQ, real time PCR, chip SEQ, statistical analysis	Tissue organization and expression of mucin 2 (MUC2) and lysozyme (LYZ) demonstrated histologic faithfulness of organoids to healthy and diseased colonic epithelium. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Tissue organization and expression of mucin 2 (MUC2) and lysozyme (LYZ) demonstrated histologic faithfulness of organoids to healthy and diseased colonic epithelium. 		Tissue organization and expression of mucin 2 (MUC2) and lysozyme (LYZ) demonstrated histologic faithfulness of organoids to healthy and diseased colonic epithelium. 	Immunohistochemical staining	Tissue organization and expression of mucin 2 (MUC2) and lysozyme (LYZ) demonstrated histologic faithfulness of organoids to healthy and diseased colonic epithelium. 			免疫组织化学,RNA-Seq,Real-time PCR,ChIP-seq,统计分析				MUC2
29983891	chr12	69345724	69347724	LYZ	Tissue organization and expression of mucin 2 (MUC2) and lysozyme (LYZ) demonstrated histologic faithfulness of organoids to healthy and diseased colonic epithelium. 	human		High+Lowthroughput	Cancer-predicting transcriptomic and epigenetic signatures revealed for ulcerative colitis in patient-derived epithelial organoids	否		Ulcerative colitis (UC)	goblet cell	E_01_0807	Immunohistochemistry, RNA SEQ, real time PCR, chip SEQ, statistical analysis	Tissue organization and expression of mucin 2 (MUC2) and lysozyme (LYZ) demonstrated histologic faithfulness of organoids to healthy and diseased colonic epithelium. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Tissue organization and expression of mucin 2 (MUC2) and lysozyme (LYZ) demonstrated histologic faithfulness of organoids to healthy and diseased colonic epithelium. 		Tissue organization and expression of mucin 2 (MUC2) and lysozyme (LYZ) demonstrated histologic faithfulness of organoids to healthy and diseased colonic epithelium. 	Immunohistochemical staining	Tissue organization and expression of mucin 2 (MUC2) and lysozyme (LYZ) demonstrated histologic faithfulness of organoids to healthy and diseased colonic epithelium. 			免疫组织化学,RNA-Seq,Real-time PCR,ChIP-seq,统计分析				LYZ
29979962	chr7	46371356	46373481	CTCF	Tridimensional enhancer-promoter interactions are mediated by DNA, RNA, and protein components, including transcription factors and chromatin-binding CTCF and Cohesin complexes (Bonev and Cavalli, 2016).	mouse		Low throughput	A Muscle-Specific Enhancer RNA Mediates Cohesin Recruitment and Regulates Transcription In trans	否	--	--	neural progenitor cell	E_02_0539	ChIRP	"To directly evaluate whether the DRReRNA 2Kb transcript could undergo splicing, we 
cloned it into the splicing reporter plasmid RHCglo.The resulting plasmid (RHCglo-DRR) or the parental vector were transiently transfected in human embryonic kidney 293 cells, in C2C12 MB or C2C12 cells induced to differentiate. RNA recovered from RHCglo-DRR-transfected cells and amplified with vector-specific primers gave rise to a single band of ~1.5Kb (Figure S1B,C), the same length observed for endogenous DRReRNA."	Enhancer	--	Western blot,RT-qPCR,ChIP	DRReRNA influences transcription of Myogenin in trans without significantly affecting that of MyoD in cis;This analysis revealed that the top two DRReRNA-enriched ChIRP regions were observed at Myogenin and DRR, whereas the MyoD gene located 5 kb downstream of DRR was devoid of DRReRNA binding.	AI503393,MYF3,MyoD,?Myod-1,bHLHc1	DRR eRNA Promotes Cohesin Recruitment and Maintenance at the Myogenin Locus	qRT-PCR	A non-coding RNA transcribed from an Enhancer region on mouse chromosome 7 (eRNA) recruits cohesin to regulate transcription of the Myogenin gene located on chromosome 1.	--	--	--	--	--	--	Myod1
29977016	chr7	50301609	50303609	IKZF1	Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.	human		High+Lowthroughput	Genetic predisposition to B-cell acute lymphoblastic leukemia at 14q11.2 is mediated by a CEBPE promoter polymorphism	是	rs2239630	Acute lymphoblastic leukemia (all)	B cell	E_01_0808	Chip SEQ, QRT PCR, RNA SEQ, flow cytometry	Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.	Immunohistochemical staining	Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.	IKZF1		ChIP-seq,qRT-PCR,RNA-Seq,流式细胞术	Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.			
29977016	chr9	36830512	36832512	PAX5	Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.	human		High+Lowthroughput	Genetic predisposition to B-cell acute lymphoblastic leukemia at 14q11.2 is mediated by a CEBPE promoter polymorphism	是	rs2239630	Acute lymphoblastic leukemia (all)	B cell	E_01_0808	Chip SEQ, QRT PCR, RNA SEQ, flow cytometry	Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.	Immunohistochemical staining	Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.	PAX5		ChIP-seq,qRT-PCR,RNA-Seq,流式细胞术	Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.			
29977016	chr14	23114856	23116856	CEBPE	Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.	human		High+Lowthroughput	Genetic predisposition to B-cell acute lymphoblastic leukemia at 14q11.2 is mediated by a CEBPE promoter polymorphism	是	rs2239630	Acute lymphoblastic leukemia (all)	B cell	E_01_0808	Chip SEQ, QRT PCR, RNA SEQ, flow cytometry	Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.	Immunohistochemical staining	Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.	CEBPE		ChIP-seq,qRT-PCR,RNA-Seq,流式细胞术	Correspondingly, crucial B-cell development transcription factors IKZF1, PAX5, and EBF1 are also the targets of frequent somatic mutation [11, 12], highlighting that GWAS signals and somatic mutations may impact upon the same genes.                                                                                                                                                                                                                                                                                                                                                                                       The rs2239630-A risk allele is associated with increased promotor activity and CEBPE expression.			
29976669	chr6	170552062	170554062	TBP	Viruses with mutations in E1A subdomains were constructed and analyzed for kinetics of early viral RNA expression and association of acetylated H3K9, K18, K27, TBP, and RNA polymerase II (Pol II) across the viral genome.	mouse		High+Lowthroughput	Adenovirus E1A Activation Domain Regulates H3 Acetylation Affecting Varied Steps in Transcription at Different Viral Promoters	否				E_02_0540	qRT-PCR,ChIP-seq	Viruses with mutations in E1A subdomains were constructed and analyzed for kinetics of early viral RNA expression and association of acetylated H3K9, K18, K27, TBP, and RNA polymerase II (Pol II) across the viral genome.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Viruses with mutations in E1A subdomains were constructed and analyzed for kinetics of early viral RNA expression and association of acetylated H3K9, K18, K27, TBP, and RNA polymerase II (Pol II) across the viral genome.		Viruses with mutations in E1A subdomains were constructed and analyzed for kinetics of early viral RNA expression and association of acetylated H3K9, K18, K27, TBP, and RNA polymerase II (Pol II) across the viral genome.	Immunohistochemical staining	Viruses with mutations in E1A subdomains were constructed and analyzed for kinetics of early viral RNA expression and association of acetylated H3K9, K18, K27, TBP, and RNA polymerase II (Pol II) across the viral genome.			qRT-PCR,ChIP-seq				TBP
29973940	chr12	54359352	54361352	GPR84	GPR84 is a member of the metabolic G protein-coupled receptor family, and its expression has been described predominantly in immune cells. 	mouse,human		High+Lowthroughput	Activation of the Immune-Metabolic Receptor GPR84 Enhances Inflammation and Phagocytosis in Macrophages	否		diabetes	macrophage	E_02_0541	FACS, Western blot, immunofluorescence staining, chemotaxis assay	GPR84 is a member of the metabolic G protein-coupled receptor family, and its expression has been described predominantly in immune cells. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	GPR84 is a member of the metabolic G protein-coupled receptor family, and its expression has been described predominantly in immune cells. 		GPR84 is a member of the metabolic G protein-coupled receptor family, and its expression has been described predominantly in immune cells. 	Immunohistochemical staining	GPR84 is a member of the metabolic G protein-coupled receptor family, and its expression has been described predominantly in immune cells. 			FACS,western blot,免疫荧光染色,Chemotaxis Assay				GPR84
29973282	chr12	78861267	78863267	SYT1	The researchers detected the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) according to kit instructions. The protein expression of brain-derived neurotrophic factor (BDNF), synaptotagmin-1 (SYT1) and cyclic adenosine monophosphate response element binding protein (CREB) in the rats hippocampi was detected by immunohistochemistry and Western blot, and the gene expression of cAMP-regulated enhancer (CRE) was detected by real-time quantitative polymerase chain reaction (PCR).                                                                                                                                                                                                                                                                                  The synaptic plasticity related proteins BDNF and SYT1 can not only promote neuronal regeneration but also regulate synaptic plasticity, thereby affecting the learning and memory functions of the brain.	mouse		High+Lowthroughput	Possible mechanism of Vitis vinifera L. flavones on neurotransmitters, synaptic transmission and related learning and memory in Alzheimer model rats	否		Alzheimer's disease (AD)		E_02_0542	Chat, ache assay, immunohistochemistry staining, Western blot, real time quantitative PCR, statistical analysis	The researchers detected the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) according to kit instructions. The protein expression of brain-derived neurotrophic factor (BDNF), synaptotagmin-1 (SYT1) and cyclic adenosine monophosphate response element binding protein (CREB) in the rats hippocampi was detected by immunohistochemistry and Western blot, and the gene expression of cAMP-regulated enhancer (CRE) was detected by real-time quantitative polymerase chain reaction (PCR).                                                                                                                                                                                                                                                                                  The synaptic plasticity related proteins BDNF and SYT1 can not only promote neuronal regeneration but also regulate synaptic plasticity, thereby affecting the learning and memory functions of the brain.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The researchers detected the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) according to kit instructions. The protein expression of brain-derived neurotrophic factor (BDNF), synaptotagmin-1 (SYT1) and cyclic adenosine monophosphate response element binding protein (CREB) in the rats hippocampi was detected by immunohistochemistry and Western blot, and the gene expression of cAMP-regulated enhancer (CRE) was detected by real-time quantitative polymerase chain reaction (PCR).                                                                                                                                                                                                                                                                                  The synaptic plasticity related proteins BDNF and SYT1 can not only promote neuronal regeneration but also regulate synaptic plasticity, thereby affecting the learning and memory functions of the brain.		The researchers detected the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) according to kit instructions. The protein expression of brain-derived neurotrophic factor (BDNF), synaptotagmin-1 (SYT1) and cyclic adenosine monophosphate response element binding protein (CREB) in the rats hippocampi was detected by immunohistochemistry and Western blot, and the gene expression of cAMP-regulated enhancer (CRE) was detected by real-time quantitative polymerase chain reaction (PCR).                                                                                                                                                                                                                                                                                  The synaptic plasticity related proteins BDNF and SYT1 can not only promote neuronal regeneration but also regulate synaptic plasticity, thereby affecting the learning and memory functions of the brain.	Immunohistochemical staining	The researchers detected the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) according to kit instructions. The protein expression of brain-derived neurotrophic factor (BDNF), synaptotagmin-1 (SYT1) and cyclic adenosine monophosphate response element binding protein (CREB) in the rats hippocampi was detected by immunohistochemistry and Western blot, and the gene expression of cAMP-regulated enhancer (CRE) was detected by real-time quantitative polymerase chain reaction (PCR).                                                                                                                                                                                                                                                                                  The synaptic plasticity related proteins BDNF and SYT1 can not only promote neuronal regeneration but also regulate synaptic plasticity, thereby affecting the learning and memory functions of the brain.			ChAT、AChE检测,Immunohistochemistry staining,Western blot,Real-time quantitative PCR,统计分析				SYT1
29973282	chr11	27652242	27654242	BDNF	The researchers detected the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) according to kit instructions. The protein expression of brain-derived neurotrophic factor (BDNF), synaptotagmin-1 (SYT1) and cyclic adenosine monophosphate response element binding protein (CREB) in the rats hippocampi was detected by immunohistochemistry and Western blot, and the gene expression of cAMP-regulated enhancer (CRE) was detected by real-time quantitative polymerase chain reaction (PCR).                                                                                                                                                                                                                                                                                  The synaptic plasticity related proteins BDNF and SYT1 can not only promote neuronal regeneration but also regulate synaptic plasticity, thereby affecting the learning and memory functions of the brain.	mouse		High+Lowthroughput	Possible mechanism of Vitis vinifera L. flavones on neurotransmitters, synaptic transmission and related learning and memory in Alzheimer model rats	否		Alzheimer's disease (AD)		E_02_0542	Chat, ache assay, immunohistochemistry staining, Western blot, real time quantitative PCR, statistical analysis	The researchers detected the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) according to kit instructions. The protein expression of brain-derived neurotrophic factor (BDNF), synaptotagmin-1 (SYT1) and cyclic adenosine monophosphate response element binding protein (CREB) in the rats hippocampi was detected by immunohistochemistry and Western blot, and the gene expression of cAMP-regulated enhancer (CRE) was detected by real-time quantitative polymerase chain reaction (PCR).                                                                                                                                                                                                                                                                                  The synaptic plasticity related proteins BDNF and SYT1 can not only promote neuronal regeneration but also regulate synaptic plasticity, thereby affecting the learning and memory functions of the brain.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The researchers detected the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) according to kit instructions. The protein expression of brain-derived neurotrophic factor (BDNF), synaptotagmin-1 (SYT1) and cyclic adenosine monophosphate response element binding protein (CREB) in the rats hippocampi was detected by immunohistochemistry and Western blot, and the gene expression of cAMP-regulated enhancer (CRE) was detected by real-time quantitative polymerase chain reaction (PCR).                                                                                                                                                                                                                                                                                  The synaptic plasticity related proteins BDNF and SYT1 can not only promote neuronal regeneration but also regulate synaptic plasticity, thereby affecting the learning and memory functions of the brain.		The researchers detected the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) according to kit instructions. The protein expression of brain-derived neurotrophic factor (BDNF), synaptotagmin-1 (SYT1) and cyclic adenosine monophosphate response element binding protein (CREB) in the rats hippocampi was detected by immunohistochemistry and Western blot, and the gene expression of cAMP-regulated enhancer (CRE) was detected by real-time quantitative polymerase chain reaction (PCR).                                                                                                                                                                                                                                                                                  The synaptic plasticity related proteins BDNF and SYT1 can not only promote neuronal regeneration but also regulate synaptic plasticity, thereby affecting the learning and memory functions of the brain.	Immunohistochemical staining	The researchers detected the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) according to kit instructions. The protein expression of brain-derived neurotrophic factor (BDNF), synaptotagmin-1 (SYT1) and cyclic adenosine monophosphate response element binding protein (CREB) in the rats hippocampi was detected by immunohistochemistry and Western blot, and the gene expression of cAMP-regulated enhancer (CRE) was detected by real-time quantitative polymerase chain reaction (PCR).                                                                                                                                                                                                                                                                                  The synaptic plasticity related proteins BDNF and SYT1 can not only promote neuronal regeneration but also regulate synaptic plasticity, thereby affecting the learning and memory functions of the brain.			ChAT、AChE检测,Immunohistochemistry staining,Western blot,Real-time quantitative PCR,统计分析				BDNF
29970899	chr7	148804543	148806543	EZH2	In addition, in accordance with the findings of the RNA-Seq analysis, SNHG1 knockdown exhibited a significant impact on the target genes that were linked to cell migration and regulation of cell proliferation, in addition to the apoptotic phenomenon. In a mechanistic manner, we also showed that SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A, and, as a result, altered the CCA cell biology.	human		High+Lowthroughput	Epigenetic silencing of tumor suppressor gene CDKN1A by oncogenic long non-coding RNA SNHG1 in cholangiocarcinoma	否		Cholangiocarcinoma (CCA)	CCA cell	E_01_0809	QRT PCR, Western blot, flow cytometry, rip assays, chip assays, immunofluorescence, statistical analysis, gene knockdown, RNA seq	In addition, in accordance with the findings of the RNA-Seq analysis, SNHG1 knockdown exhibited a significant impact on the target genes that were linked to cell migration and regulation of cell proliferation, in addition to the apoptotic phenomenon. In a mechanistic manner, we also showed that SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A, and, as a result, altered the CCA cell biology.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			In addition, in accordance with the findings of the RNA-Seq analysis, SNHG1 knockdown exhibited a significant impact on the target genes that were linked to cell migration and regulation of cell proliferation, in addition to the apoptotic phenomenon. In a mechanistic manner, we also showed that SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A, and, as a result, altered the CCA cell biology.	Immunohistochemical staining	In addition, in accordance with the findings of the RNA-Seq analysis, SNHG1 knockdown exhibited a significant impact on the target genes that were linked to cell migration and regulation of cell proliferation, in addition to the apoptotic phenomenon. In a mechanistic manner, we also showed that SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A, and, as a result, altered the CCA cell biology.	EZH2		qRT-PCR,Western blot,流式细胞术,RIP assays,ChIP assays,Immunofluorescence,统计分析,基因敲降,RNA-Seq	In addition, in accordance with the findings of the RNA-Seq analysis, SNHG1 knockdown exhibited a significant impact on the target genes that were linked to cell migration and regulation of cell proliferation, in addition to the apoptotic phenomenon. In a mechanistic manner, we also showed that SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A, and, as a result, altered the CCA cell biology.			
29970899	chr11	62848904	62850904	SNHG1	In addition, in accordance with the findings of the RNA-Seq analysis, SNHG1 knockdown exhibited a significant impact on the target genes that were linked to cell migration and regulation of cell proliferation, in addition to the apoptotic phenomenon. In a mechanistic manner, we also showed that SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A, and, as a result, altered the CCA cell biology.	human		High+Lowthroughput	Epigenetic silencing of tumor suppressor gene CDKN1A by oncogenic long non-coding RNA SNHG1 in cholangiocarcinoma	否		Cholangiocarcinoma (CCA)	CCA cell	E_01_0809	QRT PCR, Western blot, flow cytometry, rip assays, chip assays, immunofluorescence, statistical analysis, gene knockdown, RNA seq	In addition, in accordance with the findings of the RNA-Seq analysis, SNHG1 knockdown exhibited a significant impact on the target genes that were linked to cell migration and regulation of cell proliferation, in addition to the apoptotic phenomenon. In a mechanistic manner, we also showed that SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A, and, as a result, altered the CCA cell biology.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In addition, in accordance with the findings of the RNA-Seq analysis, SNHG1 knockdown exhibited a significant impact on the target genes that were linked to cell migration and regulation of cell proliferation, in addition to the apoptotic phenomenon. In a mechanistic manner, we also showed that SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A, and, as a result, altered the CCA cell biology.		In addition, in accordance with the findings of the RNA-Seq analysis, SNHG1 knockdown exhibited a significant impact on the target genes that were linked to cell migration and regulation of cell proliferation, in addition to the apoptotic phenomenon. In a mechanistic manner, we also showed that SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A, and, as a result, altered the CCA cell biology.	Immunohistochemical staining	In addition, in accordance with the findings of the RNA-Seq analysis, SNHG1 knockdown exhibited a significant impact on the target genes that were linked to cell migration and regulation of cell proliferation, in addition to the apoptotic phenomenon. In a mechanistic manner, we also showed that SNHG1 bound to the histone methyltransferase enhancer of the zeste homolog 2 (EZH2, which is regarded as the catalytic subunit of the polycomb repressive complex 2 (PRC2), which is an extremely conserved protein complex regulating gene expression with the help of methylating lysine 27 on histone H3), specifying the histone alteration pattern on the target genes, including CDKN1A, and, as a result, altered the CCA cell biology.			qRT-PCR,Western blot,流式细胞术,RIP assays,ChIP assays,Immunofluorescence,统计分析,基因敲降,RNA-Seq				SNHG1
29967281	chr17	85527960	85530660	Six3	Conditional deletion of Six3 also prevents the formation of most D2 MSNs, phenocopying the Sp8/9 mutants.                                                                                                                                                                                                                                                  SP8 and SP9 together drive expression of the transcription factor Six3 in a spatially restricted domain of the LGE subventricular zone.	mouse		Low+High throughput	SP8 and SP9 coordinately promote D2-type medium spiny neuron production by activating Six3 expression	否	--	--		E_02_0543	Luciferase Reporter Assay,ChIP-seq	We found an SP9 ChIP-Seq peak at the Six3 promoter region (?5 to +411 of the TSS) (Fig. 9C), and several additional peaks upstream of the Six3 gene (regions 1, 2 and 3) (Fig. 9C);Thus, these noncoding domains are strong candidates for the Six3 promoter and three Six3 enhancers.	Enhancer	--	ChIP-seq,Luciferase Reporter Assay	Together,the results of ChIP-seq and Dual-Luciferase assay provide evidence that SP9 promotes Six3 expression in the LGE SVZ through its direct binding to the promoter and possibly through binding to regulatory elements within the Six3 locus.	E130112M24Rika,Six3alpha,Six3b,Six3beta,?Six3	--	--	--	Six3	E130112M24Rika，Six3alpha，Six3b，Six3beta	RNA-seq,ChIP-seq	SP8 and SP9 together drive expression of the transcription factor Six3 in a spatially restricted domain of the LGE subventricular zone. Conditional deletion of Six3 also prevents the formation of most D2 MSNs, phenocopying the Sp8/9 mutants.This implies that there are additional mechanisms that regulate the generation of D2 MSNs in Sp9-KO mice, one of which was suggested by the LGE RNA-Seq analysis. We identified that expression of the TF Six3 was decreased ?5-fold in E16.5 Sp8/9-DCKO mice compared with control mice.	--	--	Six3
29967281	chr17	85527960	85530660	SP8	Conditional deletion of Six3 also prevents the formation of most D2 MSNs, phenocopying the Sp8/9 mutants.                                                                                                                                                                                                                                                  SP8 and SP9 together drive expression of the transcription factor Six3 in a spatially restricted domain of the LGE subventricular zone.	mouse		Low+High throughput	SP8 and SP9 coordinately promote D2-type medium spiny neuron production by activating Six3 expression	否	--	--		E_02_0543	Luciferase Reporter Assay,ChIP-seq	We found an SP9 ChIP-Seq peak at the Six3 promoter region (?5 to +411 of the TSS) (Fig. 9C), and several additional peaks upstream of the Six3 gene (regions 1, 2 and 3) (Fig. 9C);Thus, these noncoding domains are strong candidates for the Six3 promoter and three Six3 enhancers.	Enhancer	--	ChIP-seq,Luciferase Reporter Assay	Together,the results of ChIP-seq and Dual-Luciferase assay provide evidence that SP9 promotes Six3 expression in the LGE SVZ through its direct binding to the promoter and possibly through binding to regulatory elements within the Six3 locus.	E130112M24Rika,Six3alpha,Six3b,Six3beta,?Six3	--	--	--	Six3	E130112M24Rika，Six3alpha，Six3b，Six3beta	RNA-seq,ChIP-seq	SP8 and SP9 together drive expression of the transcription factor Six3 in a spatially restricted domain of the LGE subventricular zone. Conditional deletion of Six3 also prevents the formation of most D2 MSNs, phenocopying the Sp8/9 mutants.This implies that there are additional mechanisms that regulate the generation of D2 MSNs in Sp9-KO mice, one of which was suggested by the LGE RNA-Seq analysis. We identified that expression of the TF Six3 was decreased ?5-fold in E16.5 Sp8/9-DCKO mice compared with control mice.	--	--	Six3
29967281	chr17	85527960	85530660	SP9	Conditional deletion of Six3 also prevents the formation of most D2 MSNs, phenocopying the Sp8/9 mutants.                                                                                                                                                                                                                                                  SP8 and SP9 together drive expression of the transcription factor Six3 in a spatially restricted domain of the LGE subventricular zone.	mouse		Low+High throughput	SP8 and SP9 coordinately promote D2-type medium spiny neuron production by activating Six3 expression	否	--	--		E_02_0543	Luciferase Reporter Assay,ChIP-seq	We found an SP9 ChIP-Seq peak at the Six3 promoter region (?5 to +411 of the TSS) (Fig. 9C), and several additional peaks upstream of the Six3 gene (regions 1, 2 and 3) (Fig. 9C);Thus, these noncoding domains are strong candidates for the Six3 promoter and three Six3 enhancers.	Enhancer	--	ChIP-seq,Luciferase Reporter Assay	Together,the results of ChIP-seq and Dual-Luciferase assay provide evidence that SP9 promotes Six3 expression in the LGE SVZ through its direct binding to the promoter and possibly through binding to regulatory elements within the Six3 locus.	E130112M24Rika,Six3alpha,Six3b,Six3beta,?Six3	--	--	--	Six3	E130112M24Rika，Six3alpha，Six3b，Six3beta	RNA-seq,ChIP-seq	SP8 and SP9 together drive expression of the transcription factor Six3 in a spatially restricted domain of the LGE subventricular zone. Conditional deletion of Six3 also prevents the formation of most D2 MSNs, phenocopying the Sp8/9 mutants.This implies that there are additional mechanisms that regulate the generation of D2 MSNs in Sp9-KO mice, one of which was suggested by the LGE RNA-Seq analysis. We identified that expression of the TF Six3 was decreased ?5-fold in E16.5 Sp8/9-DCKO mice compared with control mice.	--	--	Six3
29966981	chr4	140556428	140558428	UCP1	Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.	mouse,human	adipose tissue	High+Lowthroughput	Heshouwu (Polygonum multiflorum Thunb.) ethanol extract suppresses pre-adipocytes differentiation in 3T3-L1 cells and adiposity in obese mice	否		Type 2 diabetes, obesity	3T3-L1 cell	E_02_0544	Real time PCR, Western blot, and statistical analysis	Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.		Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.	Immunohistochemical staining	Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.			real-time PCR,Western blot,统计分析				UCP1
29966981	chr1	53194183	53196183	CPT2	Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.	mouse,human	adipose tissue	High+Lowthroughput	Heshouwu (Polygonum multiflorum Thunb.) ethanol extract suppresses pre-adipocytes differentiation in 3T3-L1 cells and adiposity in obese mice	否		Type 2 diabetes, obesity	3T3-L1 cell	E_02_0544	Real time PCR, Western blot, and statistical analysis	Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.		Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.	Immunohistochemical staining	Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.			real-time PCR,Western blot,统计分析				CPT2
29966981	chr11	75756789	75758789	DGAT2	Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.	mouse,human	adipose tissue	High+Lowthroughput	Heshouwu (Polygonum multiflorum Thunb.) ethanol extract suppresses pre-adipocytes differentiation in 3T3-L1 cells and adiposity in obese mice	否		Type 2 diabetes, obesity	3T3-L1 cell	E_02_0544	Real time PCR, Western blot, and statistical analysis	Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.		Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.	Immunohistochemical staining	Furthermore, PME supplementation significantly up-regulated the PPARα, CPT1, CPT2, UCP1 and HSL mRNA levels compared with the HFD group, whereas it down-regulated expression of the PPARγ and DGAT2 genes.			real-time PCR,Western blot,统计分析				DGAT2
29966764	chrX	48519594	48521594	EBP	In contrast, enhancers of subcutaneous adipocytes show enrichment of motifs for common adipogenic transcription factors, such as C/EBP, NFI and PPAR implicating substantially disparate gene regulatory  networks in visceral and subcutaneous adipocytes.	human,mouse	adipose tissue	High+Lowthroughput	Enhancer-driven transcriptional regulation is a potential key determinant for human visceral and subcutaneous adipocytes	否		Obesity	fat cell	E_02_0545	RT-qPCR,RNA-Seq,ChIP-Seq	In contrast, enhancers of subcutaneous adipocytes show enrichment of motifs for common adipogenic transcription factors, such as C/EBP, NFI and PPAR implicating substantially disparate gene regulatory  networks in visceral and subcutaneous adipocytes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In contrast, enhancers of subcutaneous adipocytes show enrichment of motifs for common adipogenic transcription factors, such as C/EBP, NFI and PPAR implicating substantially disparate gene regulatory  networks in visceral and subcutaneous adipocytes.		In contrast, enhancers of subcutaneous adipocytes show enrichment of motifs for common adipogenic transcription factors, such as C/EBP, NFI and PPAR implicating substantially disparate gene regulatory  networks in visceral and subcutaneous adipocytes.	Immunohistochemical staining	In contrast, enhancers of subcutaneous adipocytes show enrichment of motifs for common adipogenic transcription factors, such as C/EBP, NFI and PPAR implicating substantially disparate gene regulatory  networks in visceral and subcutaneous adipocytes.			RT-qPCR,RNA-Seq,ChIP-Seq				EBP
29966306	chrX	48518772	48520772	EBP	However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.	human,mouse		High+Lowthroughput	Regulation of Expression of CEBP Genes by Variably Expressed Vitamin D Receptor and Retinoic Acid Receptor α in Human Acute Myeloid Leukemia Cell Lines	否		Myeloid leukemia cells	KG-1 cell	E_02_0546	Real time PCR, Western blot, immunofluorescence staining, statistical analysis	However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.		However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.	Immunohistochemical staining	However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.			Real-Time PCR,Western Blot,免疫荧光染色,统计分析				EBP
29966306	chr12	47838064	47840064	VDR	However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.	human,mouse		High+Lowthroughput	Regulation of Expression of CEBP Genes by Variably Expressed Vitamin D Receptor and Retinoic Acid Receptor α in Human Acute Myeloid Leukemia Cell Lines	否		Myeloid leukemia cells	KG-1 cell	E_02_0546	Real time PCR, Western blot, immunofluorescence staining, statistical analysis	However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.		However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.	Immunohistochemical staining	However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.			Real-Time PCR,Western Blot,免疫荧光染色,统计分析				VDR
29966306	chr8	47734412	47736412	CEBPD	However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.	human,mouse		High+Lowthroughput	Regulation of Expression of CEBP Genes by Variably Expressed Vitamin D Receptor and Retinoic Acid Receptor α in Human Acute Myeloid Leukemia Cell Lines	否		Myeloid leukemia cells	KG-1 cell	E_02_0546	Real time PCR, Western blot, immunofluorescence staining, statistical analysis	However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.		However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.	Immunohistochemical staining	However, precise mechanism controlling the diversification of myeloid progenitors is largely unknown, CCAAT/enhancer-binding protein (C/EBP) transcription factors have been characterized as key regulators of the development and function of the myeloid system.                                                                                                                                                                                                                                                                                                                                                    In this study, we show that in acute myeloid leukemia (AML) cells, high expression of vitamin D receptor gene (VDR) is needed for strong and sustained upregulation of CEBPB gene, while the moderate expression of VDR is sufficient for upregulation of CEBPD in response to 1,25D.			Real-Time PCR,Western Blot,免疫荧光染色,统计分析				CEBPD
29964053	chrX	67541163	67543163	AR	Specifically, eRNA MARC1 (eMARC1), transcribed from androgen receptor (AR) activated enhancer that was responsible for activation of nearby coding transcription units [20, 21], was identified as an androgen associated AR-activated eRNA [22].	human	BCA tissues	High+Lowthroughput	High expression of enhancer RNA MARC1 or its activation by DHT is associated with the malignant behavior in bladder cancer	否		Bladder cancer (BCA)	Bca cell	E_01_0810	Real time quantitative PCR, flow cytometry, statistical analysis	Specifically, eRNA MARC1 (eMARC1), transcribed from androgen receptor (AR) activated enhancer that was responsible for activation of nearby coding transcription units [20, 21], was identified as an androgen associated AR-activated eRNA [22].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Specifically, eRNA MARC1 (eMARC1), transcribed from androgen receptor (AR) activated enhancer that was responsible for activation of nearby coding transcription units [20, 21], was identified as an androgen associated AR-activated eRNA [22].	Immunohistochemical staining	Specifically, eRNA MARC1 (eMARC1), transcribed from androgen receptor (AR) activated enhancer that was responsible for activation of nearby coding transcription units [20, 21], was identified as an androgen associated AR-activated eRNA [22].	AR		Real-time quantitative PCR,流式细胞术,统计分析	Specifically, eRNA MARC1 (eMARC1), transcribed from androgen receptor (AR) activated enhancer that was responsible for activation of nearby coding transcription units [20, 21], was identified as an androgen associated AR-activated eRNA [22].			
29963192	chr1	156460745	156462745	MEF2D	In the present study, it was found that MEF2D and miR-30a were inversely correlated in lung cancer samples.	human		High+Lowthroughput	Absent expression of miR-30a promotes the growth of lung cancer cells by targeting MEF2D	否		lung cancer	A549 cell	E_01_0811	RT qPCR, Western blot, statistical analysis, flow cytometry	In the present study, it was found that MEF2D and miR-30a were inversely correlated in lung cancer samples.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the present study, it was found that MEF2D and miR-30a were inversely correlated in lung cancer samples.		In the present study, it was found that MEF2D and miR-30a were inversely correlated in lung cancer samples.	Immunohistochemical staining	In the present study, it was found that MEF2D and miR-30a were inversely correlated in lung cancer samples.			RT-qPCR,Western blot,统计分析,流式细胞术				MEF2D
29958106	chr21	34785412	34787412	RUNX1	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).	human,mouse		High+Lowthroughput	CBFβ-SMMHC Inhibition Triggers Apoptosis by Disrupting MYC Chromatin Dynamics in Acute Myeloid Leukemia	否		Myeloid leukemia	cancer cell	E_02_0547	Flow cytometry, quantitative RT-PCR, RNA SEQ, chip qPCR, chip SEQ, ATAC qPCR, ATAC SEQ, immunoblotting	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).		The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).	Immunohistochemical staining	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).			流式细胞术,Quantitative RT-PCR,RNA-seq,ChIP qPCR,ChIP-seq,ATAC-qPCR,ATAC-seq,Immunoblotting				RUNX1
29958106	chr8	127732760	127734760	MYC	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).	human,mouse		High+Lowthroughput	CBFβ-SMMHC Inhibition Triggers Apoptosis by Disrupting MYC Chromatin Dynamics in Acute Myeloid Leukemia	否		Myeloid leukemia	cancer cell	E_02_0547	Flow cytometry, quantitative RT-PCR, RNA SEQ, chip qPCR, chip SEQ, ATAC qPCR, ATAC SEQ, immunoblotting	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).		The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).	Immunohistochemical staining	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).			流式细胞术,Quantitative RT-PCR,RNA-seq,ChIP qPCR,ChIP-seq,ATAC-qPCR,ATAC-seq,Immunoblotting				MYC
29958106	chr16	67026226	67028226	CBFB	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).	human,mouse		High+Lowthroughput	CBFβ-SMMHC Inhibition Triggers Apoptosis by Disrupting MYC Chromatin Dynamics in Acute Myeloid Leukemia	否		Myeloid leukemia	cancer cell	E_02_0547	Flow cytometry, quantitative RT-PCR, RNA SEQ, chip qPCR, chip SEQ, ATAC qPCR, ATAC SEQ, immunoblotting	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).		The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).	Immunohistochemical staining	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).			流式细胞术,Quantitative RT-PCR,RNA-seq,ChIP qPCR,ChIP-seq,ATAC-qPCR,ATAC-seq,Immunoblotting				CBFB
29958106	chr16	15700466	15702466	MYH11	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).	human,mouse		High+Lowthroughput	CBFβ-SMMHC Inhibition Triggers Apoptosis by Disrupting MYC Chromatin Dynamics in Acute Myeloid Leukemia	否		Myeloid leukemia	cancer cell	E_02_0547	Flow cytometry, quantitative RT-PCR, RNA SEQ, chip qPCR, chip SEQ, ATAC qPCR, ATAC SEQ, immunoblotting	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).		The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).	Immunohistochemical staining	The fusion oncoprotein CBFβ-SMMHC, expressed in leukemia cases with chromosome 16 inversion, drives leukemia development and maintenance by altering the activity of the transcription factor RUNX1.Here we demonstrate that CBFβ-SMMHC maintains cell viability by neutralizing RUNX1-mediated repression of MYC expression.                                                                                                                                                                                                                   The chromosome inversion inv(16)(p13;q22), found in 8% of acute myeloid leukemia (AML) cases, fuses the CBFB and MYH11 genes to produce the leukemic oncoprotein CBFβ-SMMHC (Liu et al., 1993).			流式细胞术,Quantitative RT-PCR,RNA-seq,ChIP qPCR,ChIP-seq,ATAC-qPCR,ATAC-seq,Immunoblotting				MYH11
29956731	chr7	148804007	148806007	EZH2	Therefore, an increased level of EZH2 is considered to indicate propensity for metastasis and poor outcome in patients with mammary tumors (21).	human,mouse	Breast cancer tissues	High+Lowthroughput	Quercetin?3?methyl ether suppresses human breast cancer stem cell formation by inhibiting the Notch1 and PI3K/Akt signaling pathways	否		mammary cancer	Cancer stem cell	E_02_0548	Western blot, statistical analysis, flow cytometry	Therefore, an increased level of EZH2 is considered to indicate propensity for metastasis and poor outcome in patients with mammary tumors (21).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Therefore, an increased level of EZH2 is considered to indicate propensity for metastasis and poor outcome in patients with mammary tumors (21).		Therefore, an increased level of EZH2 is considered to indicate propensity for metastasis and poor outcome in patients with mammary tumors (21).	Immunohistochemical staining	Therefore, an increased level of EZH2 is considered to indicate propensity for metastasis and poor outcome in patients with mammary tumors (21).			Western blot,统计分析,流式细胞术				EZH2
29956121	chr3	189628865	189630865	TP63	Abstract Purpose Genome-wide association studies (GWAS) have led to the identification of a bladder cancer susceptibility variant (rs710521) in a non-coding intergenic region between the TP63 and LEPREL1 genes on chromosome 3q28, suggesting a role in the transcriptional regulation of these genes.	human		High+Lowthroughput	Identification of an enhancer region within the TP63/LEPREL1 locus containing genetic variants associated with bladder cancer risk	是	rs710521,rs6983267	Bladder cancer (BCA)	bladder cancer cell	E_01_0812	Faire, RT qPCR, statistical analysis	Abstract Purpose Genome-wide association studies (GWAS) have led to the identification of a bladder cancer susceptibility variant (rs710521) in a non-coding intergenic region between the TP63 and LEPREL1 genes on chromosome 3q28, suggesting a role in the transcriptional regulation of these genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Abstract Purpose Genome-wide association studies (GWAS) have led to the identification of a bladder cancer susceptibility variant (rs710521) in a non-coding intergenic region between the TP63 and LEPREL1 genes on chromosome 3q28, suggesting a role in the transcriptional regulation of these genes.	Immunohistochemical staining	Abstract Purpose Genome-wide association studies (GWAS) have led to the identification of a bladder cancer susceptibility variant (rs710521) in a non-coding intergenic region between the TP63 and LEPREL1 genes on chromosome 3q28, suggesting a role in the transcriptional regulation of these genes.	TP63		FAIRE,RT-qPCR,统计分析	Abstract Purpose Genome-wide association studies (GWAS) have led to the identification of a bladder cancer susceptibility variant (rs710521) in a non-coding intergenic region between the TP63 and LEPREL1 genes on chromosome 3q28, suggesting a role in the transcriptional regulation of these genes.			
29953980	chr4	108044755	108046755	LEF1	Overexpression of LEF1 diminished repression of Wnt signalling and reduced proliferation activity in mangiferin-treated HCC cells. The mangiferin-mediated down-regulation of LEF1 was independent of β-catenin but associated with WT1 protein.	human,mouse		High+Lowthroughput	Repression of WT1-Mediated LEF1 Transcription by Mangiferin Governs β-Catenin-Independent Wnt Signalling Inactivation in Hepatocellular Carcinoma	否		Hepatocellular carcinoma (HCC)	HCC cell	E_02_0549	Real time quantitative PCR, chromatin immunoprecipitation (chip) assay, statistical analysis, immunofluorescence staining	Overexpression of LEF1 diminished repression of Wnt signalling and reduced proliferation activity in mangiferin-treated HCC cells. The mangiferin-mediated down-regulation of LEF1 was independent of β-catenin but associated with WT1 protein.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Overexpression of LEF1 diminished repression of Wnt signalling and reduced proliferation activity in mangiferin-treated HCC cells. The mangiferin-mediated down-regulation of LEF1 was independent of β-catenin but associated with WT1 protein.		Overexpression of LEF1 diminished repression of Wnt signalling and reduced proliferation activity in mangiferin-treated HCC cells. The mangiferin-mediated down-regulation of LEF1 was independent of β-catenin but associated with WT1 protein.	Immunohistochemical staining	Overexpression of LEF1 diminished repression of Wnt signalling and reduced proliferation activity in mangiferin-treated HCC cells. The mangiferin-mediated down-regulation of LEF1 was independent of β-catenin but associated with WT1 protein.			Real-time Quantitative PCR,Chromatin immunoprecipitation (ChIP) assay,统计分析,免疫荧光染色				LEF1
29953980	chr11	32384686	32386686	WT1	Overexpression of LEF1 diminished repression of Wnt signalling and reduced proliferation activity in mangiferin-treated HCC cells. The mangiferin-mediated down-regulation of LEF1 was independent of β-catenin but associated with WT1 protein.	human,mouse		High+Lowthroughput	Repression of WT1-Mediated LEF1 Transcription by Mangiferin Governs β-Catenin-Independent Wnt Signalling Inactivation in Hepatocellular Carcinoma	否		Hepatocellular carcinoma (HCC)	HCC cell	E_02_0549	Real time quantitative PCR, chromatin immunoprecipitation (chip) assay, statistical analysis, immunofluorescence staining	Overexpression of LEF1 diminished repression of Wnt signalling and reduced proliferation activity in mangiferin-treated HCC cells. The mangiferin-mediated down-regulation of LEF1 was independent of β-catenin but associated with WT1 protein.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Overexpression of LEF1 diminished repression of Wnt signalling and reduced proliferation activity in mangiferin-treated HCC cells. The mangiferin-mediated down-regulation of LEF1 was independent of β-catenin but associated with WT1 protein.		Overexpression of LEF1 diminished repression of Wnt signalling and reduced proliferation activity in mangiferin-treated HCC cells. The mangiferin-mediated down-regulation of LEF1 was independent of β-catenin but associated with WT1 protein.	Immunohistochemical staining	Overexpression of LEF1 diminished repression of Wnt signalling and reduced proliferation activity in mangiferin-treated HCC cells. The mangiferin-mediated down-regulation of LEF1 was independent of β-catenin but associated with WT1 protein.			Real-time Quantitative PCR,Chromatin immunoprecipitation (ChIP) assay,统计分析,免疫荧光染色				WT1
29951200	chr2	26345102	26347102	Notch1	Background Notch signaling is mainly regulated by Notch1 during development of chicken germ stem cells; however, the molecular mechanisms that contribute to generation of these germ stem cells have not been thoroughly investigated.                                                                                                                                                                                                                                                                                                                                                                               Dynamic expression of transducin-like enhancer of split 3, TLE4, and C-terminal binding protein 2 during further differentiation of PGCs inhibited the dissociation of the CBF-1/RBP co-suppression complex and inhibited the expression of the downstream genes.	mouse		High+Lowthroughput	NICD-mediated notch transduction regulates the different fate of chicken primordial germ cells and spermatogonial stem cells	否			germ stem cell	E_02_0550	Western blot, CO IP, QRT PCR, indirect immunofluorescence, statistical analysis	Background Notch signaling is mainly regulated by Notch1 during development of chicken germ stem cells; however, the molecular mechanisms that contribute to generation of these germ stem cells have not been thoroughly investigated.                                                                                                                                                                                                                                                                                                                                                                               Dynamic expression of transducin-like enhancer of split 3, TLE4, and C-terminal binding protein 2 during further differentiation of PGCs inhibited the dissociation of the CBF-1/RBP co-suppression complex and inhibited the expression of the downstream genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background Notch signaling is mainly regulated by Notch1 during development of chicken germ stem cells; however, the molecular mechanisms that contribute to generation of these germ stem cells have not been thoroughly investigated.                                                                                                                                                                                                                                                                                                                                                                               Dynamic expression of transducin-like enhancer of split 3, TLE4, and C-terminal binding protein 2 during further differentiation of PGCs inhibited the dissociation of the CBF-1/RBP co-suppression complex and inhibited the expression of the downstream genes.		Background Notch signaling is mainly regulated by Notch1 during development of chicken germ stem cells; however, the molecular mechanisms that contribute to generation of these germ stem cells have not been thoroughly investigated.                                                                                                                                                                                                                                                                                                                                                                               Dynamic expression of transducin-like enhancer of split 3, TLE4, and C-terminal binding protein 2 during further differentiation of PGCs inhibited the dissociation of the CBF-1/RBP co-suppression complex and inhibited the expression of the downstream genes.	Immunohistochemical staining	Background Notch signaling is mainly regulated by Notch1 during development of chicken germ stem cells; however, the molecular mechanisms that contribute to generation of these germ stem cells have not been thoroughly investigated.                                                                                                                                                                                                                                                                                                                                                                               Dynamic expression of transducin-like enhancer of split 3, TLE4, and C-terminal binding protein 2 during further differentiation of PGCs inhibited the dissociation of the CBF-1/RBP co-suppression complex and inhibited the expression of the downstream genes.			Western blot,Co-IP,qRT-PCR,Indirect immunofluorescence,统计分析				Notch1
29951200	chr9	79569069	79571069	TLE4	Background Notch signaling is mainly regulated by Notch1 during development of chicken germ stem cells; however, the molecular mechanisms that contribute to generation of these germ stem cells have not been thoroughly investigated.                                                                                                                                                                                                                                                                                                                                                                               Dynamic expression of transducin-like enhancer of split 3, TLE4, and C-terminal binding protein 2 during further differentiation of PGCs inhibited the dissociation of the CBF-1/RBP co-suppression complex and inhibited the expression of the downstream genes.	mouse		High+Lowthroughput	NICD-mediated notch transduction regulates the different fate of chicken primordial germ cells and spermatogonial stem cells	否			germ stem cell	E_02_0550	Western blot, CO IP, QRT PCR, indirect immunofluorescence, statistical analysis	Background Notch signaling is mainly regulated by Notch1 during development of chicken germ stem cells; however, the molecular mechanisms that contribute to generation of these germ stem cells have not been thoroughly investigated.                                                                                                                                                                                                                                                                                                                                                                               Dynamic expression of transducin-like enhancer of split 3, TLE4, and C-terminal binding protein 2 during further differentiation of PGCs inhibited the dissociation of the CBF-1/RBP co-suppression complex and inhibited the expression of the downstream genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Background Notch signaling is mainly regulated by Notch1 during development of chicken germ stem cells; however, the molecular mechanisms that contribute to generation of these germ stem cells have not been thoroughly investigated.                                                                                                                                                                                                                                                                                                                                                                               Dynamic expression of transducin-like enhancer of split 3, TLE4, and C-terminal binding protein 2 during further differentiation of PGCs inhibited the dissociation of the CBF-1/RBP co-suppression complex and inhibited the expression of the downstream genes.		Background Notch signaling is mainly regulated by Notch1 during development of chicken germ stem cells; however, the molecular mechanisms that contribute to generation of these germ stem cells have not been thoroughly investigated.                                                                                                                                                                                                                                                                                                                                                                               Dynamic expression of transducin-like enhancer of split 3, TLE4, and C-terminal binding protein 2 during further differentiation of PGCs inhibited the dissociation of the CBF-1/RBP co-suppression complex and inhibited the expression of the downstream genes.	Immunohistochemical staining	Background Notch signaling is mainly regulated by Notch1 during development of chicken germ stem cells; however, the molecular mechanisms that contribute to generation of these germ stem cells have not been thoroughly investigated.                                                                                                                                                                                                                                                                                                                                                                               Dynamic expression of transducin-like enhancer of split 3, TLE4, and C-terminal binding protein 2 during further differentiation of PGCs inhibited the dissociation of the CBF-1/RBP co-suppression complex and inhibited the expression of the downstream genes.			Western blot,Co-IP,qRT-PCR,Indirect immunofluorescence,统计分析				TLE4
29949917	chr11	118744735	118746735	DDX6	Among them was the RIG-I related RNA helicase DEAD box helicase 6 (DDX6), a known component of cytoplasmic mRNA-ribonucleoprotein (mRNP) granules like P-bodies and stress granules (SGs).	human		High+Lowthroughput	The RNA Helicase DDX6 Associates with RIG-I to Augment Induction of Antiviral Signaling	否		influenza	293T cell	E_01_0813	Immunoprecipitation, quantitative RT-PCR, ELISA, statistical analysis	Among them was the RIG-I related RNA helicase DEAD box helicase 6 (DDX6), a known component of cytoplasmic mRNA-ribonucleoprotein (mRNP) granules like P-bodies and stress granules (SGs).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Among them was the RIG-I related RNA helicase DEAD box helicase 6 (DDX6), a known component of cytoplasmic mRNA-ribonucleoprotein (mRNP) granules like P-bodies and stress granules (SGs).		Among them was the RIG-I related RNA helicase DEAD box helicase 6 (DDX6), a known component of cytoplasmic mRNA-ribonucleoprotein (mRNP) granules like P-bodies and stress granules (SGs).	Immunohistochemical staining	Among them was the RIG-I related RNA helicase DEAD box helicase 6 (DDX6), a known component of cytoplasmic mRNA-ribonucleoprotein (mRNP) granules like P-bodies and stress granules (SGs).			Immunoprecipitation,Quantitative RT-PCR,ELISA,统计分析				DDX6
35121888	chr2	15938207	15940207	MYCN	Three of these subtypes recapitulated known clinical groups; namely, MYCN-amplified, MYCN non-amplified high-risk and MYCN non-amplified low-risk NBs.	human		High+Lowthroughput	Super enhancers define regulatory subtypes and cell identity in neuroblastoma	不相关		Neuroblastoma	endothelial cell,Neuroblastoma	E_01_0814	Identification of SEs and CRCs,ACE-seq,HiChIP experiments,ATAC-seq	Three of these subtypes recapitulated known clinical groups; namely, MYCN-amplified, MYCN non-amplified high-risk and MYCN non-amplified low-risk NBs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Three of these subtypes recapitulated known clinical groups; namely, MYCN-amplified, MYCN non-amplified high-risk and MYCN non-amplified low-risk NBs.	Immunohistochemical staining	Three of these subtypes recapitulated known clinical groups; namely, MYCN-amplified, MYCN non-amplified high-risk and MYCN non-amplified low-risk NBs.	MYCN		Identification of SEs and CRCs,ACE-seq,HiChIP experiments,ATAC-seq	Three of these subtypes recapitulated known clinical groups; namely, MYCN-amplified, MYCN non-amplified high-risk and MYCN non-amplified low-risk NBs.			
35121887	chr6	145159621	145161621	Kras	Kras-activating mutations display the highest incidence in pancreatic ductal adenocarcinoma.	mouse		High+Lowthroughput	Mutant Kras co-opts a proto-oncogenic enhancer network in inflammation-induced metaplastic progenitor cells to initiate pancreatic cancer	不相关		pancreatic cancer	progenitor cell	E_02_0551	Small-scale RNA-seq, scRNA-seq ，small-scale ATAC-seq,Chromatin enrichment for proteomics.Immunoblotting, immunofluorescence and IHC. 	Kras-activating mutations display the highest incidence in pancreatic ductal adenocarcinoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Kras-activating mutations display the highest incidence in pancreatic ductal adenocarcinoma.		Kras-activating mutations display the highest incidence in pancreatic ductal adenocarcinoma.	Immunohistochemical staining	Kras-activating mutations display the highest incidence in pancreatic ductal adenocarcinoma.			Small-scale RNA-seq, scRNA-seq ，small-scale ATAC-seq,Chromatin enrichment for proteomics.Immunoblotting, immunofluorescence and IHC. 				Kras
34291139	chr10	97764137	97766137	SFRP5	Secreted frizzled-related protein 5 (SFRP5) plays a pivotal role in regulating the development of many tissues and organs, however, as an inhibitor of Wnt signaling, the role of SFRP5 in vitiligo remains unknown.	mouse		High+Lowthroughput	SFRP5 inhibits melanin synthesis of melanocytes in vitiligo by suppressing the Wnt/β-catenin signaling	不相关		Vitiligo	melanocyte,B16 cell	E_02_0552		Secreted frizzled-related protein 5 (SFRP5) plays a pivotal role in regulating the development of many tissues and organs, however, as an inhibitor of Wnt signaling, the role of SFRP5 in vitiligo remains unknown.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Secreted frizzled-related protein 5 (SFRP5) plays a pivotal role in regulating the development of many tissues and organs, however, as an inhibitor of Wnt signaling, the role of SFRP5 in vitiligo remains unknown.		Secreted frizzled-related protein 5 (SFRP5) plays a pivotal role in regulating the development of many tissues and organs, however, as an inhibitor of Wnt signaling, the role of SFRP5 in vitiligo remains unknown.	Immunohistochemical staining	Secreted frizzled-related protein 5 (SFRP5) plays a pivotal role in regulating the development of many tissues and organs, however, as an inhibitor of Wnt signaling, the role of SFRP5 in vitiligo remains unknown.							SFRP5
34109280	chr12	24807287	24809287	BCAT1	In NRASG12D-mutant myeloproliferative neoplasms, EZH2 deficiency is associated with elevated expression of BCAT1.	human		High+Lowthroughput	The Bidirectional Relationship Between Cancer Epigenetics and Metabolism	不相关		cancer	cancer cell	E_01_0815	Histone methylation,	In NRASG12D-mutant myeloproliferative neoplasms, EZH2 deficiency is associated with elevated expression of BCAT1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In NRASG12D-mutant myeloproliferative neoplasms, EZH2 deficiency is associated with elevated expression of BCAT1.		In NRASG12D-mutant myeloproliferative neoplasms, EZH2 deficiency is associated with elevated expression of BCAT1.	Immunohistochemical staining	In NRASG12D-mutant myeloproliferative neoplasms, EZH2 deficiency is associated with elevated expression of BCAT1.			组蛋白甲基化,				BCAT1
33994736	chr1	245746404	245748404	SMYD3	 The role of SMYD3 in gallbladder cancer (GBC) still needs to be studied. In the present study, we examined the SMYD3 gene expression at mRNA and protein level to look its impact on risk for developing gallbladder carcinogenesis.	human		High+Lowthroughput	Analysis of SET and MYND Domain-Containing Protein 3 (SMYD3) Expression in Gallbladder Cancer: a Pilot Study	不相关		cancer	tumor cell	E_01_0816	Immunohistochemical (IHC) analysis,	 The role of SMYD3 in gallbladder cancer (GBC) still needs to be studied. In the present study, we examined the SMYD3 gene expression at mRNA and protein level to look its impact on risk for developing gallbladder carcinogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 The role of SMYD3 in gallbladder cancer (GBC) still needs to be studied. In the present study, we examined the SMYD3 gene expression at mRNA and protein level to look its impact on risk for developing gallbladder carcinogenesis.		 The role of SMYD3 in gallbladder cancer (GBC) still needs to be studied. In the present study, we examined the SMYD3 gene expression at mRNA and protein level to look its impact on risk for developing gallbladder carcinogenesis.	Immunohistochemical staining	 The role of SMYD3 in gallbladder cancer (GBC) still needs to be studied. In the present study, we examined the SMYD3 gene expression at mRNA and protein level to look its impact on risk for developing gallbladder carcinogenesis.			免疫组化 （IHC） 分析，				SMYD3
33777677	chr19	4171328	4173328	SIRT6	We designed a novel SIRT6 activator MDL-811 which remarkably inhibited inflammatory response in lipopolysaccharide (LPS)-stimulated RAW264.	human	connective tissue	High+Lowthroughput	A novel SIRT6 activator ameliorates neuroinflammation and ischemic brain injury via EZH2/FOXC1 axis	不相关		Ischemic stroke	macrophage	E_01_0817	SIRT6 protein purification and fluorescence cleavage assay (FDL), enzyme linked immunosorbent assay, Western blot analysis, chromatin immunoprecipitation (chip) assay, immunoprecipitation and immunoblotting	We designed a novel SIRT6 activator MDL-811 which remarkably inhibited inflammatory response in lipopolysaccharide (LPS)-stimulated RAW264.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We designed a novel SIRT6 activator MDL-811 which remarkably inhibited inflammatory response in lipopolysaccharide (LPS)-stimulated RAW264.		We designed a novel SIRT6 activator MDL-811 which remarkably inhibited inflammatory response in lipopolysaccharide (LPS)-stimulated RAW264.	Immunohistochemical staining	We designed a novel SIRT6 activator MDL-811 which remarkably inhibited inflammatory response in lipopolysaccharide (LPS)-stimulated RAW264.			SIRT6蛋白纯化和荧光裂解测定（FDL）,酶联免疫吸附测定,蛋白质印迹分析,染色质免疫沉淀（ChIP）测定,免疫沉淀和免疫印迹				SIRT6
33763107	chr7	148804661	148806661	EZH2	Our RNA immunoprecipitation experiment indicated that PVT1 bound histone methyltransferase enhancer of zeste homolog 2 (EZH2), and regulated the expression of target gene, including p57, and consequently altered ovarian cancer cell biology.	human		High+Lowthroughput	Ketamine Inhibits Ovarian Cancer Cell Growth by Regulating the lncRNA-PVT1/EZH2/p57 Axis	不相关		oophoroma	ovarian cancer cell	E_01_0818	Real time PCR, Western blotting, chromatin immunoprecipitation (chip)	Our RNA immunoprecipitation experiment indicated that PVT1 bound histone methyltransferase enhancer of zeste homolog 2 (EZH2), and regulated the expression of target gene, including p57, and consequently altered ovarian cancer cell biology.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our RNA immunoprecipitation experiment indicated that PVT1 bound histone methyltransferase enhancer of zeste homolog 2 (EZH2), and regulated the expression of target gene, including p57, and consequently altered ovarian cancer cell biology.	Immunohistochemical staining	Our RNA immunoprecipitation experiment indicated that PVT1 bound histone methyltransferase enhancer of zeste homolog 2 (EZH2), and regulated the expression of target gene, including p57, and consequently altered ovarian cancer cell biology.	EZH2		实时荧光定量 PCR ，蛋白质印记，染色质免疫沉淀 （ChIP）	Our RNA immunoprecipitation experiment indicated that PVT1 bound histone methyltransferase enhancer of zeste homolog 2 (EZH2), and regulated the expression of target gene, including p57, and consequently altered ovarian cancer cell biology.			
33753020	chr11	116786522	116788522	APOA5	The strongest associations in GWASs were two single-nucleotide polymorphisms (SNPs), rs964184 and rs651821,within different but adjacent genes,ZPR1 zinc finger (ZPR1) and APOA5.	human	connective tissue	High+Lowthroughput	Fine genetic mapping of the chromosome 11q23.3 region in a Han Chinese population: insights into the apolipoprotein genes underlying the blood lipid-lipoprotein variances	相关	rs964184，rs651821	Cardiovascular disease	hepatocyte	E_01_0819	 Sequencing and genotyping， Lookups of eQTL data and regulatory mechanisms. Joint fine-mapping analyses integrating functional data	The strongest associations in GWASs were two single-nucleotide polymorphisms (SNPs), rs964184 and rs651821,within different but adjacent genes,ZPR1 zinc finger (ZPR1) and APOA5.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The strongest associations in GWASs were two single-nucleotide polymorphisms (SNPs), rs964184 and rs651821,within different but adjacent genes,ZPR1 zinc finger (ZPR1) and APOA5.		The strongest associations in GWASs were two single-nucleotide polymorphisms (SNPs), rs964184 and rs651821,within different but adjacent genes,ZPR1 zinc finger (ZPR1) and APOA5.	Immunohistochemical staining	The strongest associations in GWASs were two single-nucleotide polymorphisms (SNPs), rs964184 and rs651821,within different but adjacent genes,ZPR1 zinc finger (ZPR1) and APOA5.			 Sequencing and genotyping， Lookups of eQTL data and regulatory mechanisms. Joint fine-mapping analyses integrating functional data				APOA5
33746938	chr11	72099986	72101986	Med31	We first focus on the Med31 subunit of the middle module of Mediator and find that it is required in host defense against Aspergillus fumigatus, Enterococcus faecalis, and injected but not topically-applied Metarhizium robertsii.	mouse		High+Lowthroughput	Differential Requirements for Mediator Complex Subunits in Drosophila melanogaster Host Defense Against Fungal and Bacterial Pathogens	不相关		bacterial infection	macrophage	E_02_0553	Western blot	We first focus on the Med31 subunit of the middle module of Mediator and find that it is required in host defense against Aspergillus fumigatus, Enterococcus faecalis, and injected but not topically-applied Metarhizium robertsii.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We first focus on the Med31 subunit of the middle module of Mediator and find that it is required in host defense against Aspergillus fumigatus, Enterococcus faecalis, and injected but not topically-applied Metarhizium robertsii.		We first focus on the Med31 subunit of the middle module of Mediator and find that it is required in host defense against Aspergillus fumigatus, Enterococcus faecalis, and injected but not topically-applied Metarhizium robertsii.	Immunohistochemical staining	We first focus on the Med31 subunit of the middle module of Mediator and find that it is required in host defense against Aspergillus fumigatus, Enterococcus faecalis, and injected but not topically-applied Metarhizium robertsii.			蛋白质印迹				Med31
33718109	chr7	148804493	148806493	EZH2	Enhancer of zester homolog 2 (EZH2), a histone methyl transferase that mediates H3K27me3 through polycomb repressive complex 2 (PRC2), is overexpressed in ovarian cancer and promotes malignant proliferation.	human		High+Lowthroughput	EZH2-miRNA Positive Feedback Promotes Tumor Growth in Ovarian Cancer	不相关		oophoroma	cancer cell	E_01_0820	Real time PCR, Western blot analysis, chromatin immunoprecipitation assay, immunohistochemistry	Enhancer of zester homolog 2 (EZH2), a histone methyl transferase that mediates H3K27me3 through polycomb repressive complex 2 (PRC2), is overexpressed in ovarian cancer and promotes malignant proliferation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zester homolog 2 (EZH2), a histone methyl transferase that mediates H3K27me3 through polycomb repressive complex 2 (PRC2), is overexpressed in ovarian cancer and promotes malignant proliferation.	Immunohistochemical staining	Enhancer of zester homolog 2 (EZH2), a histone methyl transferase that mediates H3K27me3 through polycomb repressive complex 2 (PRC2), is overexpressed in ovarian cancer and promotes malignant proliferation.	EZH2		实时荧光定量 PCR，蛋白质印迹分析，染色质免疫沉淀测定，免疫组化	Enhancer of zester homolog 2 (EZH2), a histone methyl transferase that mediates H3K27me3 through polycomb repressive complex 2 (PRC2), is overexpressed in ovarian cancer and promotes malignant proliferation.			
33650655	chr15	41318452	41320452	NUSAP1	As a potential oncogene, nucleolar and spindle-associated protein 1 (NUSAP1) is involved in the regulation of tumor cell proliferation, metastasis and drug resistance.	human	Musculature	High+Lowthroughput	Nucleolar and spindle?associated protein 1 promotes non?small cell lung cancer progression and serves as an effector of myocyte enhancer factor 2D	不相关		lung cancer	myocyte	E_01_0821	Luciferase assay, reverse transcription quantitative PCR (RT qPCR) analysis,	As a potential oncogene, nucleolar and spindle-associated protein 1 (NUSAP1) is involved in the regulation of tumor cell proliferation, metastasis and drug resistance.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	As a potential oncogene, nucleolar and spindle-associated protein 1 (NUSAP1) is involved in the regulation of tumor cell proliferation, metastasis and drug resistance.		As a potential oncogene, nucleolar and spindle-associated protein 1 (NUSAP1) is involved in the regulation of tumor cell proliferation, metastasis and drug resistance.	Immunohistochemical staining	As a potential oncogene, nucleolar and spindle-associated protein 1 (NUSAP1) is involved in the regulation of tumor cell proliferation, metastasis and drug resistance.			荧光素酶测定，逆转录定量 PCR （RT-qPCR） 分析，				NUSAP1
33604333	chr11	101448961	101450961	TRPC6	Transient receptor potential canonical 6 (TRPC6) channel is an important non-selective cation channel with a variety of physiological roles in the central nervous system. 	mouse	Nervous tissue	High+Lowthroughput	TRPC6 Attenuates Cortical Astrocytic Apoptosis and Inflammation in Cerebral Ischemic/Reperfusion Injury	不相关		Ischemic stroke	cortical cell	E_02_0554	TTC staining, flow cytometry, Western blot, immunofluorescence	Transient receptor potential canonical 6 (TRPC6) channel is an important non-selective cation channel with a variety of physiological roles in the central nervous system. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Transient receptor potential canonical 6 (TRPC6) channel is an important non-selective cation channel with a variety of physiological roles in the central nervous system. 		Transient receptor potential canonical 6 (TRPC6) channel is an important non-selective cation channel with a variety of physiological roles in the central nervous system. 	Immunohistochemical staining	Transient receptor potential canonical 6 (TRPC6) channel is an important non-selective cation channel with a variety of physiological roles in the central nervous system. 			TTC 染色，流式细胞术，蛋白质印迹，免疫荧光				TRPC6
33520978	chr19	47400663	47402663	MEIS3	Dual-luciferase reporter gene assay was employed to test the presence of miR-202-3p binding sites in the 3’UTR of KDM3A and chromatin immunoprecipitation (ChIP) assay to homeobox A1 (HOXA1) interaction with KDM3A and MEIS3.	human		High+Lowthroughput	Tumor-Suppressive Role of microRNA-202-3p in Hepatocellular Carcinoma Through the KDM3A/HOXA1/MEIS3 Pathway	不相关		Hepatocellular carcinoma	hepatocyte	E_01_0822	Western blot analysis, RNA extraction and quantitative real-time PCR (QRT PCR) analysis	Dual-luciferase reporter gene assay was employed to test the presence of miR-202-3p binding sites in the 3’UTR of KDM3A and chromatin immunoprecipitation (ChIP) assay to homeobox A1 (HOXA1) interaction with KDM3A and MEIS3.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Dual-luciferase reporter gene assay was employed to test the presence of miR-202-3p binding sites in the 3’UTR of KDM3A and chromatin immunoprecipitation (ChIP) assay to homeobox A1 (HOXA1) interaction with KDM3A and MEIS3.		Dual-luciferase reporter gene assay was employed to test the presence of miR-202-3p binding sites in the 3’UTR of KDM3A and chromatin immunoprecipitation (ChIP) assay to homeobox A1 (HOXA1) interaction with KDM3A and MEIS3.	Immunohistochemical staining	Dual-luciferase reporter gene assay was employed to test the presence of miR-202-3p binding sites in the 3’UTR of KDM3A and chromatin immunoprecipitation (ChIP) assay to homeobox A1 (HOXA1) interaction with KDM3A and MEIS3.			蛋白质印迹分析，RNA 提取和定量实时荧光定量 PCR （qRT-PCR） 分析				MEIS3
33519497	chr6	41680863	41682863	TFEB	We showed earlier that the transcription factor EB (TFEB) plays a role by increasing E3 ubiquitin ligase muscle really interesting new gene-finger 1(MuRF1)/tripartite motif-containing 63 (TRIM63) expression.	mouse	Musculature	High+Lowthroughput	Activation of Tripartite Motif Containing 63 Expression by Transcription Factor EB and Transcription Factor Binding to Immunoglobulin Heavy Chain Enhancer 3 Is Regulated by Protein Kinase D and Class IIa Histone Deacetylases	不相关		Muscle wasting	myocyte	E_02_0555	Luciferase reporter assay, immunofluorescence, protein extraction and Western blot analysis, coimmunoprecipitation	We showed earlier that the transcription factor EB (TFEB) plays a role by increasing E3 ubiquitin ligase muscle really interesting new gene-finger 1(MuRF1)/tripartite motif-containing 63 (TRIM63) expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We showed earlier that the transcription factor EB (TFEB) plays a role by increasing E3 ubiquitin ligase muscle really interesting new gene-finger 1(MuRF1)/tripartite motif-containing 63 (TRIM63) expression.		We showed earlier that the transcription factor EB (TFEB) plays a role by increasing E3 ubiquitin ligase muscle really interesting new gene-finger 1(MuRF1)/tripartite motif-containing 63 (TRIM63) expression.	Immunohistochemical staining	We showed earlier that the transcription factor EB (TFEB) plays a role by increasing E3 ubiquitin ligase muscle really interesting new gene-finger 1(MuRF1)/tripartite motif-containing 63 (TRIM63) expression.			荧光素酶报告检测，免疫荧光，蛋白质提取和蛋白质印迹分析，共免疫沉淀				TFEB
33068224	chr1	156461073	156463073	MEF2D	Western blot was used to detect the protein levels of matrix metallopeptidase 2 (MMP2), MMP9 and myocyte enhancer factor 2D (MEF2D). 	human		High+Lowthroughput	CircCPA4 Promotes the Malignant Phenotypes in Glioma via miR-760/MEF2D Axis.	不相关		Gliomas	Glioma cell	E_01_0823	Quantitative Real‑Time Polymerase Chain Reaction (qRT‑PCR)，Cell Transfection	Western blot was used to detect the protein levels of matrix metallopeptidase 2 (MMP2), MMP9 and myocyte enhancer factor 2D (MEF2D). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Western blot was used to detect the protein levels of matrix metallopeptidase 2 (MMP2), MMP9 and myocyte enhancer factor 2D (MEF2D). 		Western blot was used to detect the protein levels of matrix metallopeptidase 2 (MMP2), MMP9 and myocyte enhancer factor 2D (MEF2D). 	Immunohistochemical staining	Western blot was used to detect the protein levels of matrix metallopeptidase 2 (MMP2), MMP9 and myocyte enhancer factor 2D (MEF2D). 			Quantitative Real‑Time Polymerase Chain Reaction (qRT‑PCR)，Cell Transfection				MEF2D
33511127	chr7	148804442	148806442	EZH2	Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 and contains a SET domain that catalyzes histone H3 trimethylation on lysine 27 (H3K27me3) to generate an epigenetic silencing mark.	mouse	Musculature	High+Lowthroughput	RIP-Seq of EZH2 Identifies TCONS-00036665 as a Regulator of Myogenesis in Pigs	不相关			myoblast cell	E_02_0556	Rip SEQ, lincrnaseq, Western blot, quantitative real-time PCR, immunofluorescence staining of cells	Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 and contains a SET domain that catalyzes histone H3 trimethylation on lysine 27 (H3K27me3) to generate an epigenetic silencing mark.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 and contains a SET domain that catalyzes histone H3 trimethylation on lysine 27 (H3K27me3) to generate an epigenetic silencing mark.		Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 and contains a SET domain that catalyzes histone H3 trimethylation on lysine 27 (H3K27me3) to generate an epigenetic silencing mark.	Immunohistochemical staining	Enhancer of zeste homolog 2 (EZH2) is the catalytic subunit of polycomb repressive complex 2 and contains a SET domain that catalyzes histone H3 trimethylation on lysine 27 (H3K27me3) to generate an epigenetic silencing mark.			RIP-Seq，LincRNAseq，蛋白质印迹，定量实时荧光定量 PCR，细胞免疫荧光染色				EZH2
33537515	chr10	4558873	4560873	Esr1	The absence of functional estrogen receptor α (Esr1) results in an overgrowth of the epididymal fat, as observed in estrogen receptor α knockout (ERαKO) mouse.	mouse	connective tissue	High+Lowthroughput	Assessment of Adipocyte Differentiation and Maturation-related Gene Expression in the Epididymal Fat of Estrogen Receptor α Knockout (ERαKO) Mouse during Postnatal Development Period	不相关			fat cell	E_02_0557	Real time PCR	The absence of functional estrogen receptor α (Esr1) results in an overgrowth of the epididymal fat, as observed in estrogen receptor α knockout (ERαKO) mouse.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The absence of functional estrogen receptor α (Esr1) results in an overgrowth of the epididymal fat, as observed in estrogen receptor α knockout (ERαKO) mouse.		The absence of functional estrogen receptor α (Esr1) results in an overgrowth of the epididymal fat, as observed in estrogen receptor α knockout (ERαKO) mouse.	Immunohistochemical staining	The absence of functional estrogen receptor α (Esr1) results in an overgrowth of the epididymal fat, as observed in estrogen receptor α knockout (ERαKO) mouse.			实时荧光定量 PCR 				Esr1
33553989	chr10	126881408	126883408	Cyp27b1	Our recent genomic studies identified a complex kidney‐specific enhancer module located within the introns of adjacent Mettl1 (M1) and Mettl21b (M21) genes that mediate basal and PTH induction of Cyp27b1, as well as suppression by FGF23 and 1,25‐dihydroxyvitamin D3 [1,25(OH)2D3].	mouse	connective tissue	High+Lowthroughput	Genomic Mechanisms Governing Mineral Homeostasis and the Regulation and Maintenance of Vitamin D Metabolism	不相关			osteocyte,nephrocyte	E_02_0558		Our recent genomic studies identified a complex kidney‐specific enhancer module located within the introns of adjacent Mettl1 (M1) and Mettl21b (M21) genes that mediate basal and PTH induction of Cyp27b1, as well as suppression by FGF23 and 1,25‐dihydroxyvitamin D3 [1,25(OH)2D3].	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our recent genomic studies identified a complex kidney‐specific enhancer module located within the introns of adjacent Mettl1 (M1) and Mettl21b (M21) genes that mediate basal and PTH induction of Cyp27b1, as well as suppression by FGF23 and 1,25‐dihydroxyvitamin D3 [1,25(OH)2D3].		Our recent genomic studies identified a complex kidney‐specific enhancer module located within the introns of adjacent Mettl1 (M1) and Mettl21b (M21) genes that mediate basal and PTH induction of Cyp27b1, as well as suppression by FGF23 and 1,25‐dihydroxyvitamin D3 [1,25(OH)2D3].	Immunohistochemical staining	Our recent genomic studies identified a complex kidney‐specific enhancer module located within the introns of adjacent Mettl1 (M1) and Mettl21b (M21) genes that mediate basal and PTH induction of Cyp27b1, as well as suppression by FGF23 and 1,25‐dihydroxyvitamin D3 [1,25(OH)2D3].							Cyp27b1
33488675	chr16	67559628	67561628	CTCF	We assayed histone modifications and CTCF enrichment by chromatin immunoprecipitation with deep sequencing (ChIP-seq) in two sheep to determine cis-regulatory DNA elements and chromatin domain boundaries that control immunity-related gene expression.	mouse	connective tissue	High+Lowthroughput	Genome-Wide Histone Modifications and CTCF Enrichment Predict Gene Expression in Sheep Macrophages	不相关		Viruses such as small ruminant lentivirus and bacteria such as Coxiella bethesdensis	alveolar macrophage	E_02_0559	Chromatin immunoprecipitation and sequencing, chip SEQ data analysis	We assayed histone modifications and CTCF enrichment by chromatin immunoprecipitation with deep sequencing (ChIP-seq) in two sheep to determine cis-regulatory DNA elements and chromatin domain boundaries that control immunity-related gene expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We assayed histone modifications and CTCF enrichment by chromatin immunoprecipitation with deep sequencing (ChIP-seq) in two sheep to determine cis-regulatory DNA elements and chromatin domain boundaries that control immunity-related gene expression.		We assayed histone modifications and CTCF enrichment by chromatin immunoprecipitation with deep sequencing (ChIP-seq) in two sheep to determine cis-regulatory DNA elements and chromatin domain boundaries that control immunity-related gene expression.	Immunohistochemical staining	We assayed histone modifications and CTCF enrichment by chromatin immunoprecipitation with deep sequencing (ChIP-seq) in two sheep to determine cis-regulatory DNA elements and chromatin domain boundaries that control immunity-related gene expression.			染色质免疫沉淀和测序，ChIP-Seq 数据分析				CTCF
33461200	chr7	148804344	148806344	EZH2	As a histone methyltransferase, enhancer of zeste homolog 2 (EZH2), suppresses osteoblast maturation and is involved in inflammation. 	human		High+Lowthroughput	Targeting EZH2 Ameliorates the LPS-Inhibited PDLSC Osteogenesis via Wnt/β-Catenin Pathway	不相关		inflammation	Periodontal stem cell	E_01_0824	Flow cytometric analysis, cell transfection, alkaline phosphatase assay, enzyme linked immunosorbent assay, real time RT-PCR	As a histone methyltransferase, enhancer of zeste homolog 2 (EZH2), suppresses osteoblast maturation and is involved in inflammation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			As a histone methyltransferase, enhancer of zeste homolog 2 (EZH2), suppresses osteoblast maturation and is involved in inflammation. 	Immunohistochemical staining	As a histone methyltransferase, enhancer of zeste homolog 2 (EZH2), suppresses osteoblast maturation and is involved in inflammation. 	EZH2		流式细胞术分析,细胞转染，碱性磷酸酶测定，Enzyme-Linked Immunosorbent Assay，Real-Time RT-PCR	As a histone methyltransferase, enhancer of zeste homolog 2 (EZH2), suppresses osteoblast maturation and is involved in inflammation. 			
33455270	chr6	45324897	45326897	RUNX2	Runt-related transcription factor 2 (RUNX2) is a master regulator of the osteogenic commitment of hMSCs.	human		High+Lowthroughput	Intracellular Delivery of Recombinant RUNX2 Facilitated by Cell-Penetrating Protein for the Osteogenic Differentiation of hMSCs	不相关		Skull defects	mesenchymal stem cell	E_01_0825	Protein expression and purification，SDS-PAGE and western blot analysis	Runt-related transcription factor 2 (RUNX2) is a master regulator of the osteogenic commitment of hMSCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Runt-related transcription factor 2 (RUNX2) is a master regulator of the osteogenic commitment of hMSCs.	Immunohistochemical staining	Runt-related transcription factor 2 (RUNX2) is a master regulator of the osteogenic commitment of hMSCs.	RUNX2		Protein expression and purification，SDS-PAGE and western blot analysis	Runt-related transcription factor 2 (RUNX2) is a master regulator of the osteogenic commitment of hMSCs.			
33453998	chr4	108044986	108046986	LEF1	We show that ablation of HNF-1β in mIMCD3 renal epithelial cells results in activation of β-catenin and increased expression of lymphoid enhancer–binding factor 1 (LEF1), a downstream effector in the canonical Wnt signaling pathway. Increased expression and nuclear localization of LEF1 are also observed in cystic kidneys from Hnf1b mutant mice.	mouse	Epithelial tissues	High+Lowthroughput	Hepatocyte nuclear factor 1β suppresses canonical Wnt signaling through transcriptional repression of lymphoid enhancer-binding factor 1	不相关		Cystic kidney disease	kidney epithelial cell	E_02_0560	Gene knockdown, luciferase reporter assay, genome wide chip SEQ analysis	We show that ablation of HNF-1β in mIMCD3 renal epithelial cells results in activation of β-catenin and increased expression of lymphoid enhancer–binding factor 1 (LEF1), a downstream effector in the canonical Wnt signaling pathway. Increased expression and nuclear localization of LEF1 are also observed in cystic kidneys from Hnf1b mutant mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We show that ablation of HNF-1β in mIMCD3 renal epithelial cells results in activation of β-catenin and increased expression of lymphoid enhancer–binding factor 1 (LEF1), a downstream effector in the canonical Wnt signaling pathway. Increased expression and nuclear localization of LEF1 are also observed in cystic kidneys from Hnf1b mutant mice.		We show that ablation of HNF-1β in mIMCD3 renal epithelial cells results in activation of β-catenin and increased expression of lymphoid enhancer–binding factor 1 (LEF1), a downstream effector in the canonical Wnt signaling pathway. Increased expression and nuclear localization of LEF1 are also observed in cystic kidneys from Hnf1b mutant mice.	Immunohistochemical staining	We show that ablation of HNF-1β in mIMCD3 renal epithelial cells results in activation of β-catenin and increased expression of lymphoid enhancer–binding factor 1 (LEF1), a downstream effector in the canonical Wnt signaling pathway. Increased expression and nuclear localization of LEF1 are also observed in cystic kidneys from Hnf1b mutant mice.			基因敲降,荧光素酶报告检测，全基因组ChIP-Seq分析				LEF1
33454003	chr3	8726296	8728296	Hey1	Previous work has shown that loss of a basic helix-loop-helix transcription factor Hey1 in mice causes abnormal fourth PAA development and lethal great vessel anomalies resembling congenital malformations in humans.	mouse	Musculature	High+Lowthroughput	Importance of endothelial Hey1 expression for thoracic great vessel development and its distal enhancer for Notch-dependent endothelial transcription	不相关			smooth muscle cell	E_02_0561	Micro CT analysis, BAC lacZ	Previous work has shown that loss of a basic helix-loop-helix transcription factor Hey1 in mice causes abnormal fourth PAA development and lethal great vessel anomalies resembling congenital malformations in humans.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Previous work has shown that loss of a basic helix-loop-helix transcription factor Hey1 in mice causes abnormal fourth PAA development and lethal great vessel anomalies resembling congenital malformations in humans.		Previous work has shown that loss of a basic helix-loop-helix transcription factor Hey1 in mice causes abnormal fourth PAA development and lethal great vessel anomalies resembling congenital malformations in humans.	Immunohistochemical staining	Previous work has shown that loss of a basic helix-loop-helix transcription factor Hey1 in mice causes abnormal fourth PAA development and lethal great vessel anomalies resembling congenital malformations in humans.			Micro-CT分析， BAC-LacZ				Hey1
33416105	chr7	148804533	148806533	EZH2	The data revealed that hsa_circ_0026123 downregulation suppressed EZH2 expression by miR-124-3p 'sponging', which was confirmed by rescue experiments and luciferase reporter assays.	mouse		High+Lowthroughput	Downregulation of hsa_circ_0026123 suppresses ovarian cancer cell metastasis and proliferation through the miR?124?3p/EZH2 signaling pathway	不相关		oophoroma	OVA cell	E_02_0562	Reverse transcription quantitative PCR (RT qPCR), Western blot analysis, fluorescence in situ hybridization (FISH)	The data revealed that hsa_circ_0026123 downregulation suppressed EZH2 expression by miR-124-3p 'sponging', which was confirmed by rescue experiments and luciferase reporter assays.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The data revealed that hsa_circ_0026123 downregulation suppressed EZH2 expression by miR-124-3p 'sponging', which was confirmed by rescue experiments and luciferase reporter assays.		The data revealed that hsa_circ_0026123 downregulation suppressed EZH2 expression by miR-124-3p 'sponging', which was confirmed by rescue experiments and luciferase reporter assays.	Immunohistochemical staining	The data revealed that hsa_circ_0026123 downregulation suppressed EZH2 expression by miR-124-3p 'sponging', which was confirmed by rescue experiments and luciferase reporter assays.			逆转录定量 PCR （RT-qPCR），蛋白质印迹分析，荧光原位杂交 （FISH）				EZH2
33388376	chr7	148804674	148806674	EZH2	The enhancer of zest homolog-2 (EZH2) has been demonstrated to participate in the development of brain injury.	mouse		High+Lowthroughput	Knockdown EZH2 attenuates cerebral ischemia-reperfusion injury via regulating microRNA-30d-3p methylation and USP22	不相关		Cerebral ischemia-reperfusion	Brain tissue cell	E_02_0563	Methylation specific polymerase chain reaction (MSP). 2,3,5-Triphenyltetrazolium chloride (TTC) staining	The enhancer of zest homolog-2 (EZH2) has been demonstrated to participate in the development of brain injury.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The enhancer of zest homolog-2 (EZH2) has been demonstrated to participate in the development of brain injury.		The enhancer of zest homolog-2 (EZH2) has been demonstrated to participate in the development of brain injury.	Immunohistochemical staining	The enhancer of zest homolog-2 (EZH2) has been demonstrated to participate in the development of brain injury.			Methylation specific polymerase chain reaction (MSP). 2,3,5-Triphenyltetrazolium chloride (TTC) staining				EZH2
33376128	chr19	39383229	39385229	PAF1	The RNA polymerase II (RNAPII) associated factor 1 complex (Paf1C) plays critical roles in modulating the release of paused RNAPII into productive elongation. 	mouse		High+Lowthroughput	The Paf1 complex positively regulates enhancer activity in mouse embryonic stem cells	不相关		cancer	embryonic stem cell	E_02_0564	CRISPR / cas9 assisted GFP labeling, chip SEQ, QRT PCR and RNA SEQ, immunostaining for Western blotting	The RNA polymerase II (RNAPII) associated factor 1 complex (Paf1C) plays critical roles in modulating the release of paused RNAPII into productive elongation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The RNA polymerase II (RNAPII) associated factor 1 complex (Paf1C) plays critical roles in modulating the release of paused RNAPII into productive elongation. 		The RNA polymerase II (RNAPII) associated factor 1 complex (Paf1C) plays critical roles in modulating the release of paused RNAPII into productive elongation. 	Immunohistochemical staining	The RNA polymerase II (RNAPII) associated factor 1 complex (Paf1C) plays critical roles in modulating the release of paused RNAPII into productive elongation. 			CRISPR/Cas9 辅助 GFP 标记，ChIP-seq，qRT-PCR 和 RNA-seq，免疫染色蛋白质印记				PAF1
33371364	chr4	73866599	73868599	CXCL1	DEP released the C-X-C Motif Chemokine Ligand 1 (CXCL1/KC) in AM.	mouse	connective tissue	High+Lowthroughput	Diesel Exhaust Particulates Induce Neutrophilic Lung Inflammation by Modulating Endoplasmic Reticulum Stress-Mediated CXCL1/KC Expression in Alveolar Macrophages	不相关		Lung inflammation	alveolar macrophage	E_02_0565	RNA extraction and quantitative real-time polymerase chain reaction (RT qPCR), cell viability and reactive oxygen species (ROS) measurement, Western blot analysis, Western blot analysis, DEP instillation	DEP released the C-X-C Motif Chemokine Ligand 1 (CXCL1/KC) in AM.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	DEP released the C-X-C Motif Chemokine Ligand 1 (CXCL1/KC) in AM.		DEP released the C-X-C Motif Chemokine Ligand 1 (CXCL1/KC) in AM.	Immunohistochemical staining	DEP released the C-X-C Motif Chemokine Ligand 1 (CXCL1/KC) in AM.			RNA提取和定量实时聚合酶链反应（RT-qPCR），细胞活力和活性氧（ROS）测量，蛋白质印迹分析，蛋白质印迹分析，DEP灌输				CXCL1
33370552	chr7	148804266	148806266	EZH2	Our studies are aimed to investigate the expression of enhancer of zeste homolog 2 (EZH2) in IHD and regulation of cardiac NaV1.5 expression by EZH2.	human	Musculature	High+Lowthroughput	Elevated EZH2 in ischemic heart disease epigenetically mediates suppression of Na(V)1.5 expression	相关	rs6801957	ischemic heart disease	cardiac muscle cell (sensu Arthopoda)	E_01_0826	Chip qPCR, immunofluorescence staining	Our studies are aimed to investigate the expression of enhancer of zeste homolog 2 (EZH2) in IHD and regulation of cardiac NaV1.5 expression by EZH2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our studies are aimed to investigate the expression of enhancer of zeste homolog 2 (EZH2) in IHD and regulation of cardiac NaV1.5 expression by EZH2.	Immunohistochemical staining	Our studies are aimed to investigate the expression of enhancer of zeste homolog 2 (EZH2) in IHD and regulation of cardiac NaV1.5 expression by EZH2.	EZH2		ChIP-qPCR，免疫荧光染色	Our studies are aimed to investigate the expression of enhancer of zeste homolog 2 (EZH2) in IHD and regulation of cardiac NaV1.5 expression by EZH2.			
33358566	chr7	148804311	148806311	EZH2	Growing evidence shows that enhancer of zeste homolog 2 (EZH2) plays a role in various physiological functions and cancer pathogenesis. 	mouse	Epithelial tissues	High+Lowthroughput	DZNep attenuates allergic airway inflammation in an ovalbumin-induced murine model	不相关		allergic airway inflammation 	goblet cell	E_02_0566	Western blotting	Growing evidence shows that enhancer of zeste homolog 2 (EZH2) plays a role in various physiological functions and cancer pathogenesis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Growing evidence shows that enhancer of zeste homolog 2 (EZH2) plays a role in various physiological functions and cancer pathogenesis. 		Growing evidence shows that enhancer of zeste homolog 2 (EZH2) plays a role in various physiological functions and cancer pathogenesis. 	Immunohistochemical staining	Growing evidence shows that enhancer of zeste homolog 2 (EZH2) plays a role in various physiological functions and cancer pathogenesis. 			蛋白质印记				EZH2
33355129	chr22	43148897	43150897	TSPO	The complex formed by TSPO with the protein kinase A (PKA), via the A-kinase anchoring protein acyl-CoA binding domain containing 3 (ACBD3), established the tethering.	human		High+Lowthroughput	Mitochondria form contact sites with the nucleus to couple prosurvival retrograde response	不相关			cancer cell	E_01_0827	Immunohistochemistry / immunocytochemistry, Western blotting, confocal imaging, fluorescence imaging	The complex formed by TSPO with the protein kinase A (PKA), via the A-kinase anchoring protein acyl-CoA binding domain containing 3 (ACBD3), established the tethering.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The complex formed by TSPO with the protein kinase A (PKA), via the A-kinase anchoring protein acyl-CoA binding domain containing 3 (ACBD3), established the tethering.		The complex formed by TSPO with the protein kinase A (PKA), via the A-kinase anchoring protein acyl-CoA binding domain containing 3 (ACBD3), established the tethering.	Immunohistochemical staining	The complex formed by TSPO with the protein kinase A (PKA), via the A-kinase anchoring protein acyl-CoA binding domain containing 3 (ACBD3), established the tethering.			免疫组化/免疫细胞化学，蛋白质印迹，共聚焦成像，荧光成像				TSPO
33349155	chr17	39725778	39727778	MIEN1	miR-124-5p targeted MIEN1 and negatively modulated the MIEN1 expression in SGC-803 and SGC7901 cells. Silencing MIEN1 negatively regulated the metastasis and proliferation ability of SGC7901 cells.	human		High+Lowthroughput	MiR-124-5p Inhibits the Progression of Gastric Cancer by Targeting MIEN1	不相关		gastric cancer	GC cell，SGC803 cell	E_01_0828	Dual luciferase reporter assay, QRT PCR	miR-124-5p targeted MIEN1 and negatively modulated the MIEN1 expression in SGC-803 and SGC7901 cells. Silencing MIEN1 negatively regulated the metastasis and proliferation ability of SGC7901 cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	miR-124-5p targeted MIEN1 and negatively modulated the MIEN1 expression in SGC-803 and SGC7901 cells. Silencing MIEN1 negatively regulated the metastasis and proliferation ability of SGC7901 cells.		miR-124-5p targeted MIEN1 and negatively modulated the MIEN1 expression in SGC-803 and SGC7901 cells. Silencing MIEN1 negatively regulated the metastasis and proliferation ability of SGC7901 cells.	Immunohistochemical staining	miR-124-5p targeted MIEN1 and negatively modulated the MIEN1 expression in SGC-803 and SGC7901 cells. Silencing MIEN1 negatively regulated the metastasis and proliferation ability of SGC7901 cells.			双荧光素酶报告检测，qRT-PCR				MIEN1
33100045	chr3	192136683	192138683	FGF12	In human PASMCs, FGF12 expression was increased by canonical BMP signaling. FGF12 knockdown blocked the antiproliferative and prodifferentiation effect of BMP on human PASMCs, suggesting that FGF12 is required for the BMP-mediated acquisition of the quiescent and differentiated PASMC phenotype.	human	Musculature	High+Lowthroughput	FGF12 (Fibroblast Growth Factor 12) Inhibits Vascular Smooth Muscle Cell Remodeling in Pulmonary Arterial Hypertension	不相关		Pulmonary arterial hypertension	smooth muscle cell	E_01_0829	Immunofluorescence staining, Western blotting, real time RT-PCR analysis	In human PASMCs, FGF12 expression was increased by canonical BMP signaling. FGF12 knockdown blocked the antiproliferative and prodifferentiation effect of BMP on human PASMCs, suggesting that FGF12 is required for the BMP-mediated acquisition of the quiescent and differentiated PASMC phenotype.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In human PASMCs, FGF12 expression was increased by canonical BMP signaling. FGF12 knockdown blocked the antiproliferative and prodifferentiation effect of BMP on human PASMCs, suggesting that FGF12 is required for the BMP-mediated acquisition of the quiescent and differentiated PASMC phenotype.		In human PASMCs, FGF12 expression was increased by canonical BMP signaling. FGF12 knockdown blocked the antiproliferative and prodifferentiation effect of BMP on human PASMCs, suggesting that FGF12 is required for the BMP-mediated acquisition of the quiescent and differentiated PASMC phenotype.	Immunohistochemical staining	In human PASMCs, FGF12 expression was increased by canonical BMP signaling. FGF12 knockdown blocked the antiproliferative and prodifferentiation effect of BMP on human PASMCs, suggesting that FGF12 is required for the BMP-mediated acquisition of the quiescent and differentiated PASMC phenotype.			免疫荧光染色，蛋白质印记，实时 RT-PCR 分析				FGF12
33340495	chr7	148804230	148806230	EZH2	 In the mechanism exploration, we found that Lncenc1 could bind with the RNA binding protein (RBP) enhancer of zeste homologue 2 (EZH2), an identified contributor in microglial activation and neuropathic pain. Lncenc1 interacted with EZH2 and downregulated the expression of brain-specific angiogenesis inhibitor 1 (BAI1). 	mouse		High+Lowthroughput	LncRNA embryonic stem cells expressed 1 (Lncenc1) is identified as a novel regulator in neuropathic pain by interacting with EZH2 and downregulating the expression of Bai1 in mouse microglia	不相关		Neuropathic pain	embryonic stem cell	E_02_0567	SUMC data analysis，SEER data analysis	 In the mechanism exploration, we found that Lncenc1 could bind with the RNA binding protein (RBP) enhancer of zeste homologue 2 (EZH2), an identified contributor in microglial activation and neuropathic pain. Lncenc1 interacted with EZH2 and downregulated the expression of brain-specific angiogenesis inhibitor 1 (BAI1). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 In the mechanism exploration, we found that Lncenc1 could bind with the RNA binding protein (RBP) enhancer of zeste homologue 2 (EZH2), an identified contributor in microglial activation and neuropathic pain. Lncenc1 interacted with EZH2 and downregulated the expression of brain-specific angiogenesis inhibitor 1 (BAI1). 		 In the mechanism exploration, we found that Lncenc1 could bind with the RNA binding protein (RBP) enhancer of zeste homologue 2 (EZH2), an identified contributor in microglial activation and neuropathic pain. Lncenc1 interacted with EZH2 and downregulated the expression of brain-specific angiogenesis inhibitor 1 (BAI1). 	Immunohistochemical staining	 In the mechanism exploration, we found that Lncenc1 could bind with the RNA binding protein (RBP) enhancer of zeste homologue 2 (EZH2), an identified contributor in microglial activation and neuropathic pain. Lncenc1 interacted with EZH2 and downregulated the expression of brain-specific angiogenesis inhibitor 1 (BAI1). 			SUMC data analysis，SEER data analysis				EZH2
33336896	chr7	148804630	148806630	EZH2	RNA immunoprecipitation and RNA pull‐down results showed that lnc‐ATB positively regulated the expression of EZH2 via directly interacting with EZH2. 	human		High+Lowthroughput	Long noncoding RNA ATB promotes ovarian cancer tumorigenesis by mediating histone H3 lysine 27 trimethylation through binding to EZH2	不相关		cancer	A2780	E_01_0830	Western blotting, real-time PCR (RT qPCR), RNA immunoprecipitation (RIP), RNA immunoprecipitation (RIP), immunohistochemistry (IHC)	RNA immunoprecipitation and RNA pull‐down results showed that lnc‐ATB positively regulated the expression of EZH2 via directly interacting with EZH2. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			RNA immunoprecipitation and RNA pull‐down results showed that lnc‐ATB positively regulated the expression of EZH2 via directly interacting with EZH2. 	Immunohistochemical staining	RNA immunoprecipitation and RNA pull‐down results showed that lnc‐ATB positively regulated the expression of EZH2 via directly interacting with EZH2. 	EZH2		蛋白质印记，实时荧光定量 PCR （RT-qPCR），RNA免疫沉淀（RIP），RNA免疫沉淀（RIP），免疫组化（IHC）	RNA immunoprecipitation and RNA pull‐down results showed that lnc‐ATB positively regulated the expression of EZH2 via directly interacting with EZH2. 			
33334823	chr4	54096876	54098876	GSX2	 Reporter assays showed that Gsx2 mediates opposing outcomes in a DNA binding site-dependent manner: Monomer Gsx2 binding represses transcription, whereas homodimer binding stimulates gene expression. In Drosophila, the Gsx homolog, Ind, similarly represses or stimulates transcription in a site-dependent manner via an autoregulatory enhancer containing a combination of monomer and homodimer sites.	mouse		High+Lowthroughput	Conserved Gsx2/Ind homeodomain monomer versus homodimer DNA binding defines regulatory outcomes in flies and mice	不相关			Neurogenic progenitor cell	E_02_0568	Protein purification, electrophoretic mobility shift assay (EMSA), luciferase assay, chip qPCR, ribonucleic acid sequencing	 Reporter assays showed that Gsx2 mediates opposing outcomes in a DNA binding site-dependent manner: Monomer Gsx2 binding represses transcription, whereas homodimer binding stimulates gene expression. In Drosophila, the Gsx homolog, Ind, similarly represses or stimulates transcription in a site-dependent manner via an autoregulatory enhancer containing a combination of monomer and homodimer sites.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 Reporter assays showed that Gsx2 mediates opposing outcomes in a DNA binding site-dependent manner: Monomer Gsx2 binding represses transcription, whereas homodimer binding stimulates gene expression. In Drosophila, the Gsx homolog, Ind, similarly represses or stimulates transcription in a site-dependent manner via an autoregulatory enhancer containing a combination of monomer and homodimer sites.		 Reporter assays showed that Gsx2 mediates opposing outcomes in a DNA binding site-dependent manner: Monomer Gsx2 binding represses transcription, whereas homodimer binding stimulates gene expression. In Drosophila, the Gsx homolog, Ind, similarly represses or stimulates transcription in a site-dependent manner via an autoregulatory enhancer containing a combination of monomer and homodimer sites.	Immunohistochemical staining	 Reporter assays showed that Gsx2 mediates opposing outcomes in a DNA binding site-dependent manner: Monomer Gsx2 binding represses transcription, whereas homodimer binding stimulates gene expression. In Drosophila, the Gsx homolog, Ind, similarly represses or stimulates transcription in a site-dependent manner via an autoregulatory enhancer containing a combination of monomer and homodimer sites.			蛋白质纯化，电泳迁移率转移检测 （EMSA），荧光素酶检测，ChIP-qPCR，核糖核酸测序				GSX2
33334620	chr1	156461041	156463041	MEF2D	Here we hypothesized that a protein kinase D (PKD)-dependent extracellular signal-regulated kinase 5 (ERK5) pathway was able to regulate downstream myocyte enhancer factor 2D (MEF2D), affecting prohypertrophic responses to angiotensin II (Ang II).	mouse	Musculature	High+Lowthroughput	Protein kinase D participates in cardiomyocyte hypertrophy by regulating extracellular signal-regulated and myocyte enhancer factor 2D	不相关		hypertension	cardiac muscle cell (sensu Arthopoda)	E_02_0569	Western blot analysis, immunofluorescence staining, real-time quantitative polymerase chain reaction, small interfering RNA and its transfection	Here we hypothesized that a protein kinase D (PKD)-dependent extracellular signal-regulated kinase 5 (ERK5) pathway was able to regulate downstream myocyte enhancer factor 2D (MEF2D), affecting prohypertrophic responses to angiotensin II (Ang II).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we hypothesized that a protein kinase D (PKD)-dependent extracellular signal-regulated kinase 5 (ERK5) pathway was able to regulate downstream myocyte enhancer factor 2D (MEF2D), affecting prohypertrophic responses to angiotensin II (Ang II).		Here we hypothesized that a protein kinase D (PKD)-dependent extracellular signal-regulated kinase 5 (ERK5) pathway was able to regulate downstream myocyte enhancer factor 2D (MEF2D), affecting prohypertrophic responses to angiotensin II (Ang II).	Immunohistochemical staining	Here we hypothesized that a protein kinase D (PKD)-dependent extracellular signal-regulated kinase 5 (ERK5) pathway was able to regulate downstream myocyte enhancer factor 2D (MEF2D), affecting prohypertrophic responses to angiotensin II (Ang II).			蛋白质印迹分析，免疫荧光染色，实时定量聚合酶链反应，小干扰RNA及其转染				MEF2D
33334026	chr12	55964237	55966237	CDK2	Non-alcoholic fatty liver disease (NAFLD) has a large impact on global health. At the onset of disease, NAFLD is characterized by hepatic steatosis defined by the accumulation of triglycerides stored as lipid droplets.	human	hepatic tissue	High+Lowthroughput	Pluripotent Stem Cell-Derived Hepatocytes Phenotypic Screening Reveals Small Molecules Targeting the CDK2/4-C/EBPα/DGAT2 Pathway Preventing ER-Stress Induced Lipid Accumulation	不相关		Nonalcoholic fatty liver disease	pluripotent stem cell,hepatocyte	E_01_0831	Tag accumulation, staining and high content imaging, real time PCR, dendrogram – hierarchical clustering using Ward's method	Non-alcoholic fatty liver disease (NAFLD) has a large impact on global health. At the onset of disease, NAFLD is characterized by hepatic steatosis defined by the accumulation of triglycerides stored as lipid droplets.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Non-alcoholic fatty liver disease (NAFLD) has a large impact on global health. At the onset of disease, NAFLD is characterized by hepatic steatosis defined by the accumulation of triglycerides stored as lipid droplets.		Non-alcoholic fatty liver disease (NAFLD) has a large impact on global health. At the onset of disease, NAFLD is characterized by hepatic steatosis defined by the accumulation of triglycerides stored as lipid droplets.	Immunohistochemical staining	Non-alcoholic fatty liver disease (NAFLD) has a large impact on global health. At the onset of disease, NAFLD is characterized by hepatic steatosis defined by the accumulation of triglycerides stored as lipid droplets.			TAG积累，染色和高内涵成像，实时荧光定量 PCR，树状图–使用沃德方法的分层聚类				CDK2
33323375	chr5	150050709	150052709	CSF1R	Were reported to be absent in mice lacking a conserved Csf1r enhancer: the fms-intronic regulatory element (FIRE). 	mouse		High+Lowthroughput	CNS macrophages differentially rely on an intronic Csf1r enhancer for their development	不相关			microglial cell	E_02_0570	Immunostaining, ex vivo time-lapse imaging	Were reported to be absent in mice lacking a conserved Csf1r enhancer: the fms-intronic regulatory element (FIRE). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Were reported to be absent in mice lacking a conserved Csf1r enhancer: the fms-intronic regulatory element (FIRE). 		Were reported to be absent in mice lacking a conserved Csf1r enhancer: the fms-intronic regulatory element (FIRE). 	Immunohistochemical staining	Were reported to be absent in mice lacking a conserved Csf1r enhancer: the fms-intronic regulatory element (FIRE). 			免疫染色，离体延时成像				CSF1R
33322515	chrX	136144009	136146009	FHL1	The knockdown of FHL1 by siRNA stimulated cell proliferation and inhibited myogenic differentiation of myoblasts.	mouse		High+Lowthroughput	MiR-96-5p Induced by Palmitic Acid Suppresses the Myogenic Differentiation of C2C12 Myoblasts by Targeting FHL1	不相关			C2C12 cell	E_02_0571	Transfection of oligonucleotides, RNA preparation and quantitative reverse transcription polymerase chain reaction (QRT PCR), dual luciferase reporter assay, Western blot analysis, immunofluorescence analysis, Western blot analysis	The knockdown of FHL1 by siRNA stimulated cell proliferation and inhibited myogenic differentiation of myoblasts.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The knockdown of FHL1 by siRNA stimulated cell proliferation and inhibited myogenic differentiation of myoblasts.		The knockdown of FHL1 by siRNA stimulated cell proliferation and inhibited myogenic differentiation of myoblasts.	Immunohistochemical staining	The knockdown of FHL1 by siRNA stimulated cell proliferation and inhibited myogenic differentiation of myoblasts.			Transfection of Oligonucleotides，RNA制备和定量逆转录-聚合酶链反应（qRT-PCR），双荧光素酶报告基因测定，免疫印迹分析，免疫荧光分析，免疫印迹分析				FHL1
33318687	chr10	86432735	86434735	WAPL	We report that the cohesin release factor WAPL creates a pool of free cohesin, in a process known as cohesin turnover, which reloads it to cell-type specific binding sites.	mouse		High+Lowthroughput	WAPL maintains a cohesin loading cycle to preserve cell-type-specific distal gene regulation	不相关			embryonic stem cell	E_02_0572	Plasmid construction, gene targeting, Western blot, GFP quantification and cell cycle analysis, cell proliferation analysis, immunofluorescence staining, alkaline phosphatase staining, single cell colony formation assay, RT qPCR, chip SEQ riboprobes, TT SEQ, ATAC SEQ, chip SEQ analysis, ATAC SEQ analysis	We report that the cohesin release factor WAPL creates a pool of free cohesin, in a process known as cohesin turnover, which reloads it to cell-type specific binding sites.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We report that the cohesin release factor WAPL creates a pool of free cohesin, in a process known as cohesin turnover, which reloads it to cell-type specific binding sites.		We report that the cohesin release factor WAPL creates a pool of free cohesin, in a process known as cohesin turnover, which reloads it to cell-type specific binding sites.	Immunohistochemical staining	We report that the cohesin release factor WAPL creates a pool of free cohesin, in a process known as cohesin turnover, which reloads it to cell-type specific binding sites.			质粒构建，基因靶向，蛋白质印迹，GFP定量和细胞周期分析，细胞增殖分析，免疫荧光染色，碱性磷酸酶染色，单细胞集落形成测定，RT-qPCR，ChIP-seq核糖核酸序列，TT-seq，ATAC-seq，ChIP-seq 分析，ATAC-seq Analysis				WAPL
33299054	chr12	108856762	108858762	DAO	Vegetal diamine oxidase (vDAO) might be a relevant alternative owing to its histaminase activity.	human	Connective tissue, lymphoid tissue	High+Lowthroughput	Vegetal diamine oxidase alleviates histamine-induced contraction of colonic muscles	不相关		Gastrointestinal disorders	Immune cell,epithelial cell,muscle cell	E_01_0832	Immunofluorescence, purification of vdao, Dao activity assay, and study of the interaction between pyridoxal-5-phosphate (PLP) and histamine	Vegetal diamine oxidase (vDAO) might be a relevant alternative owing to its histaminase activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Vegetal diamine oxidase (vDAO) might be a relevant alternative owing to its histaminase activity.		Vegetal diamine oxidase (vDAO) might be a relevant alternative owing to its histaminase activity.	Immunohistochemical staining	Vegetal diamine oxidase (vDAO) might be a relevant alternative owing to its histaminase activity.			免疫荧光，vDAO的纯化，DAO活性测定，吡哆醛-5-磷酸（PLP）与组胺相互作用的研究				DAO
33293536	chr19	10868423	10870423	CARM1	We identify that coactivator-associated arginine methyltransferase 1 (CARM1) methylates Pontin chromatin-remodeling factor under glucose starvation, and methylated Pontin binds Forkhead Box O 3a (FOXO3a).	human		High+Lowthroughput	Pontin arginine methylation by CARM1 is crucial for epigenetic regulation of autophagy	不相关			fibroblast	E_01_0833	GST pull down assay, in vitro methylation assay, in vitro methylation assay using 3h-sam, immunodot blot assay, immunofluorescence, luciferase assay, luciferase assay, luciferase assay, ribonucleic acid sequence analysis, chip SEQ analysis, chromosome conformation capture (3C) assay	We identify that coactivator-associated arginine methyltransferase 1 (CARM1) methylates Pontin chromatin-remodeling factor under glucose starvation, and methylated Pontin binds Forkhead Box O 3a (FOXO3a).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identify that coactivator-associated arginine methyltransferase 1 (CARM1) methylates Pontin chromatin-remodeling factor under glucose starvation, and methylated Pontin binds Forkhead Box O 3a (FOXO3a).		We identify that coactivator-associated arginine methyltransferase 1 (CARM1) methylates Pontin chromatin-remodeling factor under glucose starvation, and methylated Pontin binds Forkhead Box O 3a (FOXO3a).	Immunohistochemical staining	We identify that coactivator-associated arginine methyltransferase 1 (CARM1) methylates Pontin chromatin-remodeling factor under glucose starvation, and methylated Pontin binds Forkhead Box O 3a (FOXO3a).			GST下拉测定，体外甲基化测定，体外甲基化测定使用3H-SAM，免疫点印迹测定，免疫荧光，荧光素酶测定，荧光素酶测定，荧光素酶测定，核糖核酸序列分析，ChIP-seq 分析，染色体构象捕获 （3C） 测定				CARM1
33293480	chr2	181665521	181667521	NEUROD1	Through motif enrichment analysis, we found that NEUROD1 controls iPSC differentiation to NPC by binding to the accessible regions of enhancers in cooperation with other factors such as the Hox proteins. 	human	Neural tissue-	High+Lowthroughput	NEUROD1 Intrinsically Initiates Differentiation of Induced Pluripotent Stem Cells into Neural Progenitor Cells	不相关			Neuronal progenitor,pluripotent stem cell	E_01_0834	ATAC SEQ, histone chip SEQ, RNA sequencing data processing, Hi-C data processing	Through motif enrichment analysis, we found that NEUROD1 controls iPSC differentiation to NPC by binding to the accessible regions of enhancers in cooperation with other factors such as the Hox proteins. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Through motif enrichment analysis, we found that NEUROD1 controls iPSC differentiation to NPC by binding to the accessible regions of enhancers in cooperation with other factors such as the Hox proteins. 	Immunohistochemical staining	Through motif enrichment analysis, we found that NEUROD1 controls iPSC differentiation to NPC by binding to the accessible regions of enhancers in cooperation with other factors such as the Hox proteins. 	NEUROD1		ATAC-seq，组蛋白 ChIP-seq ，RNA测序数据处理，Hi-C数据处理	Through motif enrichment analysis, we found that NEUROD1 controls iPSC differentiation to NPC by binding to the accessible regions of enhancers in cooperation with other factors such as the Hox proteins. 			
33292225	chr7	148804685	148806685	EZH2	We aimed to analyze the underlying mechanism supporting that enhancer of zeste homolog 2 (EZH2) affected the development of OC via the involvement of microRNA-139 (miR-139)/transforming growth factor beta (TGF-β)/lysophosphatidic acid-1 (LPA1) axis.	human		High+Lowthroughput	EZH2 promotes the expression of LPA1 by mediating microRNA-139 promoter methylation to accelerate the development of ovarian cancer	不相关		oophoroma	Osteoclast	E_01_0835	Immunohistochemistry, cell transfection, RNA isolation and quantification, Western blot analysis, dual luciferase reporter assay, dual luciferase reporter assay, flow cytometry	We aimed to analyze the underlying mechanism supporting that enhancer of zeste homolog 2 (EZH2) affected the development of OC via the involvement of microRNA-139 (miR-139)/transforming growth factor beta (TGF-β)/lysophosphatidic acid-1 (LPA1) axis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We aimed to analyze the underlying mechanism supporting that enhancer of zeste homolog 2 (EZH2) affected the development of OC via the involvement of microRNA-139 (miR-139)/transforming growth factor beta (TGF-β)/lysophosphatidic acid-1 (LPA1) axis.	Immunohistochemical staining	We aimed to analyze the underlying mechanism supporting that enhancer of zeste homolog 2 (EZH2) affected the development of OC via the involvement of microRNA-139 (miR-139)/transforming growth factor beta (TGF-β)/lysophosphatidic acid-1 (LPA1) axis.	EZH2		免疫组化，细胞转染，RNA 分离和定量，蛋白质印迹分析，双荧光素酶报告基因检测，双荧光素酶报告基因检测，流式细胞术	We aimed to analyze the underlying mechanism supporting that enhancer of zeste homolog 2 (EZH2) affected the development of OC via the involvement of microRNA-139 (miR-139)/transforming growth factor beta (TGF-β)/lysophosphatidic acid-1 (LPA1) axis.			
33288562	chr7	148804232	148806232	EZH2	POD24 is currently the most useful tool for the identification of poor outlook patients. EZH2 is crucial in FL biology, but the value of its protein expression is limited as a prognostic factor.	human	connective tissue	High+Lowthroughput	EZH2 Expression in Follicular Lymphoma Is Variable and Independent from the Progression of Disease Within 24 Months of First Treatment	不相关		Follicular lymphoma	B cell	E_01_0836	Immunohistochemistry.	POD24 is currently the most useful tool for the identification of poor outlook patients. EZH2 is crucial in FL biology, but the value of its protein expression is limited as a prognostic factor.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			POD24 is currently the most useful tool for the identification of poor outlook patients. EZH2 is crucial in FL biology, but the value of its protein expression is limited as a prognostic factor.	Immunohistochemical staining	POD24 is currently the most useful tool for the identification of poor outlook patients. EZH2 is crucial in FL biology, but the value of its protein expression is limited as a prognostic factor.	EZH2		Immunohistochemistry.	POD24 is currently the most useful tool for the identification of poor outlook patients. EZH2 is crucial in FL biology, but the value of its protein expression is limited as a prognostic factor.			
33287648	chr3	41191825	41193825	CTNNB1	Previous studies have suggested that there are somatic CTNNB1 mutations in APA, but the specific mechanism of CTNNB1 mutation in APA tumorigenesis and aldosterone secretion remains unclear. In the present study, human adrenocortical carcinoma cell line H295 R was used to establish stable CTNNB1 knockdown cell lines.	mouse		High+Lowthroughput	CTNNB1 Knockdown Inhibits Cell Proliferation and Aldosterone Secretion Through Inhibiting Wnt/β-Catenin Signaling in H295R Cells	不相关		Primary aldosteronism	H295Rcell,cortical cell of adrenal gland	E_02_0573	CTNNB1 Knockdown，Total RNA Extraction and qRT-PCR，Western Blot Analysis，Cell Viability Assays，Quantification of Aldosterone Using ELISA Kit	Previous studies have suggested that there are somatic CTNNB1 mutations in APA, but the specific mechanism of CTNNB1 mutation in APA tumorigenesis and aldosterone secretion remains unclear. In the present study, human adrenocortical carcinoma cell line H295 R was used to establish stable CTNNB1 knockdown cell lines.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Previous studies have suggested that there are somatic CTNNB1 mutations in APA, but the specific mechanism of CTNNB1 mutation in APA tumorigenesis and aldosterone secretion remains unclear. In the present study, human adrenocortical carcinoma cell line H295 R was used to establish stable CTNNB1 knockdown cell lines.		Previous studies have suggested that there are somatic CTNNB1 mutations in APA, but the specific mechanism of CTNNB1 mutation in APA tumorigenesis and aldosterone secretion remains unclear. In the present study, human adrenocortical carcinoma cell line H295 R was used to establish stable CTNNB1 knockdown cell lines.	Immunohistochemical staining	Previous studies have suggested that there are somatic CTNNB1 mutations in APA, but the specific mechanism of CTNNB1 mutation in APA tumorigenesis and aldosterone secretion remains unclear. In the present study, human adrenocortical carcinoma cell line H295 R was used to establish stable CTNNB1 knockdown cell lines.			CTNNB1 Knockdown，Total RNA Extraction and qRT-PCR，Western Blot Analysis，Cell Viability Assays，Quantification of Aldosterone Using ELISA Kit				CTNNB1
33281964	chr7	148804758	148806758	EZH2	The present study aimed to illustrate the role of LINC00565 in aggravating colorectal cancer (CRC) by targeting enhancer of zeste homolog 2 (EZH2). 	human		High+Lowthroughput	LINC00565 promotes the progression of colorectal cancer by upregulating EZH2	不相关		colorectal cancer 	T helper cell	E_01_0837	Reverse transcription quantitative polymerase chain reaction (RT qPCR), cell transfection, Transwell migration assay, RNA immunoprecipitation (RIP)	The present study aimed to illustrate the role of LINC00565 in aggravating colorectal cancer (CRC) by targeting enhancer of zeste homolog 2 (EZH2). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The present study aimed to illustrate the role of LINC00565 in aggravating colorectal cancer (CRC) by targeting enhancer of zeste homolog 2 (EZH2). 	Immunohistochemical staining	The present study aimed to illustrate the role of LINC00565 in aggravating colorectal cancer (CRC) by targeting enhancer of zeste homolog 2 (EZH2). 	EZH2		逆转录-定量聚合酶链反应（RT-qPCR），细胞转染，透孔迁移测定，RNA免疫沉淀（RIP）	The present study aimed to illustrate the role of LINC00565 in aggravating colorectal cancer (CRC) by targeting enhancer of zeste homolog 2 (EZH2). 			
33277782	chr7	148804134	148806134	EZH2	The enhancer of zeste homologue 2 (EZH2) is a histone H3 lysine 27 methyltransferase that promotes tumorigenesis in a variety of human malignancies by altering the expression of tumour suppressor genes.	human	Immunohistochem	High+Lowthroughput	EZH2 is a potential prognostic predictor of glioma	不相关		cancer	lymphocyte	E_01_0838	Quantitative real-time PCR (QRT PCR), Western blot, immunohistochemical staining	The enhancer of zeste homologue 2 (EZH2) is a histone H3 lysine 27 methyltransferase that promotes tumorigenesis in a variety of human malignancies by altering the expression of tumour suppressor genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The enhancer of zeste homologue 2 (EZH2) is a histone H3 lysine 27 methyltransferase that promotes tumorigenesis in a variety of human malignancies by altering the expression of tumour suppressor genes.	Immunohistochemical staining	The enhancer of zeste homologue 2 (EZH2) is a histone H3 lysine 27 methyltransferase that promotes tumorigenesis in a variety of human malignancies by altering the expression of tumour suppressor genes.	EZH2		实时荧光定量 PCR （qRT-PCR），蛋白质印迹，免疫组化染色	The enhancer of zeste homologue 2 (EZH2) is a histone H3 lysine 27 methyltransferase that promotes tumorigenesis in a variety of human malignancies by altering the expression of tumour suppressor genes.			
33275145	chr19	16352505	16354505	EPS15L1	The EPS15L1 fusion protein may regulate (Gasdermin E) GSDME, critical in pyroptosis and anti-tumor immunity. 	human		High+Lowthroughput	The landscape of long noncoding RNA-involved and tumor-specific fusions across various cancers	不相关		cancer	breast cancer cell,SKBR3 cell	E_01_0839	Proteomic and phosphoproteomic analysis, real-time PCR, Western blot analysis	The EPS15L1 fusion protein may regulate (Gasdermin E) GSDME, critical in pyroptosis and anti-tumor immunity. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The EPS15L1 fusion protein may regulate (Gasdermin E) GSDME, critical in pyroptosis and anti-tumor immunity. 		The EPS15L1 fusion protein may regulate (Gasdermin E) GSDME, critical in pyroptosis and anti-tumor immunity. 	Immunohistochemical staining	The EPS15L1 fusion protein may regulate (Gasdermin E) GSDME, critical in pyroptosis and anti-tumor immunity. 			蛋白质组学和磷酸化蛋白质组学分析，实时荧光定量 PCR，蛋白质印迹分析				EPS15L1
33264630	chr7	116521979	116523979	CAV1	CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 	mouse	lymphoid tissue	High+Lowthroughput	Rare Variant Burden Analysis within Enhancers Identifies CAV1 as an ALS Risk Gene	不相关		Amyotrophic lateral sclerosis	Lymphoblast	E_02_0574	Immunoblotting, fluorescent quantitative PCR (RT-PCR), immunocytochemistry, live cell imaging	CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 		CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 	Immunohistochemical staining	CAV1 and CAV2 organize membrane lipid rafts (MLRs) important for cell signaling and neuronal survival, and overexpression of CAV1 ameliorates ALS phenotypes in vivo. 			免疫印迹，荧光定量 PCR（RT-PCR），免疫细胞化学，活细胞成像				CAV1
33261193	chr7	117284424	117286424	CFTR	In PKD, the decreased levels of intracellular calcium and the increased levels of intracellular cAMP lead to two pathophysiological events: (i) cyclic adenosine monophosphate (cAMP)-induced chloride secretion, in part driven by cystic fibrosis transmembrane conductance regulator (CFTR), and (ii) increased cell proliferation, at least in part mediated by mammalian target of rapamycin complex 1 (mTORC1).	mouse	Kidney tissue	High+Lowthroughput	Novel Potential Application of Chitosan Oligosaccharide for Attenuation of Renal Cyst Growth in the Treatment of Polycystic Kidney Disease	不相关		Polycystic kidney disease	renal tubular cell	E_02_0575	Cell viability assay, immunoblotting, intracellular calcium measurement	In PKD, the decreased levels of intracellular calcium and the increased levels of intracellular cAMP lead to two pathophysiological events: (i) cyclic adenosine monophosphate (cAMP)-induced chloride secretion, in part driven by cystic fibrosis transmembrane conductance regulator (CFTR), and (ii) increased cell proliferation, at least in part mediated by mammalian target of rapamycin complex 1 (mTORC1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In PKD, the decreased levels of intracellular calcium and the increased levels of intracellular cAMP lead to two pathophysiological events: (i) cyclic adenosine monophosphate (cAMP)-induced chloride secretion, in part driven by cystic fibrosis transmembrane conductance regulator (CFTR), and (ii) increased cell proliferation, at least in part mediated by mammalian target of rapamycin complex 1 (mTORC1).		In PKD, the decreased levels of intracellular calcium and the increased levels of intracellular cAMP lead to two pathophysiological events: (i) cyclic adenosine monophosphate (cAMP)-induced chloride secretion, in part driven by cystic fibrosis transmembrane conductance regulator (CFTR), and (ii) increased cell proliferation, at least in part mediated by mammalian target of rapamycin complex 1 (mTORC1).	Immunohistochemical staining	In PKD, the decreased levels of intracellular calcium and the increased levels of intracellular cAMP lead to two pathophysiological events: (i) cyclic adenosine monophosphate (cAMP)-induced chloride secretion, in part driven by cystic fibrosis transmembrane conductance regulator (CFTR), and (ii) increased cell proliferation, at least in part mediated by mammalian target of rapamycin complex 1 (mTORC1).			细胞活力测定，免疫印迹，细胞内钙测量				CFTR
33260349	chr2	9485612	9487612	ADAM17	Our results revealed that TGF-β-induced CTGF expression was weakened by ADAM17 small interfering RNA (ADAM17 siRNA), TNF-α processing inhibitor-0 (TAPI-0, an ADAM17 inhibitor), U0126 (an ERK inhibitor), RSK1 siRNA, and C/EBPβ siRNA.	human	Epithelial tissues	High+Lowthroughput	TGF-β Induced CTGF Expression in Human Lung Epithelial Cells through ERK, ADAM17, RSK1, and C/EBPβ Pathways	不相关		lung cancer	epithelial cell of lung	E_01_0840	SiRNA transfection, Western blotting, chromatin immunoprecipitation assay, RNA isolation and RT-PCR	Our results revealed that TGF-β-induced CTGF expression was weakened by ADAM17 small interfering RNA (ADAM17 siRNA), TNF-α processing inhibitor-0 (TAPI-0, an ADAM17 inhibitor), U0126 (an ERK inhibitor), RSK1 siRNA, and C/EBPβ siRNA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results revealed that TGF-β-induced CTGF expression was weakened by ADAM17 small interfering RNA (ADAM17 siRNA), TNF-α processing inhibitor-0 (TAPI-0, an ADAM17 inhibitor), U0126 (an ERK inhibitor), RSK1 siRNA, and C/EBPβ siRNA.		Our results revealed that TGF-β-induced CTGF expression was weakened by ADAM17 small interfering RNA (ADAM17 siRNA), TNF-α processing inhibitor-0 (TAPI-0, an ADAM17 inhibitor), U0126 (an ERK inhibitor), RSK1 siRNA, and C/EBPβ siRNA.	Immunohistochemical staining	Our results revealed that TGF-β-induced CTGF expression was weakened by ADAM17 small interfering RNA (ADAM17 siRNA), TNF-α processing inhibitor-0 (TAPI-0, an ADAM17 inhibitor), U0126 (an ERK inhibitor), RSK1 siRNA, and C/EBPβ siRNA.			siRNA转染，蛋白质印迹，染色质免疫沉淀测定，RNA分离和RT-PCR				ADAM17
33258451	chr22	39516712	39518712	ATF4	We demonstrate that treatment with the drug-like small-molecule ISR inhibitor ISRIB reverses ISR activation in the brain, as indicated by decreased levels of activating transcription factor 4 (ATF4) and phosphorylated eukaryotic translation initiation factor eIF2. 	mouse	lymphoid tissue	High+Lowthroughput	Small molecule cognitive enhancer reverses age-related memory decline in mice	不相关		Neurodegenerative diseases	T cell	E_02_0576	Western blot analysis, electrophysiology, fluorescent spine imaging preparation, qPCR analysis, qPCR analysis	We demonstrate that treatment with the drug-like small-molecule ISR inhibitor ISRIB reverses ISR activation in the brain, as indicated by decreased levels of activating transcription factor 4 (ATF4) and phosphorylated eukaryotic translation initiation factor eIF2. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We demonstrate that treatment with the drug-like small-molecule ISR inhibitor ISRIB reverses ISR activation in the brain, as indicated by decreased levels of activating transcription factor 4 (ATF4) and phosphorylated eukaryotic translation initiation factor eIF2. 		We demonstrate that treatment with the drug-like small-molecule ISR inhibitor ISRIB reverses ISR activation in the brain, as indicated by decreased levels of activating transcription factor 4 (ATF4) and phosphorylated eukaryotic translation initiation factor eIF2. 	Immunohistochemical staining	We demonstrate that treatment with the drug-like small-molecule ISR inhibitor ISRIB reverses ISR activation in the brain, as indicated by decreased levels of activating transcription factor 4 (ATF4) and phosphorylated eukaryotic translation initiation factor eIF2. 			蛋白质印迹分析，电生理学，荧光脊柱成像准备，qPCR 分析，qPCR 分析				ATF4
33257854	chr10	112947297	112949297	TCF7L2	We also identify a stage-specific enhancer in the TCF7L2 diabetes GWAS locus that drives a transient wave of gene expression in pancreatic progenitors. 	human		High+Lowthroughput	Single-cell lineage analysis reveals extensive multimodal transcriptional control during directed beta-cell differentiation	相关	rs180988137 ，rs78025551，rs7903146	diabetes	Pancreatic progenitor cell	E_01_0841	Cell directed differentiation versus hESCs, cell directed differentiation versus hESCs, fluorescence quantitative polymerase chain reaction, sgRNA cargo, gene knockdown, GSEA functional enrichment analysis, transient transcription factor motif enrichment analysis, two wave gene analysis	We also identify a stage-specific enhancer in the TCF7L2 diabetes GWAS locus that drives a transient wave of gene expression in pancreatic progenitors. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We also identify a stage-specific enhancer in the TCF7L2 diabetes GWAS locus that drives a transient wave of gene expression in pancreatic progenitors. 	Immunohistochemical staining	We also identify a stage-specific enhancer in the TCF7L2 diabetes GWAS locus that drives a transient wave of gene expression in pancreatic progenitors. 	TCF7L2		细胞定向分化与hESCs，细胞定向分化与hESCs，荧光定量聚合酶链反应，sgRNA-CARGO，基因敲除 ，GSEA功能富集分析，瞬态转录因子基序富集分析，双波基因分析	We also identify a stage-specific enhancer in the TCF7L2 diabetes GWAS locus that drives a transient wave of gene expression in pancreatic progenitors. 			
33257422	chr5	147204073	147206073	Pdx1	Pancreatic duodenum homeobox 1 (Pdx1) expression is crucial for pancreatic organogenesis and is a key regulator of insulin gene expression. 	mouse		High+Lowthroughput	Genetically engineered pigs manifesting pancreatic agenesis with severe diabetes	不相关		diabetes	germ line cell,exocrine cell	E_02_0577	Genotyping, biochemical analysis, RNA isolation, complementary DNA (cDNA) synthesis and quantitative real-time PCR (qPCR)	Pancreatic duodenum homeobox 1 (Pdx1) expression is crucial for pancreatic organogenesis and is a key regulator of insulin gene expression. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Pancreatic duodenum homeobox 1 (Pdx1) expression is crucial for pancreatic organogenesis and is a key regulator of insulin gene expression. 		Pancreatic duodenum homeobox 1 (Pdx1) expression is crucial for pancreatic organogenesis and is a key regulator of insulin gene expression. 	Immunohistochemical staining	Pancreatic duodenum homeobox 1 (Pdx1) expression is crucial for pancreatic organogenesis and is a key regulator of insulin gene expression. 			基因分型，生化分析，RNA 分离、互补 DNA （cDNA） 合成和定量实时荧光定量 PCR （qPCR）				Pdx1
33251580	chrX	15491856	15493856	ACE2	Because epicardial adipose tissue (EAT) expresses ACE2, we wanted to identify the main factors associated with ACE2 levels and its cleavage enzyme, ADAM17, in epicardial fat.	human		High+Lowthroughput	Higher ACE2 expression levels in epicardial cells than subcutaneous stromal cells from patients with cardiovascular disease: Diabetes and obesity as possible enhancer	不相关		Cardiovascular disease	Stromal vascular cell	E_01_0842	RNA isolation, ACE1, ACE2, and ADAM17 regulation of adipogenesis by epicardial adipose stromal cells	Because epicardial adipose tissue (EAT) expresses ACE2, we wanted to identify the main factors associated with ACE2 levels and its cleavage enzyme, ADAM17, in epicardial fat.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Because epicardial adipose tissue (EAT) expresses ACE2, we wanted to identify the main factors associated with ACE2 levels and its cleavage enzyme, ADAM17, in epicardial fat.		Because epicardial adipose tissue (EAT) expresses ACE2, we wanted to identify the main factors associated with ACE2 levels and its cleavage enzyme, ADAM17, in epicardial fat.	Immunohistochemical staining	Because epicardial adipose tissue (EAT) expresses ACE2, we wanted to identify the main factors associated with ACE2 levels and its cleavage enzyme, ADAM17, in epicardial fat.			RNA 分离，ACE1，ACE2和ADAM17通过心外膜脂肪基质细胞的脂肪发生调节				ACE2
33251489	chrX	15491850	15493850	ACE2	To test whether the olfactory neuroepithelium may represent a target of the virus, we generated RNA-seq libraries from human olfactory neuroepithelia, in which we found substantial expression of the genes coding for the virus receptor angiotensin-converting enzyme-2 (ACE2) and for the virus internalization enhancer TMPRSS2. 	human		High+Lowthroughput	SARS-CoV-2 Receptors and Entry Genes Are Expressed in the Human Olfactory Neuroepithelium and Brain	不相关		New crown	Suspension cell,Olfactory single cell,Cystic cell	E_01_0843	RNA SEQ, immunohistochemistry, supplementary figures	To test whether the olfactory neuroepithelium may represent a target of the virus, we generated RNA-seq libraries from human olfactory neuroepithelia, in which we found substantial expression of the genes coding for the virus receptor angiotensin-converting enzyme-2 (ACE2) and for the virus internalization enhancer TMPRSS2. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To test whether the olfactory neuroepithelium may represent a target of the virus, we generated RNA-seq libraries from human olfactory neuroepithelia, in which we found substantial expression of the genes coding for the virus receptor angiotensin-converting enzyme-2 (ACE2) and for the virus internalization enhancer TMPRSS2. 		To test whether the olfactory neuroepithelium may represent a target of the virus, we generated RNA-seq libraries from human olfactory neuroepithelia, in which we found substantial expression of the genes coding for the virus receptor angiotensin-converting enzyme-2 (ACE2) and for the virus internalization enhancer TMPRSS2. 	Immunohistochemical staining	To test whether the olfactory neuroepithelium may represent a target of the virus, we generated RNA-seq libraries from human olfactory neuroepithelia, in which we found substantial expression of the genes coding for the virus receptor angiotensin-converting enzyme-2 (ACE2) and for the virus internalization enhancer TMPRSS2. 			RNA-seq，免疫组织化学，Supplementary Figures				ACE2
33250922	chr16	31480055	31482055	SLC5A2	Familial renal glucosuria is a rare renal tubular disorder caused by SLC5A2 gene variants.	human	connective tissue	High+Lowthroughput	Six Exonic Variants in the SLC5A2 Gene Cause Exon Skipping in a Minigene Assay	不相关		Familial renal glucosuria	leukocyte	E_01_0844	Amplification of slc5a2 genomic fragment, mini splicing assay, mini structure and site directed mutagenesis	Familial renal glucosuria is a rare renal tubular disorder caused by SLC5A2 gene variants.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Familial renal glucosuria is a rare renal tubular disorder caused by SLC5A2 gene variants.		Familial renal glucosuria is a rare renal tubular disorder caused by SLC5A2 gene variants.	Immunohistochemical staining	Familial renal glucosuria is a rare renal tubular disorder caused by SLC5A2 gene variants.			SLC5A2基因组片段的扩增，微型剪接试验，微型结构和站点导向诱变				SLC5A2
33247104	chr2	112827574	112829574	IL1B	RAS-induced de novo cohesin peaks are transcription-dependent and enriched for senescence-associated genes, exemplified by IL1B, where de novo cohesin binding is involved in new loop formation.	human		High+Lowthroughput	Transcription-dependent cohesin repositioning rewires chromatin loops in cellular senescence	不相关		be senile	fibroblast,macrophage	E_01_0845	Dna-fish, immunofluorescence, chip SEQ, quantitative reverse transcription polymerase chain reaction, Hi-C and capture Hi-C, chip SEQ analysis, ribonucleic acid sequence analysis	RAS-induced de novo cohesin peaks are transcription-dependent and enriched for senescence-associated genes, exemplified by IL1B, where de novo cohesin binding is involved in new loop formation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			RAS-induced de novo cohesin peaks are transcription-dependent and enriched for senescence-associated genes, exemplified by IL1B, where de novo cohesin binding is involved in new loop formation.	Immunohistochemical staining	RAS-induced de novo cohesin peaks are transcription-dependent and enriched for senescence-associated genes, exemplified by IL1B, where de novo cohesin binding is involved in new loop formation.	IL1B		DNA-FISH，免疫荧光，ChIP-seq，定量逆转录-聚合酶链反应，Hi-C 和 Capture Hi-C，ChIP-seq 分析，核糖核酸序列分析	RAS-induced de novo cohesin peaks are transcription-dependent and enriched for senescence-associated genes, exemplified by IL1B, where de novo cohesin binding is involved in new loop formation.			
33246552	chr16	30111578	30113578	MAPK3	We found that the schizophrenia GWAS risk variations at 16p11.2 were significantly associated with mRNA levels of multiple genes in human brain, and one of the leading eQTL genes, MAPK3, located ~200-kb away from these risk variations in the genome.	human		High+Lowthroughput	Functional Genomics Identify a Regulatory Risk Variation rs4420550 in the 16p11.2 Schizophrenia-Associated Locus	相关	rs4420550	Schizophrenia		E_01_0846	Expression quantitative trait locus analysis, identification of epigenomic features, luciferase reporter assays, chromatin conformation capture, homology directed genome editing by CRISPR / cas9 (clustered regularly interspaced short palindromic repeats / cas9), RNA sequencing, and ATAC SEQ (assay for transposase accessible chromatin using sequencing)	We found that the schizophrenia GWAS risk variations at 16p11.2 were significantly associated with mRNA levels of multiple genes in human brain, and one of the leading eQTL genes, MAPK3, located ~200-kb away from these risk variations in the genome.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found that the schizophrenia GWAS risk variations at 16p11.2 were significantly associated with mRNA levels of multiple genes in human brain, and one of the leading eQTL genes, MAPK3, located ~200-kb away from these risk variations in the genome.		We found that the schizophrenia GWAS risk variations at 16p11.2 were significantly associated with mRNA levels of multiple genes in human brain, and one of the leading eQTL genes, MAPK3, located ~200-kb away from these risk variations in the genome.	Immunohistochemical staining	We found that the schizophrenia GWAS risk variations at 16p11.2 were significantly associated with mRNA levels of multiple genes in human brain, and one of the leading eQTL genes, MAPK3, located ~200-kb away from these risk variations in the genome.			表达定量性状位点分析，表观基因组特征鉴定，荧光素酶报告基因测定，染色质构象捕获，通过CRISPR / Cas9（聚集的有规律间隔的短回文重复序列/ Cas9）的同源定向基因组编辑，RNA测序和ATAC-Seq（使用测序测定转座酶可访问的染色质）				MAPK3
33246486	chr8	37692893	37694893	ZNF703	It is known that the transcription factor zinc finger protein 703 (ZNF703) plays an important role in physiological functions and the occurrence and development of various tumors.	human	Cancer tissues	High+Lowthroughput	ZNF703 promotes tumor progression in ovarian cancer by interacting with HE4 and epigenetically regulating PEA15	不相关		cancer	ovarian cancer cell	E_01_0847	Immunohistochemistry and immunocytochemistry, fast polymerase chain reaction, Western blot, Western blot, coimmunoprecipitation, immunofluorescence and immunofluorescence colocalization, chromatin immunoprecipitation sequencing (chip SEQ)	It is known that the transcription factor zinc finger protein 703 (ZNF703) plays an important role in physiological functions and the occurrence and development of various tumors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	It is known that the transcription factor zinc finger protein 703 (ZNF703) plays an important role in physiological functions and the occurrence and development of various tumors.		It is known that the transcription factor zinc finger protein 703 (ZNF703) plays an important role in physiological functions and the occurrence and development of various tumors.	Immunohistochemical staining	It is known that the transcription factor zinc finger protein 703 (ZNF703) plays an important role in physiological functions and the occurrence and development of various tumors.			免疫组化和免疫细胞化学，快速聚合酶链反应，蛋白质印迹，蛋白质印迹，共免疫沉淀，免疫荧光和免疫荧光共定位，染色质免疫沉淀测序（ChIP-seq）				ZNF703
33240378	chr3	12284469	12286469	PPARG	Peroxisome proliferator-activated receptor-γ (PPARG) mainly regulates lipid and glucose metabolisms while it is constitutively expressed in rat primary microglial cultures. 	mouse	connective tissue	High+Lowthroughput	Impact of Proliferator-Activated Receptor γ Gene Polymorphisms on Risk of Schizophrenia: A Case-Control Study and Computational Analyses	相关	rs1801282，rs3856806	Schizophrenia	Fat cell (adipocyte),macrophage	E_02_0578	Genotyping	Peroxisome proliferator-activated receptor-γ (PPARG) mainly regulates lipid and glucose metabolisms while it is constitutively expressed in rat primary microglial cultures. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Peroxisome proliferator-activated receptor-γ (PPARG) mainly regulates lipid and glucose metabolisms while it is constitutively expressed in rat primary microglial cultures. 		Peroxisome proliferator-activated receptor-γ (PPARG) mainly regulates lipid and glucose metabolisms while it is constitutively expressed in rat primary microglial cultures. 	Immunohistochemical staining	Peroxisome proliferator-activated receptor-γ (PPARG) mainly regulates lipid and glucose metabolisms while it is constitutively expressed in rat primary microglial cultures. 			基因分型				PPARG
33239431	chr22	23784215	23786215	SMARCB1	SMARCB1, known initially as a bona fide tumor suppressor gene, was investigated in liver cancer. 	human	Cancer tissues	High+Lowthroughput	Nucleoporin 210 Serves a Key Scaffold for SMARCB1 in Liver Cancer	不相关		liver cancer	HCC cell	E_01_0848	ShRNA infection, transient transfection, RNA extraction and reverse transcription polymerase chain reaction, chromatin immunoprecipitation assay (chip) and re chromatin, chip sequencing, chip sequencing, Western blot analysis, immunoprecipitation, faire qPCR	SMARCB1, known initially as a bona fide tumor suppressor gene, was investigated in liver cancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SMARCB1, known initially as a bona fide tumor suppressor gene, was investigated in liver cancer. 		SMARCB1, known initially as a bona fide tumor suppressor gene, was investigated in liver cancer. 	Immunohistochemical staining	SMARCB1, known initially as a bona fide tumor suppressor gene, was investigated in liver cancer. 			shRNA 感染，瞬时转染，RNA 提取和逆转录聚合酶链反应，染色质免疫沉淀测定 （ChIP） 和再染色质，ChIP测序，ChIP测序，蛋白质印迹分析，免疫沉淀，FAIRE qPCR				SMARCB1
33238114	chr2	25224801	25226801	DNMT3A	Mutations in DNA methyltransferase 3A (DNMT3A) have been detected in autism and related disorders, but how these mutations disrupt nervous system function is unknown.	mouse		High+Lowthroughput	DNMT3A Haploinsufficiency Results in Behavioral Deficits and Global Epigenomic Dysregulation Shared across Neurodevelopmental Disorders	不相关		autism	immune cell	E_02_0579	Immunocytochemistry, in vitro radioactive methyltransferase assay, Western blot, chromatin immunoprecipitation, RNA sequencing analysis	Mutations in DNA methyltransferase 3A (DNMT3A) have been detected in autism and related disorders, but how these mutations disrupt nervous system function is unknown.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mutations in DNA methyltransferase 3A (DNMT3A) have been detected in autism and related disorders, but how these mutations disrupt nervous system function is unknown.		Mutations in DNA methyltransferase 3A (DNMT3A) have been detected in autism and related disorders, but how these mutations disrupt nervous system function is unknown.	Immunohistochemical staining	Mutations in DNA methyltransferase 3A (DNMT3A) have been detected in autism and related disorders, but how these mutations disrupt nervous system function is unknown.			免疫细胞化学，体外放射性甲基转移酶测定，蛋白质印迹，染色质免疫沉淀，RNA测序分析				DNMT3A
33234727	chr10	117470772	117472772	EMX2OS	 EMX2OS downregulation was significantly associated with higher histological grade, advanced stage, and poorer prognosis.	human	Kidney tissue	High+Lowthroughput	Downregulation of enhancer RNA EMX2OS is associated with poor prognosis in kidney renal clear cell carcinoma	不相关		Renal clear cell carcinoma	Renal cell	E_01_0849	RT-qPCR	 EMX2OS downregulation was significantly associated with higher histological grade, advanced stage, and poorer prognosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 EMX2OS downregulation was significantly associated with higher histological grade, advanced stage, and poorer prognosis.		 EMX2OS downregulation was significantly associated with higher histological grade, advanced stage, and poorer prognosis.	Immunohistochemical staining	 EMX2OS downregulation was significantly associated with higher histological grade, advanced stage, and poorer prognosis.			RT-qPCR				EMX2OS
33232675	chr19	47605479	47607479	BICRA	We have identified 12 individuals with rare variants (10 loss-of-function, 2 missense) in the BICRA (BRD4 interacting chromatin remodeling complex-associated protein) gene, also known as GLTSCR1, which encodes a subunit of the non-canonical BAF (ncBAF) complex.	mouse	Nervous tissue	High+Lowthroughput	BICRA, a SWI/SNF Complex Member, Is Associated with BAF-Disorder Related Phenotypes in Humans and Model Organisms	不相关		Intellectual disability	neuroglioform cell,neuron	E_02_0580	Immunoprecipitation mass spectrometry	We have identified 12 individuals with rare variants (10 loss-of-function, 2 missense) in the BICRA (BRD4 interacting chromatin remodeling complex-associated protein) gene, also known as GLTSCR1, which encodes a subunit of the non-canonical BAF (ncBAF) complex.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We have identified 12 individuals with rare variants (10 loss-of-function, 2 missense) in the BICRA (BRD4 interacting chromatin remodeling complex-associated protein) gene, also known as GLTSCR1, which encodes a subunit of the non-canonical BAF (ncBAF) complex.		We have identified 12 individuals with rare variants (10 loss-of-function, 2 missense) in the BICRA (BRD4 interacting chromatin remodeling complex-associated protein) gene, also known as GLTSCR1, which encodes a subunit of the non-canonical BAF (ncBAF) complex.	Immunohistochemical staining	We have identified 12 individuals with rare variants (10 loss-of-function, 2 missense) in the BICRA (BRD4 interacting chromatin remodeling complex-associated protein) gene, also known as GLTSCR1, which encodes a subunit of the non-canonical BAF (ncBAF) complex.			免疫沉淀-质谱				BICRA
33232656	chr3	187718918	187720918	BCL6	Here we show that OCA-B, a B cell-specific coactivator essential for germinal center (GC) formation, forms a ternary complex with the lymphoid-enriched OCT2 and GC-specific MEF2B transcription factors, and that this complex occupies and activates an LCR that regulates the BCL6 proto-oncogene and is uniquely required by normal and malignant GC B-cells.	mouse	lymphoid tissue	High+Lowthroughput	Unique Immune Cell Coactivators Specify Locus Control Region Function and Cell Stage	不相关		B cell lymphoma	B cell,lymphocyte	E_02_0581	Cross linked chromatin immunoprecipitation (chip), gene knockdown, CRISPR / cas9, RNA isolation, cDNA preparation and quantitative real-time PCR (qPCR), luciferase assay, immunoprecipitation and immunoprecipitation mass spectrometry (ip-ms), electrophoretic mobility shift assay (EMSA	Here we show that OCA-B, a B cell-specific coactivator essential for germinal center (GC) formation, forms a ternary complex with the lymphoid-enriched OCT2 and GC-specific MEF2B transcription factors, and that this complex occupies and activates an LCR that regulates the BCL6 proto-oncogene and is uniquely required by normal and malignant GC B-cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we show that OCA-B, a B cell-specific coactivator essential for germinal center (GC) formation, forms a ternary complex with the lymphoid-enriched OCT2 and GC-specific MEF2B transcription factors, and that this complex occupies and activates an LCR that regulates the BCL6 proto-oncogene and is uniquely required by normal and malignant GC B-cells.		Here we show that OCA-B, a B cell-specific coactivator essential for germinal center (GC) formation, forms a ternary complex with the lymphoid-enriched OCT2 and GC-specific MEF2B transcription factors, and that this complex occupies and activates an LCR that regulates the BCL6 proto-oncogene and is uniquely required by normal and malignant GC B-cells.	Immunohistochemical staining	Here we show that OCA-B, a B cell-specific coactivator essential for germinal center (GC) formation, forms a ternary complex with the lymphoid-enriched OCT2 and GC-specific MEF2B transcription factors, and that this complex occupies and activates an LCR that regulates the BCL6 proto-oncogene and is uniquely required by normal and malignant GC B-cells.			交联染色质免疫沉淀 （ChIP），基因敲降，CRISPR/Cas9，RNA 分离、cDNA 制备和定量实时荧光定量 PCR （qPCR），荧光素酶测定，免疫沉淀和免疫沉淀质谱（IP-MS），电泳迁移率转移测定 （EMSA）				BCL6
33224573	chr5	88714545	88716545	MEF2C	Emerging evidence suggests existence of three prognostically relevant molecular entities among immature T-ALL-early thymic precursor ALL (ETP-ALL), T-ALL with the absence of biallelic deletion of TCRγ chains (ABD) and MEF2C (Myocyte Enhancer Factor 2C) high T-ALL.	human	Lymphoid tissue, muscle tissue	High+Lowthroughput	MEF2C expression, but not absence of bi-allelic deletion of TCR gamma chains (ABD), is a predictor of patient outcome in Indian T-acute lymphoblastic leukemia	不相关		T-acute lymphoblastic leukemia	T cell progenitor cell,myocyte	E_01_0850	Determination of MEF2C expression	Emerging evidence suggests existence of three prognostically relevant molecular entities among immature T-ALL-early thymic precursor ALL (ETP-ALL), T-ALL with the absence of biallelic deletion of TCRγ chains (ABD) and MEF2C (Myocyte Enhancer Factor 2C) high T-ALL.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Emerging evidence suggests existence of three prognostically relevant molecular entities among immature T-ALL-early thymic precursor ALL (ETP-ALL), T-ALL with the absence of biallelic deletion of TCRγ chains (ABD) and MEF2C (Myocyte Enhancer Factor 2C) high T-ALL.	Immunohistochemical staining	Emerging evidence suggests existence of three prognostically relevant molecular entities among immature T-ALL-early thymic precursor ALL (ETP-ALL), T-ALL with the absence of biallelic deletion of TCRγ chains (ABD) and MEF2C (Myocyte Enhancer Factor 2C) high T-ALL.	MEF2C		MEF2C表达的测定	Emerging evidence suggests existence of three prognostically relevant molecular entities among immature T-ALL-early thymic precursor ALL (ETP-ALL), T-ALL with the absence of biallelic deletion of TCRγ chains (ABD) and MEF2C (Myocyte Enhancer Factor 2C) high T-ALL.			
33224311	chr7	44101749	44103749	AEBP1	Tumor-related databases and bioinformatics analysis revealed that AEBP1 was highly expressed in GBM and indicated poor outcome of patients; its high expression that was also confirmed in GBM tissues and cell lines was closely related to the tumor size. 	human	Connective tissue, cancer tissue	High+Lowthroughput	AEBP1 Promotes Glioblastoma Progression and Activates the Classical NF-κB Pathway	不相关		Glioblastoma	fat cell,Glioblastoma cell	E_01_0851	Plasmid cell transfection, real-time QRT PCR, Western blot, cell migration, invasion assays, NF- κ B activity measurements	Tumor-related databases and bioinformatics analysis revealed that AEBP1 was highly expressed in GBM and indicated poor outcome of patients; its high expression that was also confirmed in GBM tissues and cell lines was closely related to the tumor size. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Tumor-related databases and bioinformatics analysis revealed that AEBP1 was highly expressed in GBM and indicated poor outcome of patients; its high expression that was also confirmed in GBM tissues and cell lines was closely related to the tumor size. 		Tumor-related databases and bioinformatics analysis revealed that AEBP1 was highly expressed in GBM and indicated poor outcome of patients; its high expression that was also confirmed in GBM tissues and cell lines was closely related to the tumor size. 	Immunohistochemical staining	Tumor-related databases and bioinformatics analysis revealed that AEBP1 was highly expressed in GBM and indicated poor outcome of patients; its high expression that was also confirmed in GBM tissues and cell lines was closely related to the tumor size. 			质粒细胞转染，实时 qRT-PCR，蛋白质印迹，细胞迁移、侵袭分析，NF-κB 活性测量				AEBP1
33222501	chr14	24332849	24334849	RIPK3	Upstream of the RIPK3-MLKL necroptotic machinery lies RIPK1 (receptor-interacting serine/threonine-protein kinase 1), which acts as a master switch that controls whether the cell undergoes NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells)–dependent inflammation, caspase-dependent apoptosis, or necroptosis in response to extracellular stimuli.	mouse	Lymphoid tissues, epithelial tissues	High+Lowthroughput	RIPK1 Expression Associates With Inflammation in Early Atherosclerosis in Humans and Can Be Therapeutically Silenced to Reduce NF-κB Activation and Atherogenesis in Mice	不相关		atherosclerosis	endothelial cell,macrophage	E_02_0582	Western blot, cell viability assay, NF- κ B luciferase assay, immunofluorescence of HUVECs	Upstream of the RIPK3-MLKL necroptotic machinery lies RIPK1 (receptor-interacting serine/threonine-protein kinase 1), which acts as a master switch that controls whether the cell undergoes NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells)–dependent inflammation, caspase-dependent apoptosis, or necroptosis in response to extracellular stimuli.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Upstream of the RIPK3-MLKL necroptotic machinery lies RIPK1 (receptor-interacting serine/threonine-protein kinase 1), which acts as a master switch that controls whether the cell undergoes NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells)–dependent inflammation, caspase-dependent apoptosis, or necroptosis in response to extracellular stimuli.		Upstream of the RIPK3-MLKL necroptotic machinery lies RIPK1 (receptor-interacting serine/threonine-protein kinase 1), which acts as a master switch that controls whether the cell undergoes NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells)–dependent inflammation, caspase-dependent apoptosis, or necroptosis in response to extracellular stimuli.	Immunohistochemical staining	Upstream of the RIPK3-MLKL necroptotic machinery lies RIPK1 (receptor-interacting serine/threonine-protein kinase 1), which acts as a master switch that controls whether the cell undergoes NF-κB (nuclear factor κ-light-chain-enhancer of activated B cells)–dependent inflammation, caspase-dependent apoptosis, or necroptosis in response to extracellular stimuli.			蛋白质印迹，细胞活力检测，NF-κB荧光素酶测定，HUVECs的免疫荧光				RIPK3
33221539	chr12	114351443	114353443	TBX5	T-box 5 (TBX5) protein belongs to the T-box family whose members play a crucial role in cell-type specification, morphogenesis and organogenesis.	human	Musculature	High+Lowthroughput	Transcriptional regulation of human T-box 5 gene (TBX5) by bone- and cardiac-related transcription factors	不相关			myocyte	E_01_0852	Amplification of TBX5 promoter fragments，Construction of promoter-luciferase reporter vectors ，Transcription factor expressing vectors ，Transient transfection and luciferase assays	T-box 5 (TBX5) protein belongs to the T-box family whose members play a crucial role in cell-type specification, morphogenesis and organogenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			T-box 5 (TBX5) protein belongs to the T-box family whose members play a crucial role in cell-type specification, morphogenesis and organogenesis.	Immunohistochemical staining	T-box 5 (TBX5) protein belongs to the T-box family whose members play a crucial role in cell-type specification, morphogenesis and organogenesis.	TBX5		Amplification of TBX5 promoter fragments，Construction of promoter-luciferase reporter vectors ，Transcription factor expressing vectors ，Transient transfection and luciferase assays	T-box 5 (TBX5) protein belongs to the T-box family whose members play a crucial role in cell-type specification, morphogenesis and organogenesis.			
33221504	chr1	156461106	156463106	MEF2D	MEF2D-fusions have recently been identified as one of the major oncogenic drivers in precursor B-cell acute lymphoblastic leukemia (B-ALL). 	human	lymphoid tissue	High+Lowthroughput	Purification, crystallization, and X-ray diffraction analysis of myocyte enhancer factor 2D and DNA complex	不相关		acute lymphoblastic leukemia	B cell	E_01_0853	Electrophoretic mobility shift assays 	MEF2D-fusions have recently been identified as one of the major oncogenic drivers in precursor B-cell acute lymphoblastic leukemia (B-ALL). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MEF2D-fusions have recently been identified as one of the major oncogenic drivers in precursor B-cell acute lymphoblastic leukemia (B-ALL). 		MEF2D-fusions have recently been identified as one of the major oncogenic drivers in precursor B-cell acute lymphoblastic leukemia (B-ALL). 	Immunohistochemical staining	MEF2D-fusions have recently been identified as one of the major oncogenic drivers in precursor B-cell acute lymphoblastic leukemia (B-ALL). 			Electrophoretic mobility shift assays 				MEF2D
33212152	chr3	70952083	70954083	FOXP1	We prioritized three loci with putative regulation events (FGFR2 enhancer in BCC, intragenic regulation of FOXP1 in SCC, and WNT5A promoter in both subtypes) and validated our findings with published gene expression data.	human		High+Lowthroughput	Epigenetic Alterations in Keratinocyte Carcinoma	不相关		cancer	keratinocyte cell	E_01_0854	ChIP-seq of Keratinocyte Carcinoma，Differentially enhancer definition，Dimensionality reduction and visualization，Gene set enrichment analysis，Transcription factor motif analysis	We prioritized three loci with putative regulation events (FGFR2 enhancer in BCC, intragenic regulation of FOXP1 in SCC, and WNT5A promoter in both subtypes) and validated our findings with published gene expression data.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We prioritized three loci with putative regulation events (FGFR2 enhancer in BCC, intragenic regulation of FOXP1 in SCC, and WNT5A promoter in both subtypes) and validated our findings with published gene expression data.	Immunohistochemical staining	We prioritized three loci with putative regulation events (FGFR2 enhancer in BCC, intragenic regulation of FOXP1 in SCC, and WNT5A promoter in both subtypes) and validated our findings with published gene expression data.	FOXP1		ChIP-seq of Keratinocyte Carcinoma，Differentially enhancer definition，Dimensionality reduction and visualization，Gene set enrichment analysis，Transcription factor motif analysis	We prioritized three loci with putative regulation events (FGFR2 enhancer in BCC, intragenic regulation of FOXP1 in SCC, and WNT5A promoter in both subtypes) and validated our findings with published gene expression data.			
33199729	chr11	69768295	69770295	FGF4	Of these tumours, SDH-deficient (characterized by the loss of SDHB) and quadruple WT GIST (KIT/PDGFRA/SDH/RAS-P WT) subgroups were reported to display a marked overexpression of FGF4, identifying a putative common therapeutic target for the first time.	human		High+Lowthroughput	Gene duplication, rather than epigenetic changes, drives FGF4 overexpression in KIT/PDGFRA/SDH/RAS-P WT GIST	相关	rs3168175，rs9666584	Gastrointestinal cancers		E_01_0855	Global methylation profile, target methylation analysis, Sanger sequencing	Of these tumours, SDH-deficient (characterized by the loss of SDHB) and quadruple WT GIST (KIT/PDGFRA/SDH/RAS-P WT) subgroups were reported to display a marked overexpression of FGF4, identifying a putative common therapeutic target for the first time.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Of these tumours, SDH-deficient (characterized by the loss of SDHB) and quadruple WT GIST (KIT/PDGFRA/SDH/RAS-P WT) subgroups were reported to display a marked overexpression of FGF4, identifying a putative common therapeutic target for the first time.		Of these tumours, SDH-deficient (characterized by the loss of SDHB) and quadruple WT GIST (KIT/PDGFRA/SDH/RAS-P WT) subgroups were reported to display a marked overexpression of FGF4, identifying a putative common therapeutic target for the first time.	Immunohistochemical staining	Of these tumours, SDH-deficient (characterized by the loss of SDHB) and quadruple WT GIST (KIT/PDGFRA/SDH/RAS-P WT) subgroups were reported to display a marked overexpression of FGF4, identifying a putative common therapeutic target for the first time.			全球甲基化概况，靶标甲基化分析，桑格测序				FGF4
33199677	chr2	15937777	15939777	MYCN	MYCN amplification drives one in six cases of neuroblastoma.	human	Nervous tissue	High+Lowthroughput	Enhancer hijacking determines extrachromosomal circular MYCN amplicon architecture in neuroblastoma	不相关		Neuroblastoma	neuroblast 	E_01_0856	RNA SEQ, chip SEQ, ATAC SEQ, fluorescence in situ hybridization	MYCN amplification drives one in six cases of neuroblastoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MYCN amplification drives one in six cases of neuroblastoma.	Immunohistochemical staining	MYCN amplification drives one in six cases of neuroblastoma.	MYCN		核糖核酸序列，ChIP-seq，ATAC-seq，荧光原位杂交	MYCN amplification drives one in six cases of neuroblastoma.			
33197296	chr19	33296873	33298873	CEBPA	CCAAT/enhancer-binding protein α (CEBPA) is an essential transcription factor for myeloid differentiation. 	human	lymphoid tissue	High+Lowthroughput	A regulatory element in the 3'-untranslated region of CEBPA is associated with myeloid/NK/T-cell leukemia	不相关		leukemia	T cell	E_01_0857	DNA methylation analysis, real time PCR, electrophoretic mobility shift assay (EMSA)	CCAAT/enhancer-binding protein α (CEBPA) is an essential transcription factor for myeloid differentiation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			CCAAT/enhancer-binding protein α (CEBPA) is an essential transcription factor for myeloid differentiation. 	Immunohistochemical staining	CCAAT/enhancer-binding protein α (CEBPA) is an essential transcription factor for myeloid differentiation. 	CEBPA		DNA甲基化分析，Real-time PCR，Electrophoretic mobility shift assay (EMSA)	CCAAT/enhancer-binding protein α (CEBPA) is an essential transcription factor for myeloid differentiation. 			
33196849	chr16	67559614	67561614	CTCF	Using RNA-seq and ChIP-seq, we identified for the first time that neurotensin (NTS) serves as a key oncogene in uveal melanoma and that CTCF interacts with the upstream enhancer of NTS and orchestrates an 800 kb chromosomal loop between the promoter and enhancer. 	human		High+Lowthroughput	Generation of onco-enhancer enhances chromosomal remodeling and accelerates tumorigenesis	不相关		tumour	embryonic stem cell	E_01_0858	RNA extraction, library construction and Illumina sequencing (RNA SEQ)	Using RNA-seq and ChIP-seq, we identified for the first time that neurotensin (NTS) serves as a key oncogene in uveal melanoma and that CTCF interacts with the upstream enhancer of NTS and orchestrates an 800 kb chromosomal loop between the promoter and enhancer. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Using RNA-seq and ChIP-seq, we identified for the first time that neurotensin (NTS) serves as a key oncogene in uveal melanoma and that CTCF interacts with the upstream enhancer of NTS and orchestrates an 800 kb chromosomal loop between the promoter and enhancer. 	Immunohistochemical staining	Using RNA-seq and ChIP-seq, we identified for the first time that neurotensin (NTS) serves as a key oncogene in uveal melanoma and that CTCF interacts with the upstream enhancer of NTS and orchestrates an 800 kb chromosomal loop between the promoter and enhancer. 	CTCF		RNA 提取、文库构建和 Illumina 测序 （RNA-seq）	Using RNA-seq and ChIP-seq, we identified for the first time that neurotensin (NTS) serves as a key oncogene in uveal melanoma and that CTCF interacts with the upstream enhancer of NTS and orchestrates an 800 kb chromosomal loop between the promoter and enhancer. 			
33195520	chr1	109306543	109308543	SORT1	Although culture with POA, OA, and LA led to lower very low density lipoprotein (VLDL) concentration in cell culture medium, POA and OA led to greater concentrations of triacylglycerol, protein abundance of sterol regulatory element-binding protein 1c, fatty acid synthase, acetyl coenzyme A carboxylase 1, ApoB100, and sortilin 1 (SORT1).	mouse	hepatic tissue	High+Lowthroughput	Lipid Accumulation and Injury in Primary Calf Hepatocytes Challenged With Different Long-Chain Fatty Acids	不相关		Nonalcoholic fatty liver disease	hepatocyte	E_02_0583	Ribonucleic acid extraction and polymerase chain reaction, Western blot assay, biochemical and oxidative stress index assays, lipid droplet confocal microscopy, reactive oxygen species (ROS) assay	Although culture with POA, OA, and LA led to lower very low density lipoprotein (VLDL) concentration in cell culture medium, POA and OA led to greater concentrations of triacylglycerol, protein abundance of sterol regulatory element-binding protein 1c, fatty acid synthase, acetyl coenzyme A carboxylase 1, ApoB100, and sortilin 1 (SORT1).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Although culture with POA, OA, and LA led to lower very low density lipoprotein (VLDL) concentration in cell culture medium, POA and OA led to greater concentrations of triacylglycerol, protein abundance of sterol regulatory element-binding protein 1c, fatty acid synthase, acetyl coenzyme A carboxylase 1, ApoB100, and sortilin 1 (SORT1).		Although culture with POA, OA, and LA led to lower very low density lipoprotein (VLDL) concentration in cell culture medium, POA and OA led to greater concentrations of triacylglycerol, protein abundance of sterol regulatory element-binding protein 1c, fatty acid synthase, acetyl coenzyme A carboxylase 1, ApoB100, and sortilin 1 (SORT1).	Immunohistochemical staining	Although culture with POA, OA, and LA led to lower very low density lipoprotein (VLDL) concentration in cell culture medium, POA and OA led to greater concentrations of triacylglycerol, protein abundance of sterol regulatory element-binding protein 1c, fatty acid synthase, acetyl coenzyme A carboxylase 1, ApoB100, and sortilin 1 (SORT1).			核糖核酸提取和聚合酶链反应，蛋白质印迹测定，生化和氧化应激指数检测，脂滴共聚焦显微镜，活性氧 （ROS） 测定				SORT1
33195246	chr4	108044684	108046684	LEF1	This effect is mediated by RSPO2, a WNT/b-catenin agonist, and lymphoid enhancer binding factor 1 (LEF1), an essential nuclear effector of the WNT/b-catenin pathway, via conserved LEF1/T-cell factor binding sites in the Pitx3 promoter.	mouse	Nervous tissue	High+Lowthroughput	Dose-Dependent and Subset-Specific Regulation of Midbrain Dopaminergic Neuron Differentiation by LEF1-Mediated WNT1/b-Catenin Signaling	不相关		Parkinson's disease	neural cell	E_02_0584	Microarray analysis, immunohistochemistry / immunocytochemistry, VM primary cultures and rspo2 / edu treatment, Western blotting, chromatin immunoprecipitation polymerase chain reaction, transfection, luciferase reporter assays and site directed mutagenesis, fast polymerase chain reaction	This effect is mediated by RSPO2, a WNT/b-catenin agonist, and lymphoid enhancer binding factor 1 (LEF1), an essential nuclear effector of the WNT/b-catenin pathway, via conserved LEF1/T-cell factor binding sites in the Pitx3 promoter.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This effect is mediated by RSPO2, a WNT/b-catenin agonist, and lymphoid enhancer binding factor 1 (LEF1), an essential nuclear effector of the WNT/b-catenin pathway, via conserved LEF1/T-cell factor binding sites in the Pitx3 promoter.		This effect is mediated by RSPO2, a WNT/b-catenin agonist, and lymphoid enhancer binding factor 1 (LEF1), an essential nuclear effector of the WNT/b-catenin pathway, via conserved LEF1/T-cell factor binding sites in the Pitx3 promoter.	Immunohistochemical staining	This effect is mediated by RSPO2, a WNT/b-catenin agonist, and lymphoid enhancer binding factor 1 (LEF1), an essential nuclear effector of the WNT/b-catenin pathway, via conserved LEF1/T-cell factor binding sites in the Pitx3 promoter.			微阵列分析，免疫组化/免疫细胞化学，VM 原代培养和 RSPO2/EdU 治疗，蛋白质印迹，染色质免疫沉淀-聚合酶链反应，转染、荧光素酶报告检测和定点诱变，快速聚合酶链反应				LEF1
33193627	chr12	9749885	9751885	CD69	The CD69 gene encodes a C-type lectin glycoprotein with immune regulatory properties which is expressed on the cell surfaces of all activated hematopoietic cells.	human		High+Lowthroughput	Functional Characterization of a Dual Enhancer/Promoter Regulatory Element Leading Human CD69 Expression	不相关			hematopoietic cell,lymphocyte	E_01_0859	Luciferase assays, crispr-cas9 deletion, RNA extraction and RT qPCR, Erna profiling by qPCR, chromatin immunoprecipitation	The CD69 gene encodes a C-type lectin glycoprotein with immune regulatory properties which is expressed on the cell surfaces of all activated hematopoietic cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The CD69 gene encodes a C-type lectin glycoprotein with immune regulatory properties which is expressed on the cell surfaces of all activated hematopoietic cells.		The CD69 gene encodes a C-type lectin glycoprotein with immune regulatory properties which is expressed on the cell surfaces of all activated hematopoietic cells.	Immunohistochemical staining	The CD69 gene encodes a C-type lectin glycoprotein with immune regulatory properties which is expressed on the cell surfaces of all activated hematopoietic cells.			荧光素酶检测，CRISPR-Cas9 删除，RNA 提取和 RT-qPCR，通过 qPCR 进行 eRNA 分析，染色质免疫沉淀				CD69
33188077	chr11	53519379	53521379	Il13	Mast cells express Il13 mRNA and produce IL-13 protein in response to antigenic stimulation.	mouse	lymphoid tissue	High+Lowthroughput	The Clusters of Transcription Factors NFATC2, STAT5, GATA2, AP1, RUNX1 and EGR2 Binding Sites at the Induced Il13 Enhancers Mediate Il13 Gene Transcription in Response to Antigenic Stimulation	不相关		Allergic inflammation	leukocyte	E_02_0585	Chromatin immunoprecipitation chip, Omni ATAC SEQ, transcription factor binding motif analysis, cell transfection	Mast cells express Il13 mRNA and produce IL-13 protein in response to antigenic stimulation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mast cells express Il13 mRNA and produce IL-13 protein in response to antigenic stimulation.		Mast cells express Il13 mRNA and produce IL-13 protein in response to antigenic stimulation.	Immunohistochemical staining	Mast cells express Il13 mRNA and produce IL-13 protein in response to antigenic stimulation.			染色质免疫沉淀 ChIP，Omni-ATAC-seq，转录因子结合基序分析，细胞转染				Il13
33187138	chr6	47504488	47506488	Ezh2	Ezh2 is a catalytic subunit of the polycomb repressive complex 2 (PRC2) which mediates epigenetic gene silencing through depositing the mark histone H3 lysine 27 trimethylation (H3K27me3) at target genomic sequences. 	mouse	Nervous tissue	High+Lowthroughput	Downregulation of the Polycomb-Associated Methyltransferase Ezh2 during Maturation of Hippocampal Neurons Is Mediated by MicroRNAs Let-7 and miR-124	不相关			neuronal stem cell,neuron	E_02_0586	MicroRNA expression analysis using microarrays, microRNA quantification, transient transfection, reverse transcriptase and real-time quantitative fluorescent PCR (RT qPCR), luciferase reporter assays	Ezh2 is a catalytic subunit of the polycomb repressive complex 2 (PRC2) which mediates epigenetic gene silencing through depositing the mark histone H3 lysine 27 trimethylation (H3K27me3) at target genomic sequences. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ezh2 is a catalytic subunit of the polycomb repressive complex 2 (PRC2) which mediates epigenetic gene silencing through depositing the mark histone H3 lysine 27 trimethylation (H3K27me3) at target genomic sequences. 		Ezh2 is a catalytic subunit of the polycomb repressive complex 2 (PRC2) which mediates epigenetic gene silencing through depositing the mark histone H3 lysine 27 trimethylation (H3K27me3) at target genomic sequences. 	Immunohistochemical staining	Ezh2 is a catalytic subunit of the polycomb repressive complex 2 (PRC2) which mediates epigenetic gene silencing through depositing the mark histone H3 lysine 27 trimethylation (H3K27me3) at target genomic sequences. 			使用微阵列的MicroRNA表达分析，微量RNA定量，瞬时转染，逆转录酶和实时定量荧光定量 PCR （RT-qPCR），荧光素酶报告基因测定				Ezh2
33184061	chr9	70381623	70383623	KLF9	Some genes, including Krüppel-like factor 9 (KLF9), a putative transcriptional repressor, demonstrate conserved responses.	human	Epithelial tissues	High+Lowthroughput	Genomic determinants implicated in the glucocorticoid-mediated induction of KLF9 in pulmonary epithelial cells	不相关			epithelial cell	E_01_0860	RNA isolation, cDNA synthesis, and SYBR green real-time PCR	Some genes, including Krüppel-like factor 9 (KLF9), a putative transcriptional repressor, demonstrate conserved responses.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Some genes, including Krüppel-like factor 9 (KLF9), a putative transcriptional repressor, demonstrate conserved responses.	Immunohistochemical staining	Some genes, including Krüppel-like factor 9 (KLF9), a putative transcriptional repressor, demonstrate conserved responses.	KLF9		RNA isolation, cDNA synthesis, and SYBR green real-time PCR	Some genes, including Krüppel-like factor 9 (KLF9), a putative transcriptional repressor, demonstrate conserved responses.			
33183330	chr1	247412986	247414986	NLRP3	Inflammatory NFκB [54–56] and MAPK [55, 57] signaling increase the expression of the scaffold protein NOD-like receptor pyrin domain-containing 3 (NLRP3).	mouse		High+Lowthroughput	Adenosine A(3) receptor as a novel therapeutic target to reduce secondary events and improve neurocognitive functions following traumatic brain injury	不相关		Traumatic brain injury	astrocyte, granulocyte 	E_02_0587	Western blot analysis, immunofluorescence staining	Inflammatory NFκB [54–56] and MAPK [55, 57] signaling increase the expression of the scaffold protein NOD-like receptor pyrin domain-containing 3 (NLRP3).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Inflammatory NFκB [54–56] and MAPK [55, 57] signaling increase the expression of the scaffold protein NOD-like receptor pyrin domain-containing 3 (NLRP3).		Inflammatory NFκB [54–56] and MAPK [55, 57] signaling increase the expression of the scaffold protein NOD-like receptor pyrin domain-containing 3 (NLRP3).	Immunohistochemical staining	Inflammatory NFκB [54–56] and MAPK [55, 57] signaling increase the expression of the scaffold protein NOD-like receptor pyrin domain-containing 3 (NLRP3).			蛋白质印迹分析，免疫荧光染色				NLRP3
33182063	chr1	247413256	247415256	NLRP3	The findings may suggest that MyD88/NF-κB pathway is an upstream regulator of NLRP3 inflammasome underlying smoking-induced atherosclerosis.	human		High+Lowthroughput	Molecular insights of cigarette smoke condensate-activated NLRP3 inflammasome in THP-1 cells in a stage-specific atherogenesis	不相关		Atherosclerosis	THP-1	E_01_0861	Transcriptional profiling，Immunocytochemistry，Cytokine assays，qPCR array	The findings may suggest that MyD88/NF-κB pathway is an upstream regulator of NLRP3 inflammasome underlying smoking-induced atherosclerosis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The findings may suggest that MyD88/NF-κB pathway is an upstream regulator of NLRP3 inflammasome underlying smoking-induced atherosclerosis.		The findings may suggest that MyD88/NF-κB pathway is an upstream regulator of NLRP3 inflammasome underlying smoking-induced atherosclerosis.	Immunohistochemical staining	The findings may suggest that MyD88/NF-κB pathway is an upstream regulator of NLRP3 inflammasome underlying smoking-induced atherosclerosis.			Transcriptional profiling，Immunocytochemistry，Cytokine assays，qPCR array				NLRP3
33179113	chr18	76371869	76373869	Smad2	The endothelial-mesenchymal transition (EndMT) serves a key role in a number of diseases with an important role in cardiac fibrosis and the activin/Smad2 and 3 signaling pathway is involved in regulating the EndMT. 	human	Epithelial tissues	High+Lowthroughput	Activation of activin/Smad2 and 3 signaling pathway and the&nbsp;potential involvement of endothelial?mesenchymal transition in the valvular damage due to rheumatic heart disease	不相关		Rheumatic heart disease	endothelial cell	E_01_0862	Histochemistry, reverse transcription quantitative (rt-q) PCR, Western blot analysis	The endothelial-mesenchymal transition (EndMT) serves a key role in a number of diseases with an important role in cardiac fibrosis and the activin/Smad2 and 3 signaling pathway is involved in regulating the EndMT. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The endothelial-mesenchymal transition (EndMT) serves a key role in a number of diseases with an important role in cardiac fibrosis and the activin/Smad2 and 3 signaling pathway is involved in regulating the EndMT. 		The endothelial-mesenchymal transition (EndMT) serves a key role in a number of diseases with an important role in cardiac fibrosis and the activin/Smad2 and 3 signaling pathway is involved in regulating the EndMT. 	Immunohistochemical staining	The endothelial-mesenchymal transition (EndMT) serves a key role in a number of diseases with an important role in cardiac fibrosis and the activin/Smad2 and 3 signaling pathway is involved in regulating the EndMT. 			组织化学，逆转录定量 （RT-q） PCR，蛋白质印迹分析				Smad2
33176148	chr1	26690137	26692137	ARID1A	ARID1A mutations are observed in deeply invasive forms of the disease, often correlating with malignancy. 	human		High+Lowthroughput	ARID1A Mutations Promote P300-Dependent Endometrial Invasion through Super-Enhancer Hyperacetylation	不相关		Chromatin immunoprecipitation	endometrial cell	E_01_0863	Histology and immunohistochemistry, cell transfection, cell viability assay, annexin V assay, chromatin immunoprecipitation	ARID1A mutations are observed in deeply invasive forms of the disease, often correlating with malignancy. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			ARID1A mutations are observed in deeply invasive forms of the disease, often correlating with malignancy. 	Immunohistochemical staining	ARID1A mutations are observed in deeply invasive forms of the disease, often correlating with malignancy. 	ARID1A		组织学和免疫组织化学，细胞转染，细胞活力测定，膜联蛋白V测定，染色质免疫沉淀	ARID1A mutations are observed in deeply invasive forms of the disease, often correlating with malignancy. 			
33175598	chr5	115564894	115566894	Msi1	Evolutionarily conserved RNA-binding protein Musashi1 (Msi1) can regulate developmentally relevant genes. 	mouse	Epithelial tissues	High+Lowthroughput	Constitutive Musashi1 expression impairs mouse postnatal development and intestinal homeostasis	不相关		cancer	epithelial cell, goblet cell	E_02_0588	Gene knockdown, immunofluorescence, immunoperoxidase staining, RNA in situ hybridization, cDNA generation, and gene expression analysis	Evolutionarily conserved RNA-binding protein Musashi1 (Msi1) can regulate developmentally relevant genes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Evolutionarily conserved RNA-binding protein Musashi1 (Msi1) can regulate developmentally relevant genes. 		Evolutionarily conserved RNA-binding protein Musashi1 (Msi1) can regulate developmentally relevant genes. 	Immunohistochemical staining	Evolutionarily conserved RNA-binding protein Musashi1 (Msi1) can regulate developmentally relevant genes. 			基因敲降，免疫荧光，免疫过氧化物酶染色，RNA原位杂交，cDNA生成和基因表达分析				Msi1
33171905	chr6	143937411	143939411	PLAGL1	The most enriched transcription factor, PLAGL1 had a predicted motif in 233 regions that were significantly associated with vasculature development and response to insulin stimulus genes. 	mouse	Epithelial tissues	High+Lowthroughput	Transcription Factor PLAGL1 Is Associated with Angiogenic Gene Expression in the Placenta	不相关		Gestational diabetes mellitus	endothelial cell	E_02_0589	Immunohistochemical staining, siRNA knockdown and qPCR, htr-8 / svneo RNA seq	The most enriched transcription factor, PLAGL1 had a predicted motif in 233 regions that were significantly associated with vasculature development and response to insulin stimulus genes. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The most enriched transcription factor, PLAGL1 had a predicted motif in 233 regions that were significantly associated with vasculature development and response to insulin stimulus genes. 		The most enriched transcription factor, PLAGL1 had a predicted motif in 233 regions that were significantly associated with vasculature development and response to insulin stimulus genes. 	Immunohistochemical staining	The most enriched transcription factor, PLAGL1 had a predicted motif in 233 regions that were significantly associated with vasculature development and response to insulin stimulus genes. 			免疫组化染色，siRNA敲低和qPCR，HTR-8/SVneo RNA-seq				PLAGL1
33167400	chr7	16913285	16915285	AHR	Recent studies indicate that PM2.5 generated by combustion activates the Aryl Hydrocarbon Receptor (AHR) and inflammatory cytokines contributing to PM2.5-mediated atherogenesis. 	human	Lymphoid tissues, epithelial tissues	High+Lowthroughput	AHR Signaling Interacting with Nutritional Factors Regulating the Expression of Markers in Vascular Inflammation and Atherogenesis	不相关		Vascular inflammation and atherosclerosis	macrophage, endothelial cell	E_01_0864	RNA isolation and quantitative real-time RT-PCR (qPCR), transfection experiments and luciferase assays, gel mobility shift assay (GMSA)	Recent studies indicate that PM2.5 generated by combustion activates the Aryl Hydrocarbon Receptor (AHR) and inflammatory cytokines contributing to PM2.5-mediated atherogenesis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Recent studies indicate that PM2.5 generated by combustion activates the Aryl Hydrocarbon Receptor (AHR) and inflammatory cytokines contributing to PM2.5-mediated atherogenesis. 	Immunohistochemical staining	Recent studies indicate that PM2.5 generated by combustion activates the Aryl Hydrocarbon Receptor (AHR) and inflammatory cytokines contributing to PM2.5-mediated atherogenesis. 	AHR		RNA分离和定量实时RT-PCR（qPCR），转染实验和荧光素酶测定，凝胶迁移率转移分析（GMSA）	Recent studies indicate that PM2.5 generated by combustion activates the Aryl Hydrocarbon Receptor (AHR) and inflammatory cytokines contributing to PM2.5-mediated atherogenesis. 			
33164433	chr9	117701684	117703684	TLR4	Its protection mechanism may be related to inhibiting TLR4 signaling pathways.	human	Epithelial tissues	High+Lowthroughput	[Effect of baicalin on inflammatory response and TLR4/NF-κB signaling pathway of human brain microvascular endothelial cell after hypoxia-reoxygenation injury]	不相关		cerebral apoplexy	microvascular endothelial cell	E_01_0865	Immunofluorescence assay, Western blot	Its protection mechanism may be related to inhibiting TLR4 signaling pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Its protection mechanism may be related to inhibiting TLR4 signaling pathways.	Immunohistochemical staining	Its protection mechanism may be related to inhibiting TLR4 signaling pathways.	TLR4		免疫荧光法检测， Western blot 	Its protection mechanism may be related to inhibiting TLR4 signaling pathways.			
33163273	chr19	33371055	33373055	CEBPG	High CEBPG expression is regulated by the ESCC specific transcription factor TP63 and serves as a prognostic factor for poor survival in ESCC patients.	human	cancer cell	High+Lowthroughput	CEBPG promotes esophageal squamous cell carcinoma progression by enhancing PI3K-AKT signaling	不相关		Esophageal squamous cell carcinoma	ESCC	E_01_0866	RNA extraction and QRT PCR analysis, Western blotting, siRNA and transfection, chromatin immunoprecipitation polymerase chain (chip PCR)	High CEBPG expression is regulated by the ESCC specific transcription factor TP63 and serves as a prognostic factor for poor survival in ESCC patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			High CEBPG expression is regulated by the ESCC specific transcription factor TP63 and serves as a prognostic factor for poor survival in ESCC patients.	Immunohistochemical staining	High CEBPG expression is regulated by the ESCC specific transcription factor TP63 and serves as a prognostic factor for poor survival in ESCC patients.	CEBPG		RNA 提取和 qRT-PCR 分析，蛋白质印记，siRNA 和转染，染色质免疫沉淀聚合酶链 （ChIP-PCR）	High CEBPG expression is regulated by the ESCC specific transcription factor TP63 and serves as a prognostic factor for poor survival in ESCC patients.			
33148375	chrX	136143924	136145924	FHL1	Long-chain SFA palmitic acid (PA) drastically reduced myogenic transcription factors, such as myoblast determination protein (MyoD), myogenin (MyoG), and myocyte enhancer factor 2C (MEF2C), and inhibited FHL1 expression and myogenic differentiation of C2C12 myoblasts, accompanied by the induction of miR-183-5p.	human	Musculature	High+Lowthroughput	MiR-183-5p induced by saturated fatty acids regulates the myogenic differentiation by directly targeting FHL1 in C2C12 myoblasts	不相关			myoblast cell	E_01_0867	Gene knockdown, immunofluorescence staining	Long-chain SFA palmitic acid (PA) drastically reduced myogenic transcription factors, such as myoblast determination protein (MyoD), myogenin (MyoG), and myocyte enhancer factor 2C (MEF2C), and inhibited FHL1 expression and myogenic differentiation of C2C12 myoblasts, accompanied by the induction of miR-183-5p.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Long-chain SFA palmitic acid (PA) drastically reduced myogenic transcription factors, such as myoblast determination protein (MyoD), myogenin (MyoG), and myocyte enhancer factor 2C (MEF2C), and inhibited FHL1 expression and myogenic differentiation of C2C12 myoblasts, accompanied by the induction of miR-183-5p.		Long-chain SFA palmitic acid (PA) drastically reduced myogenic transcription factors, such as myoblast determination protein (MyoD), myogenin (MyoG), and myocyte enhancer factor 2C (MEF2C), and inhibited FHL1 expression and myogenic differentiation of C2C12 myoblasts, accompanied by the induction of miR-183-5p.	Immunohistochemical staining	Long-chain SFA palmitic acid (PA) drastically reduced myogenic transcription factors, such as myoblast determination protein (MyoD), myogenin (MyoG), and myocyte enhancer factor 2C (MEF2C), and inhibited FHL1 expression and myogenic differentiation of C2C12 myoblasts, accompanied by the induction of miR-183-5p.			基因敲降，免疫荧光染色				FHL1
33146943	chr9	117701168	117703168	TLR4	Li‐EVs reduced posthypoxic and postischemic TLR4 abundance, resulting in an inhibition of the nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) signaling pathway, decreased proteasomal activity, and declined both inducible NO synthase and cyclooxygenase‐2 expression, all of which culminated in reduced levels of poststroke cerebral inflammation. 	mouse		High+Lowthroughput	Lithium modulates miR-1906 levels of mesenchymal stem cell-derived extracellular vesicles contributing to poststroke neuroprotection by toll-like receptor 4 regulation	不相关		cerebral ischemia	mesenchymal stem cell	E_02_0590	Preparation of EVs using regulatory media of polyethylene glycol, characterization of MSC derived EVs, measurement of proteasome activity, Western blot analysis, real-time polymerase chain reaction	Li‐EVs reduced posthypoxic and postischemic TLR4 abundance, resulting in an inhibition of the nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) signaling pathway, decreased proteasomal activity, and declined both inducible NO synthase and cyclooxygenase‐2 expression, all of which culminated in reduced levels of poststroke cerebral inflammation. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Li‐EVs reduced posthypoxic and postischemic TLR4 abundance, resulting in an inhibition of the nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) signaling pathway, decreased proteasomal activity, and declined both inducible NO synthase and cyclooxygenase‐2 expression, all of which culminated in reduced levels of poststroke cerebral inflammation. 		Li‐EVs reduced posthypoxic and postischemic TLR4 abundance, resulting in an inhibition of the nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) signaling pathway, decreased proteasomal activity, and declined both inducible NO synthase and cyclooxygenase‐2 expression, all of which culminated in reduced levels of poststroke cerebral inflammation. 	Immunohistochemical staining	Li‐EVs reduced posthypoxic and postischemic TLR4 abundance, resulting in an inhibition of the nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) signaling pathway, decreased proteasomal activity, and declined both inducible NO synthase and cyclooxygenase‐2 expression, all of which culminated in reduced levels of poststroke cerebral inflammation. 			使用聚乙二醇的调节介质制备EV，MSC衍生EV的表征，蛋白酶体活性的测量，蛋白质印记分析，实时聚合酶链反应				TLR4
33145887	chr5	138462973	138464973	EGR1	EGR1‐activated linc01503 could epigenetically silence DUSP5/CDKN1A expression to mediate cell cycle progression and tumorigenesis, implicating it as a prospective target for GC therapeutics.	human	hepatic tissue	High+Lowthroughput	EGR1-mediated linc01503 promotes cell cycle progression and tumorigenesis in gastric cancer	不相关		gastric cancer	hepatocyte	E_01_0868	RT qPCR analysis, cell transfection, RNA immunoprecipitation (RIP), chromatin immunoprecipitation test (chip), subcellular fractionation, and fluorescence in situ hybridization (FISH) assay	EGR1‐activated linc01503 could epigenetically silence DUSP5/CDKN1A expression to mediate cell cycle progression and tumorigenesis, implicating it as a prospective target for GC therapeutics.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EGR1‐activated linc01503 could epigenetically silence DUSP5/CDKN1A expression to mediate cell cycle progression and tumorigenesis, implicating it as a prospective target for GC therapeutics.	Immunohistochemical staining	EGR1‐activated linc01503 could epigenetically silence DUSP5/CDKN1A expression to mediate cell cycle progression and tumorigenesis, implicating it as a prospective target for GC therapeutics.	EGR1		RT-qPCR分析，细胞转染，RNA免疫沉淀（RIP），染色质免疫沉淀测试（ChIP）,亚细胞分离和荧光原位杂交（FISH）测定	EGR1‐activated linc01503 could epigenetically silence DUSP5/CDKN1A expression to mediate cell cycle progression and tumorigenesis, implicating it as a prospective target for GC therapeutics.			
33144667	chr6	89923787	89925787	BACH2	The transcription factor BACH2 functions as a pervasive regulator of T cell differentiation, promoting development of CD4 T+reg cells and suppressing the effector functions of multiple effector T cell (Teff) lineages.	mouse	lymphoid tissue	High+Lowthroughput	A cell-based bioluminescence assay reveals dose-dependent and contextual repression of AP-1-driven gene expression by BACH2	不相关		cancer	T cell	E_02_0591	Sanger sequencing and data analysis, luciferase assay, Western blot, rgfp966 inhibitor treatment	The transcription factor BACH2 functions as a pervasive regulator of T cell differentiation, promoting development of CD4 T+reg cells and suppressing the effector functions of multiple effector T cell (Teff) lineages.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcription factor BACH2 functions as a pervasive regulator of T cell differentiation, promoting development of CD4 T+reg cells and suppressing the effector functions of multiple effector T cell (Teff) lineages.		The transcription factor BACH2 functions as a pervasive regulator of T cell differentiation, promoting development of CD4 T+reg cells and suppressing the effector functions of multiple effector T cell (Teff) lineages.	Immunohistochemical staining	The transcription factor BACH2 functions as a pervasive regulator of T cell differentiation, promoting development of CD4 T+reg cells and suppressing the effector functions of multiple effector T cell (Teff) lineages.			桑格测序和数据分析，荧光素酶测定，蛋白质印迹，RGFP966 抑制剂治疗				BACH2
33143661	chr18	38066305	38068305	Hdac3	The present study revealed that Hdac3 activated the EZH1-p65-Pgf axis through inhibiting miR-17 in the miR-17-92 cluster, leading to accelerated abnormal pulmonary angiogenesis and alveolarization of BPD mice.	mouse		High+Lowthroughput	Involvement of Hdac3-mediated inhibition of microRNA cluster 17-92 in bronchopulmonary dysplasia development	不相关		Bronchial dysplasia	desmocyte，lung cancer cell	E_02_0592	Immunohistochemistry, immunofluorescence staining of microvessel density (MVD), RNA extraction and gene expression extraction, Western blot analysis, chromatin immunoprecipitation (chip) assay	The present study revealed that Hdac3 activated the EZH1-p65-Pgf axis through inhibiting miR-17 in the miR-17-92 cluster, leading to accelerated abnormal pulmonary angiogenesis and alveolarization of BPD mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The present study revealed that Hdac3 activated the EZH1-p65-Pgf axis through inhibiting miR-17 in the miR-17-92 cluster, leading to accelerated abnormal pulmonary angiogenesis and alveolarization of BPD mice.		The present study revealed that Hdac3 activated the EZH1-p65-Pgf axis through inhibiting miR-17 in the miR-17-92 cluster, leading to accelerated abnormal pulmonary angiogenesis and alveolarization of BPD mice.	Immunohistochemical staining	The present study revealed that Hdac3 activated the EZH1-p65-Pgf axis through inhibiting miR-17 in the miR-17-92 cluster, leading to accelerated abnormal pulmonary angiogenesis and alveolarization of BPD mice.			免疫组化，微血管密度（MVD）的免疫荧光染色，RNA提取和基因表达提取，蛋白质印记分析，染色质免疫沉淀（ChIP）测定				Hdac3
33143524	chr10	13096741	13098741	OPTN	OPTN (optineurin), a macroautophagy/autophagy (hereinafter referred to as autophagy) receptor, is found to play a pivotal role in selective autophagy, coupling autophagy with bone metabolism. However, its role in osteogenesis is still mysterious. 	mouse		High+Lowthroughput	Autophagy receptor OPTN (optineurin) regulates mesenchymal stem cell fate and bone-fat balance during aging by clearing FABP3	不相关		Senile osteoporosis	mesenchymal stem cell，bone cell	E_02_0593	Three point bending test, LC-MS analysis and data analysis, ROS detection, QRT PCR, enzyme-linked immunosorbent assay (ELISA), sa-glb1 staining. Histochemical and immunohistochemical staining, Western blot analysis, CO immunoprecipitation analysis	OPTN (optineurin), a macroautophagy/autophagy (hereinafter referred to as autophagy) receptor, is found to play a pivotal role in selective autophagy, coupling autophagy with bone metabolism. However, its role in osteogenesis is still mysterious. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	OPTN (optineurin), a macroautophagy/autophagy (hereinafter referred to as autophagy) receptor, is found to play a pivotal role in selective autophagy, coupling autophagy with bone metabolism. However, its role in osteogenesis is still mysterious. 		OPTN (optineurin), a macroautophagy/autophagy (hereinafter referred to as autophagy) receptor, is found to play a pivotal role in selective autophagy, coupling autophagy with bone metabolism. However, its role in osteogenesis is still mysterious. 	Immunohistochemical staining	OPTN (optineurin), a macroautophagy/autophagy (hereinafter referred to as autophagy) receptor, is found to play a pivotal role in selective autophagy, coupling autophagy with bone metabolism. However, its role in osteogenesis is still mysterious. 			三点弯曲试验，LC-MS 分析和数据分析，ROS 检测，qRT-PCR，酶联免疫吸附测定 （ELISA），SA-GLB1 染色。组织化学和免疫组织化学染色，免疫印迹分析，共免疫沉淀分析				OPTN
33139491	chrX	7437220	7439220	Foxp3	During Treg differentiation, a CpG-rich Foxp3 intronic enhancer, conserved noncoding sequence 2 (CNS2), is activated via DNA demethylation to establish epigenetic memory of Foxp3 expression to protect Treg identity. 	mouse	lymphoid tissue	High+Lowthroughput	Cutting Edge: CRISPR-Based Transcriptional Regulators Reveal Transcription-Dependent Establishment of Epigenetic Memory of Foxp3 in Regulatory T Cells	不相关		Immune disorders	T cell	E_02_0594	Retroviral transduction, in vitro suppression assay	During Treg differentiation, a CpG-rich Foxp3 intronic enhancer, conserved noncoding sequence 2 (CNS2), is activated via DNA demethylation to establish epigenetic memory of Foxp3 expression to protect Treg identity. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	During Treg differentiation, a CpG-rich Foxp3 intronic enhancer, conserved noncoding sequence 2 (CNS2), is activated via DNA demethylation to establish epigenetic memory of Foxp3 expression to protect Treg identity. 		During Treg differentiation, a CpG-rich Foxp3 intronic enhancer, conserved noncoding sequence 2 (CNS2), is activated via DNA demethylation to establish epigenetic memory of Foxp3 expression to protect Treg identity. 	Immunohistochemical staining	During Treg differentiation, a CpG-rich Foxp3 intronic enhancer, conserved noncoding sequence 2 (CNS2), is activated via DNA demethylation to establish epigenetic memory of Foxp3 expression to protect Treg identity. 			逆转录病毒转导，体外抑制试验				Foxp3
33137873	chr7	148804266	148806266	EZH2	β-Cells were protected against glucolipotoxicity-induced ER stress and apoptosis by EZH2 attenuation.	human	lymphoid tissue	High+Lowthroughput	Enhancer of Zeste Homolog 2 (EZH2) Mediates Glucolipotoxicity-Induced Apoptosis in β-Cells	不相关		diabetes	B cell	E_01_0869	Small molecule inhibitors, gene knockdown, mRNA microarray, real-time PCR, immunoblot analysis	β-Cells were protected against glucolipotoxicity-induced ER stress and apoptosis by EZH2 attenuation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			β-Cells were protected against glucolipotoxicity-induced ER stress and apoptosis by EZH2 attenuation.	Immunohistochemical staining	β-Cells were protected against glucolipotoxicity-induced ER stress and apoptosis by EZH2 attenuation.	EZH2		小分子抑制剂，基因敲降，mRNA微阵列，实时荧光定量 PCR，免疫印迹分析	β-Cells were protected against glucolipotoxicity-induced ER stress and apoptosis by EZH2 attenuation.			
33137828	chr19	33792836	33794836	KCTD15	We identified miR-381, which specifically targets the 3′ untranslated region (3′ UTR) of potassium channel tetramerization-domain-containing 15 (KCTD15) , and verified the mechanism regulating its expression and participation in adipogenesis. We used a dual luciferase-reporter assay and transfection-mediated miR-381 overexpression and inhibition in Yanbian yellow cattle preadipocytes to investigate the role of miR-381 in adipogenesis. 	mouse	connective tissue	High+Lowthroughput	miR-381 Targets KCTD15 to Regulate Bovine Preadipocyte Differentiation In Vitro	不相关			fat cell	E_02_0595	Cell transfection, dual luciferase reporter assay, RNA extraction and qPCR analysis	We identified miR-381, which specifically targets the 3′ untranslated region (3′ UTR) of potassium channel tetramerization-domain-containing 15 (KCTD15) , and verified the mechanism regulating its expression and participation in adipogenesis. We used a dual luciferase-reporter assay and transfection-mediated miR-381 overexpression and inhibition in Yanbian yellow cattle preadipocytes to investigate the role of miR-381 in adipogenesis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identified miR-381, which specifically targets the 3′ untranslated region (3′ UTR) of potassium channel tetramerization-domain-containing 15 (KCTD15) , and verified the mechanism regulating its expression and participation in adipogenesis. We used a dual luciferase-reporter assay and transfection-mediated miR-381 overexpression and inhibition in Yanbian yellow cattle preadipocytes to investigate the role of miR-381 in adipogenesis. 		We identified miR-381, which specifically targets the 3′ untranslated region (3′ UTR) of potassium channel tetramerization-domain-containing 15 (KCTD15) , and verified the mechanism regulating its expression and participation in adipogenesis. We used a dual luciferase-reporter assay and transfection-mediated miR-381 overexpression and inhibition in Yanbian yellow cattle preadipocytes to investigate the role of miR-381 in adipogenesis. 	Immunohistochemical staining	We identified miR-381, which specifically targets the 3′ untranslated region (3′ UTR) of potassium channel tetramerization-domain-containing 15 (KCTD15) , and verified the mechanism regulating its expression and participation in adipogenesis. We used a dual luciferase-reporter assay and transfection-mediated miR-381 overexpression and inhibition in Yanbian yellow cattle preadipocytes to investigate the role of miR-381 in adipogenesis. 			细胞转染，Dual luciferase-reporter assay，RNA extraction and qPCR analysis				KCTD15
33134376	chr1	11931678	11933678	PLOD1	Our results indicated that PLOD1 promoted proliferation, migration, and invasion of osteosarcoma cells.	human		High+Lowthroughput	PLOD1 Is a Prognostic Biomarker and Mediator of Proliferation and Invasion in Osteosarcoma	不相关		Osteosarcoma	U-2OS cell，MG-63 cell	E_01_0870	Cell culture and interfering RNA transfection, Western blot analysis, RNA isolation and RT-PCR, TCF / lef luciferase reporter assay, immunofluorescence staining	Our results indicated that PLOD1 promoted proliferation, migration, and invasion of osteosarcoma cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our results indicated that PLOD1 promoted proliferation, migration, and invasion of osteosarcoma cells.		Our results indicated that PLOD1 promoted proliferation, migration, and invasion of osteosarcoma cells.	Immunohistochemical staining	Our results indicated that PLOD1 promoted proliferation, migration, and invasion of osteosarcoma cells.			细胞培养和干扰RNA转染，蛋白质印记分析，RNA分离和RT-PCR，TCF/LEF萤光素酶报告分析，免疫荧光染色				PLOD1
33129761	chr14	104766534	104768534	AKT1	The mechanistic analysis showed that SETD5 contributes BC progression by interacting with AKT1 pathway. 	human	Lymphoid tissue, cancer tissue	High+Lowthroughput	Su(var)3-9, Enhancer of Zeste, and Trithorax Domain-Containing 5 Facilitates Tumor Growth and Pulmonary Metastasis through Up-Regulation of AKT1 Signaling in Breast Cancer	不相关		mammary cancer	macrophage，breast cancer cell	E_01_0871	Cell transfection, IHC, Western blot, immunofluorescence, migration and invasion assays, semi quantitative analysis of immunostaining	The mechanistic analysis showed that SETD5 contributes BC progression by interacting with AKT1 pathway. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The mechanistic analysis showed that SETD5 contributes BC progression by interacting with AKT1 pathway. 	Immunohistochemical staining	The mechanistic analysis showed that SETD5 contributes BC progression by interacting with AKT1 pathway. 	AKT1		细胞转染，IHC, western blot, immunofluorescence, migration and invasion assays，Semi-quantitative analysis of immunostaining	The mechanistic analysis showed that SETD5 contributes BC progression by interacting with AKT1 pathway. 			
33126652	chr5	176808090	176810090	UNC5A	Our data support the hypothesis that O-GlcNAcylation could represent one link between nutrition and epigenetic downregulation of key tumor suppressor genes governing colon carcinogenesis including UNC5A.	mouse	Cancer tissues	High+Lowthroughput	O-GlcNAcylation Links Nutrition to the Epigenetic Downregulation of UNC5A during Colon Carcinogenesis	不相关		Colon cancer	colon cancer cell	E_02_0596	Immunohistochemical staining, quantification, RT-PCR quantification, extraction of total and chromatin bound proteins, Western blotting and antibodies, luciferase promoter activity assay, CO immunoprecipitation	Our data support the hypothesis that O-GlcNAcylation could represent one link between nutrition and epigenetic downregulation of key tumor suppressor genes governing colon carcinogenesis including UNC5A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our data support the hypothesis that O-GlcNAcylation could represent one link between nutrition and epigenetic downregulation of key tumor suppressor genes governing colon carcinogenesis including UNC5A.		Our data support the hypothesis that O-GlcNAcylation could represent one link between nutrition and epigenetic downregulation of key tumor suppressor genes governing colon carcinogenesis including UNC5A.	Immunohistochemical staining	Our data support the hypothesis that O-GlcNAcylation could represent one link between nutrition and epigenetic downregulation of key tumor suppressor genes governing colon carcinogenesis including UNC5A.			免疫组织化学染色、定量，RT-PCR定量分析，总蛋白和染色质结合蛋白的提取，蛋白质印迹和抗体，荧光素酶启动子活性测定，共免疫沉淀				UNC5A
33125094	chr2	69642193	69644193	ANXA4	Annexin IV (ANXA4) is highly expressed in ovarian clear cell carcinoma (OCCC); however, its underlying molecular mechanism in OCCC remains unknown. 	human	Lymphoid tissue, cancer tissue	High+Lowthroughput	p53 and ANXA4/NF?κB p50 complexes regulate cell proliferation, apoptosis and tumor progression in ovarian clear cell carcinoma	不相关		Ovarian clear cell carcinoma	B cell，Ovarian Clear cell carcinoma	E_01_0872	Immunohistochemistry, cell transfection, CO immunoprecipitation, Western blotting, flow cytometry	Annexin IV (ANXA4) is highly expressed in ovarian clear cell carcinoma (OCCC); however, its underlying molecular mechanism in OCCC remains unknown. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Annexin IV (ANXA4) is highly expressed in ovarian clear cell carcinoma (OCCC); however, its underlying molecular mechanism in OCCC remains unknown. 		Annexin IV (ANXA4) is highly expressed in ovarian clear cell carcinoma (OCCC); however, its underlying molecular mechanism in OCCC remains unknown. 	Immunohistochemical staining	Annexin IV (ANXA4) is highly expressed in ovarian clear cell carcinoma (OCCC); however, its underlying molecular mechanism in OCCC remains unknown. 			免疫组化，细胞转染，共免疫沉淀，蛋白质印记，流式细胞术				ANXA4
33124053	chr10	103084318	103086318	NT5C2	A recent genomewide association study has identified germline polymorphisms (e.g., rs72846714) in the NT5C2 gene associated with 6-MP metabolism in patients with ALL. However, the full spectrum of genetic variation in NT5C2 is unclear and its impact on 6-MP drug activation has not been comprehensively examined.	human	lymphoid tissue	High+Lowthroughput	Effects of NT5C2 Germline Variants on 6-Mecaptopurine Metabolism in Children With Acute Lymphoblastic Leukemia	相关	rs10883841，rs12256506，rs7091462，rs12240508	acute lymphoblastic leukemia	erythrocyte	E_01_0873	NT5C2 recombinant protein production and 5’-nucleotidase activity assay	A recent genomewide association study has identified germline polymorphisms (e.g., rs72846714) in the NT5C2 gene associated with 6-MP metabolism in patients with ALL. However, the full spectrum of genetic variation in NT5C2 is unclear and its impact on 6-MP drug activation has not been comprehensively examined.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A recent genomewide association study has identified germline polymorphisms (e.g., rs72846714) in the NT5C2 gene associated with 6-MP metabolism in patients with ALL. However, the full spectrum of genetic variation in NT5C2 is unclear and its impact on 6-MP drug activation has not been comprehensively examined.		A recent genomewide association study has identified germline polymorphisms (e.g., rs72846714) in the NT5C2 gene associated with 6-MP metabolism in patients with ALL. However, the full spectrum of genetic variation in NT5C2 is unclear and its impact on 6-MP drug activation has not been comprehensively examined.	Immunohistochemical staining	A recent genomewide association study has identified germline polymorphisms (e.g., rs72846714) in the NT5C2 gene associated with 6-MP metabolism in patients with ALL. However, the full spectrum of genetic variation in NT5C2 is unclear and its impact on 6-MP drug activation has not been comprehensively examined.			NT5C2 recombinant protein production and 5’-nucleotidase activity assay				NT5C2
33121685	chr18	40386919	40388919	Kctd16	In this study, we identified a novel gene regulatory genomic element in mouse primary spermatocytes, DES-K16, in an intron of the Kctd16 gene.	human		High+Lowthroughput	A dual enhancer-silencer element, DES-K16, in mouse spermatocyte-derived GC-2spd(ts) cells	不相关				E_01_0874	Cell culture, transfection, and reporter gene assay，qRT-PCR analysis，ChIP-sequencing data analysis	In this study, we identified a novel gene regulatory genomic element in mouse primary spermatocytes, DES-K16, in an intron of the Kctd16 gene.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, we identified a novel gene regulatory genomic element in mouse primary spermatocytes, DES-K16, in an intron of the Kctd16 gene.		In this study, we identified a novel gene regulatory genomic element in mouse primary spermatocytes, DES-K16, in an intron of the Kctd16 gene.	Immunohistochemical staining	In this study, we identified a novel gene regulatory genomic element in mouse primary spermatocytes, DES-K16, in an intron of the Kctd16 gene.			Cell culture, transfection, and reporter gene assay，qRT-PCR analysis，ChIP-sequencing data analysis				Kctd16
33121524	chr7	148804652	148806652	EZH2	Our study revealed that UPK1A-AS1 promotes HCC development by accelerating cell cycle progression through interaction with EZH2 and sponging of miR-138-5p, suggesting that UPK1A-AS1 possesses substantial potential as a novel biomarker for HCC prognosis and therapy.	human	Cancer tissues	High+Lowthroughput	Long noncoding RNA UPK1A-AS1 indicates poor prognosis of hepatocellular carcinoma and promotes cell proliferation through interaction with EZH2	不相关		Hepatocellular carcinoma	hepatocellular carcinoma cell	E_01_0875	Edu assay, flow cytometry, Western blot and xenograft assay, bioinformatics analysis and quantitative polymerase chain reaction (QRT PCR), RNA immunoprecipitation (RIP), RNA pull-down assay, QRT PCR assay, luciferase reporter	Our study revealed that UPK1A-AS1 promotes HCC development by accelerating cell cycle progression through interaction with EZH2 and sponging of miR-138-5p, suggesting that UPK1A-AS1 possesses substantial potential as a novel biomarker for HCC prognosis and therapy.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our study revealed that UPK1A-AS1 promotes HCC development by accelerating cell cycle progression through interaction with EZH2 and sponging of miR-138-5p, suggesting that UPK1A-AS1 possesses substantial potential as a novel biomarker for HCC prognosis and therapy.	Immunohistochemical staining	Our study revealed that UPK1A-AS1 promotes HCC development by accelerating cell cycle progression through interaction with EZH2 and sponging of miR-138-5p, suggesting that UPK1A-AS1 possesses substantial potential as a novel biomarker for HCC prognosis and therapy.	EZH2		EdU测定，流式细胞术，蛋白质印迹和异种移植测定，生物信息学分析和定量聚合酶链反应（qRT-PCR），RNA免疫沉淀（RIP）、RNA下拉测定、qRT-PCR检测，荧光素酶报告	Our study revealed that UPK1A-AS1 promotes HCC development by accelerating cell cycle progression through interaction with EZH2 and sponging of miR-138-5p, suggesting that UPK1A-AS1 possesses substantial potential as a novel biomarker for HCC prognosis and therapy.			
33116876	chr2	25730681	25732681	ASXL2	"These results showed that ASXL2 could induce cell proliferation, which was associated with poor prognosis of CRC patients, suggesting that ASXL2 might be a new therapeutic target for CRC.
"	human	Cancer tissues	High+Lowthroughput	Elevated Expression of ASXL2 is Associated with Poor Prognosis in Colorectal Cancer by Enhancing Tumorigenesis and Inducing Cell Proliferation	不相关		colorectal cancer 	Human colorectal carcinoma cell	E_01_0876	Quantitative real-time polymerase chain reaction (QRT PCR), Western blot analysis and immunohistochemistry (IHC)	"These results showed that ASXL2 could induce cell proliferation, which was associated with poor prognosis of CRC patients, suggesting that ASXL2 might be a new therapeutic target for CRC.
"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"These results showed that ASXL2 could induce cell proliferation, which was associated with poor prognosis of CRC patients, suggesting that ASXL2 might be a new therapeutic target for CRC.
"	Immunohistochemical staining	"These results showed that ASXL2 could induce cell proliferation, which was associated with poor prognosis of CRC patients, suggesting that ASXL2 might be a new therapeutic target for CRC.
"	ASXL2		定量实时聚合酶链反应（qRT-PCR）、蛋白质印迹分析和免疫组化（IHC）	"These results showed that ASXL2 could induce cell proliferation, which was associated with poor prognosis of CRC patients, suggesting that ASXL2 might be a new therapeutic target for CRC.
"			
33113374	chr16	67559229	67561229	CTCF	We propose that CTCF functions as a typical insulator on inactive alleles, but facilitates transcription through enhancer-linking on active allele of MAE genes, indicating widespread allele-specific regulatory roles of CTCF.	human	lymphoid tissue	High+Lowthroughput	CTCF-Mediated Genome Architecture Regulates the Dosage of Mitotically Stable Mono-allelic Expression of Autosomal Genes	不相关			T cell	E_01_0877	Western blotting, single-molecule fluorescence in situ hybridization (smfish)	We propose that CTCF functions as a typical insulator on inactive alleles, but facilitates transcription through enhancer-linking on active allele of MAE genes, indicating widespread allele-specific regulatory roles of CTCF.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We propose that CTCF functions as a typical insulator on inactive alleles, but facilitates transcription through enhancer-linking on active allele of MAE genes, indicating widespread allele-specific regulatory roles of CTCF.	Immunohistochemical staining	We propose that CTCF functions as a typical insulator on inactive alleles, but facilitates transcription through enhancer-linking on active allele of MAE genes, indicating widespread allele-specific regulatory roles of CTCF.	CTCF		蛋白质印记，单分子荧光原位杂交（smFISH）	We propose that CTCF functions as a typical insulator on inactive alleles, but facilitates transcription through enhancer-linking on active allele of MAE genes, indicating widespread allele-specific regulatory roles of CTCF.			
33110425	chr1	41503769	41505769	HIVEP3	We found that HIVEP3 gene and LINC RNA are potentially correlated with femoral neck BMC.	human	connective tissue	High+Lowthroughput	Association of HIVEP3 Gene and Lnc RNA with Femoral Neck Bone Mineral Content and Hip Geometry by Genome-Wide Association Analysis in Chinese People	相关	rs35282355，rs7071262，rs7907051，rs187172215，rs12152026	Osteoporosis you	cementoblast	E_01_0878	Genotype imputation, BMD, and hip geometry parameter measurements	We found that HIVEP3 gene and LINC RNA are potentially correlated with femoral neck BMC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found that HIVEP3 gene and LINC RNA are potentially correlated with femoral neck BMC.		We found that HIVEP3 gene and LINC RNA are potentially correlated with femoral neck BMC.	Immunohistochemical staining	We found that HIVEP3 gene and LINC RNA are potentially correlated with femoral neck BMC.			基因型插补，BMD和髋关节几何参数测量				HIVEP3
33099542	chr20	46005995	46007995	MMP9	Allele C rs3918249 MMP9 decreased risk for XFG (OR = 0.75), and allele G of the rs2250889 MMP9 locus increased risk for XFG (OR = 1.59-1.68) in the Caucasian population of Central Russia.	human	Nervous tissue	High+Lowthroughput	Novel Data about Association of the Functionally Significant Polymorphisms of the MMP9 Gene with Exfoliation Glaucoma in the Caucasian Population of Central Russia	相关	rs3918242，rs3918249，rs17576，rs3787268，rs2250889，rs17577	Exfoliative glaucoma (xfg) in the central Russian Caucasian population	retinal ganglion cell	E_01_0879	DNA isolation and genotyping assays, functional SNPs	Allele C rs3918249 MMP9 decreased risk for XFG (OR = 0.75), and allele G of the rs2250889 MMP9 locus increased risk for XFG (OR = 1.59-1.68) in the Caucasian population of Central Russia.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Allele C rs3918249 MMP9 decreased risk for XFG (OR = 0.75), and allele G of the rs2250889 MMP9 locus increased risk for XFG (OR = 1.59-1.68) in the Caucasian population of Central Russia.	Immunohistochemical staining	Allele C rs3918249 MMP9 decreased risk for XFG (OR = 0.75), and allele G of the rs2250889 MMP9 locus increased risk for XFG (OR = 1.59-1.68) in the Caucasian population of Central Russia.	MMP9		DNA 分离和基因分型检测，功能性 SNP	Allele C rs3918249 MMP9 decreased risk for XFG (OR = 0.75), and allele G of the rs2250889 MMP9 locus increased risk for XFG (OR = 1.59-1.68) in the Caucasian population of Central Russia.			
33097694	chr3	147382975	147384975	ZIC4	Inactivation of tumor suppressor gene played critical roles in the development and progression of human hepatocellular carcinoma (HCC). Zic family member 4 (ZIC4) is transcription factor and plays an important role in the developmental process.	human,mouse	Cancer tissues	High+Lowthroughput	Epigenetic silencing of ZIC4 contributes to cancer progression in hepatocellular carcinoma	不相关		Hepatocellular carcinoma	hepatocellular carcinoma cell	E_02_0597	Transfection of shRNA, DNA methylation analysis, RNA extraction and quantitative reverse transcription polymerase chain reaction (QRT PCR), Western blot analysis, chromatin immunoprecipitation discovery, flow cytometry	Inactivation of tumor suppressor gene played critical roles in the development and progression of human hepatocellular carcinoma (HCC). Zic family member 4 (ZIC4) is transcription factor and plays an important role in the developmental process.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Inactivation of tumor suppressor gene played critical roles in the development and progression of human hepatocellular carcinoma (HCC). Zic family member 4 (ZIC4) is transcription factor and plays an important role in the developmental process.		Inactivation of tumor suppressor gene played critical roles in the development and progression of human hepatocellular carcinoma (HCC). Zic family member 4 (ZIC4) is transcription factor and plays an important role in the developmental process.	Immunohistochemical staining	Inactivation of tumor suppressor gene played critical roles in the development and progression of human hepatocellular carcinoma (HCC). Zic family member 4 (ZIC4) is transcription factor and plays an important role in the developmental process.			转染 shRNA，DNA甲基化分析，RNA提取和定量逆转录-聚合酶链反应（qRT-PCR），蛋白质印记分析，染色质免疫沉淀发现，流式细胞术				ZIC4
33096182	chr14	35275853	35277853	PSMA6	It was also found that the transcription factors CCAAT/enhancer-binding protein alpha (CEBPA) and peroxisome proliferator-activated receptor gamma (PPARG), as well as the key genes related to adipogenesis, were upregulated, while the genes related to fat oxidation were significantly downregulated, which indicated that the PSMA6 gene could stimulate the differentiation of preadipocytes.	mouse	connective tissue	High+Lowthroughput	The potential role of PSMA6 in modulating fat deposition in pigs by promoting preadipocyte proliferation and differentiation	不相关		Fat deposition	adipocyte ，desmocyte	E_02_0598	Oil Red O staining，cDNA preparation and quantitative real-time PCR (qRT-PCR) assay	It was also found that the transcription factors CCAAT/enhancer-binding protein alpha (CEBPA) and peroxisome proliferator-activated receptor gamma (PPARG), as well as the key genes related to adipogenesis, were upregulated, while the genes related to fat oxidation were significantly downregulated, which indicated that the PSMA6 gene could stimulate the differentiation of preadipocytes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	It was also found that the transcription factors CCAAT/enhancer-binding protein alpha (CEBPA) and peroxisome proliferator-activated receptor gamma (PPARG), as well as the key genes related to adipogenesis, were upregulated, while the genes related to fat oxidation were significantly downregulated, which indicated that the PSMA6 gene could stimulate the differentiation of preadipocytes.		It was also found that the transcription factors CCAAT/enhancer-binding protein alpha (CEBPA) and peroxisome proliferator-activated receptor gamma (PPARG), as well as the key genes related to adipogenesis, were upregulated, while the genes related to fat oxidation were significantly downregulated, which indicated that the PSMA6 gene could stimulate the differentiation of preadipocytes.	Immunohistochemical staining	It was also found that the transcription factors CCAAT/enhancer-binding protein alpha (CEBPA) and peroxisome proliferator-activated receptor gamma (PPARG), as well as the key genes related to adipogenesis, were upregulated, while the genes related to fat oxidation were significantly downregulated, which indicated that the PSMA6 gene could stimulate the differentiation of preadipocytes.			Oil Red O staining，cDNA preparation and quantitative real-time PCR (qRT-PCR) assay				PSMA6
33096543	chr2	74831227	74833227	HK2	In dual-luciferase enhancer reporter system experiments, we found that inserting the minor allele of rs9315202 in a human kidney cell line HK-2 genomic DNA resulted in a change in KL transcriptional activities, likely operating via long noncoding RNA in this region. 	human	PTSD brain bank，DNA, DNAm, and related statistical procedures	High+Lowthroughput	Klotho, PTSD, and advanced epigenetic age in cortical tissue	相关	rs9315202	PTSD	astrocyte,endothelial stalk cell，gitter cell ，The mural cell，nerve cell，oligodendroglia cell，erythrocyte	E_01_0880	RNA sequencing, DNA emergence, dual luciferase reporter	In dual-luciferase enhancer reporter system experiments, we found that inserting the minor allele of rs9315202 in a human kidney cell line HK-2 genomic DNA resulted in a change in KL transcriptional activities, likely operating via long noncoding RNA in this region. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In dual-luciferase enhancer reporter system experiments, we found that inserting the minor allele of rs9315202 in a human kidney cell line HK-2 genomic DNA resulted in a change in KL transcriptional activities, likely operating via long noncoding RNA in this region. 		In dual-luciferase enhancer reporter system experiments, we found that inserting the minor allele of rs9315202 in a human kidney cell line HK-2 genomic DNA resulted in a change in KL transcriptional activities, likely operating via long noncoding RNA in this region. 	Immunohistochemical staining	In dual-luciferase enhancer reporter system experiments, we found that inserting the minor allele of rs9315202 in a human kidney cell line HK-2 genomic DNA resulted in a change in KL transcriptional activities, likely operating via long noncoding RNA in this region. 			RNA测序，DNA出现，双荧光素酶报告				HK2
33086062	chr12	49016248	49018248	KMT2D	Histone methyltransferase KMT2D harbors frequent loss-of-function somatic point mutations in several tumor types, including melanoma.	mouse		High+Lowthroughput	Enhancer Reprogramming Confers Dependence on Glycolysis and IGF Signaling in KMT2D Mutant Melanoma	不相关		tumour	melanocyte，melanoma cell	E_02_0599	Inhibitor treatment experiments, chip SEQ chromatin immunoprecipitation, TCGA RNA SEQ data analysis, immunohistochemistry	Histone methyltransferase KMT2D harbors frequent loss-of-function somatic point mutations in several tumor types, including melanoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Histone methyltransferase KMT2D harbors frequent loss-of-function somatic point mutations in several tumor types, including melanoma.		Histone methyltransferase KMT2D harbors frequent loss-of-function somatic point mutations in several tumor types, including melanoma.	Immunohistochemical staining	Histone methyltransferase KMT2D harbors frequent loss-of-function somatic point mutations in several tumor types, including melanoma.			抑制剂治疗实验，ChIP-Seq染色质免疫沉淀，TCGA RNA-Seq数据分析，免疫组化				KMT2D
33084574	chr1	26690504	26692504	ARID1A	In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 	human,mouse	Lymphoid tissue, liver tissue	High+Lowthroughput	ARID1A loss in adult hepatocytes activates β-catenin-mediated erythropoietin transcription	不相关			erythrocyte，stem cell	E_02_0600	Immunohistochemistry and in situ hybridization experiments, enzyme-linked immunosorbent assay (ELISA), cell transfection, stimulation and luciferase assays, RNA extraction and quantitative RT-PCR, protein extracts and Western blotting, electrophoretic mobility shift assay (EMSA), flow cytometry and forming unit erythroid (CFU-E) assays, chromatin immunoprecipitation (chip) and ATAC qPCR assays were performed	In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 		In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 	Immunohistochemical staining	In mice with Apc-Arid1a gene invalidations in single hepatocytes, Epo de novo synthesis led to its secretion, to splenic erythropoiesis and to dramatic erythrocytosis. 			免疫组化和原位杂交实验，酶联免疫吸附测定（ELISA），细胞转染、刺激和荧光素酶检测，RNA 提取和定量 RT-PCR，蛋白质提取物和蛋白质印迹，电泳迁移率移位测定 （EMSA），流式细胞术和成形单元红系 （CFU-E） 检测，染色质免疫沉淀 （ChIP） 和 ATAC-qPCR 检测				ARID1A
33083767	chr17	27055027	27057027	Nkx2-5	We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.	mouse	Musculature	High+Lowthroughput	Divergent Transcription of the Nkx2-5 Locus Generates Two Enhancer RNAs with Opposing Functions	不相关		heart failure	cardiac muscle cell (sensu Arthopoda)	E_02_0601	RNA sequencing (RNA SEQ), quantitative PCR (qPCR), cell fractionation, rna-fish, Western blotting, fluorescent immunoassay	We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.		We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.	Immunohistochemical staining	We have identified an autoregulatory loop controlling expression of the master cardiac TF NKX2-5, in which one eRNA represses transcription.			RNA测序（RNA-seq），定量PCR（qPCR），细胞分馏，RNA-FISH，蛋白质印记，荧光免疫分析				Nkx2-5
33078455	chr13	73052160	73054160	KLF5	These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.	mouse	connective tissue	High+Lowthroughput	Regulation of adipocyte differentiation by clusterin-mediated Krüppel-like factor 5 stabilization	不相关			fat cell，mesenchymal stem cell	E_02_0602	RNA isolation and quantitative real_x0002_time PCR (qRT-PCR)，Luciferase reporter assay，20S proteasome activity assay	These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.		These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.	Immunohistochemical staining	These results suggest that CLU is a novel regulator of adipocyte differentiation by modulating the protein stability of the adipogenic transcription factor KLF5.			RNA isolation and quantitative real_x0002_time PCR (qRT-PCR)，Luciferase reporter assay，20S proteasome activity assay				KLF5
33067396	chr3	47013497	47015497	SETD2	We demonstrate that H3.3 G34 oncohistones selectively promote PRC2 activity by interfering with SETD2-mediated H3K36 methylation. We propose that PRC2-mediated silencing of enhancers involved in cell differentiation represents a potential mechanism by which H3.3 G34 mutations drive these tumors.	human		High+Lowthroughput	Histone H3.3 G34 mutations promote aberrant PRC2 activity and drive tumor progression	不相关		Tumour stones	mesenchymal stem cell,stromal cell,osteoblast	E_01_0881	Chip SEQ analysis, histone methyltransferase (HMT) assay	We demonstrate that H3.3 G34 oncohistones selectively promote PRC2 activity by interfering with SETD2-mediated H3K36 methylation. We propose that PRC2-mediated silencing of enhancers involved in cell differentiation represents a potential mechanism by which H3.3 G34 mutations drive these tumors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We demonstrate that H3.3 G34 oncohistones selectively promote PRC2 activity by interfering with SETD2-mediated H3K36 methylation. We propose that PRC2-mediated silencing of enhancers involved in cell differentiation represents a potential mechanism by which H3.3 G34 mutations drive these tumors.		We demonstrate that H3.3 G34 oncohistones selectively promote PRC2 activity by interfering with SETD2-mediated H3K36 methylation. We propose that PRC2-mediated silencing of enhancers involved in cell differentiation represents a potential mechanism by which H3.3 G34 mutations drive these tumors.	Immunohistochemical staining	We demonstrate that H3.3 G34 oncohistones selectively promote PRC2 activity by interfering with SETD2-mediated H3K36 methylation. We propose that PRC2-mediated silencing of enhancers involved in cell differentiation represents a potential mechanism by which H3.3 G34 mutations drive these tumors.			ChIP-Seq Analysis，组蛋白甲基转移酶（HMT）测定				SETD2
33055097	chr9	27532950	27534950	C9orf72	The GGGGCC hexanucleotide expansion in C9orf72 (C9) is the most frequent known cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), yet a clear understanding of how C9 fits into the broader context of ALS/FTD pathology has remained lacking.	human		High+Lowthroughput	Widespread intron retention impairs protein homeostasis in C9orf72 ALS brains	不相关		Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD)	HEK 293T	E_01_0882	RNA SEQ, analysis of intron identity, gene ontology analysis, analysis of hnrnph clip SEQ data	The GGGGCC hexanucleotide expansion in C9orf72 (C9) is the most frequent known cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), yet a clear understanding of how C9 fits into the broader context of ALS/FTD pathology has remained lacking.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The GGGGCC hexanucleotide expansion in C9orf72 (C9) is the most frequent known cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), yet a clear understanding of how C9 fits into the broader context of ALS/FTD pathology has remained lacking.		The GGGGCC hexanucleotide expansion in C9orf72 (C9) is the most frequent known cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), yet a clear understanding of how C9 fits into the broader context of ALS/FTD pathology has remained lacking.	Immunohistochemical staining	The GGGGCC hexanucleotide expansion in C9orf72 (C9) is the most frequent known cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD), yet a clear understanding of how C9 fits into the broader context of ALS/FTD pathology has remained lacking.			核糖核酸序列数据，RNA-seq，内含子特性分析，基因本体分析，分析 hnRNPH CLIP-seq 数据				C9orf72
33051686	chr8	127732617	127734617	MYC	MYC thus interacts with its flanking enhancers in a mutually exclusive manner documenting that enhancer hubs impinging on MYC detected in large cell populations likely do not exist in single cells.	human	Cancer tissues	High+Lowthroughput	MYC as a driver of stochastic chromatin networks: implications for the fitness of cancer cells	不相关		cancer	colon cancer cell	E_01_0883	3D DNA FISH analysis	MYC thus interacts with its flanking enhancers in a mutually exclusive manner documenting that enhancer hubs impinging on MYC detected in large cell populations likely do not exist in single cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MYC thus interacts with its flanking enhancers in a mutually exclusive manner documenting that enhancer hubs impinging on MYC detected in large cell populations likely do not exist in single cells.	Immunohistochemical staining	MYC thus interacts with its flanking enhancers in a mutually exclusive manner documenting that enhancer hubs impinging on MYC detected in large cell populations likely do not exist in single cells.	MYC		3D DNA FISH 分析	MYC thus interacts with its flanking enhancers in a mutually exclusive manner documenting that enhancer hubs impinging on MYC detected in large cell populations likely do not exist in single cells.			
33051488	chrX	31095139	31097139	DMD	Dystrophin Dp71 is the smallest isoform of the DMD gene, mutations in which cause Duchenne muscular dystrophy (DMD).	human		High+Lowthroughput	Dystrophin Dp71ab is monoclonally expressed in human satellite cells and enhances proliferation of myoblast cells	不相关		Duchenne muscular dystrophy	stem cell,sarcoblast	E_01_0884	MRNA analysis, protein analysis, cell proliferation assay, cell number assay	Dystrophin Dp71 is the smallest isoform of the DMD gene, mutations in which cause Duchenne muscular dystrophy (DMD).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Dystrophin Dp71 is the smallest isoform of the DMD gene, mutations in which cause Duchenne muscular dystrophy (DMD).		Dystrophin Dp71 is the smallest isoform of the DMD gene, mutations in which cause Duchenne muscular dystrophy (DMD).	Immunohistochemical staining	Dystrophin Dp71 is the smallest isoform of the DMD gene, mutations in which cause Duchenne muscular dystrophy (DMD).			mRNA 分析，蛋白质分析，细胞增殖测定，细胞数测定				DMD
33048369	chr7	99753898	99755898	CYP3A4	The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.	human		High+Lowthroughput	DNA methylation determines the regulation of pregnane X receptor on CYP3A4 expression	不相关			HepG2 cell	E_01_0885	Plasmid construction，In vitro methylation，Luciferase reporter assay，Transfection and rifampicin induction，RNA isolation and real-time quantitative polymerase chain reaction (RT-qPCR) ，ChIP assay	The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.		The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.	Immunohistochemical staining	The expression and activity of CYP3A4 vary among individuals. With the development of epigenetics, it is now possible to elucidate interindividual differences in drug-metabolizing enzymes.			Plasmid construction，In vitro methylation，Luciferase reporter assay，Transfection and rifampicin induction，RNA isolation and real-time quantitative polymerase chain reaction (RT-qPCR) ，ChIP assay				CYP3A4
33033262	chr9	107482552	107484552	KLF4	Establishes a multifaceted role for JMJD3, placing it as a key partner of KLF4 and a scaffold that assists chromatin interactions and activates gene transcription.	mouse		High+Lowthroughput	JMJD3 acts in tandem with KLF4 to facilitate reprogramming to pluripotency	不相关			fibroblast	E_02_0603	IPSC generation and EPISC to naive PSC transition, plasmid and molecular cloning, ribonucleic acid isolation and RT qPCR, immunofluorescence, Western blot and co immunoprecipitation, flow cytometry analysis, ribonucleic acid sequencing and analysis, chip qPCR and chip SEQ, chip SEQ analysis, chip SEQ analysis, chip SEQ analysis, chip SEQ analysis	Establishes a multifaceted role for JMJD3, placing it as a key partner of KLF4 and a scaffold that assists chromatin interactions and activates gene transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Establishes a multifaceted role for JMJD3, placing it as a key partner of KLF4 and a scaffold that assists chromatin interactions and activates gene transcription.		Establishes a multifaceted role for JMJD3, placing it as a key partner of KLF4 and a scaffold that assists chromatin interactions and activates gene transcription.	Immunohistochemical staining	Establishes a multifaceted role for JMJD3, placing it as a key partner of KLF4 and a scaffold that assists chromatin interactions and activates gene transcription.			iPSC 生成和 EpiSC 到幼稚 PSC 的过渡，质粒和分子克隆，核糖核酸分离和 RT-qPCR，免疫荧光，蛋白质印迹和共免疫沉淀，流式细胞术分析，核糖核酸序列和分析，ChIP-qPCR 和 ChIP-seq，ChIP-seq 分析，ChIP-seq 分析，ChIP-seq 分析				KLF4
33029258	chr16	67559853	67561853	CTCF	We investigated whether CTCF played a role in mediating the transcriptional regulation network. eRNAs, especially those that regulate androgen response genes, may be candidates for prognostic biomarkers and therapy targets.	human		High+Lowthroughput	eRNAs and Superenhancer lncRNAs Are Functional in Human Prostate Cancer	不相关		prostatic cancer	human prostatic cancer cell	E_01_0886	Microarray design, microarray analysis, data analysis, identification of Ernas and Se lncrnas, prediction of Erna target genes, functional enrichment analysis of target genes, TCGA data analysis, QRT PCR analysis, prediction of transcription factors (TFs) and construction of interaction networks, CTCF chip SEQ data analysis	We investigated whether CTCF played a role in mediating the transcriptional regulation network. eRNAs, especially those that regulate androgen response genes, may be candidates for prognostic biomarkers and therapy targets.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We investigated whether CTCF played a role in mediating the transcriptional regulation network. eRNAs, especially those that regulate androgen response genes, may be candidates for prognostic biomarkers and therapy targets.	Immunohistochemical staining	We investigated whether CTCF played a role in mediating the transcriptional regulation network. eRNAs, especially those that regulate androgen response genes, may be candidates for prognostic biomarkers and therapy targets.	CTCF		微阵列设计，微阵列分析、数据分析，eRNA和SE-lncRNA的鉴定，eRNA靶基因的预测，靶基因的功能富集分析，TCGA数据分析，qRT-PCR分析，转录因子（TF）的预测与交互网络的构建，CTCF ChIP-seq数据分析	We investigated whether CTCF played a role in mediating the transcriptional regulation network. eRNAs, especially those that regulate androgen response genes, may be candidates for prognostic biomarkers and therapy targets.			
31470645	chr8	94246733	94248733	GEM	In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).	human,and,mouse	liver	High+Lowthroughput	A Novel Bacterium-Like Particle Vaccine Displaying the MERS-CoV Receptor-Binding Domain Induces Specific Mucosal and Systemic Immune Responses in Mice.	否	无	Respiratory disease	Huh 7 cell	E_02_0604	PCR, flow cytometry, gene knockdown, Western blot, gel electrophoresis, immunofluorescence staining	In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).		In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).	Immunohistochemical staining	In this study, a bacterium (Lactococcus lactis)- like particle (BLP) vaccine displaying the MERS-CoV receptor-binding domain (RBD) was  developed, and gram-positive enhancer matrix (GEM) particles were used as substrates to  externally bind to the MERS-CoV RBD through a protein anchor (PA).			PCR,流式细胞术,基因敲降,Western blot,凝胶电泳,免疫荧光染色				GEM
31469428	chr3	51382539	51384539	MANF	Mesencephalic astrocyte-derived  neurotrophic factor (MANF) is an ER stress-inducible secretion  protein that inhibits inflammation by interacting with the key  subunit of nuclear factor kappa light chain enhancer of acti_x005f_x0002_vated B cells (NF-κB) p65.	human,and,mouse		High+Lowthroughput	Mesencephalic Astrocyte-Derived Neurotrophic Factor Inhibits Liver Cancer Through Small Ubiquitin-Related Modifier (SUMO)ylation-Related Suppression of NF-κB/Snail Signaling Pathway and Epithelial-Mesenchymal Transition.	否	无	Alzheimer's disease		E_02_0605	PCR, Western blot, gene knockdown, gel electrophoresis	Mesencephalic astrocyte-derived  neurotrophic factor (MANF) is an ER stress-inducible secretion  protein that inhibits inflammation by interacting with the key  subunit of nuclear factor kappa light chain enhancer of acti_x005f_x0002_vated B cells (NF-κB) p65.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mesencephalic astrocyte-derived  neurotrophic factor (MANF) is an ER stress-inducible secretion  protein that inhibits inflammation by interacting with the key  subunit of nuclear factor kappa light chain enhancer of acti_x005f_x0002_vated B cells (NF-κB) p65.		Mesencephalic astrocyte-derived  neurotrophic factor (MANF) is an ER stress-inducible secretion  protein that inhibits inflammation by interacting with the key  subunit of nuclear factor kappa light chain enhancer of acti_x005f_x0002_vated B cells (NF-κB) p65.	Immunohistochemical staining	Mesencephalic astrocyte-derived  neurotrophic factor (MANF) is an ER stress-inducible secretion  protein that inhibits inflammation by interacting with the key  subunit of nuclear factor kappa light chain enhancer of acti_x005f_x0002_vated B cells (NF-κB) p65.			PCR,Western blot,基因敲降,凝胶电泳				MANF
31467880	chr12	113389693	113391693	SDS	Equal amounts (20 _x005f_xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.	human,and,mouse		High+Lowthroughput	The Antiobesity Effects of Buginawa in 3T3-L1 Preadipocytes and in a Mouse Model of High-Fat Diet-Induced Obesity.	否	无	Heart disease	mesenchymal stem cell	E_02_0606	PCR, Western blot, gel electrophoresis	Equal amounts (20 _x005f_xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Equal amounts (20 _x005f_xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.		Equal amounts (20 _x005f_xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.	Immunohistochemical staining	Equal amounts (20 _x005f_xd835_g) of protein sample were separated on a sodium dodecyl sulfate (SDS) polyacrylamide gel, fol_x0002_lowed by being transferred onto a polyvinylidene fuoride (PVDF) membrane.			PCR,Western blot,凝胶电泳				SDS
31467629	chr17	42310510	42312510	STAT3	One report indicated that the activation of the STAT3 pathway was involved in radiation-induced endothelial inflammation [54], and the DNA-binding activity of STAT3 and the level of phospho_x005f_x0002_Stat3 Tyr (705), but not phospho-Stat3 Ser (727), was reduced in HUVECs after 3 Gy irradiation.	human,and,mouse	Epithelial tissues	High+Lowthroughput	Gamma Radiation-Induced Disruption of Cellular Junctions in HUVECs Is Mediated through Affecting MAPK/NF-κB Inflammatory Pathways.	否	无	Cardiovascular disease	endothelial cell	E_02_0607	PCR, Western blot, gene knockdown, gel electrophoresis	One report indicated that the activation of the STAT3 pathway was involved in radiation-induced endothelial inflammation [54], and the DNA-binding activity of STAT3 and the level of phospho_x005f_x0002_Stat3 Tyr (705), but not phospho-Stat3 Ser (727), was reduced in HUVECs after 3 Gy irradiation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	One report indicated that the activation of the STAT3 pathway was involved in radiation-induced endothelial inflammation [54], and the DNA-binding activity of STAT3 and the level of phospho_x005f_x0002_Stat3 Tyr (705), but not phospho-Stat3 Ser (727), was reduced in HUVECs after 3 Gy irradiation.		One report indicated that the activation of the STAT3 pathway was involved in radiation-induced endothelial inflammation [54], and the DNA-binding activity of STAT3 and the level of phospho_x005f_x0002_Stat3 Tyr (705), but not phospho-Stat3 Ser (727), was reduced in HUVECs after 3 Gy irradiation.	Immunohistochemical staining	One report indicated that the activation of the STAT3 pathway was involved in radiation-induced endothelial inflammation [54], and the DNA-binding activity of STAT3 and the level of phospho_x005f_x0002_Stat3 Tyr (705), but not phospho-Stat3 Ser (727), was reduced in HUVECs after 3 Gy irradiation.			PCR,Western blot,基因敲降,凝胶电泳				STAT3
31467598	chr15	51205539	51207539	CYP19A1	Characterization of the endogenous retrovirus insertion in CYP19A1 associated with henny feathering in chicken.	mouse		High+Lowthroughput	Characterization of the endogenous retrovirus insertion in CYP19A1 associated with henny feathering in chicken.	否	无	nothing		E_02_0608	PCR, Western blot, gel electrophoresis	Characterization of the endogenous retrovirus insertion in CYP19A1 associated with henny feathering in chicken.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Characterization of the endogenous retrovirus insertion in CYP19A1 associated with henny feathering in chicken.		Characterization of the endogenous retrovirus insertion in CYP19A1 associated with henny feathering in chicken.	Immunohistochemical staining	Characterization of the endogenous retrovirus insertion in CYP19A1 associated with henny feathering in chicken.			PCR,Western blot,凝胶电泳				CYP19A1
31467127	chr9	136491743	136493743	NOTCH1	Genomic alterations in high-risk chronic lymphocytic leukemia frequently affect cell cycle key regulators and NOTCH1-regulated transcription.	human	tumour	High+Lowthroughput	Genomic alterations in high-risk chronic lymphocytic leukemia frequently affect cell cycle key regulators and NOTCH1-regulated transcription.	是	无	Lymphocytic leukemia	cancer cell	E_01_0887	PCR, gel electrophoresis	Genomic alterations in high-risk chronic lymphocytic leukemia frequently affect cell cycle key regulators and NOTCH1-regulated transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Genomic alterations in high-risk chronic lymphocytic leukemia frequently affect cell cycle key regulators and NOTCH1-regulated transcription.	Immunohistochemical staining	Genomic alterations in high-risk chronic lymphocytic leukemia frequently affect cell cycle key regulators and NOTCH1-regulated transcription.	NOTCH1		PCR,凝胶电泳	Genomic alterations in high-risk chronic lymphocytic leukemia frequently affect cell cycle key regulators and NOTCH1-regulated transcription.			
31466317	chr12	9749793	9751793	CD69	The Conserved Non-Coding Sequence 2 (CNS2) Enhances CD69 Transcription through Cooperation between the Transcription Factors Oct1 and RUNX1.	human,and,mouse	lymph	High+Lowthroughput	The Conserved Non-Coding Sequence 2 (CNS2) Enhances CD69 Transcription through Cooperation between the Transcription Factors Oct1 and RUNX1.	否	无	Autoimmune disease	Jurkat cell	E_02_0609	PCR, gel electrophoresis	The Conserved Non-Coding Sequence 2 (CNS2) Enhances CD69 Transcription through Cooperation between the Transcription Factors Oct1 and RUNX1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The Conserved Non-Coding Sequence 2 (CNS2) Enhances CD69 Transcription through Cooperation between the Transcription Factors Oct1 and RUNX1.		The Conserved Non-Coding Sequence 2 (CNS2) Enhances CD69 Transcription through Cooperation between the Transcription Factors Oct1 and RUNX1.	Immunohistochemical staining	The Conserved Non-Coding Sequence 2 (CNS2) Enhances CD69 Transcription through Cooperation between the Transcription Factors Oct1 and RUNX1.			PCR,凝胶电泳				CD69
31465963	chr3	181709146	181711146	SOX2	Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.	human,and,mouse		High+Lowthroughput	Landscape of Enhancer-Enhancer Cooperative Regulation during Human Cardiac Commitment.	否	无	Heart disease		E_02_0610	ChIP-seq,RNA-seq	Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.		Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.	Immunohistochemical staining	Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.			ChIP-seq,RNA-seq				SOX2
31465963	chr6	31161583	31163583	POU5F1	Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.	human,and,mouse		High+Lowthroughput	Landscape of Enhancer-Enhancer Cooperative Regulation during Human Cardiac Commitment.	否	无	Heart disease		E_02_0610	ChIP-seq,RNA-seq	Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.		Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.	Immunohistochemical staining	Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.			ChIP-seq,RNA-seq				POU5F1
31465963	chr12	7784849	7786849	NANOG	Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.	human,and,mouse		High+Lowthroughput	Landscape of Enhancer-Enhancer Cooperative Regulation during Human Cardiac Commitment.	否	无	Heart disease		E_02_0610	ChIP-seq,RNA-seq	Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.		Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.	Immunohistochemical staining	Enhancers of undifferentiated ESCs cooperatively regulate pluripotency genes, such as POU5F1/ OCT4, NANOG, and SOX2 (Table 1; Figure 6D), which are pluripo_x005f_x0002_tent master transcription factors that can bind enhancer elements and recruit Mediator to activate much of the gene expression program of pluripotent ESCs.			ChIP-seq,RNA-seq				NANOG
31462713	chr10	22318328	22320328	BMI1	BMI1 is directly regulated by androgen receptor to promote castration-resistance in prostate cancer.	human,and,mouse	Epithelial tissues	High+Lowthroughput	BMI1 is directly regulated by androgen receptor to promote castration-resistance in prostate cancer.	否	无	During disease (heart disease in pregnancy)	epithelial cell	E_02_0611	Chip SEQ, PCR, Western blot, gel electrophoresis	BMI1 is directly regulated by androgen receptor to promote castration-resistance in prostate cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	BMI1 is directly regulated by androgen receptor to promote castration-resistance in prostate cancer.		BMI1 is directly regulated by androgen receptor to promote castration-resistance in prostate cancer.	Immunohistochemical staining	BMI1 is directly regulated by androgen receptor to promote castration-resistance in prostate cancer.			ChIP-seq,PCR,Western blot,凝胶电泳				BMI1
31462429	chr6	36591375	36593375	SRSF3	SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.	human,and,mouse	kidney	High+Lowthroughput	SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.	否	无	Tumour	HEK293T cell	E_02_0612	Western blot, gel electrophoresis, clip seq	SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.		SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.	Immunohistochemical staining	SRSF3-Regulated RNA Alternative Splicing Promotes Glioblastoma Tumorigenicity by Affecting Multiple Cellular Processes.			Western blot,凝胶电泳,CLIP-seq				SRSF3
31461843	chr20	3079786	3081786	AVP	Arginine-vasopressin (AVP) promotes muscle differentiation, hypertrophy, and regeneration through the combined activation of the calcineurin and Calcium/Calmodulin-dependent Protein Kinase (CaMK) pathways.	human,and,mouse	Myotome	High+Lowthroughput	Inhibition of Phosphoinositide 3-Kinase/Protein Kinase B Signaling Hampers the Vasopressin-dependent Stimulation of Myogenic Differentiation.	否	无	Neuromuscular diseases (certain neuromuscular disorders)	L6 cell	E_02_0613	PCR, Western blot, gene knockdown, gel electrophoresis	Arginine-vasopressin (AVP) promotes muscle differentiation, hypertrophy, and regeneration through the combined activation of the calcineurin and Calcium/Calmodulin-dependent Protein Kinase (CaMK) pathways.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Arginine-vasopressin (AVP) promotes muscle differentiation, hypertrophy, and regeneration through the combined activation of the calcineurin and Calcium/Calmodulin-dependent Protein Kinase (CaMK) pathways.		Arginine-vasopressin (AVP) promotes muscle differentiation, hypertrophy, and regeneration through the combined activation of the calcineurin and Calcium/Calmodulin-dependent Protein Kinase (CaMK) pathways.	Immunohistochemical staining	Arginine-vasopressin (AVP) promotes muscle differentiation, hypertrophy, and regeneration through the combined activation of the calcineurin and Calcium/Calmodulin-dependent Protein Kinase (CaMK) pathways.			PCR,Western blot,基因敲降,凝胶电泳				AVP
31461456	chr3	160396511	160398511	SMC4	ChIP-Seq was therefore performed on WT and sir2Δ strains in which the condensin subunit Smc4 was C-terminally tagged (13xMyc).	human,and,mouse		High+Lowthroughput	A Sir2-regulated locus control region in the recombination enhancer of Saccharomyces cerevisiae specifies chromosome III structure.	否	无	nothing	Haploid Cell	E_02_0614	PCR, Western blot, gel electrophoresis	ChIP-Seq was therefore performed on WT and sir2Δ strains in which the condensin subunit Smc4 was C-terminally tagged (13xMyc).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ChIP-Seq was therefore performed on WT and sir2Δ strains in which the condensin subunit Smc4 was C-terminally tagged (13xMyc).		ChIP-Seq was therefore performed on WT and sir2Δ strains in which the condensin subunit Smc4 was C-terminally tagged (13xMyc).	Immunohistochemical staining	ChIP-Seq was therefore performed on WT and sir2Δ strains in which the condensin subunit Smc4 was C-terminally tagged (13xMyc).			PCR,Western blot,凝胶电泳				SMC4
31456359	chr7	148804691	148806691	EZH2	The aims of this study were to investigate the link between enhancer  of zeste homolog 2 (EZH2) and histone deacetylase (HDAC) in preclinical studies  and in human lung cancer tissue microarrays.	human,and,mouse	lung	High+Lowthroughput	Oncogenic enhancer of zeste homolog 2 is an actionable target in patients with non-small cell lung cancer.	否	无	Lung adenocarcinoma	Lung adenocarcinoma cell	E_02_0615	PCR, Western blot, gel electrophoresis	The aims of this study were to investigate the link between enhancer  of zeste homolog 2 (EZH2) and histone deacetylase (HDAC) in preclinical studies  and in human lung cancer tissue microarrays.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The aims of this study were to investigate the link between enhancer  of zeste homolog 2 (EZH2) and histone deacetylase (HDAC) in preclinical studies  and in human lung cancer tissue microarrays.		The aims of this study were to investigate the link between enhancer  of zeste homolog 2 (EZH2) and histone deacetylase (HDAC) in preclinical studies  and in human lung cancer tissue microarrays.	Immunohistochemical staining	The aims of this study were to investigate the link between enhancer  of zeste homolog 2 (EZH2) and histone deacetylase (HDAC) in preclinical studies  and in human lung cancer tissue microarrays.			PCR,Western blot,凝胶电泳				EZH2
31455793	chr3	149159715	149161715	CP	At the heart  of the proteasome is the barrel-shaped 20S core particle (CP), which contains two β-rings sandwiched  between two α-rings.	human,and,mouse	Immunohistochem	High+Lowthroughput	Proteasome subunit α1 overexpression preferentially drives canonical proteasome biogenesis and enhances stress tolerance in yeast.	否	无	nothing	Immune cell	E_02_0616	Immunofluorescence staining, PCR, Western blot, gel electrophoresis	At the heart  of the proteasome is the barrel-shaped 20S core particle (CP), which contains two β-rings sandwiched  between two α-rings.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	At the heart  of the proteasome is the barrel-shaped 20S core particle (CP), which contains two β-rings sandwiched  between two α-rings.		At the heart  of the proteasome is the barrel-shaped 20S core particle (CP), which contains two β-rings sandwiched  between two α-rings.	Immunohistochemical staining	At the heart  of the proteasome is the barrel-shaped 20S core particle (CP), which contains two β-rings sandwiched  between two α-rings.			免疫荧光染色,PCR,Western blot,凝胶电泳				CP
31454988	chr9	127782849	127784849	CDK9	Transcription Repressor Hes1 Contributes to Neuropathic Pain Development by Modifying CDK9/RNAPII-Dependent Spinal mGluR5 Transcription.	mouse	Immunohistochem	High+Lowthroughput	Transcription Repressor Hes1 Contributes to Neuropathic Pain Development by Modifying CDK9/RNAPII-Dependent Spinal mGluR5 Transcription	否	无	Alzheimer's disease	Immune cell	E_02_0617	Knockdown, Western blot, PCR, gel electrophoresis	Transcription Repressor Hes1 Contributes to Neuropathic Pain Development by Modifying CDK9/RNAPII-Dependent Spinal mGluR5 Transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Transcription Repressor Hes1 Contributes to Neuropathic Pain Development by Modifying CDK9/RNAPII-Dependent Spinal mGluR5 Transcription.		Transcription Repressor Hes1 Contributes to Neuropathic Pain Development by Modifying CDK9/RNAPII-Dependent Spinal mGluR5 Transcription.	Immunohistochemical staining	Transcription Repressor Hes1 Contributes to Neuropathic Pain Development by Modifying CDK9/RNAPII-Dependent Spinal mGluR5 Transcription.			基因敲降,Western blot,PCR,凝胶电泳				CDK9
31452712	chr4	71739025	71741025	GC	Accumulating evidence suggests that the epigenetic  alterations caused by histone modifications have important  roles in the genesis of gastric cancer (GC), particularly the  well-studied acetylation and methylation modifications.	human,and,mouse	tumour	High+Lowthroughput	Comprehensive analysis of histone modification-associated genes on differential gene expression and prognosis in gastric cancer	否	无	Cancer (cancer)	glioma cell line	E_02_0618	Flow cytometry, PCR, gel electrophoresis	Accumulating evidence suggests that the epigenetic  alterations caused by histone modifications have important  roles in the genesis of gastric cancer (GC), particularly the  well-studied acetylation and methylation modifications.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Accumulating evidence suggests that the epigenetic  alterations caused by histone modifications have important  roles in the genesis of gastric cancer (GC), particularly the  well-studied acetylation and methylation modifications.		Accumulating evidence suggests that the epigenetic  alterations caused by histone modifications have important  roles in the genesis of gastric cancer (GC), particularly the  well-studied acetylation and methylation modifications.	Immunohistochemical staining	Accumulating evidence suggests that the epigenetic  alterations caused by histone modifications have important  roles in the genesis of gastric cancer (GC), particularly the  well-studied acetylation and methylation modifications.			流式细胞术,PCR,凝胶电泳				GC
31452712	chr6	151653994	151655994	ESR1	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.	human,and,mouse		High+Lowthroughput	Comprehensive analysis of histone modification-associated genes on differential gene expression and prognosis in gastric cancer	否	无	Cancer (cancer)		E_02_0618	Flow cytometry, PCR, gel electrophoresis	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.		Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.	Immunohistochemical staining	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.			流式细胞术,PCR,凝胶电泳				ESR1
31452712	chr19	49672955	49674955	PRMT1	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.	human,and,mouse		High+Lowthroughput	Comprehensive analysis of histone modification-associated genes on differential gene expression and prognosis in gastric cancer	否	无	Cancer (cancer)		E_02_0618	Flow cytometry, PCR, gel electrophoresis	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.		Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.	Immunohistochemical staining	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.			流式细胞术,PCR,凝胶电泳				PRMT1
31452712	chr2	24488304	24490304	NCOA1	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.	human,and,mouse		High+Lowthroughput	Comprehensive analysis of histone modification-associated genes on differential gene expression and prognosis in gastric cancer	否	无	Cancer (cancer)		E_02_0618	Flow cytometry, PCR, gel electrophoresis	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.		Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.	Immunohistochemical staining	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.			流式细胞术,PCR,凝胶电泳				NCOA1
31452712	chr17	42110322	42112322	KAT2A	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.	human,and,mouse		High+Lowthroughput	Comprehensive analysis of histone modification-associated genes on differential gene expression and prognosis in gastric cancer	否	无	Cancer (cancer)		E_02_0618	Flow cytometry, PCR, gel electrophoresis	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.		Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.	Immunohistochemical staining	Correlation analysis and protein-protein interaction network analysis  indicated a close association between ATAD2 and estrogen  receptor 1 (ESR1), PRMT1, NCOA1 and KAT2A.			流式细胞术,PCR,凝胶电泳				KAT2A
31451355	chr16	67559754	67561754	CTCF	CCCTC-binding factor (CTCF), cohesion (SMC1), and mediator (MED12) are the top three factors that have been reported as both essential for cellular functions and correlated with a specific looping interaction using chromosome conformation capture (3C) technology.	human	tumour	High+Lowthroughput	A Cohesin-Mediated Intrachromosomal Loop Drives Oncogenic ROR lncRNA to Accelerate Tumorigenesis	否	无	Cancer (cancer)	cancer cell	E_01_0888	Western blot, PCR, gel electrophoresis	CCCTC-binding factor (CTCF), cohesion (SMC1), and mediator (MED12) are the top three factors that have been reported as both essential for cellular functions and correlated with a specific looping interaction using chromosome conformation capture (3C) technology.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			CCCTC-binding factor (CTCF), cohesion (SMC1), and mediator (MED12) are the top three factors that have been reported as both essential for cellular functions and correlated with a specific looping interaction using chromosome conformation capture (3C) technology.	Immunohistochemical staining	CCCTC-binding factor (CTCF), cohesion (SMC1), and mediator (MED12) are the top three factors that have been reported as both essential for cellular functions and correlated with a specific looping interaction using chromosome conformation capture (3C) technology.	CTCF		Western blot,PCR,凝胶电泳	CCCTC-binding factor (CTCF), cohesion (SMC1), and mediator (MED12) are the top three factors that have been reported as both essential for cellular functions and correlated with a specific looping interaction using chromosome conformation capture (3C) technology.			
31451060	chr6	106042562	106044562	ATG5	m(6)A mRNA methylation controls autophagy and adipogenesis by targeting Atg5 and Atg7	human,and,mouse	embryo	High+Lowthroughput	m(6)A mRNA methylation controls autophagy and adipogenesis by targeting Atg5 and Atg7	否	无	Cancer (cancer)	3T3-L1 cell	E_02_0619	Knockdown, Western blot, PCR, gel electrophoresis	m(6)A mRNA methylation controls autophagy and adipogenesis by targeting Atg5 and Atg7	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	m(6)A mRNA methylation controls autophagy and adipogenesis by targeting Atg5 and Atg7		m(6)A mRNA methylation controls autophagy and adipogenesis by targeting Atg5 and Atg7	Immunohistochemical staining	m(6)A mRNA methylation controls autophagy and adipogenesis by targeting Atg5 and Atg7			基因敲降,Western blot,PCR,凝胶电泳				ATG5
31451060	chr3	11269426	11271426	ATG7	m(6)A mRNA methylation controls autophagy and adipogenesis by targeting Atg5 and Atg7	human,and,mouse	embryo	High+Lowthroughput	m(6)A mRNA methylation controls autophagy and adipogenesis by targeting Atg5 and Atg7	否	无	Cancer (cancer)	3T3-L1 cell	E_02_0619	Knockdown, Western blot, PCR, gel electrophoresis	m(6)A mRNA methylation controls autophagy and adipogenesis by targeting Atg5 and Atg7	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	m(6)A mRNA methylation controls autophagy and adipogenesis by targeting Atg5 and Atg7		m(6)A mRNA methylation controls autophagy and adipogenesis by targeting Atg5 and Atg7	Immunohistochemical staining	m(6)A mRNA methylation controls autophagy and adipogenesis by targeting Atg5 and Atg7			基因敲降,Western blot,PCR,凝胶电泳				ATG7
31445429	chr6	88137074	88139074	CNR1	Numerous studies have shown that expression of the gene encoding CB1 (CNR1) is highly dynamic with changes in the tissue specific expression of CNR1 associated with brain homeostasis and disease progression.	human,and,mouse		High+Lowthroughput	Disruption of an enhancer associated with addictive behaviour within the cannabinoid receptor-1 gene suggests a possible role in alcohol intake, cannabinoid response and anxiety-related behaviour	是	2023239	Cancer (cancer)	hippocampal neuron cell	E_02_0620	PCR, gel electrophoresis	Numerous studies have shown that expression of the gene encoding CB1 (CNR1) is highly dynamic with changes in the tissue specific expression of CNR1 associated with brain homeostasis and disease progression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Numerous studies have shown that expression of the gene encoding CB1 (CNR1) is highly dynamic with changes in the tissue specific expression of CNR1 associated with brain homeostasis and disease progression.		Numerous studies have shown that expression of the gene encoding CB1 (CNR1) is highly dynamic with changes in the tissue specific expression of CNR1 associated with brain homeostasis and disease progression.	Immunohistochemical staining	Numerous studies have shown that expression of the gene encoding CB1 (CNR1) is highly dynamic with changes in the tissue specific expression of CNR1 associated with brain homeostasis and disease progression.			PCR,凝胶电泳				CNR1
31444346	chr2	25157892	25159892	POMC	Two pituitary lineages express the hormone precursor pro_x005f_x0002_opiomelanocortin (POMC), the melanotropes and corticotropes.	human,and,mouse		High+Lowthroughput	Pioneer and nonpioneer factor cooperation drives lineage specific chromatin opening	否	无	Cushing disease (Cushing disease)	melanophore	E_02_0621	RNA-seq,ATAC-seq,ChIP-seq	Two pituitary lineages express the hormone precursor pro_x005f_x0002_opiomelanocortin (POMC), the melanotropes and corticotropes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Two pituitary lineages express the hormone precursor pro_x005f_x0002_opiomelanocortin (POMC), the melanotropes and corticotropes.		Two pituitary lineages express the hormone precursor pro_x005f_x0002_opiomelanocortin (POMC), the melanotropes and corticotropes.	Immunohistochemical staining	Two pituitary lineages express the hormone precursor pro_x005f_x0002_opiomelanocortin (POMC), the melanotropes and corticotropes.			RNA-seq,ATAC-seq,ChIP-seq				POMC
31444232	chr7	55016353	55018353	EGFR	Intron 1-Mediated Regulation of EGFR Expression in EGFR-Dependent Malignancies Is Mediated by AP-1 and BET Proteins.	human	Epithelial tissues	High+Lowthroughput	Intron 1-Mediated Regulation of EGFR Expression in EGFR-Dependent Malignancies Is Mediated by AP-1 and BET Proteins	否	无	Neck squamous cell carcinoma	Neck squamous epithelial cell	E_01_0889	Flow cytometry, Western blot, PCR, gel electrophoresis	Intron 1-Mediated Regulation of EGFR Expression in EGFR-Dependent Malignancies Is Mediated by AP-1 and BET Proteins.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Intron 1-Mediated Regulation of EGFR Expression in EGFR-Dependent Malignancies Is Mediated by AP-1 and BET Proteins.	Immunohistochemical staining	Intron 1-Mediated Regulation of EGFR Expression in EGFR-Dependent Malignancies Is Mediated by AP-1 and BET Proteins.	EGFR		流式细胞术,Western blot,PCR,凝胶电泳	Intron 1-Mediated Regulation of EGFR Expression in EGFR-Dependent Malignancies Is Mediated by AP-1 and BET Proteins.			
31443565	chr4	140556841	140558841	UCP1	This process, the non-shivering thermogenesis, is mediated by the mitochondrial uncoupling  protein 1 (UCP1), which shunts the proton circuit and leads to heat production instead of ATP.	human,and,mouse	embryo	High+Lowthroughput	Bitter Orange (Citrus aurantium Linné) Improves Obesity by Regulating Adipogenesis and Thermogenesis through AMPK Activation	否	无	Cardiovascular diseases (CVD)	3T3-L1 cell	E_02_0622	Western blot, PCR, gel electrophoresis	This process, the non-shivering thermogenesis, is mediated by the mitochondrial uncoupling  protein 1 (UCP1), which shunts the proton circuit and leads to heat production instead of ATP.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	This process, the non-shivering thermogenesis, is mediated by the mitochondrial uncoupling  protein 1 (UCP1), which shunts the proton circuit and leads to heat production instead of ATP.		This process, the non-shivering thermogenesis, is mediated by the mitochondrial uncoupling  protein 1 (UCP1), which shunts the proton circuit and leads to heat production instead of ATP.	Immunohistochemical staining	This process, the non-shivering thermogenesis, is mediated by the mitochondrial uncoupling  protein 1 (UCP1), which shunts the proton circuit and leads to heat production instead of ATP.			Western blot,PCR,凝胶电泳				UCP1
31441598	chr11	18263505	18265505	SAA1	We reported earlier that the acute-phase protein serum amyloid A1 (SAA1) is increased and accumulates in muscle of ICUAW patients, but its relevance was unknown.	human	tumour	High+Lowthroughput	Serum amyloid A1 mediates myotube atrophy via Toll-like receptors	否	无	Cancer (cancer)	cancer cell	E_01_0890	Western blot, PCR, gel electrophoresis	We reported earlier that the acute-phase protein serum amyloid A1 (SAA1) is increased and accumulates in muscle of ICUAW patients, but its relevance was unknown.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We reported earlier that the acute-phase protein serum amyloid A1 (SAA1) is increased and accumulates in muscle of ICUAW patients, but its relevance was unknown.		We reported earlier that the acute-phase protein serum amyloid A1 (SAA1) is increased and accumulates in muscle of ICUAW patients, but its relevance was unknown.	Immunohistochemical staining	We reported earlier that the acute-phase protein serum amyloid A1 (SAA1) is increased and accumulates in muscle of ICUAW patients, but its relevance was unknown.			Western blot,PCR,凝胶电泳				SAA1
31441382	chr5	179803964	179805964	SQSTM1	SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence.	human	Myotome	High+Lowthroughput	SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence	否	无	Alzheimer disease	muscle cell	E_01_0891	Knockdown, Western blot, PCR, gel electrophoresis	SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence.		SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence.	Immunohistochemical staining	SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence.			基因敲降,Western blot,PCR,凝胶电泳				SQSTM1
31441382	chr4	23752069	23754069	PPARGC1A	SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence.	human	Myotome	High+Lowthroughput	SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence	否	无	Alzheimer disease	muscle cell	E_01_0891	Knockdown, Western blot, PCR, gel electrophoresis	SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence.	Immunohistochemical staining	SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence.	PPARGC1A		基因敲降,Western blot,PCR,凝胶电泳	SQSTM1/p62 and PPARGC1A/PGC-1alpha at the interface of autophagy and vascular senescence.			
31432184	chr3	38136163	38138163	MYD88	Disrupting myddosome assembly in diffuse large B?cell lymphoma cells using the MYD88 dimerization inhibitor ST2825.	human	lymph	High+Lowthroughput	Disrupting myddosome assembly in diffuse large B?cell lymphoma cells using the MYD88 dimerization inhibitor ST2825	否	无	Cancer (cancer)	Diffuse large B-cell lymphoma	E_01_0892	Immunofluorescence staining, Western blot, PCR, gel electrophoresis	Disrupting myddosome assembly in diffuse large B?cell lymphoma cells using the MYD88 dimerization inhibitor ST2825.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Disrupting myddosome assembly in diffuse large B?cell lymphoma cells using the MYD88 dimerization inhibitor ST2825.		Disrupting myddosome assembly in diffuse large B?cell lymphoma cells using the MYD88 dimerization inhibitor ST2825.	Immunohistochemical staining	Disrupting myddosome assembly in diffuse large B?cell lymphoma cells using the MYD88 dimerization inhibitor ST2825.			免疫荧光染色,Western blot,PCR,凝胶电泳				MYD88
31431927	chr4	122448607	122450607	IL2	Melibiosamine, a novel oligosaccharide, suppresses mitogen-induced IL-2 production via inactivation of NFAT and NFκB in Jurkat cells.	human		High+Lowthroughput	Melibiosamine, a novel oligosaccharide, suppresses mitogen-induced IL-2 production via inactivation of NFAT and NFκB in Jurkat cells	否	无	Leukemia	Jurkat cell	E_01_0893	Western blot, PCR, gel electrophoresis	Melibiosamine, a novel oligosaccharide, suppresses mitogen-induced IL-2 production via inactivation of NFAT and NFκB in Jurkat cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Melibiosamine, a novel oligosaccharide, suppresses mitogen-induced IL-2 production via inactivation of NFAT and NFκB in Jurkat cells.	Immunohistochemical staining	Melibiosamine, a novel oligosaccharide, suppresses mitogen-induced IL-2 production via inactivation of NFAT and NFκB in Jurkat cells.	IL2		Western blot,PCR,凝胶电泳	Melibiosamine, a novel oligosaccharide, suppresses mitogen-induced IL-2 production via inactivation of NFAT and NFκB in Jurkat cells.			
31431802	chr3	181709285	181711285	SOX2	Sox2-Dependent 3D Chromatin Interactomes in Transcription, Neural Stem Cell Proliferation and Neurodevelopmental Diseases.	human	Nervous tissue	High+Lowthroughput	Sox2-Dependent 3D Chromatin Interactomes in Transcription, Neural Stem Cell Proliferation and Neurodevelopmental Diseases	否	无	Neural disease (CNS disease)	neural stem cell	E_01_0894	ChIP-seq	Sox2-Dependent 3D Chromatin Interactomes in Transcription, Neural Stem Cell Proliferation and Neurodevelopmental Diseases.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Sox2-Dependent 3D Chromatin Interactomes in Transcription, Neural Stem Cell Proliferation and Neurodevelopmental Diseases.	Immunohistochemical staining	Sox2-Dependent 3D Chromatin Interactomes in Transcription, Neural Stem Cell Proliferation and Neurodevelopmental Diseases.	SOX2		ChIP-seq	Sox2-Dependent 3D Chromatin Interactomes in Transcription, Neural Stem Cell Proliferation and Neurodevelopmental Diseases.			
31431624	chr2	113213024	113215024	PAX8	PAX8 activates metabolic genes via enhancer elements in Renal Cell Carcinoma.	human,and,mouse	kidney	High+Lowthroughput	PAX8 activates metabolic genes via enhancer elements in Renal Cell Carcinoma	是	无	Kidney disease	renal cell	E_02_0623	RNA SEQ, ATAC SEQ, chip SEQ, PCR, gel electrophoresis	PAX8 activates metabolic genes via enhancer elements in Renal Cell Carcinoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	PAX8 activates metabolic genes via enhancer elements in Renal Cell Carcinoma.		PAX8 activates metabolic genes via enhancer elements in Renal Cell Carcinoma.	Immunohistochemical staining	PAX8 activates metabolic genes via enhancer elements in Renal Cell Carcinoma.			RNA-seq,ATAC-seq,ChIP-seq,PCR,凝胶电泳				PAX8
31430278	chr17	76709990	76711990	JMJD6	Promotion of adipogenesis by JMJD6 requires the AT hook-like domain and is independent of its catalytic function.	human,and,mouse		High+Lowthroughput	Promotion of adipogenesis by JMJD6 requires the AT hook-like domain and is independent of its catalytic function	否	无	nothing	HEK293 cell	E_02_0624	Western blot, PCR, gel electrophoresis	Promotion of adipogenesis by JMJD6 requires the AT hook-like domain and is independent of its catalytic function.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Promotion of adipogenesis by JMJD6 requires the AT hook-like domain and is independent of its catalytic function.		Promotion of adipogenesis by JMJD6 requires the AT hook-like domain and is independent of its catalytic function.	Immunohistochemical staining	Promotion of adipogenesis by JMJD6 requires the AT hook-like domain and is independent of its catalytic function.			Western blot,PCR,凝胶电泳				JMJD6
31428587	chr5	68213148	68215148	PIK3R1	Amongst these genes, PIK3R1 encodes for regulatory subunit alpha of PI3-Kinase, p85α.	human	prostate	High+Lowthroughput	LSD1 Activates PI3K/AKT Signaling Through Regulating p85 Expression in Prostate Cancer Cells	否	无	Prostate disease (prostate cancer)	LNCaP cell	E_01_0895	RNA SEQ, chip SEQ, PCR, gel electrophoresis, Western blot	Amongst these genes, PIK3R1 encodes for regulatory subunit alpha of PI3-Kinase, p85α.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Amongst these genes, PIK3R1 encodes for regulatory subunit alpha of PI3-Kinase, p85α.		Amongst these genes, PIK3R1 encodes for regulatory subunit alpha of PI3-Kinase, p85α.	Immunohistochemical staining	Amongst these genes, PIK3R1 encodes for regulatory subunit alpha of PI3-Kinase, p85α.			RNA-seq,ChIP-seq,PCR,凝胶电泳,Western blot				PIK3R1
31423236	chr1	153659151	153661151	ILF2	ILF2 promotes anchorage independence through direct regulation of PTEN.	human,and,mouse	tumour	High+Lowthroughput	ILF2 promotes anchorage independence through direct regulation of PTEN	否	无	Lung cancr (lung cancer)	cancer cell	E_02_0625	Western blot, PCR, gel electrophoresis	ILF2 promotes anchorage independence through direct regulation of PTEN.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ILF2 promotes anchorage independence through direct regulation of PTEN.		ILF2 promotes anchorage independence through direct regulation of PTEN.	Immunohistochemical staining	ILF2 promotes anchorage independence through direct regulation of PTEN.			Western blot,PCR,凝胶电泳				ILF2
31423236	chr10	87859816	87861816	PTEN	ILF2 promotes anchorage independence through direct regulation of PTEN.	human,and,mouse	tumour	High+Lowthroughput	ILF2 promotes anchorage independence through direct regulation of PTEN	否	无	Lung cancr (lung cancer)	cancer cell	E_02_0625	Western blot, PCR, gel electrophoresis	ILF2 promotes anchorage independence through direct regulation of PTEN.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ILF2 promotes anchorage independence through direct regulation of PTEN.		ILF2 promotes anchorage independence through direct regulation of PTEN.	Immunohistochemical staining	ILF2 promotes anchorage independence through direct regulation of PTEN.			Western blot,PCR,凝胶电泳				PTEN
31423206	chr7	148804518	148806518	EZH2	The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.	human		High+Lowthroughput	Clinical significance of enhancer of zeste homolog 2 and histone deacetylases 1 and 2 expression in peripheral T-cell lymphoma	否	无	nothing	NK cell	E_01_0896		The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.	Immunohistochemical staining	The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.	EZH2			The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.			
31423206	chr1	32289108	32291108	HDAC1	The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.	human		High+Lowthroughput	Clinical significance of enhancer of zeste homolog 2 and histone deacetylases 1 and 2 expression in peripheral T-cell lymphoma	否	无	nothing	NK cell	E_01_0896		The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.	Immunohistochemical staining	The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.	HDAC1			The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.			
31423206	chr6	113930181	113932181	HDAC2	The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.	human		High+Lowthroughput	Clinical significance of enhancer of zeste homolog 2 and histone deacetylases 1 and 2 expression in peripheral T-cell lymphoma	否	无	nothing	NK cell	E_01_0896		The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.		The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.	Immunohistochemical staining	The purpose of the present study was  to investigate the clinical significance of enhancer of zeste  homolog 2 (EZH2) and histone deacetylase 1 and 2 (HDAC1/2)  expression in PTCL.							HDAC2
31422875	chr17	39401623	39403623	MED1	Dynamic DNA methylation is co-regulated with MED1 recruitment and H3K27ac level.	human		High+Lowthroughput	Dynamic Enhancer DNA Methylation as Basis for Transcriptional and Cellular Heterogeneity of ESCs	是	无	Cancer (cancer)	embryonic stem cell	E_01_0897	Flow cytometry, gene knockdown, PCR, chip SEQ, RNA seq	Dynamic DNA methylation is co-regulated with MED1 recruitment and H3K27ac level.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Dynamic DNA methylation is co-regulated with MED1 recruitment and H3K27ac level.	Immunohistochemical staining	Dynamic DNA methylation is co-regulated with MED1 recruitment and H3K27ac level.	MED1		流式细胞术,基因敲降,PCR,ChIP-seq,RNA-seq	Dynamic DNA methylation is co-regulated with MED1 recruitment and H3K27ac level.			
31420918	chr2	45002618	45004618	SIX2	Transcription factor Six2 induces a stem cell-like phenotype in renal cell carcinoma cells	human	kidney	High+Lowthroughput	Transcription factor Six2 induces a stem cell-like phenotype in renal cell carcinoma cells	否	无	Renal cell carcinoma	renal cell	E_01_0898	Western blot, PCR, gel electrophoresis	Transcription factor Six2 induces a stem cell-like phenotype in renal cell carcinoma cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Transcription factor Six2 induces a stem cell-like phenotype in renal cell carcinoma cells		Transcription factor Six2 induces a stem cell-like phenotype in renal cell carcinoma cells	Immunohistochemical staining	Transcription factor Six2 induces a stem cell-like phenotype in renal cell carcinoma cells			Western blot,PCR,凝胶电泳				SIX2
31420455	chr1	156460657	156462657	MEF2D	Neuronal Myocyte-Specific Enhancer Factor 2D (MEF2D) Is Required for Normal Circadian and Sleep Behavior in Mice.	mouse		High+Lowthroughput	Neuronal Myocyte-Specific Enhancer Factor 2D (MEF2D) Is Required for Normal Circadian and Sleep Behavior in Mice	否	无	nothing	HEK293A cell	E_02_0626	PCR, gel electrophoresis	Neuronal Myocyte-Specific Enhancer Factor 2D (MEF2D) Is Required for Normal Circadian and Sleep Behavior in Mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Neuronal Myocyte-Specific Enhancer Factor 2D (MEF2D) Is Required for Normal Circadian and Sleep Behavior in Mice.		Neuronal Myocyte-Specific Enhancer Factor 2D (MEF2D) Is Required for Normal Circadian and Sleep Behavior in Mice.	Immunohistochemical staining	Neuronal Myocyte-Specific Enhancer Factor 2D (MEF2D) Is Required for Normal Circadian and Sleep Behavior in Mice.			PCR,凝胶电泳				MEF2D
31419226	chr7	148803950	148805950	EZH2	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	human	lymph	High+Lowthroughput	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations	否	无	Cancer (cancer)	lymphoma cell	E_01_0899	PCR, gel electrophoresis	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	Immunohistochemical staining	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	EZH2		PCR,凝胶电泳	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.			
31419226	chr8	127732563	127734563	MYC	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	human	lymph	High+Lowthroughput	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations	否	无	Cancer (cancer)	lymphoma cell	E_01_0899	PCR, gel electrophoresis	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	Immunohistochemical staining	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	MYC		PCR,凝胶电泳	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.			
31419226	chr18	63120577	63122577	BCL2	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	human	lymph	High+Lowthroughput	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations	否	无	Cancer (cancer)	lymphoma cell	E_01_0899	PCR, gel electrophoresis	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	Immunohistochemical staining	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	BCL2		PCR,凝胶电泳	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.			
31419226	chr3	187719120	187721120	BCL6	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	human	lymph	High+Lowthroughput	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations	否	无	Cancer (cancer)	lymphoma cell	E_01_0899	PCR, gel electrophoresis	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	Immunohistochemical staining	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.	BCL6		PCR,凝胶电泳	DZNep-mediated apoptosis in B-cell lymphoma is independent of the lymphoma type, EZH2 mutation status and MYC, BCL2 or BCL6 translocations.			
31417366	chr5	102751125	102753125	PAM	The sgRNA we designed showed high efficiency to guide Cas9 to the PAM sequence, as we observed all editing occurred 30 downstream from the PAM site.	human,and,mouse		High+Lowthroughput	Functional Dissection of C. elegans bZip-Protein CEBP-1 Reveals Novel Structural Motifs Required for Axon Regeneration and Nuclear Import	否	无	Cancer (cancer)	somatic cell	E_02_0627	Gene knockdown	The sgRNA we designed showed high efficiency to guide Cas9 to the PAM sequence, as we observed all editing occurred 30 downstream from the PAM site.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The sgRNA we designed showed high efficiency to guide Cas9 to the PAM sequence, as we observed all editing occurred 30 downstream from the PAM site.		The sgRNA we designed showed high efficiency to guide Cas9 to the PAM sequence, as we observed all editing occurred 30 downstream from the PAM site.	Immunohistochemical staining	The sgRNA we designed showed high efficiency to guide Cas9 to the PAM sequence, as we observed all editing occurred 30 downstream from the PAM site.			基因敲降				PAM
31415587	chr20	46005862	46007862	MMP9	Occludin de_x005f_x0002_gradation and matrix metalloproteinase-9 (MMP-9) activity were significantly increased in infected mice than in uninfected mice.	human,and,mouse	Epithelial tissues	High+Lowthroughput	Proteasome serves as pivotal regulator in Angiostrongylus cantonensis-induced eosinophilic meningoencephalitis	否	无	Meningoencephalitis (viral meningoencephalitis)	epithelial cell	E_02_0628	Knockdown, Western blot, PCR, gel electrophoresis	Occludin de_x005f_x0002_gradation and matrix metalloproteinase-9 (MMP-9) activity were significantly increased in infected mice than in uninfected mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Occludin de_x005f_x0002_gradation and matrix metalloproteinase-9 (MMP-9) activity were significantly increased in infected mice than in uninfected mice.		Occludin de_x005f_x0002_gradation and matrix metalloproteinase-9 (MMP-9) activity were significantly increased in infected mice than in uninfected mice.	Immunohistochemical staining	Occludin de_x005f_x0002_gradation and matrix metalloproteinase-9 (MMP-9) activity were significantly increased in infected mice than in uninfected mice.			基因敲降,Western blot,PCR,凝胶电泳				MMP9
31415393	chr20	50188140	50190140	CEBPB	The crucial genes Signal transducer and activator of transcription 5A (STAT5A), CCAAT/enhancer-binding protein beta (CEBPB), Myc proto-oncogene protein (MYC), and REL-associated protein (RELA) were identified and showed increased expression in sepsis survivors.	human	Immune cells	High+Lowthroughput	Identifying crucial genes for prognosis in septic patients: Gene integration study based on PRISMA guidelines	否	无	Infectious disease	NK cell	E_01_0900	Flow cytometry	The crucial genes Signal transducer and activator of transcription 5A (STAT5A), CCAAT/enhancer-binding protein beta (CEBPB), Myc proto-oncogene protein (MYC), and REL-associated protein (RELA) were identified and showed increased expression in sepsis survivors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The crucial genes Signal transducer and activator of transcription 5A (STAT5A), CCAAT/enhancer-binding protein beta (CEBPB), Myc proto-oncogene protein (MYC), and REL-associated protein (RELA) were identified and showed increased expression in sepsis survivors.	Immunohistochemical staining	The crucial genes Signal transducer and activator of transcription 5A (STAT5A), CCAAT/enhancer-binding protein beta (CEBPB), Myc proto-oncogene protein (MYC), and REL-associated protein (RELA) were identified and showed increased expression in sepsis survivors.	CEBPB		流式细胞术	The crucial genes Signal transducer and activator of transcription 5A (STAT5A), CCAAT/enhancer-binding protein beta (CEBPB), Myc proto-oncogene protein (MYC), and REL-associated protein (RELA) were identified and showed increased expression in sepsis survivors.			
31413586	chr4	98876674	98878674	EIF4E	AEG-1 promotes the growth of gastric cancer through the upregulation of eIF4E expression.	human,and,mouse	stomach	High+Lowthroughput	AEG-1 promotes the growth of gastric cancer through the upregulation of eIF4E expression	否	无	Gastric cancer	SGC-7901 cell	E_02_0629	Western blot, PCR, gel electrophoresis	AEG-1 promotes the growth of gastric cancer through the upregulation of eIF4E expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	AEG-1 promotes the growth of gastric cancer through the upregulation of eIF4E expression.		AEG-1 promotes the growth of gastric cancer through the upregulation of eIF4E expression.	Immunohistochemical staining	AEG-1 promotes the growth of gastric cancer through the upregulation of eIF4E expression.			Western blot,PCR,凝胶电泳				EIF4E
31413151	chr14	95083182	95085182	DICER1	We also observed distinct expres_x005f_x0002_sion patterns for Alu elements in specific tissue types (e.g., testis) (Supplemental Fig. S5D,E) or associated with specific factors (e.g., DICER1) (Supplemental Material).	human		High+Lowthroughput	Genome-wide analysis of polymerase III-transcribed Alu elements suggests cell-type-specific enhancer function	否	无	Leukemia	somatic cell	E_01_0901	RNA SEQ, chip SEQ, PCR, gel electrophoresis	We also observed distinct expres_x005f_x0002_sion patterns for Alu elements in specific tissue types (e.g., testis) (Supplemental Fig. S5D,E) or associated with specific factors (e.g., DICER1) (Supplemental Material).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We also observed distinct expres_x005f_x0002_sion patterns for Alu elements in specific tissue types (e.g., testis) (Supplemental Fig. S5D,E) or associated with specific factors (e.g., DICER1) (Supplemental Material).	Immunohistochemical staining	We also observed distinct expres_x005f_x0002_sion patterns for Alu elements in specific tissue types (e.g., testis) (Supplemental Fig. S5D,E) or associated with specific factors (e.g., DICER1) (Supplemental Material).	DICER1		RNA-seq,ChIP-seq,PCR,凝胶电泳	We also observed distinct expres_x005f_x0002_sion patterns for Alu elements in specific tissue types (e.g., testis) (Supplemental Fig. S5D,E) or associated with specific factors (e.g., DICER1) (Supplemental Material).			
31413137	chr5	179611470	179613470	HNRNPH1	HnRNPH1 depletion and mutation of a prominent viral RNA hnRNPH1 binding site decreased use of splice acceptor A1, causing a deficit in Vif expression and replicative fitness.	human,and,mouse	kidney	High+Lowthroughput	Genome-Wide Analysis of Heterogeneous Nuclear Ribonucleoprotein (hnRNP) Binding to HIV-1 RNA Reveals a Key Role for hnRNP H1 in Alternative Viral mRNA Splicing	否	无	Leukemia	HEK293T cell	E_02_0630	Clip SEQ, PCR, Western blot, gel electrophoresis	HnRNPH1 depletion and mutation of a prominent viral RNA hnRNPH1 binding site decreased use of splice acceptor A1, causing a deficit in Vif expression and replicative fitness.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HnRNPH1 depletion and mutation of a prominent viral RNA hnRNPH1 binding site decreased use of splice acceptor A1, causing a deficit in Vif expression and replicative fitness.		HnRNPH1 depletion and mutation of a prominent viral RNA hnRNPH1 binding site decreased use of splice acceptor A1, causing a deficit in Vif expression and replicative fitness.	Immunohistochemical staining	HnRNPH1 depletion and mutation of a prominent viral RNA hnRNPH1 binding site decreased use of splice acceptor A1, causing a deficit in Vif expression and replicative fitness.			CLIP-seq,PCR,Western blot,凝胶电泳				HNRNPH1
31413137	chr12	54277146	54279146	HNRNPA1	Notably, hnRNPA1, hnRNPA2 and hnRNPB1 bound to many dispersed sites across viral mRNAs.	human,and,mouse	lymph	High+Lowthroughput	Genome-Wide Analysis of Heterogeneous Nuclear Ribonucleoprotein (hnRNP) Binding to HIV-1 RNA Reveals a Key Role for hnRNP H1 in Alternative Viral mRNA Splicing	否	无	Leukemia	MT4 cell	E_02_0630	Clip SEQ, PCR, Western blot, gel electrophoresis	Notably, hnRNPA1, hnRNPA2 and hnRNPB1 bound to many dispersed sites across viral mRNAs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Notably, hnRNPA1, hnRNPA2 and hnRNPB1 bound to many dispersed sites across viral mRNAs.		Notably, hnRNPA1, hnRNPA2 and hnRNPB1 bound to many dispersed sites across viral mRNAs.	Immunohistochemical staining	Notably, hnRNPA1, hnRNPA2 and hnRNPB1 bound to many dispersed sites across viral mRNAs.			CLIP-seq,PCR,Western blot,凝胶电泳				HNRNPA1
31412725	chr2	42491888	42493888	MTA3	The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.	human,and,mouse	Epithelial tissues	High+Lowthroughput	Nuclear S-Nitrosylation Defines an Optimal Zone for Inducing Pluripotency	否	无	Lung disease	endothelial cell	E_02_0631	PCR, Western blot, gel electrophoresis	The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.		The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.	Immunohistochemical staining	The effect of NO on DNA accessibility is mediated in part by S_x005f_x0002_nitrosylation of nuclear proteins, including MTA3, a subunit of Nucleosome Remodeling  Deacetylase (NuRD) complex.			PCR,Western blot,凝胶电泳				MTA3
31412252	chr3	181709008	181711008	SOX2	p63 and SOX2 Dictate Glucose Reliance and Metabolic Vulnerabilities in Squamous Cell Carcinomas.	human,and,mouse	Epithelial tissues	High+Lowthroughput	p63 and SOX2 Dictate Glucose Reliance and Metabolic Vulnerabilities in Squamous Cell Carcinomas	否	无	Cancer (cancer)	squamous cell(pinacocyte)	E_02_0632	Chip SEQ, RNA SEQ, gene knockdown, PCR, Western blot, gel electrophoresis	p63 and SOX2 Dictate Glucose Reliance and Metabolic Vulnerabilities in Squamous Cell Carcinomas.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	p63 and SOX2 Dictate Glucose Reliance and Metabolic Vulnerabilities in Squamous Cell Carcinomas.		p63 and SOX2 Dictate Glucose Reliance and Metabolic Vulnerabilities in Squamous Cell Carcinomas.	Immunohistochemical staining	p63 and SOX2 Dictate Glucose Reliance and Metabolic Vulnerabilities in Squamous Cell Carcinomas.			ChIP-seq,RNA-seq,基因敲降,PCR,Western blot,凝胶电泳				SOX2
31410149	chr4	108045179	108047179	LEF1	MicroRNA-6852 suppresses glioma A172 cell proliferation and invasion by targeting LEF1.	human		High+Lowthroughput	MicroRNA-6852 suppresses glioma A172 cell proliferation and invasion by targeting LEF1	否	无	Cancer (cancer)	glioblastoma cell	E_01_0902	PCR, gel electrophoresis	MicroRNA-6852 suppresses glioma A172 cell proliferation and invasion by targeting LEF1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			MicroRNA-6852 suppresses glioma A172 cell proliferation and invasion by targeting LEF1.	Immunohistochemical staining	MicroRNA-6852 suppresses glioma A172 cell proliferation and invasion by targeting LEF1.	LEF1		PCR,凝胶电泳	MicroRNA-6852 suppresses glioma A172 cell proliferation and invasion by targeting LEF1.			
31409603	chr22	30237461	30239461	LIF	We found widespread and pervasive alterations  of the (super)-enhancer reservoir in both subtypes of  oesophageal cancer, leading to transcriptional activation  of a myriad of novel oncogenes and signalling pathways,  some of which may be exploited pharmacologically (eg,  leukemia inhibitory factor (LIF) pathway).	human,and,mouse	Epithelial tissues	High+Lowthroughput	Master transcription factors form interconnected circuitry and orchestrate transcriptional networks in oesophageal adenocarcinoma	否	无	Digestive disease	squamous cell(pinacocyte)	E_02_0633	ATAC SEQ, chip SEQ, PCR, Western blot, gel electrophoresis	We found widespread and pervasive alterations  of the (super)-enhancer reservoir in both subtypes of  oesophageal cancer, leading to transcriptional activation  of a myriad of novel oncogenes and signalling pathways,  some of which may be exploited pharmacologically (eg,  leukemia inhibitory factor (LIF) pathway).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found widespread and pervasive alterations  of the (super)-enhancer reservoir in both subtypes of  oesophageal cancer, leading to transcriptional activation  of a myriad of novel oncogenes and signalling pathways,  some of which may be exploited pharmacologically (eg,  leukemia inhibitory factor (LIF) pathway).		We found widespread and pervasive alterations  of the (super)-enhancer reservoir in both subtypes of  oesophageal cancer, leading to transcriptional activation  of a myriad of novel oncogenes and signalling pathways,  some of which may be exploited pharmacologically (eg,  leukemia inhibitory factor (LIF) pathway).	Immunohistochemical staining	We found widespread and pervasive alterations  of the (super)-enhancer reservoir in both subtypes of  oesophageal cancer, leading to transcriptional activation  of a myriad of novel oncogenes and signalling pathways,  some of which may be exploited pharmacologically (eg,  leukemia inhibitory factor (LIF) pathway).			ATAC-seq,ChIP-seq,PCR,Western blot,凝胶电泳				LIF
31408468	chr10	100732618	100734618	PAX2	In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.	human,and,mouse	Epithelial tissues	High+Lowthroughput	The genomic landscape of estrogen receptor α binding sites in mouse mammary gland	否	无	Breast cancer (breast cancer)	epithelial cell	E_02_0634	RNA-seq,ChIP-seq	In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.		In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.	Immunohistochemical staining	In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.			RNA-seq,ChIP-seq				PAX2
31408468	chr14	76307838	76309838	ESRRB	In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.	human,and,mouse	Epithelial tissues	High+Lowthroughput	The genomic landscape of estrogen receptor α binding sites in mouse mammary gland	否	无	Breast cancer (breast cancer)	epithelial cell	E_02_0634	RNA-seq,ChIP-seq	In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.		In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.	Immunohistochemical staining	In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.			RNA-seq,ChIP-seq				ESRRB
31408468	chr11	64762102	64764102	SF1	In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.	human,and,mouse	Epithelial tissues	High+Lowthroughput	The genomic landscape of estrogen receptor α binding sites in mouse mammary gland	否	无	Breast cancer (breast cancer)	epithelial cell	E_02_0634	RNA-seq,ChIP-seq	In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.		In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.	Immunohistochemical staining	In the distal regions (up and down) of ERα binding sites contained a canonical ERE and other motifs including PAX2, ESRRB, SF1, and AP1 motifs as the most highly enriched (p-value <10−30) cis-elements.			RNA-seq,ChIP-seq				SF1
31406377	chr6	106967367	106969367	CD24	BM from Zbtb46gfp/+ mice was analyzed by flow cytometry  to identify pre-cDC1s as defined by Zbtb46–GFP or CD24 expression.	human,and,mouse	Immunohistochem	High+Lowthroughput	An Nfil3-Zeb2-Id2 pathway imposes Irf8 enhancer switching during cDC1 development	否	无	Cancer (cancer)	dendritic cell	E_02_0635	Flow cytometry, ATAC SEQ, RNA SEQ, scrna seq	BM from Zbtb46gfp/+ mice was analyzed by flow cytometry  to identify pre-cDC1s as defined by Zbtb46–GFP or CD24 expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	BM from Zbtb46gfp/+ mice was analyzed by flow cytometry  to identify pre-cDC1s as defined by Zbtb46–GFP or CD24 expression.		BM from Zbtb46gfp/+ mice was analyzed by flow cytometry  to identify pre-cDC1s as defined by Zbtb46–GFP or CD24 expression.	Immunohistochemical staining	BM from Zbtb46gfp/+ mice was analyzed by flow cytometry  to identify pre-cDC1s as defined by Zbtb46–GFP or CD24 expression.			流式细胞术,ATAC-seq,RNA-seq,scRNA-seq				CD24
31406023	chr8	132864337	132866337	TG	Moreover, inhibition of ER stress by 4-phenylbutyrate (4-PBA) attenuated thapsigargin-(TG, ER stress agonist) or LPS-induced reduction of Cyp19al and E2, pro-inflammatory cytokines expression (IL-1β, IL-6, IL-8, and TNF-a), and the expression of CHOP and GRP78.  	human,and,mouse		High+Lowthroughput	Role of endoplasmic reticulum stress in lipopolysaccharide-inhibited mouse granulosa cell estradiol production	否	无	Metabolic disease (metabolic disease)	granulosa cell	E_02_0636	PCR, Western blot, gel electrophoresis	Moreover, inhibition of ER stress by 4-phenylbutyrate (4-PBA) attenuated thapsigargin-(TG, ER stress agonist) or LPS-induced reduction of Cyp19al and E2, pro-inflammatory cytokines expression (IL-1β, IL-6, IL-8, and TNF-a), and the expression of CHOP and GRP78.  	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Moreover, inhibition of ER stress by 4-phenylbutyrate (4-PBA) attenuated thapsigargin-(TG, ER stress agonist) or LPS-induced reduction of Cyp19al and E2, pro-inflammatory cytokines expression (IL-1β, IL-6, IL-8, and TNF-a), and the expression of CHOP and GRP78.  		Moreover, inhibition of ER stress by 4-phenylbutyrate (4-PBA) attenuated thapsigargin-(TG, ER stress agonist) or LPS-induced reduction of Cyp19al and E2, pro-inflammatory cytokines expression (IL-1β, IL-6, IL-8, and TNF-a), and the expression of CHOP and GRP78.  	Immunohistochemical staining	Moreover, inhibition of ER stress by 4-phenylbutyrate (4-PBA) attenuated thapsigargin-(TG, ER stress agonist) or LPS-induced reduction of Cyp19al and E2, pro-inflammatory cytokines expression (IL-1β, IL-6, IL-8, and TNF-a), and the expression of CHOP and GRP78.  			PCR,Western blot,凝胶电泳				TG
31405024	chr21	41461360	41463360	TMPRSS2	Androgen Receptor-Activated Enhancers Simultaneously Regulate Oncogene TMPRSS2 and lncRNA PRCAT38 in Prostate Cancer.	human,and,mouse	prostate	High+Lowthroughput	Androgen Receptor-Activated Enhancers Simultaneously Regulate Oncogene TMPRSS2 and lncRNA PRCAT38 in Prostate Cancer	是	无	Prostate cancer	prostate cancer cell	E_02_0637	Chip SEQ, PCR, Western blot, gel electrophoresis	Androgen Receptor-Activated Enhancers Simultaneously Regulate Oncogene TMPRSS2 and lncRNA PRCAT38 in Prostate Cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Androgen Receptor-Activated Enhancers Simultaneously Regulate Oncogene TMPRSS2 and lncRNA PRCAT38 in Prostate Cancer.		Androgen Receptor-Activated Enhancers Simultaneously Regulate Oncogene TMPRSS2 and lncRNA PRCAT38 in Prostate Cancer.	Immunohistochemical staining	Androgen Receptor-Activated Enhancers Simultaneously Regulate Oncogene TMPRSS2 and lncRNA PRCAT38 in Prostate Cancer.			ChIP-seq,PCR,Western blot,凝胶电泳				TMPRSS2
31402092	chr3	133743447	133745447	TF	Functional annotation was evaluated via epigenetic data, including DNase I hypersensitive sites and TF ChIP-seq binding peaks, from both ENCODE and Roadmap.	human	Epithelial tissues	High+Lowthroughput	Identifying Putative Susceptibility Genes and Evaluating Their Associations with Somatic Mutations in Human Cancers	是	7902587	Cancer (cancer)	Squamous cell	E_01_0903	Chip SEQ, RNA SEQ, PCR, gel electrophoresis	Functional annotation was evaluated via epigenetic data, including DNase I hypersensitive sites and TF ChIP-seq binding peaks, from both ENCODE and Roadmap.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Functional annotation was evaluated via epigenetic data, including DNase I hypersensitive sites and TF ChIP-seq binding peaks, from both ENCODE and Roadmap.		Functional annotation was evaluated via epigenetic data, including DNase I hypersensitive sites and TF ChIP-seq binding peaks, from both ENCODE and Roadmap.	Immunohistochemical staining	Functional annotation was evaluated via epigenetic data, including DNase I hypersensitive sites and TF ChIP-seq binding peaks, from both ENCODE and Roadmap.			ChIP-seq,RNA-seq,PCR,凝胶电泳				TF
31400158	chr2	219051311	219053311	IHH	Multiple passages of immortalized human hepatocytes (IHH) generated a transformed and tumorigenic phenotype, named as THH.	human,and,mouse	liver	High+Lowthroughput	Hepatitis C Virus Mediated Inhibition of miR-181c Activates ATM Signaling and Promotes Hepatocyte Growth	否	无	Prostate cancer	hepatoma cell	E_02_0638	PCR, Western blot, gel electrophoresis	Multiple passages of immortalized human hepatocytes (IHH) generated a transformed and tumorigenic phenotype, named as THH.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Multiple passages of immortalized human hepatocytes (IHH) generated a transformed and tumorigenic phenotype, named as THH.		Multiple passages of immortalized human hepatocytes (IHH) generated a transformed and tumorigenic phenotype, named as THH.	Immunohistochemical staining	Multiple passages of immortalized human hepatocytes (IHH) generated a transformed and tumorigenic phenotype, named as THH.			PCR,Western blot,凝胶电泳				IHH
31399571	chr9	127782971	127784971	CDK9	Gene activation generally requires the activity of the P-TEFb kinase CDK9, which decreases the duration of Pol II pausing and thereby enables an increase in the productive initiation frequency.	human	bone marrow	High+Lowthroughput	The pause-initiation limit restricts transcription activation in human cells	否	无	Cancer (cancer)	K562 cell	E_01_0904	PCR, RT qPCR, RNA SEQ, gel electrophoresis	Gene activation generally requires the activity of the P-TEFb kinase CDK9, which decreases the duration of Pol II pausing and thereby enables an increase in the productive initiation frequency.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Gene activation generally requires the activity of the P-TEFb kinase CDK9, which decreases the duration of Pol II pausing and thereby enables an increase in the productive initiation frequency.	Immunohistochemical staining	Gene activation generally requires the activity of the P-TEFb kinase CDK9, which decreases the duration of Pol II pausing and thereby enables an increase in the productive initiation frequency.	CDK9		PCR,RT-qPCR,RNA-seq,凝胶电泳	Gene activation generally requires the activity of the P-TEFb kinase CDK9, which decreases the duration of Pol II pausing and thereby enables an increase in the productive initiation frequency.			
31399550	chr4	71739194	71741194	GC	GC exposure induced changes in DNAm at 27,812 CpG dinucleotides and in the expression of 3,857 transcripts.	human,and,mouse		High+Lowthroughput	Glucocorticoid exposure during hippocampal neurogenesis primes future stress response by inducing changes in DNA methylation	否	无	Cancer (cancer)		E_02_0639	Western blot, QRT PCR, chip SEQ, gel electrophoresis	GC exposure induced changes in DNAm at 27,812 CpG dinucleotides and in the expression of 3,857 transcripts.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	GC exposure induced changes in DNAm at 27,812 CpG dinucleotides and in the expression of 3,857 transcripts.		GC exposure induced changes in DNAm at 27,812 CpG dinucleotides and in the expression of 3,857 transcripts.	Immunohistochemical staining	GC exposure induced changes in DNAm at 27,812 CpG dinucleotides and in the expression of 3,857 transcripts.			Western blot,qRT-PCR,ChIP-seq,凝胶电泳				GC
31399133	chr7	140716650	140718650	BRAF	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells.	human,and,mouse		High+Lowthroughput	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells	是	无	Genetic disease	embryonic stem cell	E_02_0640	Chip SEQ, RNA SEQ, Western blot, PCR, gel electrophoresis	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells.		MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells.	Immunohistochemical staining	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells.			ChIP-seq,RNA-seq,Western blot,PCR,凝胶电泳				BRAF
31399133	chr22	37968111	37970111	SOX10	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells.	human,and,mouse		High+Lowthroughput	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells	是	无	Genetic disease	embryonic stem cell	E_02_0640	Chip SEQ, RNA SEQ, Western blot, PCR, gel electrophoresis	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells.		MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells.	Immunohistochemical staining	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells.			ChIP-seq,RNA-seq,Western blot,PCR,凝胶电泳				SOX10
31399133	chr3	181709082	181711082	SOX2	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)	human,and,mouse	Nervous tissue	High+Lowthroughput	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells	是	无	Genetic disease	neural progenitor cell(immortalized neural progenitor cell)	E_02_0640	Chip SEQ, RNA SEQ, Western blot, PCR, gel electrophoresis	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)		Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)	Immunohistochemical staining	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)			ChIP-seq,RNA-seq,Western blot,PCR,凝胶电泳				SOX2
31399133	chr12	23526327	23528327	SOX5	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)	human,and,mouse	Nervous tissue	High+Lowthroughput	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells	是	无	Genetic disease	neural progenitor cell(immortalized neural progenitor cell)	E_02_0640	Chip SEQ, RNA SEQ, Western blot, PCR, gel electrophoresis	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)		Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)	Immunohistochemical staining	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)			ChIP-seq,RNA-seq,Western blot,PCR,凝胶电泳				SOX5
31399133	chr11	15963682	15965682	SOX6	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)	human,and,mouse	Nervous tissue	High+Lowthroughput	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells	是	无	Genetic disease	neural progenitor cell(immortalized neural progenitor cell)	E_02_0640	Chip SEQ, RNA SEQ, Western blot, PCR, gel electrophoresis	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)		Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)	Immunohistochemical staining	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)			ChIP-seq,RNA-seq,Western blot,PCR,凝胶电泳				SOX6
31399133	chr17	72118611	72120611	SOX9	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)	human,and,mouse	Nervous tissue	High+Lowthroughput	MEK inhibition remodels the active chromatin landscape and induces SOX10 genomic recruitment in BRAF(V600E) mutant melanoma cells	是	无	Genetic disease	neural progenitor cell(immortalized neural progenitor cell)	E_02_0640	Chip SEQ, RNA SEQ, Western blot, PCR, gel electrophoresis	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)		Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)	Immunohistochemical staining	Super-enhancers exhibit an exceptionally high density of binding for numerous factors, including the multiprotein Media_x005f_x0002_tor complex and BRG chromatin remodeling complex,transcriptional cofactors, and lineage-determining transcription factors, including members of the SOX transcription factor family in embryonic stem cells(SOX2), neural progenitor cells (SOX2), chondrocytes(SOX9, SOX5/6), and hair follicle stem cells (SOX9)			ChIP-seq,RNA-seq,Western blot,PCR,凝胶电泳				SOX9
31398323	chr3	133743662	133745662	TF	We show that DNA sequences encoding TF binding site number, density, and affinity above sharply defined thresholds drive condensation of TFs and coactiva_x005f_x0002_tors.	human,and,mouse		High+Lowthroughput	Enhancer Features that Drive Formation of Transcriptional Condensates	否	无	Cancer (cancer)	Molecular Cell	E_02_0641	Flow cytometry, gene knockdown, chip SEQ, PCR, gel electrophoresis	We show that DNA sequences encoding TF binding site number, density, and affinity above sharply defined thresholds drive condensation of TFs and coactiva_x005f_x0002_tors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We show that DNA sequences encoding TF binding site number, density, and affinity above sharply defined thresholds drive condensation of TFs and coactiva_x005f_x0002_tors.		We show that DNA sequences encoding TF binding site number, density, and affinity above sharply defined thresholds drive condensation of TFs and coactiva_x005f_x0002_tors.	Immunohistochemical staining	We show that DNA sequences encoding TF binding site number, density, and affinity above sharply defined thresholds drive condensation of TFs and coactiva_x005f_x0002_tors.			流式细胞术,基因敲降,ChIP-seq,PCR,凝胶电泳				TF
31397521	chr1	93990596	93992596	ABCA4	Identification of splice defects due to noncanonical splice site or deep-intronic variants in ABCA4.	human	kidney	High+Lowthroughput	Identification of splice defects due to noncanonical splice site or deep-intronic variants in ABCA4	是	无	Retinal disease	HEK293T cell	E_01_0905	Western blot, RT-PCR, gel electrophoresis	Identification of splice defects due to noncanonical splice site or deep-intronic variants in ABCA4.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Identification of splice defects due to noncanonical splice site or deep-intronic variants in ABCA4.		Identification of splice defects due to noncanonical splice site or deep-intronic variants in ABCA4.	Immunohistochemical staining	Identification of splice defects due to noncanonical splice site or deep-intronic variants in ABCA4.			Western blot,RT-PCR,凝胶电泳				ABCA4
31396576	chr15	98347480	98349480	Olfr281	However, some exceptions were noted for class II genes: the number of the most ventral class II gene Olfr281- and Olfr124-expressing OSNs increased.	mouse		High+Lowthroughput	Bcl11b controls odorant receptor class choice in mice	否	无	nothing	progenitor cell	E_02_0642	Gene knockdown, flow cytometry, PCR, RNA SEQ, gel electrophoresis	However, some exceptions were noted for class II genes: the number of the most ventral class II gene Olfr281- and Olfr124-expressing OSNs increased.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, some exceptions were noted for class II genes: the number of the most ventral class II gene Olfr281- and Olfr124-expressing OSNs increased.		However, some exceptions were noted for class II genes: the number of the most ventral class II gene Olfr281- and Olfr124-expressing OSNs increased.	Immunohistochemical staining	However, some exceptions were noted for class II genes: the number of the most ventral class II gene Olfr281- and Olfr124-expressing OSNs increased.			基因敲降,流式细胞术,PCR,RNA-seq,凝胶电泳				Olfr281
31396576	chr17	38107804	38109804	Olfr124	However, some exceptions were noted for class II genes: the number of the most ventral class II gene Olfr281- and Olfr124-expressing OSNs increased.	mouse		High+Lowthroughput	Bcl11b controls odorant receptor class choice in mice	否	无	nothing	progenitor cell	E_02_0642	Gene knockdown, flow cytometry, PCR, RNA SEQ, gel electrophoresis	However, some exceptions were noted for class II genes: the number of the most ventral class II gene Olfr281- and Olfr124-expressing OSNs increased.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	However, some exceptions were noted for class II genes: the number of the most ventral class II gene Olfr281- and Olfr124-expressing OSNs increased.		However, some exceptions were noted for class II genes: the number of the most ventral class II gene Olfr281- and Olfr124-expressing OSNs increased.	Immunohistochemical staining	However, some exceptions were noted for class II genes: the number of the most ventral class II gene Olfr281- and Olfr124-expressing OSNs increased.			基因敲降,流式细胞术,PCR,RNA-seq,凝胶电泳				Olfr124
31396342	chr6	125744718	125746718	HEY2	HEY2 acting as a co-repressor with smad3 and smad4 interferes with the response of TGF-beta in hepatocellular carcinoma.	human,and,mouse	liver	High+Lowthroughput	HEY2 acting as a co-repressor with smad3 and smad4 interferes with the response of TGF-beta in hepatocellular carcinoma	否	无	Liver cancer	hepatocyte	E_02_0643	PCR, Western blot, gene knockdown, gel electrophoresis	HEY2 acting as a co-repressor with smad3 and smad4 interferes with the response of TGF-beta in hepatocellular carcinoma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	HEY2 acting as a co-repressor with smad3 and smad4 interferes with the response of TGF-beta in hepatocellular carcinoma.		HEY2 acting as a co-repressor with smad3 and smad4 interferes with the response of TGF-beta in hepatocellular carcinoma.	Immunohistochemical staining	HEY2 acting as a co-repressor with smad3 and smad4 interferes with the response of TGF-beta in hepatocellular carcinoma.			PCR,Western blot,基因敲降,凝胶电泳				HEY2
31396089	chr18	63120684	63122684	BCL2	Ad libitum HRW consumption also had an inhibitory effect on the METH-induced increase in the expression of Bax/Bcl-2, cleaved caspase-3, glucose-related protein 78 (GRP 78), CCAAT/enhancer-binding protein  homologous protein (CHOP), and p-NF-kB p65 expression and elevation of Provisional interleukin (IL)-6 and tumor necrosis factor (TNF)- levels in the hippocampus.	human,and,mouse	Nervous tissue	High+Lowthroughput	Effects of Molecular Hydrogen on Methamphetamine-Induced Neurotoxicity and Spatial Memory Impairment	否	无	Neurodegenerative disease	Neuronal Cell	E_02_0644	PCR, Western blot, gel electrophoresis	Ad libitum HRW consumption also had an inhibitory effect on the METH-induced increase in the expression of Bax/Bcl-2, cleaved caspase-3, glucose-related protein 78 (GRP 78), CCAAT/enhancer-binding protein  homologous protein (CHOP), and p-NF-kB p65 expression and elevation of Provisional interleukin (IL)-6 and tumor necrosis factor (TNF)- levels in the hippocampus.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ad libitum HRW consumption also had an inhibitory effect on the METH-induced increase in the expression of Bax/Bcl-2, cleaved caspase-3, glucose-related protein 78 (GRP 78), CCAAT/enhancer-binding protein  homologous protein (CHOP), and p-NF-kB p65 expression and elevation of Provisional interleukin (IL)-6 and tumor necrosis factor (TNF)- levels in the hippocampus.		Ad libitum HRW consumption also had an inhibitory effect on the METH-induced increase in the expression of Bax/Bcl-2, cleaved caspase-3, glucose-related protein 78 (GRP 78), CCAAT/enhancer-binding protein  homologous protein (CHOP), and p-NF-kB p65 expression and elevation of Provisional interleukin (IL)-6 and tumor necrosis factor (TNF)- levels in the hippocampus.	Immunohistochemical staining	Ad libitum HRW consumption also had an inhibitory effect on the METH-induced increase in the expression of Bax/Bcl-2, cleaved caspase-3, glucose-related protein 78 (GRP 78), CCAAT/enhancer-binding protein  homologous protein (CHOP), and p-NF-kB p65 expression and elevation of Provisional interleukin (IL)-6 and tumor necrosis factor (TNF)- levels in the hippocampus.			PCR,Western blot,凝胶电泳				BCL2
31396089	chr19	48952451	48954451	BAX	Ad libitum HRW consumption also had an inhibitory effect on the METH-induced increase in the expression of Bax/Bcl-2, cleaved caspase-3, glucose-related protein 78 (GRP 78), CCAAT/enhancer-binding protein  homologous protein (CHOP), and p-NF-kB p65 expression and elevation of Provisional interleukin (IL)-6 and tumor necrosis factor (TNF)- levels in the hippocampus.	human,and,mouse	Nervous tissue	High+Lowthroughput	Effects of Molecular Hydrogen on Methamphetamine-Induced Neurotoxicity and Spatial Memory Impairment	否	无	Neurodegenerative disease	Neuronal Cell	E_02_0644	PCR, Western blot, gel electrophoresis	Ad libitum HRW consumption also had an inhibitory effect on the METH-induced increase in the expression of Bax/Bcl-2, cleaved caspase-3, glucose-related protein 78 (GRP 78), CCAAT/enhancer-binding protein  homologous protein (CHOP), and p-NF-kB p65 expression and elevation of Provisional interleukin (IL)-6 and tumor necrosis factor (TNF)- levels in the hippocampus.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Ad libitum HRW consumption also had an inhibitory effect on the METH-induced increase in the expression of Bax/Bcl-2, cleaved caspase-3, glucose-related protein 78 (GRP 78), CCAAT/enhancer-binding protein  homologous protein (CHOP), and p-NF-kB p65 expression and elevation of Provisional interleukin (IL)-6 and tumor necrosis factor (TNF)- levels in the hippocampus.		Ad libitum HRW consumption also had an inhibitory effect on the METH-induced increase in the expression of Bax/Bcl-2, cleaved caspase-3, glucose-related protein 78 (GRP 78), CCAAT/enhancer-binding protein  homologous protein (CHOP), and p-NF-kB p65 expression and elevation of Provisional interleukin (IL)-6 and tumor necrosis factor (TNF)- levels in the hippocampus.	Immunohistochemical staining	Ad libitum HRW consumption also had an inhibitory effect on the METH-induced increase in the expression of Bax/Bcl-2, cleaved caspase-3, glucose-related protein 78 (GRP 78), CCAAT/enhancer-binding protein  homologous protein (CHOP), and p-NF-kB p65 expression and elevation of Provisional interleukin (IL)-6 and tumor necrosis factor (TNF)- levels in the hippocampus.			PCR,Western blot,凝胶电泳				BAX
31395913	chr12	113389560	113391560	SDS	We determined the efect of the maceration bufer and the addition of the membrane destabilizer sodium  dodecyl sulfate (SDS) or PMA Enhancer during PMA treatments. Suspensions of E. amylovora live, dead, and  a mixture of live and dead cells were prepared in plant macerates obtained in either AMB or tenfold diluted  AMB (0.1xAMB).	mouse		High+Lowthroughput	Development of a viability digital PCR protocol for the selective detection and quantification of live Erwinia amylovora cells in cankers	否	无	plant disease	Phytophthora pyrus cell	E_02_0645	RNA SEQ, PCR, flow cytometry, gel electrophoresis	We determined the efect of the maceration bufer and the addition of the membrane destabilizer sodium  dodecyl sulfate (SDS) or PMA Enhancer during PMA treatments. Suspensions of E. amylovora live, dead, and  a mixture of live and dead cells were prepared in plant macerates obtained in either AMB or tenfold diluted  AMB (0.1xAMB).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We determined the efect of the maceration bufer and the addition of the membrane destabilizer sodium  dodecyl sulfate (SDS) or PMA Enhancer during PMA treatments. Suspensions of E. amylovora live, dead, and  a mixture of live and dead cells were prepared in plant macerates obtained in either AMB or tenfold diluted  AMB (0.1xAMB).		We determined the efect of the maceration bufer and the addition of the membrane destabilizer sodium  dodecyl sulfate (SDS) or PMA Enhancer during PMA treatments. Suspensions of E. amylovora live, dead, and  a mixture of live and dead cells were prepared in plant macerates obtained in either AMB or tenfold diluted  AMB (0.1xAMB).	Immunohistochemical staining	We determined the efect of the maceration bufer and the addition of the membrane destabilizer sodium  dodecyl sulfate (SDS) or PMA Enhancer during PMA treatments. Suspensions of E. amylovora live, dead, and  a mixture of live and dead cells were prepared in plant macerates obtained in either AMB or tenfold diluted  AMB (0.1xAMB).			RNA-seq,PCR,流式细胞术,凝胶电泳				SDS
31395854	chr17	72287441	72289441	LINC00511	The transcriptional landscape of lncRNAs reveals the oncogenic function of LINC00511 in ER-negative breast cancer.	human,and,mouse	breast	High+Lowthroughput	The transcriptional landscape of lncRNAs reveals the oncogenic function of LINC00511 in ER-negative breast cancer	否	无	Breast cancer (breast cancer)	breast cancer cell	E_02_0646	PCR, flow cytometry, gel electrophoresis	The transcriptional landscape of lncRNAs reveals the oncogenic function of LINC00511 in ER-negative breast cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcriptional landscape of lncRNAs reveals the oncogenic function of LINC00511 in ER-negative breast cancer.		The transcriptional landscape of lncRNAs reveals the oncogenic function of LINC00511 in ER-negative breast cancer.	Immunohistochemical staining	The transcriptional landscape of lncRNAs reveals the oncogenic function of LINC00511 in ER-negative breast cancer.			PCR,流式细胞术,凝胶电泳				LINC00511
31395079	chr7	36386993	36388993	ANLN	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.	human,and,mouse	tumour	High+Lowthroughput	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis	否	无	Pancreatic cancer		E_02_0647	PCR, Western blot, gel electrophoresis	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.		ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.	Immunohistochemical staining	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.			PCR,Western blot,凝胶电泳				ANLN
31395079	chr7	148804368	148806368	EZH2	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.	human,and,mouse	tumour	High+Lowthroughput	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis	否	无	Pancreatic cancer		E_02_0647	PCR, Western blot, gel electrophoresis	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.		ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.	Immunohistochemical staining	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.			PCR,Western blot,凝胶电泳				EZH2
31395079	chr17	38867006	38869006	LASP1	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.	human,and,mouse	tumour	High+Lowthroughput	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis	否	无	Pancreatic cancer		E_02_0647	PCR, Western blot, gel electrophoresis	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.		ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.	Immunohistochemical staining	ANLN-induced EZH2 upregulation promotes pancreatic cancer progression by mediating miR-218-5p/LASP1 signaling axis.			PCR,Western blot,凝胶电泳				LASP1
31391075	chr3	133743131	133745131	TF	Nr5a1 gene (also called Sf-1 or Ad4BP) is a transcription factor (TF) belonging to the nuclear receptor superfamily.	human,and,mouse	hormone	High+Lowthroughput	Identification of a pituitary ERα-activated enhancer triggering the expression of Nr5a1, the earliest gonadotrope lineage-specific transcription factor	否	无	Breast cancer (breast cancer)	Gonadotrope cell	E_02_0648	Chip SEQ, ATAC SEQ, PCR, gel electrophoresis	Nr5a1 gene (also called Sf-1 or Ad4BP) is a transcription factor (TF) belonging to the nuclear receptor superfamily.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Nr5a1 gene (also called Sf-1 or Ad4BP) is a transcription factor (TF) belonging to the nuclear receptor superfamily.		Nr5a1 gene (also called Sf-1 or Ad4BP) is a transcription factor (TF) belonging to the nuclear receptor superfamily.	Immunohistochemical staining	Nr5a1 gene (also called Sf-1 or Ad4BP) is a transcription factor (TF) belonging to the nuclear receptor superfamily.			ChIP-seq,ATAC-seq,PCR,凝胶电泳				TF
31391075	chr1	168278318	168280318	TBX19	Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.	human,and,mouse		High+Lowthroughput	Identification of a pituitary ERα-activated enhancer triggering the expression of Nr5a2, the earliest gonadotrope lineage-specific transcription factor	否	无	Breast cancer (breast cancer)	Stem Cell	E_02_0648	Chip SEQ, ATAC SEQ, PCR, gel electrophoresis	Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.		Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.	Immunohistochemical staining	Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.			ChIP-seq,ATAC-seq,PCR,凝胶电泳				TBX19
31391075	chr1	18628174	18630174	PAX7	Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.	human,and,mouse		High+Lowthroughput	Identification of a pituitary ERα-activated enhancer triggering the expression of Nr5a2, the earliest gonadotrope lineage-specific transcription factor	否	无	Breast cancer (breast cancer)	Stem Cell	E_02_0648	Chip SEQ, ATAC SEQ, PCR, gel electrophoresis	Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.		Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.	Immunohistochemical staining	Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.			ChIP-seq,ATAC-seq,PCR,凝胶电泳				PAX7
31391075	chr3	87256708	87258708	POU1F1	Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.	human,and,mouse		High+Lowthroughput	Identification of a pituitary ERα-activated enhancer triggering the expression of Nr5a2, the earliest gonadotrope lineage-specific transcription factor	否	无	Breast cancer (breast cancer)	Stem Cell	E_02_0648	Chip SEQ, ATAC SEQ, PCR, gel electrophoresis	Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.		Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.	Immunohistochemical staining	Several TFs are known to promote pituitary stem  cells diferentiation into a specifc endocrine lineage:  POU1F1 is mandatory for the thyrotrope, somatotrope  and lactotrope lineages , TBX19 for the corticotrope, PAX7 for the melanotrope and Nr5a1 for the gon_x005f_x0002_adotrope lineage.			ChIP-seq,ATAC-seq,PCR,凝胶电泳				POU1F1
31390360	chr12	111440987	111442987	ATXN2	Calcium-responsive transactivator (CREST) toxicity is rescued by loss of PBP1/ATXN2 function in a novel yeast proteinopathy model and in transgenic flies.	human	Nervous tissue	High+Lowthroughput	Calcium-responsive transactivator (CREST) toxicity is rescued by loss of PBP1/ATXN2 function in a novel yeast proteinopathy model and in transgenic flies	否	无	Neurodegenerative disease	retinal ganglion cell	E_01_0906	Gene knockdown, gel electrophoresis, Western blot	Calcium-responsive transactivator (CREST) toxicity is rescued by loss of PBP1/ATXN2 function in a novel yeast proteinopathy model and in transgenic flies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Calcium-responsive transactivator (CREST) toxicity is rescued by loss of PBP1/ATXN2 function in a novel yeast proteinopathy model and in transgenic flies.		Calcium-responsive transactivator (CREST) toxicity is rescued by loss of PBP1/ATXN2 function in a novel yeast proteinopathy model and in transgenic flies.	Immunohistochemical staining	Calcium-responsive transactivator (CREST) toxicity is rescued by loss of PBP1/ATXN2 function in a novel yeast proteinopathy model and in transgenic flies.			基因敲降,凝胶电泳,Western blot				ATXN2
31388625	chr10	88950960	88952960	FAS	Antibodies to fatty acid synthase  (FAS), stearoyl-coenzyme A (CoA) desaturase 1  (SCD1), and acetyl-CoA carboxylase were from  Cell Signaling (Danvers, MA).	human,and,mouse		High+Lowthroughput	Liver Proliferation Is an Essential Driver of Fibrosis in Mouse Models of Nonalcoholic Fatty Liver Disease	否	无	Liver disease		E_02_0649	RNA SEQ, PCR, Western blot, gel electrophoresis	Antibodies to fatty acid synthase  (FAS), stearoyl-coenzyme A (CoA) desaturase 1  (SCD1), and acetyl-CoA carboxylase were from  Cell Signaling (Danvers, MA).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Antibodies to fatty acid synthase  (FAS), stearoyl-coenzyme A (CoA) desaturase 1  (SCD1), and acetyl-CoA carboxylase were from  Cell Signaling (Danvers, MA).		Antibodies to fatty acid synthase  (FAS), stearoyl-coenzyme A (CoA) desaturase 1  (SCD1), and acetyl-CoA carboxylase were from  Cell Signaling (Danvers, MA).	Immunohistochemical staining	Antibodies to fatty acid synthase  (FAS), stearoyl-coenzyme A (CoA) desaturase 1  (SCD1), and acetyl-CoA carboxylase were from  Cell Signaling (Danvers, MA).			RNA-seq,PCR,Western blot,凝胶电泳				FAS
31387996	chr16	69561910	69563910	NFAT5	TonEBP/NFAT5 promotes obesity and insulin resistance by epigenetic suppression of white adipose tissue beiging.	human,and,mouse	Loose connective tissue	High+Lowthroughput	TonEBP/NFAT5 promotes obesity and insulin resistance by epigenetic suppression of white adipose tissue beiging	否	无	Metabolic disease (metabolic disease)	3T3-L1 cell	E_02_0650	Western blot, PCR, gel electrophoresis	TonEBP/NFAT5 promotes obesity and insulin resistance by epigenetic suppression of white adipose tissue beiging.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	TonEBP/NFAT5 promotes obesity and insulin resistance by epigenetic suppression of white adipose tissue beiging.		TonEBP/NFAT5 promotes obesity and insulin resistance by epigenetic suppression of white adipose tissue beiging.	Immunohistochemical staining	TonEBP/NFAT5 promotes obesity and insulin resistance by epigenetic suppression of white adipose tissue beiging.			Western blot,PCR,凝胶电泳				NFAT5
31380279	chr7	148803898	148805898	EZH2	EZH2 Phosphorylation Promotes Self-Renewal of Glioma Stem-Like Cells Through NF-κB Methylation.	human	tumour	High+Lowthroughput	EZH2 Phosphorylation Promotes Self-Renewal of Glioma Stem-Like Cells Through NF-κB Methylation	否	无	Cancer (cancer)	cancer cell	E_01_0907	PCR, Western blot, gene knockdown, gel electrophoresis	EZH2 Phosphorylation Promotes Self-Renewal of Glioma Stem-Like Cells Through NF-κB Methylation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2 Phosphorylation Promotes Self-Renewal of Glioma Stem-Like Cells Through NF-κB Methylation.	Immunohistochemical staining	EZH2 Phosphorylation Promotes Self-Renewal of Glioma Stem-Like Cells Through NF-κB Methylation.	EZH2		PCR,Western blot,基因敲降,凝胶电泳	EZH2 Phosphorylation Promotes Self-Renewal of Glioma Stem-Like Cells Through NF-κB Methylation.			
31380279	chr9	36570059	36572059	MELK	Oncogenic roles of maternal embryonic leucine-zipper kinase (MELK) and enhancer of zeste homolog 2 (EZH2) have been reported to play a crucial role in glioma tumorigenesis.	human		High+Lowthroughput	EZH3 Phosphorylation Promotes Self-Renewal of Glioma Stem-Like Cells Through NF-κB Methylation	否	无	Cancer (cancer)	Cancer stem-like cell	E_01_0907	PCR, Western blot, gene knockdown, gel electrophoresis	Oncogenic roles of maternal embryonic leucine-zipper kinase (MELK) and enhancer of zeste homolog 2 (EZH2) have been reported to play a crucial role in glioma tumorigenesis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Oncogenic roles of maternal embryonic leucine-zipper kinase (MELK) and enhancer of zeste homolog 2 (EZH2) have been reported to play a crucial role in glioma tumorigenesis.		Oncogenic roles of maternal embryonic leucine-zipper kinase (MELK) and enhancer of zeste homolog 2 (EZH2) have been reported to play a crucial role in glioma tumorigenesis.	Immunohistochemical staining	Oncogenic roles of maternal embryonic leucine-zipper kinase (MELK) and enhancer of zeste homolog 2 (EZH2) have been reported to play a crucial role in glioma tumorigenesis.			PCR,Western blot,基因敲降,凝胶电泳				MELK
31380269	chr6	108557326	108559326	FOXO3	Cardiomyocyte hypertrophy and fibrosis were assessed by histology at week 19. qRT-PCR was performed to measure the gene expression changes of miR-212 and forkhead box O3 (FOXO3) in all follow-up time points.	human,and,mouse	Myotome	High+Lowthroughput	Selective Heart Irradiation Induces Cardiac Overexpression of the Pro-hypertrophic miR-212	否	无	Heart disease	Cardiac muscle cell	E_02_0651	PCR, Western blot, gel electrophoresis	Cardiomyocyte hypertrophy and fibrosis were assessed by histology at week 19. qRT-PCR was performed to measure the gene expression changes of miR-212 and forkhead box O3 (FOXO3) in all follow-up time points.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cardiomyocyte hypertrophy and fibrosis were assessed by histology at week 19. qRT-PCR was performed to measure the gene expression changes of miR-212 and forkhead box O3 (FOXO3) in all follow-up time points.		Cardiomyocyte hypertrophy and fibrosis were assessed by histology at week 19. qRT-PCR was performed to measure the gene expression changes of miR-212 and forkhead box O3 (FOXO3) in all follow-up time points.	Immunohistochemical staining	Cardiomyocyte hypertrophy and fibrosis were assessed by histology at week 19. qRT-PCR was performed to measure the gene expression changes of miR-212 and forkhead box O3 (FOXO3) in all follow-up time points.			PCR,Western blot,凝胶电泳				FOXO3
31376680	chr20	5111752	5113752	PCNA	TonEBP Regulates PCNA Polyubiquitination in Response to DNA Damage through Interaction with SHPRH and USP1.	human,and,mouse		High+Lowthroughput	TonEBP Regulates PCNA Polyubiquitination in Response to DNA Damage through Interaction with SHPRH and USP1	否	无	Inflammatory disease	HEK293 cell	E_02_0652	PCR, Western blot, gene knockdown, gel electrophoresis	TonEBP Regulates PCNA Polyubiquitination in Response to DNA Damage through Interaction with SHPRH and USP1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	TonEBP Regulates PCNA Polyubiquitination in Response to DNA Damage through Interaction with SHPRH and USP1.		TonEBP Regulates PCNA Polyubiquitination in Response to DNA Damage through Interaction with SHPRH and USP1.	Immunohistochemical staining	TonEBP Regulates PCNA Polyubiquitination in Response to DNA Damage through Interaction with SHPRH and USP1.			PCR,Western blot,基因敲降,凝胶电泳				PCNA
31376680	chr6	145861359	145863359	SHPRH	TonEBP Regulates PCNA Polyubiquitination in Response to DNA Damage through Interaction with SHPRH and USP1.	human,and,mouse		High+Lowthroughput	TonEBP Regulates PCNA Polyubiquitination in Response to DNA Damage through Interaction with SHPRH and USP1	否	无	Inflammatory disease	HEK293 cell	E_02_0652	PCR, Western blot, gene knockdown, gel electrophoresis	TonEBP Regulates PCNA Polyubiquitination in Response to DNA Damage through Interaction with SHPRH and USP1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	TonEBP Regulates PCNA Polyubiquitination in Response to DNA Damage through Interaction with SHPRH and USP1.		TonEBP Regulates PCNA Polyubiquitination in Response to DNA Damage through Interaction with SHPRH and USP1.	Immunohistochemical staining	TonEBP Regulates PCNA Polyubiquitination in Response to DNA Damage through Interaction with SHPRH and USP1.			PCR,Western blot,基因敲降,凝胶电泳				SHPRH
31376159	chr7	22723332	22725332	IL6	The expression of  the M1 marker genes interleukin 1β (IL1β) and interleukin 6 (IL6) along with the M2 markers  arginase-1 and chitinase-like 3 (Chil3 or YM1) were evaluated by real time polymerase chain  reaction.	human,and,mouse		High+Lowthroughput	Platelet-rich fibrin elicits an anti-inflammatory response in macrophages in vitro	否	无	Infectious disease	dendritic cell	E_02_0653	PCR, gene knockdown, gel electrophoresis	The expression of  the M1 marker genes interleukin 1β (IL1β) and interleukin 6 (IL6) along with the M2 markers  arginase-1 and chitinase-like 3 (Chil3 or YM1) were evaluated by real time polymerase chain  reaction.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The expression of  the M1 marker genes interleukin 1β (IL1β) and interleukin 6 (IL6) along with the M2 markers  arginase-1 and chitinase-like 3 (Chil3 or YM1) were evaluated by real time polymerase chain  reaction.		The expression of  the M1 marker genes interleukin 1β (IL1β) and interleukin 6 (IL6) along with the M2 markers  arginase-1 and chitinase-like 3 (Chil3 or YM1) were evaluated by real time polymerase chain  reaction.	Immunohistochemical staining	The expression of  the M1 marker genes interleukin 1β (IL1β) and interleukin 6 (IL6) along with the M2 markers  arginase-1 and chitinase-like 3 (Chil3 or YM1) were evaluated by real time polymerase chain  reaction.			PCR,基因敲降,凝胶电泳				IL6
31375813	chr8	94246708	94248708	GEM	Transposed nuclei are then loaded onto a microfluidic chip for gel bead in emulsion (GEM) generation.	human,and,mouse	Immunohistochem	High+Lowthroughput	Massively parallel single-cell chromatin landscapes of human immune cell development and intratumoral T cell exhaustion	是	无	Autoimmune diseases (autoimmune diseases)	Immune cell	E_02_0654	Flow cytometry, ATAC SEQ, RNA sseq	Transposed nuclei are then loaded onto a microfluidic chip for gel bead in emulsion (GEM) generation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Transposed nuclei are then loaded onto a microfluidic chip for gel bead in emulsion (GEM) generation.		Transposed nuclei are then loaded onto a microfluidic chip for gel bead in emulsion (GEM) generation.	Immunohistochemical staining	Transposed nuclei are then loaded onto a microfluidic chip for gel bead in emulsion (GEM) generation.			流式细胞术,ATAC-seq,RNA-Sseq				GEM
31375262	chr3	181709143	181711143	SOX2	Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.	human,and,mouse	Nervous tissue	High+Lowthroughput	Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA4	否	无	Cancer (cancer)	neural stem cell	E_02_0655	Gene knockdown, PCR, gel electrophoresis, Western blot	Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.		Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.	Immunohistochemical staining	Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.			基因敲降,PCR,凝胶电泳,Western blot				SOX2
31375262	chr11	31782340	31784340	PAX6	Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.	human,and,mouse	Nervous tissue	High+Lowthroughput	Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA4	否	无	Cancer (cancer)	neural stem cell	E_02_0655	Gene knockdown, PCR, gel electrophoresis, Western blot	Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.		Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.	Immunohistochemical staining	Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.			基因敲降,PCR,凝胶电泳,Western blot				PAX6
31375262	chr2	5689341	5691341	SOX11	Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.	human,and,mouse	Nervous tissue	High+Lowthroughput	Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA4	否	无	Cancer (cancer)	neural stem cell	E_02_0655	Gene knockdown, PCR, gel electrophoresis, Western blot	Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.		Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.	Immunohistochemical staining	Loss of neural differentiation is accom_x005f_x0002_panied by changes in gene expression, including loss of the neu_x0002_ral-specific factors SOX2 and SOX3 and the downstream targets PAX6 and SOX11.			基因敲降,PCR,凝胶电泳,Western blot				SOX11
31375262	chr9	1977953	1979953	SMARCA2	Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA4.	human,and,mouse		High+Lowthroughput	Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA5	否	无	Cancer (cancer)		E_02_0655	Gene knockdown, PCR, gel electrophoresis, Western blot	Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA4.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA4.		Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA4.	Immunohistochemical staining	Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA4.			基因敲降,PCR,凝胶电泳,Western blot				SMARCA2
31375262	chr19	10958588	10960588	SMARCA4	Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA4.	human,and,mouse		High+Lowthroughput	Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA5	否	无	Cancer (cancer)		E_02_0655	Gene knockdown, PCR, gel electrophoresis, Western blot	Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA4.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA4.		Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA4.	Immunohistochemical staining	Heterozygous Mutations in SMARCA2 Reprogram the Enhancer Landscape by Global Retargeting of SMARCA4.			基因敲降,PCR,凝胶电泳,Western blot				SMARCA4
31374988	chr15	99563212	99565212	MEF2A	The vertebrate genes compose four distinct subfamilies designated MEF2A, -B, -C, and -D. There are multiple mef2 genes in the common carp (Cyprinus carpio).	human	Nervous tissue	High+Lowthroughput	Common Carp mef2 Genes: Evolution and Expression	否	无	nothing	Neural crest cell	E_01_0908	PCR, gel electrophoresis	The vertebrate genes compose four distinct subfamilies designated MEF2A, -B, -C, and -D. There are multiple mef2 genes in the common carp (Cyprinus carpio).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The vertebrate genes compose four distinct subfamilies designated MEF2A, -B, -C, and -D. There are multiple mef2 genes in the common carp (Cyprinus carpio).	Immunohistochemical staining	The vertebrate genes compose four distinct subfamilies designated MEF2A, -B, -C, and -D. There are multiple mef2 genes in the common carp (Cyprinus carpio).	MEF2A		PCR,凝胶电泳	The vertebrate genes compose four distinct subfamilies designated MEF2A, -B, -C, and -D. There are multiple mef2 genes in the common carp (Cyprinus carpio).			
31373033	chr16	67559225	67561225	CTCF	Genome-wide studies have shown that the architectural proteins CTCF and its frequent associated partner cohesin are important for partition of the genome into largely conserved topologically associating domains or TADs on the mega_x005f_x0002_base.	human,and,mouse	breast	High+Lowthroughput	C/EBPα mediates the growth inhibitory effect of progestins on breast cancer cells	否	无	Breast cancer (breast cancer)	breast cancer cell	E_02_0656	Western blot, PCR, gel electrophoresis, chip SEQ, RNA seq	Genome-wide studies have shown that the architectural proteins CTCF and its frequent associated partner cohesin are important for partition of the genome into largely conserved topologically associating domains or TADs on the mega_x005f_x0002_base.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genome-wide studies have shown that the architectural proteins CTCF and its frequent associated partner cohesin are important for partition of the genome into largely conserved topologically associating domains or TADs on the mega_x005f_x0002_base.		Genome-wide studies have shown that the architectural proteins CTCF and its frequent associated partner cohesin are important for partition of the genome into largely conserved topologically associating domains or TADs on the mega_x005f_x0002_base.	Immunohistochemical staining	Genome-wide studies have shown that the architectural proteins CTCF and its frequent associated partner cohesin are important for partition of the genome into largely conserved topologically associating domains or TADs on the mega_x005f_x0002_base.			Western blot,PCR,凝胶电泳,ChIP-seq,RNA-seq				CTCF
31372638	chr16	67559785	67561785	CTCF	A CRISPR-Cas9 screen identifies essential CTCF anchor sites for estrogen receptor-driven breast cancer cell proliferation.	human	breast	High+Lowthroughput	A CRISPR-Cas9 screen identifies essential CTCF anchor sites for estrogen receptor-driven breast cancer cell proliferation	否	无	Breast cancer (breast cancer)	breast cancer cell	E_01_0909	RNA SEQ, chip SEQ, flow cytometry, Western blot, PCR, gel electrophoresis	A CRISPR-Cas9 screen identifies essential CTCF anchor sites for estrogen receptor-driven breast cancer cell proliferation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			A CRISPR-Cas9 screen identifies essential CTCF anchor sites for estrogen receptor-driven breast cancer cell proliferation.	Immunohistochemical staining	A CRISPR-Cas9 screen identifies essential CTCF anchor sites for estrogen receptor-driven breast cancer cell proliferation.	CTCF		RNA-seq,ChIP-seq,流式细胞术,Western blot,PCR,凝胶电泳	A CRISPR-Cas9 screen identifies essential CTCF anchor sites for estrogen receptor-driven breast cancer cell proliferation.			
31372457	chr17	63925228	63927228	CD79B	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	human	Myotome	High+Lowthroughput	Data showing atherosclerosis-associated differentially methylated regions are often at enhancers	否	无	Louisiana Cancer (Louisiana Cancer)	Smooth muscle cell	E_01_0910	RNA-seq,DNA-seq	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).		Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	Immunohistochemical staining	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).			RNA-seq,DNA-seq				CD79B
31372457	chr4	2790567	2792567	SH3BP2	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	human	Myotome	High+Lowthroughput	Data showing atherosclerosis-associated differentially methylated regions are often at enhancers	否	无	Louisiana Cancer (Louisiana Cancer)	Smooth muscle cell	E_01_0910	RNA-seq,DNA-seq	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	Immunohistochemical staining	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	SH3BP2		RNA-seq,DNA-seq	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).			
31372457	chr7	35199773	35201773	TBX20	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	human	Myotome	High+Lowthroughput	Data showing atherosclerosis-associated differentially methylated regions are often at enhancers	否	无	Louisiana Cancer (Louisiana Cancer)	Smooth muscle cell	E_01_0910	RNA-seq,DNA-seq	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	Immunohistochemical staining	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	TBX20		RNA-seq,DNA-seq	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).			
31372457	chr15	67061460	67063460	SMAD3	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	human	Myotome	High+Lowthroughput	Data showing atherosclerosis-associated differentially methylated regions are often at enhancers	否	无	Louisiana Cancer (Louisiana Cancer)	Smooth muscle cell	E_01_0910	RNA-seq,DNA-seq	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	Immunohistochemical staining	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).	SMAD3		RNA-seq,DNA-seq	Athero hypomethylated and hypermethylated DMRs as well as epigenetic and transcription profiles are described for the following genes: ACTA2, MYH10,MYH11 (SMC-associated genes); SMAD3 (a signaling gene for SMCs and other cell types); CD79B and SH3BP2(leukocyte-associated genes); and TBX20 and genes in the HOXA, HOXB, HOXC, and HOXD clusters (T-box and homeobox developmental genes).			
31371786	chr10	72689789	72691789	MCU	Photoreceptor dysfunction and degeneration occur when intracellular Ca2+ homeostasis is disrupted. Ca2+ homeostasis is maintained partly by mitochondrial Ca2+ uptake through the mitochondrial Ca2+ uniporter (MCU), which can influence cytosolic Ca2+ signals, stimulate energy production, and trigger apoptosis. Here we discovered that zebrafish cone photoreceptors express unusually low levels of MCU.	human,and,mouse	Nervous tissue	High+Lowthroughput	Increasing Ca(2+) in photoreceptor mitochondria alters metabolites, accelerates photoresponse recovery, and reveals adaptations to mitochondrial stress	否	无	Retinal disease	Cone Cell	E_02_0657	Gene knockdown, PCR, Western blot, gel electrophoresis	Photoreceptor dysfunction and degeneration occur when intracellular Ca2+ homeostasis is disrupted. Ca2+ homeostasis is maintained partly by mitochondrial Ca2+ uptake through the mitochondrial Ca2+ uniporter (MCU), which can influence cytosolic Ca2+ signals, stimulate energy production, and trigger apoptosis. Here we discovered that zebrafish cone photoreceptors express unusually low levels of MCU.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Photoreceptor dysfunction and degeneration occur when intracellular Ca2+ homeostasis is disrupted. Ca2+ homeostasis is maintained partly by mitochondrial Ca2+ uptake through the mitochondrial Ca2+ uniporter (MCU), which can influence cytosolic Ca2+ signals, stimulate energy production, and trigger apoptosis. Here we discovered that zebrafish cone photoreceptors express unusually low levels of MCU.		Photoreceptor dysfunction and degeneration occur when intracellular Ca2+ homeostasis is disrupted. Ca2+ homeostasis is maintained partly by mitochondrial Ca2+ uptake through the mitochondrial Ca2+ uniporter (MCU), which can influence cytosolic Ca2+ signals, stimulate energy production, and trigger apoptosis. Here we discovered that zebrafish cone photoreceptors express unusually low levels of MCU.	Immunohistochemical staining	Photoreceptor dysfunction and degeneration occur when intracellular Ca2+ homeostasis is disrupted. Ca2+ homeostasis is maintained partly by mitochondrial Ca2+ uptake through the mitochondrial Ca2+ uniporter (MCU), which can influence cytosolic Ca2+ signals, stimulate energy production, and trigger apoptosis. Here we discovered that zebrafish cone photoreceptors express unusually low levels of MCU.			基因敲降,PCR,Western blot,凝胶电泳				MCU
31371771	chr16	14520680	14522680	Snai2	A new transgenic reporter line reveals Wnt-dependent Snai2 re-expression and cranial neural crest differentiation in Xenopus.	mouse	Nervous tissue	High+Lowthroughput	A new transgenic reporter line reveals Wnt-dependent Snai2 re-expression and cranial neural crest differentiation in Xenopus	否	无	Cancer (cancer)	Neural crest cell	E_02_0658	Gene knockdown, PCR, gel electrophoresis	A new transgenic reporter line reveals Wnt-dependent Snai2 re-expression and cranial neural crest differentiation in Xenopus.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A new transgenic reporter line reveals Wnt-dependent Snai2 re-expression and cranial neural crest differentiation in Xenopus.		A new transgenic reporter line reveals Wnt-dependent Snai2 re-expression and cranial neural crest differentiation in Xenopus.	Immunohistochemical staining	A new transgenic reporter line reveals Wnt-dependent Snai2 re-expression and cranial neural crest differentiation in Xenopus.			基因敲降,PCR,凝胶电泳				Snai2
31371698	chr8	127791948	127793948	PVT1	Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.	human,and,mouse	tumour	High+Lowthroughput	Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1	否	无	Renal disease	cancer cell	E_02_0659	Flow cytometry, gene knockdown, PCR, Western blot, gel electrophoresis	Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.		Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.	Immunohistochemical staining	Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.			流式细胞术,基因敲降,PCR,Western blot,凝胶电泳				PVT1
31371698	chr14	37587213	37589213	FOXA1	Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.	human,and,mouse	tumour	High+Lowthroughput	Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1	否	无	Renal disease	cancer cell	E_02_0659	Flow cytometry, gene knockdown, PCR, Western blot, gel electrophoresis	Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.		Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.	Immunohistochemical staining	Silencing of long noncoding RNA PVT1 inhibits podocyte damage and apoptosis in diabetic nephropathy by upregulating FOXA1.			流式细胞术,基因敲降,PCR,Western blot,凝胶电泳				FOXA1
31370857	chr21	34785179	34787179	RUNX1	RUNX1 promotes tumour metastasis by activating the Wnt/β-catenin signalling pathway and EMT in colorectal cancer.	human,and,mouse	colon	High+Lowthroughput	RUNX1 promotes tumour metastasis by activating the Wnt/β-catenin signalling pathway and EMT in colorectal cancer	否	无	Colorectal cancer		E_02_0660	PCR, Western blot, gene knockdown, gel electrophoresis	RUNX1 promotes tumour metastasis by activating the Wnt/β-catenin signalling pathway and EMT in colorectal cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RUNX1 promotes tumour metastasis by activating the Wnt/β-catenin signalling pathway and EMT in colorectal cancer.		RUNX1 promotes tumour metastasis by activating the Wnt/β-catenin signalling pathway and EMT in colorectal cancer.	Immunohistochemical staining	RUNX1 promotes tumour metastasis by activating the Wnt/β-catenin signalling pathway and EMT in colorectal cancer.			PCR,Western blot,基因敲降,凝胶电泳				RUNX1
31235524	chr22	23067631	23069631	GNAZ	Briefly, the GNAZ gene in previously established HEK293 cells devoid of three Gα families (the Gαs, the Gαq, and the Gα12 families) was mutated by a CRISPR/ Cas9 system using a GNAZ sgRNA-targeting sequence (5’-GATGCGGGTCAGCGAGTCGATGG-3’; including a NGG PAM sequence). Introduction of a 5-bp deletion (frame-shift mutation) into the GNAZ gene was verified by direct sequencing as described elsewhere.	mouse	kidney	High+Lowthroughput	WNT-3A-induced β-catenin signaling does not require signaling through heterotrimeric G proteins	否	无	Cancer (cancer)	HEK293 cell	E_02_0661	PCR, Western blot, gel electrophoresis	Briefly, the GNAZ gene in previously established HEK293 cells devoid of three Gα families (the Gαs, the Gαq, and the Gα12 families) was mutated by a CRISPR/ Cas9 system using a GNAZ sgRNA-targeting sequence (5’-GATGCGGGTCAGCGAGTCGATGG-3’; including a NGG PAM sequence). Introduction of a 5-bp deletion (frame-shift mutation) into the GNAZ gene was verified by direct sequencing as described elsewhere.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Briefly, the GNAZ gene in previously established HEK293 cells devoid of three Gα families (the Gαs, the Gαq, and the Gα12 families) was mutated by a CRISPR/ Cas9 system using a GNAZ sgRNA-targeting sequence (5’-GATGCGGGTCAGCGAGTCGATGG-3’; including a NGG PAM sequence). Introduction of a 5-bp deletion (frame-shift mutation) into the GNAZ gene was verified by direct sequencing as described elsewhere.		Briefly, the GNAZ gene in previously established HEK293 cells devoid of three Gα families (the Gαs, the Gαq, and the Gα12 families) was mutated by a CRISPR/ Cas9 system using a GNAZ sgRNA-targeting sequence (5’-GATGCGGGTCAGCGAGTCGATGG-3’; including a NGG PAM sequence). Introduction of a 5-bp deletion (frame-shift mutation) into the GNAZ gene was verified by direct sequencing as described elsewhere.	Immunohistochemical staining	Briefly, the GNAZ gene in previously established HEK293 cells devoid of three Gα families (the Gαs, the Gαq, and the Gα12 families) was mutated by a CRISPR/ Cas9 system using a GNAZ sgRNA-targeting sequence (5’-GATGCGGGTCAGCGAGTCGATGG-3’; including a NGG PAM sequence). Introduction of a 5-bp deletion (frame-shift mutation) into the GNAZ gene was verified by direct sequencing as described elsewhere.			PCR,Western blot,凝胶电泳				GNAZ
31234917	chrX	67541427	67543427	AR	ASC-J9? increases the bladder cancer chemotherapy efficacy via altering the androgen receptor (AR) and NF-κB survival signals.	human,and,mouse	bladder	High+Lowthroughput	ASC-J9? increases the bladder cancer chemotherapy efficacy via altering the androgen receptor (AR) and NF-κB survival signals	否	无	Muscle invasive disease (muscle invasive disease)	TCC-SUP cell	E_02_0662	PCR, Western blot, gel electrophoresis	ASC-J9? increases the bladder cancer chemotherapy efficacy via altering the androgen receptor (AR) and NF-κB survival signals.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ASC-J9? increases the bladder cancer chemotherapy efficacy via altering the androgen receptor (AR) and NF-κB survival signals.		ASC-J9? increases the bladder cancer chemotherapy efficacy via altering the androgen receptor (AR) and NF-κB survival signals.	Immunohistochemical staining	ASC-J9? increases the bladder cancer chemotherapy efficacy via altering the androgen receptor (AR) and NF-κB survival signals.			PCR,Western blot,凝胶电泳				AR
31234917	chr18	63120491	63122491	BCL2	The combined therapy increases the expression of the pro-apoptosis BAX gene and cell cycle inhibitor p21 gene, yet suppresses the expression of the pro-survival BCL2 gene in miBCa cells.	human,and,mouse		High+Lowthroughput	ASC-J9? increases the bladder cancer chemotherapy efficacy via altering the androgen receptor (AR) and NF-κB survival signals	否	无	Muscle invasive disease (muscle invasive disease)		E_02_0662	PCR, Western blot, gel electrophoresis	The combined therapy increases the expression of the pro-apoptosis BAX gene and cell cycle inhibitor p21 gene, yet suppresses the expression of the pro-survival BCL2 gene in miBCa cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The combined therapy increases the expression of the pro-apoptosis BAX gene and cell cycle inhibitor p21 gene, yet suppresses the expression of the pro-survival BCL2 gene in miBCa cells.		The combined therapy increases the expression of the pro-apoptosis BAX gene and cell cycle inhibitor p21 gene, yet suppresses the expression of the pro-survival BCL2 gene in miBCa cells.	Immunohistochemical staining	The combined therapy increases the expression of the pro-apoptosis BAX gene and cell cycle inhibitor p21 gene, yet suppresses the expression of the pro-survival BCL2 gene in miBCa cells.			PCR,Western blot,凝胶电泳				BCL2
31234917	chr19	48951880	48953880	BAX	The combined therapy increases the expression of the pro-apoptosis BAX gene and cell cycle inhibitor p21 gene, yet suppresses the expression of the pro-survival BCL2 gene in miBCa cells.	human,and,mouse		High+Lowthroughput	ASC-J9? increases the bladder cancer chemotherapy efficacy via altering the androgen receptor (AR) and NF-κB survival signals	否	无	Muscle invasive disease (muscle invasive disease)		E_02_0662	PCR, Western blot, gel electrophoresis	The combined therapy increases the expression of the pro-apoptosis BAX gene and cell cycle inhibitor p21 gene, yet suppresses the expression of the pro-survival BCL2 gene in miBCa cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The combined therapy increases the expression of the pro-apoptosis BAX gene and cell cycle inhibitor p21 gene, yet suppresses the expression of the pro-survival BCL2 gene in miBCa cells.		The combined therapy increases the expression of the pro-apoptosis BAX gene and cell cycle inhibitor p21 gene, yet suppresses the expression of the pro-survival BCL2 gene in miBCa cells.	Immunohistochemical staining	The combined therapy increases the expression of the pro-apoptosis BAX gene and cell cycle inhibitor p21 gene, yet suppresses the expression of the pro-survival BCL2 gene in miBCa cells.			PCR,Western blot,凝胶电泳				BAX
31368839	chr7	22723271	22725271	IL6	The acute response was measured 6 h after ASO administration, via evaluation for increased plasma production of in_x0002_terleukin 6 (IL6), IL10, monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1b(MIP-1b).	human,and,mouse		High+Lowthroughput	Hybrid Mouse Diversity Panel Identifies Genetic Architecture Associated with the Acute Antisense Oligonucleotide-Mediated Inflammatory Response to a 2'-O-Methoxyethyl Antisense Oligonucleotide	是	13479604	Neurological disease	Primary cell	E_02_0663	PCR, flow cytometry	The acute response was measured 6 h after ASO administration, via evaluation for increased plasma production of in_x0002_terleukin 6 (IL6), IL10, monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1b(MIP-1b).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The acute response was measured 6 h after ASO administration, via evaluation for increased plasma production of in_x0002_terleukin 6 (IL6), IL10, monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1b(MIP-1b).		The acute response was measured 6 h after ASO administration, via evaluation for increased plasma production of in_x0002_terleukin 6 (IL6), IL10, monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1b(MIP-1b).	Immunohistochemical staining	The acute response was measured 6 h after ASO administration, via evaluation for increased plasma production of in_x0002_terleukin 6 (IL6), IL10, monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1b(MIP-1b).			PCR,流式细胞术				IL6
31368839	chr1	206765026	206767026	IL10	The acute response was measured 6 h after ASO administration, via evaluation for increased plasma production of in_x0002_terleukin 6 (IL6), IL10, monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1b(MIP-1b).	human,and,mouse		High+Lowthroughput	Hybrid Mouse Diversity Panel Identifies Genetic Architecture Associated with the Acute Antisense Oligonucleotide-Mediated Inflammatory Response to a 2'-O-Methoxyethyl Antisense Oligonucleotide	是	13479604	Neurological disease	Primary cell	E_02_0663	PCR, flow cytometry	The acute response was measured 6 h after ASO administration, via evaluation for increased plasma production of in_x0002_terleukin 6 (IL6), IL10, monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1b(MIP-1b).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The acute response was measured 6 h after ASO administration, via evaluation for increased plasma production of in_x0002_terleukin 6 (IL6), IL10, monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1b(MIP-1b).		The acute response was measured 6 h after ASO administration, via evaluation for increased plasma production of in_x0002_terleukin 6 (IL6), IL10, monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1b(MIP-1b).	Immunohistochemical staining	The acute response was measured 6 h after ASO administration, via evaluation for increased plasma production of in_x0002_terleukin 6 (IL6), IL10, monocyte chemoattractant protein 1 (MCP-1) and macrophage inflammatory protein-1b(MIP-1b).			PCR,流式细胞术				IL10
31368152	chr7	148804623	148806623	EZH2	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.	human,and,mouse	Epithelial tissues	High+Lowthroughput	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells	否	无	Oral diseases	OSCC cell	E_02_0664	Western blot, PCR, gel electrophoresis, flow cytometry	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.		EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.	Immunohistochemical staining	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.			Western blot,PCR,凝胶电泳,流式细胞术				EZH2
31368152	chr17	42310280	42312280	STAT3	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.	human,and,mouse	Epithelial tissues	High+Lowthroughput	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells	否	无	Oral diseases	OSCC cell	E_02_0664	Western blot, PCR, gel electrophoresis, flow cytometry	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.		EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.	Immunohistochemical staining	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.			Western blot,PCR,凝胶电泳,流式细胞术				STAT3
31368152	chr13	40552864	40554864	FOXO1	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.	human,and,mouse	Epithelial tissues	High+Lowthroughput	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells	否	无	Oral diseases	OSCC cell	E_02_0664	Western blot, PCR, gel electrophoresis, flow cytometry	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.		EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.	Immunohistochemical staining	EZH2 promotes invasion and tumour glycolysis by regulating STAT3 and FoxO1 signalling in human OSCC cells.			Western blot,PCR,凝胶电泳,流式细胞术				FOXO1
31367252	chr6	4703582	4705582	CDYL	CDYL promotes the chemoresistance of small cell lung cancer by regulating H3K27 trimethylation at the CDKN1C promoter.	human,and,mouse	lung	High+Lowthroughput	CDYL promotes the chemoresistance of small cell lung cancer by regulating H3K27 trimethylation at the CDKN1C promoter	否	无	Lung cancer	H446 cell	E_02_0665	Western blot, PCR, gene knockdown, gel electrophoresis, flow cytometry	CDYL promotes the chemoresistance of small cell lung cancer by regulating H3K27 trimethylation at the CDKN1C promoter.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CDYL promotes the chemoresistance of small cell lung cancer by regulating H3K27 trimethylation at the CDKN1C promoter.		CDYL promotes the chemoresistance of small cell lung cancer by regulating H3K27 trimethylation at the CDKN1C promoter.	Immunohistochemical staining	CDYL promotes the chemoresistance of small cell lung cancer by regulating H3K27 trimethylation at the CDKN1C promoter.			Western blot,PCR,基因敲降,凝胶电泳,流式细胞术				CDYL
31364785	chr20	50188097	50190097	CEBPB	Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A.	human	tumour	High+Lowthroughput	Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A	否	无	Cancer (cancer)	MG‐63 cell	E_01_0911	Western blot, PCR, gel electrophoresis	Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A.	Immunohistochemical staining	Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A.	CEBPB		Western blot,PCR,凝胶电泳	Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A.			
31364785	chr7	141924226	141926226	CLEC5A	Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A.	human	tumour	High+Lowthroughput	Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A	否	无	Cancer (cancer)	MG‐63 cell	E_01_0911	Western blot, PCR, gel electrophoresis	Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A.		Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A.	Immunohistochemical staining	Transcription factor CEBPB inhibits the proliferation of osteosarcoma by regulating downstream target gene CLEC5A.			Western blot,PCR,凝胶电泳				CLEC5A
31364312	chr16	88640347	88642347	CYBA	The second patient, with autosomal CGD, has  a mutation in the donor splice site of intron 1 of CYBA that activates a cryptic donor  splice site downstream in intron 1, causing the insertion of intronic sequences in the  mRNA.	human		High+Lowthroughput	Activation of cryptic splice sites in three patients with chronic granulomatous disease	否	无	Chronic granulomatous disease	stem cell	E_01_0912	PCR, flow cytometry	The second patient, with autosomal CGD, has  a mutation in the donor splice site of intron 1 of CYBA that activates a cryptic donor  splice site downstream in intron 1, causing the insertion of intronic sequences in the  mRNA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The second patient, with autosomal CGD, has  a mutation in the donor splice site of intron 1 of CYBA that activates a cryptic donor  splice site downstream in intron 1, causing the insertion of intronic sequences in the  mRNA.		The second patient, with autosomal CGD, has  a mutation in the donor splice site of intron 1 of CYBA that activates a cryptic donor  splice site downstream in intron 1, causing the insertion of intronic sequences in the  mRNA.	Immunohistochemical staining	The second patient, with autosomal CGD, has  a mutation in the donor splice site of intron 1 of CYBA that activates a cryptic donor  splice site downstream in intron 1, causing the insertion of intronic sequences in the  mRNA.			PCR,流式细胞术				CYBA
31363085	chr3	8772830	8774830	RAD18	Stimulation of CRISPR-mediated homology-directed repair by an engineered RAD18 variant.	human,and,mouse	embryo	High+Lowthroughput	Stimulation of CRISPR-mediated homology-directed repair by an engineered RAD18 variant	是	无	Genetic disease	HEK293T cell	E_02_0666	Gene knockdown, PCR, flow cytometry	Stimulation of CRISPR-mediated homology-directed repair by an engineered RAD18 variant.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Stimulation of CRISPR-mediated homology-directed repair by an engineered RAD18 variant.		Stimulation of CRISPR-mediated homology-directed repair by an engineered RAD18 variant.	Immunohistochemical staining	Stimulation of CRISPR-mediated homology-directed repair by an engineered RAD18 variant.			基因敲降,PCR,流式细胞术				RAD18
31362988	chr1	56491656	56493656	PLPP3	Regulation of PLPP3 gene expression by NF-κB family transcription factors.	human,and,mouse	Epithelial tissues	High+Lowthroughput	Regulation of PLPP3 gene expression by NF-κB family transcription factors	否	无	Coronary artery disease (CHD)	endothelial cell	E_02_0667	Chip SEQ, Western blot, PCR, gel electrophoresis	Regulation of PLPP3 gene expression by NF-κB family transcription factors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Regulation of PLPP3 gene expression by NF-κB family transcription factors.		Regulation of PLPP3 gene expression by NF-κB family transcription factors.	Immunohistochemical staining	Regulation of PLPP3 gene expression by NF-κB family transcription factors.			ChIP-seq,Western blot,PCR,凝胶电泳				PLPP3
31361039	chr8	127732770	127734770	MYC	Divergent lncRNA MYMLR regulates MYC by eliciting DNA looping and promoter-enhancer interaction.	human	tumour	High+Lowthroughput	Divergent lncRNA MYMLR regulates MYC by eliciting DNA looping and promoter-enhancer interaction	是	无	Cancer (cancer)	cancer cell	E_01_0913	RNA SEQ, Western blot, PCR, gel electrophoresis	Divergent lncRNA MYMLR regulates MYC by eliciting DNA looping and promoter-enhancer interaction.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Divergent lncRNA MYMLR regulates MYC by eliciting DNA looping and promoter-enhancer interaction.	Immunohistochemical staining	Divergent lncRNA MYMLR regulates MYC by eliciting DNA looping and promoter-enhancer interaction.	MYC		RNA-seq,Western blot,PCR,凝胶电泳	Divergent lncRNA MYMLR regulates MYC by eliciting DNA looping and promoter-enhancer interaction.			
31360115	chr13	73052103	73054103	KLF5	Inhibition of super enhancer downregulates the expression of KLF5 in basal-like breast cancers.	human	tumour	High+Lowthroughput	Inhibition of super enhancer downregulates the expression of KLF5 in basal-like breast cancers	否	无	Breast cancer (breast cancer)	HCC1937 cell	E_01_0914	Western blot, PCR, gene knockdown, gel electrophoresis	Inhibition of super enhancer downregulates the expression of KLF5 in basal-like breast cancers.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Inhibition of super enhancer downregulates the expression of KLF5 in basal-like breast cancers.		Inhibition of super enhancer downregulates the expression of KLF5 in basal-like breast cancers.	Immunohistochemical staining	Inhibition of super enhancer downregulates the expression of KLF5 in basal-like breast cancers.			Western blot,PCR,基因敲降,凝胶电泳				KLF5
31360066	chr13	50079217	50081217	DLEU1	Long noncoding RNA DLEU1 aggravates glioma progression via the miR-421/MEF2D axis.	human,and,mouse		High+Lowthroughput	Long noncoding RNA DLEU1 aggravates glioma progression via the miR-421/MEF2D axis	否	无	Cancer (cancer)	glioma cell line	E_02_0668	Western blot, PCR, flow cytometry, gel electrophoresis	Long noncoding RNA DLEU1 aggravates glioma progression via the miR-421/MEF2D axis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Long noncoding RNA DLEU1 aggravates glioma progression via the miR-421/MEF2D axis.		Long noncoding RNA DLEU1 aggravates glioma progression via the miR-421/MEF2D axis.	Immunohistochemical staining	Long noncoding RNA DLEU1 aggravates glioma progression via the miR-421/MEF2D axis.			Western blot,PCR,流式细胞术,凝胶电泳				DLEU1
32311345	chr1	156461010	156463010	MEF2D	Further investigation revealed that myocyte enhancer factor 2D (MEF2D) was the direct target of miR-217.	human	muscle tissue	High+Lowthroughput	miR-217-regulated MEF2D-HDAC5/ND6 signaling pathway participates in the oxidative stress and inflammatory response after cerebral ischemia	不相关	无	cerebral ischemic injury	myocyte	E_01_0915	ChIP-qPCR，Western blot，chromatin immunoprecipitation	Further investigation revealed that myocyte enhancer factor 2D (MEF2D) was the direct target of miR-217.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Further investigation revealed that myocyte enhancer factor 2D (MEF2D) was the direct target of miR-217.		Further investigation revealed that myocyte enhancer factor 2D (MEF2D) was the direct target of miR-217.	Immunohistochemical staining	Further investigation revealed that myocyte enhancer factor 2D (MEF2D) was the direct target of miR-217.			ChIP-qPCR，Western blot，chromatin immunoprecipitation				MEF2D
32309326	chr8	72017196	72019196	TRPA1	The cells were divided into the dorsal root ganglion (DRG) group, mast cell group, DRG + mast cell group, TRPA1 inhibitor or enhancer group, mast cell stabilizer or enhancer group, CCK1-R inhibitor or enhancer group. 	human,mouse	colonic tissue	High+Lowthroughput	Early oral nutrition improves postoperative ileus through the TRPA1/CCK1-R-mediated mast cell-nerve axis	不相关	无	ileus	mast cell	E_02_0669	Western blot,immunofluorescence,RT-qPCR,Real-Time PCR	The cells were divided into the dorsal root ganglion (DRG) group, mast cell group, DRG + mast cell group, TRPA1 inhibitor or enhancer group, mast cell stabilizer or enhancer group, CCK1-R inhibitor or enhancer group. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The cells were divided into the dorsal root ganglion (DRG) group, mast cell group, DRG + mast cell group, TRPA1 inhibitor or enhancer group, mast cell stabilizer or enhancer group, CCK1-R inhibitor or enhancer group. 		The cells were divided into the dorsal root ganglion (DRG) group, mast cell group, DRG + mast cell group, TRPA1 inhibitor or enhancer group, mast cell stabilizer or enhancer group, CCK1-R inhibitor or enhancer group. 	Immunohistochemical staining	The cells were divided into the dorsal root ganglion (DRG) group, mast cell group, DRG + mast cell group, TRPA1 inhibitor or enhancer group, mast cell stabilizer or enhancer group, CCK1-R inhibitor or enhancer group. 			Western blot,immunofluorescence,RT-qPCR,Real-Time PCR				TRPA1
32308692	chr6	118561329	118563329	Cacna1c	Both knockdown of hypoxia inducible factor 1α (HIF-1α) and inactivation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NFКB) pathway inhibited over-expression of miR-711.	human,mouse	heart tissues	High+Lowthroughput	The role of miR-711 in cardiac cells in response to oxidative stress and its biogenesis: a study on H9C2 cells	不相关	无	heart diseases	Cardiac cell	E_02_0670	qRT-PCR,Western blotting,flow cytometry	Both knockdown of hypoxia inducible factor 1α (HIF-1α) and inactivation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NFКB) pathway inhibited over-expression of miR-711.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Both knockdown of hypoxia inducible factor 1α (HIF-1α) and inactivation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NFКB) pathway inhibited over-expression of miR-711.		Both knockdown of hypoxia inducible factor 1α (HIF-1α) and inactivation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NFКB) pathway inhibited over-expression of miR-711.	Immunohistochemical staining	Both knockdown of hypoxia inducible factor 1α (HIF-1α) and inactivation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NFКB) pathway inhibited over-expression of miR-711.			qRT-PCR,Western blotting,flow cytometry				Cacna1c
32308692	chr13	101707700	101709700	FGF14	Both knockdown of hypoxia inducible factor 1α (HIF-1α) and inactivation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NFКB) pathway inhibited over-expression of miR-711.	human,mouse	heart tissues	High+Lowthroughput	The role of miR-711 in cardiac cells in response to oxidative stress and its biogenesis: a study on H9C2 cells	不相关	无	heart diseases	Cardiac cell	E_02_0670	qRT-PCR,Western blotting,flow cytometry	Both knockdown of hypoxia inducible factor 1α (HIF-1α) and inactivation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NFКB) pathway inhibited over-expression of miR-711.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Both knockdown of hypoxia inducible factor 1α (HIF-1α) and inactivation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NFКB) pathway inhibited over-expression of miR-711.		Both knockdown of hypoxia inducible factor 1α (HIF-1α) and inactivation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NFКB) pathway inhibited over-expression of miR-711.	Immunohistochemical staining	Both knockdown of hypoxia inducible factor 1α (HIF-1α) and inactivation of the nuclear factor kappa-light-chain-enhancer of activated B cells (NFКB) pathway inhibited over-expression of miR-711.			qRT-PCR,Western blotting,flow cytometry				FGF14
32308561	chr11	2880343	2882343	CDKN1C	his study proposed a potential therapeutic target lncRNA growth arrest-specific transcript 5 (GAS5) for melanoma, due to its crucial role in oxidative stress and apoptosis of melanoma cells by regulating the enhancer of zeste homolog 2 (EZH2)-mediated CDKN1C expression.	human	melanoma tissues	High+Lowthroughput	Long non-coding RNA GAS5 accelerates oxidative stress in melanoma cells by rescuing EZH2-mediated CDKN1C downregulation	不相关	无	melanoma	melanoma cells	E_01_0916	Fluorescence in situ hybridization,Western blot,RNA immunoprecipitation ,ChIP	his study proposed a potential therapeutic target lncRNA growth arrest-specific transcript 5 (GAS5) for melanoma, due to its crucial role in oxidative stress and apoptosis of melanoma cells by regulating the enhancer of zeste homolog 2 (EZH2)-mediated CDKN1C expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	his study proposed a potential therapeutic target lncRNA growth arrest-specific transcript 5 (GAS5) for melanoma, due to its crucial role in oxidative stress and apoptosis of melanoma cells by regulating the enhancer of zeste homolog 2 (EZH2)-mediated CDKN1C expression.		his study proposed a potential therapeutic target lncRNA growth arrest-specific transcript 5 (GAS5) for melanoma, due to its crucial role in oxidative stress and apoptosis of melanoma cells by regulating the enhancer of zeste homolog 2 (EZH2)-mediated CDKN1C expression.	Immunohistochemical staining	his study proposed a potential therapeutic target lncRNA growth arrest-specific transcript 5 (GAS5) for melanoma, due to its crucial role in oxidative stress and apoptosis of melanoma cells by regulating the enhancer of zeste homolog 2 (EZH2)-mediated CDKN1C expression.			Fluorescence in situ hybridization,Western blot,RNA immunoprecipitation ,ChIP				CDKN1C
32308561	chr7	148804332	148806332	EZH2	his study proposed a potential therapeutic target lncRNA growth arrest-specific transcript 5 (GAS5) for melanoma, due to its crucial role in oxidative stress and apoptosis of melanoma cells by regulating the enhancer of zeste homolog 2 (EZH2)-mediated CDKN1C expression.	human	melanoma tissues	High+Lowthroughput	Long non-coding RNA GAS5 accelerates oxidative stress in melanoma cells by rescuing EZH2-mediated CDKN1C downregulation	不相关	无	melanoma	melanoma cells	E_01_0916	Fluorescence in situ hybridization,Western blot,RNA immunoprecipitation ,ChIP	his study proposed a potential therapeutic target lncRNA growth arrest-specific transcript 5 (GAS5) for melanoma, due to its crucial role in oxidative stress and apoptosis of melanoma cells by regulating the enhancer of zeste homolog 2 (EZH2)-mediated CDKN1C expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			his study proposed a potential therapeutic target lncRNA growth arrest-specific transcript 5 (GAS5) for melanoma, due to its crucial role in oxidative stress and apoptosis of melanoma cells by regulating the enhancer of zeste homolog 2 (EZH2)-mediated CDKN1C expression.	Immunohistochemical staining	his study proposed a potential therapeutic target lncRNA growth arrest-specific transcript 5 (GAS5) for melanoma, due to its crucial role in oxidative stress and apoptosis of melanoma cells by regulating the enhancer of zeste homolog 2 (EZH2)-mediated CDKN1C expression.	EZH2		Fluorescence in situ hybridization,Western blot,RNA immunoprecipitation ,ChIP	his study proposed a potential therapeutic target lncRNA growth arrest-specific transcript 5 (GAS5) for melanoma, due to its crucial role in oxidative stress and apoptosis of melanoma cells by regulating the enhancer of zeste homolog 2 (EZH2)-mediated CDKN1C expression.			
32308428	chr17	72118080	72120080	SOX9	Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1), a highly conserved and newly discovered long non-coding RNA, has been reported to be upregulated and correlated with poor prognosis in colon cancer, but the exact role of it remains uncertain.	human	colon cancer tissue	High+Lowthroughput	Long Non-Coding RNA LEF1-AS1 Promotes Migration, Invasion and Metastasis of Colon Cancer Cells Through miR-30-5p/SOX9 Axis	不相关	无	colon cancer	colon cancer cell	E_01_0917	Western blot,viability assay, colony formation assay, scratch wound healing assay	Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1), a highly conserved and newly discovered long non-coding RNA, has been reported to be upregulated and correlated with poor prognosis in colon cancer, but the exact role of it remains uncertain.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1), a highly conserved and newly discovered long non-coding RNA, has been reported to be upregulated and correlated with poor prognosis in colon cancer, but the exact role of it remains uncertain.	Immunohistochemical staining	Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1), a highly conserved and newly discovered long non-coding RNA, has been reported to be upregulated and correlated with poor prognosis in colon cancer, but the exact role of it remains uncertain.	SOX9		Western blot,viability assay, colony formation assay, scratch wound healing assay	Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1), a highly conserved and newly discovered long non-coding RNA, has been reported to be upregulated and correlated with poor prognosis in colon cancer, but the exact role of it remains uncertain.			
32308428	chr4	108164794	108166794	LEF1-AS1	Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1), a highly conserved and newly discovered long non-coding RNA, has been reported to be upregulated and correlated with poor prognosis in colon cancer, but the exact role of it remains uncertain.	human	colon cancer tissue	High+Lowthroughput	Long Non-Coding RNA LEF1-AS1 Promotes Migration, Invasion and Metastasis of Colon Cancer Cells Through miR-30-5p/SOX9 Axis	不相关	无	colon cancer	colon cancer cell	E_01_0917	Western blot,viability assay, colony formation assay, scratch wound healing assay	Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1), a highly conserved and newly discovered long non-coding RNA, has been reported to be upregulated and correlated with poor prognosis in colon cancer, but the exact role of it remains uncertain.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1), a highly conserved and newly discovered long non-coding RNA, has been reported to be upregulated and correlated with poor prognosis in colon cancer, but the exact role of it remains uncertain.		Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1), a highly conserved and newly discovered long non-coding RNA, has been reported to be upregulated and correlated with poor prognosis in colon cancer, but the exact role of it remains uncertain.	Immunohistochemical staining	Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1), a highly conserved and newly discovered long non-coding RNA, has been reported to be upregulated and correlated with poor prognosis in colon cancer, but the exact role of it remains uncertain.			Western blot,viability assay, colony formation assay, scratch wound healing assay				LEF1-AS1
32305636	chr5	149403478	149405478	CARMN	The results of our study suggested that CARMN variations may affect the risk of esophageal cancer.	human	cancer tissue	High+Lowthroughput	Genetic variations of CARMN affect risk of esophageal cancer in northwest China	相关	rs13177623, rs12654195, rs11168100, rs353303, rs353300, rs353299	esophageal cancer	Esophageal cancer-promoting cell	E_01_0918		The results of our study suggested that CARMN variations may affect the risk of esophageal cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The results of our study suggested that CARMN variations may affect the risk of esophageal cancer.		The results of our study suggested that CARMN variations may affect the risk of esophageal cancer.	Immunohistochemical staining	The results of our study suggested that CARMN variations may affect the risk of esophageal cancer.							CARMN
32303902	chr7	148804273	148806273	EZH2	 Enhancer of zeste homolog 2 (EZH2), the catalytic part of the Polycomb repressive complex 2 (PRC2), has a prognostic role in renal cell carcinoma (RCC) and was recently shown to modulate the immune response by reducing tumor cell immunogenicity.	human	tumor tissue	High+Lowthroughput	High level of EZH2 expression is linked to high density of CD8-positive T-lymphocytes and an aggressive phenotype in renal cell carcinoma	不相关	无	renal cell carcinomas	tumor cell	E_01_0919	immunostaining	 Enhancer of zeste homolog 2 (EZH2), the catalytic part of the Polycomb repressive complex 2 (PRC2), has a prognostic role in renal cell carcinoma (RCC) and was recently shown to modulate the immune response by reducing tumor cell immunogenicity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			 Enhancer of zeste homolog 2 (EZH2), the catalytic part of the Polycomb repressive complex 2 (PRC2), has a prognostic role in renal cell carcinoma (RCC) and was recently shown to modulate the immune response by reducing tumor cell immunogenicity.	Immunohistochemical staining	 Enhancer of zeste homolog 2 (EZH2), the catalytic part of the Polycomb repressive complex 2 (PRC2), has a prognostic role in renal cell carcinoma (RCC) and was recently shown to modulate the immune response by reducing tumor cell immunogenicity.	EZH2		immunostaining	 Enhancer of zeste homolog 2 (EZH2), the catalytic part of the Polycomb repressive complex 2 (PRC2), has a prognostic role in renal cell carcinoma (RCC) and was recently shown to modulate the immune response by reducing tumor cell immunogenicity.			
32286743	chr11	46853685	46855685	LRP4	Using advanced in silico prediction tools of splice-site alterations, including Alamut Visual software, we have demonstrated that the c.1048+6T>C LRP4 variant affects the native donor site and impairs an SC35 enhancer activity.	human	Blood tissue	High+Lowthroughput	A novel biallelic splice-site variant in the LRP4 gene causes sclerosteosis 2	不相关	无	isolated syndactyly		E_01_0920	RT-PCR, qPCR	Using advanced in silico prediction tools of splice-site alterations, including Alamut Visual software, we have demonstrated that the c.1048+6T>C LRP4 variant affects the native donor site and impairs an SC35 enhancer activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Using advanced in silico prediction tools of splice-site alterations, including Alamut Visual software, we have demonstrated that the c.1048+6T>C LRP4 variant affects the native donor site and impairs an SC35 enhancer activity.		Using advanced in silico prediction tools of splice-site alterations, including Alamut Visual software, we have demonstrated that the c.1048+6T>C LRP4 variant affects the native donor site and impairs an SC35 enhancer activity.	Immunohistochemical staining	Using advanced in silico prediction tools of splice-site alterations, including Alamut Visual software, we have demonstrated that the c.1048+6T>C LRP4 variant affects the native donor site and impairs an SC35 enhancer activity.			RT-PCR, qPCR				LRP4
32278790	chr4	102498878	102500878	NFKB1	To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling.	human		High+Lowthroughput	Characterization of the clinical and immunologic phenotype and management of 157 individuals with 56 distinct heterozygous NFKB1 mutations	不相关	无	inborn error of immunity with immune dysregulation	B cell	E_01_0921	Western blotting	To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling.	Immunohistochemical staining	To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling.	NFKB1		Western blotting	To provide evidence for pathogenicity, each variant was assessed in silico; in addition, 32 variants were assessed by functional in vitro testing of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB) signaling.			
32271438	chr7	148804248	148806248	EZH2	EZH2 was highly expressed in glioma cells and EZH2-mediated H3K27me3 enrichment on the MEG3 promoter regulated the growth and metastasis of glioma cells by targeting miR-21-3p. It potentially provided a new therapeutic marker targeting glioma.	human	glioma tissue	High+Lowthroughput	EZH2-mediated H3K27me3 enrichment on the lncRNA MEG3 promoter regulates the growth and metastasis of glioma cells by regulating miR-21-3p	不相关	无	Glioma	glioma cell	E_01_0922	qPCR，Western Blot，ChIP-Real-time PCR	EZH2 was highly expressed in glioma cells and EZH2-mediated H3K27me3 enrichment on the MEG3 promoter regulated the growth and metastasis of glioma cells by targeting miR-21-3p. It potentially provided a new therapeutic marker targeting glioma.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			EZH2 was highly expressed in glioma cells and EZH2-mediated H3K27me3 enrichment on the MEG3 promoter regulated the growth and metastasis of glioma cells by targeting miR-21-3p. It potentially provided a new therapeutic marker targeting glioma.	Immunohistochemical staining	EZH2 was highly expressed in glioma cells and EZH2-mediated H3K27me3 enrichment on the MEG3 promoter regulated the growth and metastasis of glioma cells by targeting miR-21-3p. It potentially provided a new therapeutic marker targeting glioma.	EZH2		qPCR，Western Blot，ChIP-Real-time PCR	EZH2 was highly expressed in glioma cells and EZH2-mediated H3K27me3 enrichment on the MEG3 promoter regulated the growth and metastasis of glioma cells by targeting miR-21-3p. It potentially provided a new therapeutic marker targeting glioma.			
32266019	chr6	3061360	3063360	RIPK1	RIPK1 regulates the survival of Human melanocytes upon endoplasmic reticulum stress	human		High+Lowthroughput	RIPK1 regulates the survival of Human melanocytes upon endoplasmic reticulum stress	不相关	无	Vitiligo	melanocyte	E_01_0923	RT-PCR, Western blot	RIPK1 regulates the survival of Human melanocytes upon endoplasmic reticulum stress	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	RIPK1 regulates the survival of Human melanocytes upon endoplasmic reticulum stress		RIPK1 regulates the survival of Human melanocytes upon endoplasmic reticulum stress	Immunohistochemical staining	RIPK1 regulates the survival of Human melanocytes upon endoplasmic reticulum stress			RT-PCR, Western blot				RIPK1
32265994	chr18	55219283	55221283	TCF4	A huge array of function is played by the Wnt/β-catenin signaling pathway in development by balancing gene expression through the modulation of cell-specific DNA binding downstream effectors such as T-cell factor/lymphoid enhancer factor (TCF/LEF). 	human	tumor tissue	High+Lowthroughput	TCF 4 tumor suppressor: a molecular target in the prognosis of sporadic colorectal cancer in Humans	相关	无	sporadic colorectal cancer	Enterocyte	E_01_0924	qRT-PCR，immunohistochemistry ，western blot	A huge array of function is played by the Wnt/β-catenin signaling pathway in development by balancing gene expression through the modulation of cell-specific DNA binding downstream effectors such as T-cell factor/lymphoid enhancer factor (TCF/LEF). 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			A huge array of function is played by the Wnt/β-catenin signaling pathway in development by balancing gene expression through the modulation of cell-specific DNA binding downstream effectors such as T-cell factor/lymphoid enhancer factor (TCF/LEF). 	Immunohistochemical staining	A huge array of function is played by the Wnt/β-catenin signaling pathway in development by balancing gene expression through the modulation of cell-specific DNA binding downstream effectors such as T-cell factor/lymphoid enhancer factor (TCF/LEF). 	TCF4		qRT-PCR，immunohistochemistry ，western blot	A huge array of function is played by the Wnt/β-catenin signaling pathway in development by balancing gene expression through the modulation of cell-specific DNA binding downstream effectors such as T-cell factor/lymphoid enhancer factor (TCF/LEF). 			
32248974	chr4	108164550	108166550	LEF1-AS1	Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1) was a recently identified lncRNA. 	human	colorectal cancer tissue	High+Lowthroughput	CREB1-induced lncRNA LEF1-AS1 contributes to colorectal cancer progression via the miR-489/DIAPH1 axis	不相关	无	colorectal cancer	Human colorectal carcinoma cell	E_01_0925	Western blot,flow cytometry	Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1) was a recently identified lncRNA. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1) was a recently identified lncRNA. 		Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1) was a recently identified lncRNA. 	Immunohistochemical staining	Lymphoid enhancer-binding factor 1 antisense RNA 1 (LEF1-AS1) was a recently identified lncRNA. 			Western blot,flow cytometry				LEF1-AS1
32242051	chr4	15960268	15962268	PROM1	H3K79me2/3 controls enhancer–promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells	human	fetal tissue	High+Lowthroughput	H3K79me2/3 controls enhancer-promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells	不相关	无	leukemia	Pan-cancer stem cell,leukemia cell	E_01_0926	qRT-PCR,qPCR,flow cytometry,western blot,Immunofluorescence	H3K79me2/3 controls enhancer–promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	H3K79me2/3 controls enhancer–promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells		H3K79me2/3 controls enhancer–promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells	Immunohistochemical staining	H3K79me2/3 controls enhancer–promoter interactions and activation of the pan-cancer stem cell marker PROM1/CD133 in MLL-AF4 leukemia cells			qRT-PCR,qPCR,flow cytometry,western blot,Immunofluorescence				PROM1
32239644	chr6	137863759	137865759	TNFAIP3	By studying the lead expression‐modulating SNP, we uncovered an NF‐κB‐driven regulatory circuit which constrains T‐cell activation through the dynamic formation of a super‐enhancer that upregulates TNFAIP3 (A20), a key NF‐κB inhibitor.	human	primary tissues	High+Lowthroughput	Resolving mechanisms of immune-mediated disease in primary CD4 T cells	相关	rs6759298, rs4672505 and rs13001372，rs1736137	immune disease	T cell	E_01_0927	PCR， qPCR	By studying the lead expression‐modulating SNP, we uncovered an NF‐κB‐driven regulatory circuit which constrains T‐cell activation through the dynamic formation of a super‐enhancer that upregulates TNFAIP3 (A20), a key NF‐κB inhibitor.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			By studying the lead expression‐modulating SNP, we uncovered an NF‐κB‐driven regulatory circuit which constrains T‐cell activation through the dynamic formation of a super‐enhancer that upregulates TNFAIP3 (A20), a key NF‐κB inhibitor.	Immunohistochemical staining	By studying the lead expression‐modulating SNP, we uncovered an NF‐κB‐driven regulatory circuit which constrains T‐cell activation through the dynamic formation of a super‐enhancer that upregulates TNFAIP3 (A20), a key NF‐κB inhibitor.	TNFAIP3		PCR， qPCR	By studying the lead expression‐modulating SNP, we uncovered an NF‐κB‐driven regulatory circuit which constrains T‐cell activation through the dynamic formation of a super‐enhancer that upregulates TNFAIP3 (A20), a key NF‐κB inhibitor.			
32238924	chr19	49082627	49084627	SNRNP70	Acute depletion of U1 snRNA or of the U1 snRNP protein component SNRNP70 markedly reduces the chromatin association of hundreds of lncRNAs and unstable transcripts,without altering the overall transcription rate in cells	human		High+Lowthroughput	U1 snRNP regulates chromatin retention of noncoding RNAs	不相关	无		stem cell	E_01_0928	qPCR，RT-qPCR，ChIP-qPCR，western immunoblot，Flow Cytometry	Acute depletion of U1 snRNA or of the U1 snRNP protein component SNRNP70 markedly reduces the chromatin association of hundreds of lncRNAs and unstable transcripts,without altering the overall transcription rate in cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Acute depletion of U1 snRNA or of the U1 snRNP protein component SNRNP70 markedly reduces the chromatin association of hundreds of lncRNAs and unstable transcripts,without altering the overall transcription rate in cells		Acute depletion of U1 snRNA or of the U1 snRNP protein component SNRNP70 markedly reduces the chromatin association of hundreds of lncRNAs and unstable transcripts,without altering the overall transcription rate in cells	Immunohistochemical staining	Acute depletion of U1 snRNA or of the U1 snRNP protein component SNRNP70 markedly reduces the chromatin association of hundreds of lncRNAs and unstable transcripts,without altering the overall transcription rate in cells			qPCR，RT-qPCR，ChIP-qPCR，western immunoblot，Flow Cytometry				SNRNP70
32237968	chr6	160528481	160530481	LPA	Rs76735376 is an expression quantitative trait loci for the LPA gene and could affect expression by altering enhancer activity.	human	liver tissue	High+Lowthroughput	DNA methylation profiling identifies a high effect genetic variant for lipoprotein(a) levels	相关	rs76735376,rs76735376			E_01_0929	PCR	Rs76735376 is an expression quantitative trait loci for the LPA gene and could affect expression by altering enhancer activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Rs76735376 is an expression quantitative trait loci for the LPA gene and could affect expression by altering enhancer activity.		Rs76735376 is an expression quantitative trait loci for the LPA gene and could affect expression by altering enhancer activity.	Immunohistochemical staining	Rs76735376 is an expression quantitative trait loci for the LPA gene and could affect expression by altering enhancer activity.			PCR				LPA
32231199	chr5	141399891	141401891	PCDHGA9	Laser confocal techniques and western blotting revealed that PCDHGA9 inhibited the nuclear translocation of β-catenin, regulated T cell factor (TCF)/ /lymphoid enhancer factor (LEF) transcriptional activity, directly impacted the signal transmission of the TGF-β/Smad2/3 pathway, strengthened the adhesion complex, weakened the effects of TGF-β, and blocked the activation of the Wnt pathway.	human	cancer tissues	High+Lowthroughput	PCDHGA9 represses epithelial-mesenchymal transition and metastatic potential in gastric cancer cells by reducing β-catenin transcriptional activity	不相关	无	Gastric cancer	gastric cancer cell	E_01_0930	qRT-PCR,qPCR,western blotting	Laser confocal techniques and western blotting revealed that PCDHGA9 inhibited the nuclear translocation of β-catenin, regulated T cell factor (TCF)/ /lymphoid enhancer factor (LEF) transcriptional activity, directly impacted the signal transmission of the TGF-β/Smad2/3 pathway, strengthened the adhesion complex, weakened the effects of TGF-β, and blocked the activation of the Wnt pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Laser confocal techniques and western blotting revealed that PCDHGA9 inhibited the nuclear translocation of β-catenin, regulated T cell factor (TCF)/ /lymphoid enhancer factor (LEF) transcriptional activity, directly impacted the signal transmission of the TGF-β/Smad2/3 pathway, strengthened the adhesion complex, weakened the effects of TGF-β, and blocked the activation of the Wnt pathway.		Laser confocal techniques and western blotting revealed that PCDHGA9 inhibited the nuclear translocation of β-catenin, regulated T cell factor (TCF)/ /lymphoid enhancer factor (LEF) transcriptional activity, directly impacted the signal transmission of the TGF-β/Smad2/3 pathway, strengthened the adhesion complex, weakened the effects of TGF-β, and blocked the activation of the Wnt pathway.	Immunohistochemical staining	Laser confocal techniques and western blotting revealed that PCDHGA9 inhibited the nuclear translocation of β-catenin, regulated T cell factor (TCF)/ /lymphoid enhancer factor (LEF) transcriptional activity, directly impacted the signal transmission of the TGF-β/Smad2/3 pathway, strengthened the adhesion complex, weakened the effects of TGF-β, and blocked the activation of the Wnt pathway.			qRT-PCR,qPCR,western blotting				PCDHGA9
32229255	chr7	30909169	30911169	AQP1	At immunoblotting, HG or HM blunted insulin ability to activate the PI3K/AKT/eNOS pathway, which was reverted through a silencing of aquaporin 1 (AQP1) and Tonicity enhancer binding protein (TonEBP), while inducing p-P38 and pERK1/2.	human	endothelial tissue	High+Lowthroughput	Simulated hyperglycemia impairs insulin signaling in endothelial cells through a hyperosmolar mechanism	不相关	无	Diabetes	endothelial cell	E_01_0931	Immunoblotting	At immunoblotting, HG or HM blunted insulin ability to activate the PI3K/AKT/eNOS pathway, which was reverted through a silencing of aquaporin 1 (AQP1) and Tonicity enhancer binding protein (TonEBP), while inducing p-P38 and pERK1/2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	At immunoblotting, HG or HM blunted insulin ability to activate the PI3K/AKT/eNOS pathway, which was reverted through a silencing of aquaporin 1 (AQP1) and Tonicity enhancer binding protein (TonEBP), while inducing p-P38 and pERK1/2.		At immunoblotting, HG or HM blunted insulin ability to activate the PI3K/AKT/eNOS pathway, which was reverted through a silencing of aquaporin 1 (AQP1) and Tonicity enhancer binding protein (TonEBP), while inducing p-P38 and pERK1/2.	Immunohistochemical staining	At immunoblotting, HG or HM blunted insulin ability to activate the PI3K/AKT/eNOS pathway, which was reverted through a silencing of aquaporin 1 (AQP1) and Tonicity enhancer binding protein (TonEBP), while inducing p-P38 and pERK1/2.			Immunoblotting				AQP1
32226522	chr4	108045215	108047215	LEF1	Our previous studies reported that lymphoid enhancer-binding factor 1 (LEF1) was upregulated in esophageal squamous cell carcinoma (ESCC) and the positive expression of LEF1 was correlated with aberrant clinicopathological characteristics in ESCC patients.	human	esophageal squamous cell carcinoma tissue	High+Lowthroughput	MiR-34a-5p Inhibits Proliferation, Migration, Invasion and Epithelial-mesenchymal Transition in Esophageal Squamous Cell Carcinoma by Targeting LEF1 and Inactivation of the Hippo-YAP1/TAZ Signaling Pathway	不相关	无	esophageal squamous cell carcinoma	oesophageal squamous cell	E_01_0932	qRT-PCR,Western blotting	Our previous studies reported that lymphoid enhancer-binding factor 1 (LEF1) was upregulated in esophageal squamous cell carcinoma (ESCC) and the positive expression of LEF1 was correlated with aberrant clinicopathological characteristics in ESCC patients.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Our previous studies reported that lymphoid enhancer-binding factor 1 (LEF1) was upregulated in esophageal squamous cell carcinoma (ESCC) and the positive expression of LEF1 was correlated with aberrant clinicopathological characteristics in ESCC patients.	Immunohistochemical staining	Our previous studies reported that lymphoid enhancer-binding factor 1 (LEF1) was upregulated in esophageal squamous cell carcinoma (ESCC) and the positive expression of LEF1 was correlated with aberrant clinicopathological characteristics in ESCC patients.	LEF1		qRT-PCR,Western blotting	Our previous studies reported that lymphoid enhancer-binding factor 1 (LEF1) was upregulated in esophageal squamous cell carcinoma (ESCC) and the positive expression of LEF1 was correlated with aberrant clinicopathological characteristics in ESCC patients.			
32619460	chr3	189629192	189631192	TP63	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines	human,mouse	Esophageal Squamous Cell Carcinoma Cell Lines tissue	High+Lowthroughput	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines	不相关	无	esophageal squamous cell carcinoma	Esophageal Squamous Cell Carcinoma Cell	E_02_0671	Immunoprecipitation, Immunoblots, Immunohistochemistry	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines		TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines	Immunohistochemical staining	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines			Immunoprecipitation, Immunoblots, Immunohistochemistry				TP63
32619460	chr3	181709381	181711381	SOX2	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines	human,mouse	Esophageal Squamous Cell Carcinoma Cell Lines tissue	High+Lowthroughput	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines	不相关	无	esophageal squamous cell carcinoma	Esophageal Squamous Cell Carcinoma Cell	E_02_0671	Immunoprecipitation, Immunoblots, Immunohistochemistry	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines		TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines	Immunohistochemical staining	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines			Immunoprecipitation, Immunoblots, Immunohistochemistry				SOX2
32619460	chr13	73052025	73054025	KLF5	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines	human,mouse	Esophageal Squamous Cell Carcinoma Cell Lines tissue	High+Lowthroughput	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines	不相关	无	esophageal squamous cell carcinoma	Esophageal Squamous Cell Carcinoma Cell	E_02_0671	Immunoprecipitation, Immunoblots, Immunohistochemistry	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines		TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines	Immunohistochemical staining	TP63, SOX2, and KLF5 Establish a Core Regulatory Circuitry That Controls Epigenetic and Transcription Patterns in Esophageal Squamous Cell Carcinoma Cell Lines			Immunoprecipitation, Immunoblots, Immunohistochemistry				KLF5
32596374	chr18	63121061	63123061	BCL2	Treatment with nicotine resulted in aggravated expressions of the mRNA or protein level of antiapoptotic (BCL2-associated X protein, B-cell lymphoma-extralarge, and caspase 3), anti-inflammatory (nuclear factor kappa-light-chain-enhancer of activated B cells and tumor necrosis factor-alpha), and vasculogenic (vascular endothelial growth factor-alpha, insulin-like growth factor-1, alpha smooth muscle actin, transforming growth factor-beta 1, and hypoxia inducible factor-1 alpha) factors in the embryo and yolk sac placenta.	human,mouse	Paraplast-embedded tissues	High+Lowthroughput	Protection of Lycopene against Embryonic Anomalies and Yolk Sac Placental Vasculogenic Disorders Induced by Nicotine Exposure	不相关	无	embryonic anomalies		E_02_0672	Real-Time PCR,Western Blotting	Treatment with nicotine resulted in aggravated expressions of the mRNA or protein level of antiapoptotic (BCL2-associated X protein, B-cell lymphoma-extralarge, and caspase 3), anti-inflammatory (nuclear factor kappa-light-chain-enhancer of activated B cells and tumor necrosis factor-alpha), and vasculogenic (vascular endothelial growth factor-alpha, insulin-like growth factor-1, alpha smooth muscle actin, transforming growth factor-beta 1, and hypoxia inducible factor-1 alpha) factors in the embryo and yolk sac placenta.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Treatment with nicotine resulted in aggravated expressions of the mRNA or protein level of antiapoptotic (BCL2-associated X protein, B-cell lymphoma-extralarge, and caspase 3), anti-inflammatory (nuclear factor kappa-light-chain-enhancer of activated B cells and tumor necrosis factor-alpha), and vasculogenic (vascular endothelial growth factor-alpha, insulin-like growth factor-1, alpha smooth muscle actin, transforming growth factor-beta 1, and hypoxia inducible factor-1 alpha) factors in the embryo and yolk sac placenta.		Treatment with nicotine resulted in aggravated expressions of the mRNA or protein level of antiapoptotic (BCL2-associated X protein, B-cell lymphoma-extralarge, and caspase 3), anti-inflammatory (nuclear factor kappa-light-chain-enhancer of activated B cells and tumor necrosis factor-alpha), and vasculogenic (vascular endothelial growth factor-alpha, insulin-like growth factor-1, alpha smooth muscle actin, transforming growth factor-beta 1, and hypoxia inducible factor-1 alpha) factors in the embryo and yolk sac placenta.	Immunohistochemical staining	Treatment with nicotine resulted in aggravated expressions of the mRNA or protein level of antiapoptotic (BCL2-associated X protein, B-cell lymphoma-extralarge, and caspase 3), anti-inflammatory (nuclear factor kappa-light-chain-enhancer of activated B cells and tumor necrosis factor-alpha), and vasculogenic (vascular endothelial growth factor-alpha, insulin-like growth factor-1, alpha smooth muscle actin, transforming growth factor-beta 1, and hypoxia inducible factor-1 alpha) factors in the embryo and yolk sac placenta.			Real-Time PCR,Western Blotting				BCL2
32594099	chr6	88167556	88169556	Gata2	Gata2 −77 enhancer regulates adult hematopoietic stem cell survival	human,mouse	hematopoietic tissues	High+Lowthroughput	Gata2 -77 enhancer regulates adult hematopoietic stem cell survival	不相关	无	leukemogenesis	hematopoietic stem cell	E_02_0673	qRT-PCR,Flow Cytometry	Gata2 −77 enhancer regulates adult hematopoietic stem cell survival	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Gata2 −77 enhancer regulates adult hematopoietic stem cell survival		Gata2 −77 enhancer regulates adult hematopoietic stem cell survival	Immunohistochemical staining	Gata2 −77 enhancer regulates adult hematopoietic stem cell survival			qRT-PCR,Flow Cytometry				Gata2
32562050	chr14	30871818	30873818	COCH	COCH is the most abundantly expressed gene in the cochlea.	human,mouse		High+Lowthroughput	Novel loss-of-function mutations in COCH cause autosomal recessive nonsyndromic hearing loss	相关	无	Nonsyndromic Hearing Loss	MDCK cell	E_02_0674	RT-PCR，PCR	COCH is the most abundantly expressed gene in the cochlea.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	COCH is the most abundantly expressed gene in the cochlea.		COCH is the most abundantly expressed gene in the cochlea.	Immunohistochemical staining	COCH is the most abundantly expressed gene in the cochlea.			RT-PCR，PCR				COCH
32552830	chr4	8842747	8844747	HMX1	uplications involving the long range HMX1 enhancer are associated with Human isolated bilateral concha-type microtia	human,mouse		High+Lowthroughput	Duplications involving the long range HMX1 enhancer are associated with Human isolated bilateral concha-type microtia	相关	rs16891285，rs4696668	Microtia	mesenchymal cell	E_02_0675	qPCR，Gap-PCR	uplications involving the long range HMX1 enhancer are associated with Human isolated bilateral concha-type microtia	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	uplications involving the long range HMX1 enhancer are associated with Human isolated bilateral concha-type microtia		uplications involving the long range HMX1 enhancer are associated with Human isolated bilateral concha-type microtia	Immunohistochemical staining	uplications involving the long range HMX1 enhancer are associated with Human isolated bilateral concha-type microtia			qPCR，Gap-PCR				HMX1
32541005	chr14	56797530	56799530	OTX2	The transcription factor Otx2 is required for photoreceptor and bipolar cell formation in the retina.	human,mouse		High+Lowthroughput	Simultaneous deletion of Prdm1 and Vsx2 enhancers in the retina alters photoreceptor and bipolar cell fate specification, yet differs from deleting both genes	不相关	无		Bipolar cell	E_02_0676	Immunohistochemistry	The transcription factor Otx2 is required for photoreceptor and bipolar cell formation in the retina.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The transcription factor Otx2 is required for photoreceptor and bipolar cell formation in the retina.		The transcription factor Otx2 is required for photoreceptor and bipolar cell formation in the retina.	Immunohistochemical staining	The transcription factor Otx2 is required for photoreceptor and bipolar cell formation in the retina.			Immunohistochemistry				OTX2
32540969	chr8	142907978	142909978	CYP11B2	Effects of intron conversion in the Human CYP11B2 gene on its transcription and blood pressure regulation in transgenic mice	human,mouse	brain tissues	High+Lowthroughput	Effects of intron conversion in the Human CYP11B2 gene on its transcription and blood pressure regulation in transgenic mice	相关	rs1799998，rs13257680，rs542092383，rs1563881467	Hypertension	H295R cell	E_02_0677	real-time PCR，qPCR ，Western blotting，chromatin immunoprecipitation，Immunoblotting	Effects of intron conversion in the Human CYP11B2 gene on its transcription and blood pressure regulation in transgenic mice	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Effects of intron conversion in the Human CYP11B2 gene on its transcription and blood pressure regulation in transgenic mice		Effects of intron conversion in the Human CYP11B2 gene on its transcription and blood pressure regulation in transgenic mice	Immunohistochemical staining	Effects of intron conversion in the Human CYP11B2 gene on its transcription and blood pressure regulation in transgenic mice			real-time PCR，qPCR ，Western blotting，chromatin immunoprecipitation，Immunoblotting				CYP11B2
32538140	chr2	68971694	68973694	GKN1	Coordinate expression loss of GKN1 and GKN2 in gastric cancer via impairment of a glucocorticoid-responsive enhancer	human,mouse	gastric epithelial tissues	High+Lowthroughput	Coordinate expression loss of GKN1 and GKN2 in gastric cancer via impairment of a glucocorticoid-responsive enhancer	不相关	无	gastric cancer	Epithelial cell of stomach	E_02_0678	 QRT-PCR,Immunohistochemistry	Coordinate expression loss of GKN1 and GKN2 in gastric cancer via impairment of a glucocorticoid-responsive enhancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Coordinate expression loss of GKN1 and GKN2 in gastric cancer via impairment of a glucocorticoid-responsive enhancer		Coordinate expression loss of GKN1 and GKN2 in gastric cancer via impairment of a glucocorticoid-responsive enhancer	Immunohistochemical staining	Coordinate expression loss of GKN1 and GKN2 in gastric cancer via impairment of a glucocorticoid-responsive enhancer			 QRT-PCR,Immunohistochemistry				GKN1
32538140	chr2	68942231	68944231	GKN2	Coordinate expression loss of GKN1 and GKN2 in gastric cancer via impairment of a glucocorticoid-responsive enhancer	human,mouse	gastric epithelial tissues	High+Lowthroughput	Coordinate expression loss of GKN1 and GKN2 in gastric cancer via impairment of a glucocorticoid-responsive enhancer	不相关	无	gastric cancer	Epithelial cell of stomach	E_02_0678	 QRT-PCR,Immunohistochemistry	Coordinate expression loss of GKN1 and GKN2 in gastric cancer via impairment of a glucocorticoid-responsive enhancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Coordinate expression loss of GKN1 and GKN2 in gastric cancer via impairment of a glucocorticoid-responsive enhancer		Coordinate expression loss of GKN1 and GKN2 in gastric cancer via impairment of a glucocorticoid-responsive enhancer	Immunohistochemical staining	Coordinate expression loss of GKN1 and GKN2 in gastric cancer via impairment of a glucocorticoid-responsive enhancer			 QRT-PCR,Immunohistochemistry				GKN2
32499518	chr16	69561736	69563736	NFAT5	Here, we report that the tonicity_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_responsive enhancer-binding protein (TonEBP or NFAT5), a Rel family protein involved in the pathogenesis of autoimmune disease and inflammation, is required for maturation and function of DCs.	human,mouse	synovial tissue	High+Lowthroughput	TonEBP in dendritic cells mediates pro-inflammatory maturation and Th1/Th17 responses	不相关	无	rheumatoid arthritis	dendritic cell	E_02_0679	RT-PCR,qPCR	Here, we report that the tonicity_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_responsive enhancer-binding protein (TonEBP or NFAT5), a Rel family protein involved in the pathogenesis of autoimmune disease and inflammation, is required for maturation and function of DCs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here, we report that the tonicity_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_responsive enhancer-binding protein (TonEBP or NFAT5), a Rel family protein involved in the pathogenesis of autoimmune disease and inflammation, is required for maturation and function of DCs.		Here, we report that the tonicity_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_responsive enhancer-binding protein (TonEBP or NFAT5), a Rel family protein involved in the pathogenesis of autoimmune disease and inflammation, is required for maturation and function of DCs.	Immunohistochemical staining	Here, we report that the tonicity_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_responsive enhancer-binding protein (TonEBP or NFAT5), a Rel family protein involved in the pathogenesis of autoimmune disease and inflammation, is required for maturation and function of DCs.			RT-PCR,qPCR				NFAT5
32493933	chr3	108040258	108042258	CD47	Using ATAC-seq and ChIP-seq, we found that acti_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_vation of JUN rendered promoters and enhancers of CD47 and PD-L1 accessible. We furtherdetect increased IL-6 that amplified JUN-mediated CD47 enhancer activity and protein expression.	human,mouse	fibrotic lung tissues.	High+Lowthroughput	Activation of JUN in fibroblasts promotes pro-fibrotic programme and modulates protective immunity	不相关	无	pulmonary fibrosis	stem cell	E_02_0680	ATAC-seq,ChIP-seq,Q-PCR	Using ATAC-seq and ChIP-seq, we found that acti_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_vation of JUN rendered promoters and enhancers of CD47 and PD-L1 accessible. We furtherdetect increased IL-6 that amplified JUN-mediated CD47 enhancer activity and protein expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Using ATAC-seq and ChIP-seq, we found that acti_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_vation of JUN rendered promoters and enhancers of CD47 and PD-L1 accessible. We furtherdetect increased IL-6 that amplified JUN-mediated CD47 enhancer activity and protein expression.		Using ATAC-seq and ChIP-seq, we found that acti_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_vation of JUN rendered promoters and enhancers of CD47 and PD-L1 accessible. We furtherdetect increased IL-6 that amplified JUN-mediated CD47 enhancer activity and protein expression.	Immunohistochemical staining	Using ATAC-seq and ChIP-seq, we found that acti_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_vation of JUN rendered promoters and enhancers of CD47 and PD-L1 accessible. We furtherdetect increased IL-6 that amplified JUN-mediated CD47 enhancer activity and protein expression.			ATAC-seq,ChIP-seq,Q-PCR				CD47
32493794	chrX	49247714	49249714	FOXP3	Targeted insertion of a robust enhancer/promoter proximal to the first coding exon bypassed epigenetic silencing, permitting stable and robust expression of endogenous FOXP3.	human,mouse	lymphoid tissues	High+Lowthroughput	Gene editing to induce FOXP3 expression in Human CD4(+) T cells leads to a stable regulatory phenotype and function	不相关	无	autoimmune disease	T cell	E_02_0681	PCR	Targeted insertion of a robust enhancer/promoter proximal to the first coding exon bypassed epigenetic silencing, permitting stable and robust expression of endogenous FOXP3.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Targeted insertion of a robust enhancer/promoter proximal to the first coding exon bypassed epigenetic silencing, permitting stable and robust expression of endogenous FOXP3.		Targeted insertion of a robust enhancer/promoter proximal to the first coding exon bypassed epigenetic silencing, permitting stable and robust expression of endogenous FOXP3.	Immunohistochemical staining	Targeted insertion of a robust enhancer/promoter proximal to the first coding exon bypassed epigenetic silencing, permitting stable and robust expression of endogenous FOXP3.			PCR				FOXP3
32458986	chr3	4300716	4302716	SETMAR	Mechanistically, RR cells upregulate the Su(var)3-9/enhancer-of-zeste/trithorax (SET) domain and mar_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_iner transposase fusion gene (SETMAR), mediating high levels of H3K36me2 and global euchromatization.	human,mouse		High+Lowthroughput	Inhibition of SETMAR-H3K36me2-NHEJ repair axis in residual disease cells prevents glioblastoma recurrence	不相关	无	Residual disease of glioblastoma	Residual cell	E_02_0682	real-time PCR	Mechanistically, RR cells upregulate the Su(var)3-9/enhancer-of-zeste/trithorax (SET) domain and mar_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_iner transposase fusion gene (SETMAR), mediating high levels of H3K36me2 and global euchromatization.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mechanistically, RR cells upregulate the Su(var)3-9/enhancer-of-zeste/trithorax (SET) domain and mar_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_iner transposase fusion gene (SETMAR), mediating high levels of H3K36me2 and global euchromatization.		Mechanistically, RR cells upregulate the Su(var)3-9/enhancer-of-zeste/trithorax (SET) domain and mar_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_iner transposase fusion gene (SETMAR), mediating high levels of H3K36me2 and global euchromatization.	Immunohistochemical staining	Mechanistically, RR cells upregulate the Su(var)3-9/enhancer-of-zeste/trithorax (SET) domain and mar_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_iner transposase fusion gene (SETMAR), mediating high levels of H3K36me2 and global euchromatization.			real-time PCR				SETMAR
32438714	chr8	11674830	11676830	GATA4	These progenitors derive froma mesodermal lineage characterized by the expression of Gata4 under control of the enhancer G2	human,mouse		High+Lowthroughput	Contribution of a GATA4-Expressing Hematopoietic Progenitor Lineage to the Adult Mouse Endothelium	不相关	无		Blastoderm cell	E_02_0683	Flow Cytometry， Immunofluorescence	These progenitors derive froma mesodermal lineage characterized by the expression of Gata4 under control of the enhancer G2	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These progenitors derive froma mesodermal lineage characterized by the expression of Gata4 under control of the enhancer G2		These progenitors derive froma mesodermal lineage characterized by the expression of Gata4 under control of the enhancer G2	Immunohistochemical staining	These progenitors derive froma mesodermal lineage characterized by the expression of Gata4 under control of the enhancer G2			Flow Cytometry， Immunofluorescence				GATA4
32424849	chr3	119521736	119523736	CD80	"RNA sequencing re_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_vealed that treatment with galectin-1 increased the expression of CCAAT/enhancer
binding protein β and CD163, but decreased the expression of CD80 on BMDMs."	human,mouse	colonic tissues	High+Lowthroughput	Oligosaccharide-dependent anti-inflammatory role of galectin-1 for macrophages in ulcerative colitis	不相关	无	colitis	macrophage	E_02_0684	RT-PCR，qPCR，Western blotting，Flow cytometric	"RNA sequencing re_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_vealed that treatment with galectin-1 increased the expression of CCAAT/enhancer
binding protein β and CD163, but decreased the expression of CD80 on BMDMs."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"RNA sequencing re_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_vealed that treatment with galectin-1 increased the expression of CCAAT/enhancer
binding protein β and CD163, but decreased the expression of CD80 on BMDMs."		"RNA sequencing re_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_vealed that treatment with galectin-1 increased the expression of CCAAT/enhancer
binding protein β and CD163, but decreased the expression of CD80 on BMDMs."	Immunohistochemical staining	"RNA sequencing re_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_vealed that treatment with galectin-1 increased the expression of CCAAT/enhancer
binding protein β and CD163, but decreased the expression of CD80 on BMDMs."			RT-PCR，qPCR，Western blotting，Flow cytometric				CD80
32417536	chr6	60706042	60708042	Snca	Here we tested the hypothesis that Snca deletion in mesenchymal progenitors using the Prrx1Cre (Prrx1, Paired-related homeobox 1) limb enhancer would protect bone mass after OVX.	human,mouse	neural tissue	High+Lowthroughput	Deletion of α-Synuclein in Prrx1-positive cells causes partial loss of function in the central nervous system (CNS) but does not affect ovariectomy induced bone loss	不相关	无	Bone loss	osteoblasts, proerythroblast，macrophage	E_02_0685	RT-qPCR，Western blotting	Here we tested the hypothesis that Snca deletion in mesenchymal progenitors using the Prrx1Cre (Prrx1, Paired-related homeobox 1) limb enhancer would protect bone mass after OVX.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here we tested the hypothesis that Snca deletion in mesenchymal progenitors using the Prrx1Cre (Prrx1, Paired-related homeobox 1) limb enhancer would protect bone mass after OVX.		Here we tested the hypothesis that Snca deletion in mesenchymal progenitors using the Prrx1Cre (Prrx1, Paired-related homeobox 1) limb enhancer would protect bone mass after OVX.	Immunohistochemical staining	Here we tested the hypothesis that Snca deletion in mesenchymal progenitors using the Prrx1Cre (Prrx1, Paired-related homeobox 1) limb enhancer would protect bone mass after OVX.			RT-qPCR，Western blotting				Snca
32405722	chr11	69286483	69288483	Kdm6b	our data support a model whereby Kdm6b induction upon neural commitment relies on an intronic  enhancer the activity of which is defned by its TET3-mediated 5-hmC level.	human,mouse		High+Lowthroughput	TET3 controls the expression of the H3K27me3 demethylase Kdm6b during neural commitment	不相关	无		embryonic stem cell	E_02_0686	real-time PCR，qPCR，Western blotting	our data support a model whereby Kdm6b induction upon neural commitment relies on an intronic  enhancer the activity of which is defned by its TET3-mediated 5-hmC level.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	our data support a model whereby Kdm6b induction upon neural commitment relies on an intronic  enhancer the activity of which is defned by its TET3-mediated 5-hmC level.		our data support a model whereby Kdm6b induction upon neural commitment relies on an intronic  enhancer the activity of which is defned by its TET3-mediated 5-hmC level.	Immunohistochemical staining	our data support a model whereby Kdm6b induction upon neural commitment relies on an intronic  enhancer the activity of which is defned by its TET3-mediated 5-hmC level.			real-time PCR，qPCR，Western blotting				Kdm6b
32403381	chr1	115283607	115285607	NGF	These findings suggest that this combination may be a potential nootropic cognitive enhancer via the induction of NGF and NGF-dependent activities.	human,mouse	Brain Tissue	High+Lowthroughput	The Mixture of Gotu Kola, Cnidium Fruit, and Goji Berry Enhances Memory Functions by Inducing Nerve-Growth-Factor-Mediated Actions Both In Vitro and In Vivo	不相关	无		neuronal cell	E_02_0687	Immunohistochemistry，	These findings suggest that this combination may be a potential nootropic cognitive enhancer via the induction of NGF and NGF-dependent activities.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings suggest that this combination may be a potential nootropic cognitive enhancer via the induction of NGF and NGF-dependent activities.		These findings suggest that this combination may be a potential nootropic cognitive enhancer via the induction of NGF and NGF-dependent activities.	Immunohistochemical staining	These findings suggest that this combination may be a potential nootropic cognitive enhancer via the induction of NGF and NGF-dependent activities.			Immunohistochemistry，				NGF
32398354	chr7	136792610	136794610	Ebf3	Screening enhancer-trap lines of zebrafish allowed us to identify Ebf3 as a transcription factor marking tenocytes and connective tissue cells in skeletal muscle of embryos.	human,mouse	sternum tissues	High+Lowthroughput	Transient and lineage-restricted requirement of Ebf3 for sternum ossification	不相关	无	sternum ossification	mesenchymal cell	E_02_0688	RT-PCR，RNA-seq，Immunostaining	Screening enhancer-trap lines of zebrafish allowed us to identify Ebf3 as a transcription factor marking tenocytes and connective tissue cells in skeletal muscle of embryos.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Screening enhancer-trap lines of zebrafish allowed us to identify Ebf3 as a transcription factor marking tenocytes and connective tissue cells in skeletal muscle of embryos.		Screening enhancer-trap lines of zebrafish allowed us to identify Ebf3 as a transcription factor marking tenocytes and connective tissue cells in skeletal muscle of embryos.	Immunohistochemical staining	Screening enhancer-trap lines of zebrafish allowed us to identify Ebf3 as a transcription factor marking tenocytes and connective tissue cells in skeletal muscle of embryos.			RT-PCR，RNA-seq，Immunostaining				Ebf3
32385306	chr17	72118341	72120341	SOX9	A highly conserved SOX9-binding enhancer located in intron 1 was necessary to drive transcription of Snorc in the Mouse, rat, and Human.	human,mouse	bone tissue	High+Lowthroughput	Biochemical characteristics of the chondrocyte-enriched SNORC protein and its transcriptional regulation by SOX9	不相关	无	 Cartilage		E_02_0689	Real-time qPCR， western blotting	A highly conserved SOX9-binding enhancer located in intron 1 was necessary to drive transcription of Snorc in the Mouse, rat, and Human.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A highly conserved SOX9-binding enhancer located in intron 1 was necessary to drive transcription of Snorc in the Mouse, rat, and Human.		A highly conserved SOX9-binding enhancer located in intron 1 was necessary to drive transcription of Snorc in the Mouse, rat, and Human.	Immunohistochemical staining	A highly conserved SOX9-binding enhancer located in intron 1 was necessary to drive transcription of Snorc in the Mouse, rat, and Human.			Real-time qPCR， western blotting				SOX9
32353178	chr11	65420453	65422453	NEAT1	Intergenic SNP rs12789028 acts as allele-specific long-range enhancer for NEAT1 via chromatin interactions.	human,mouse		High+Lowthroughput	lncRNA Neat1 Stimulates Osteoclastogenesis Via Sponging miR-7	不相关	无	osteoporosis	peripheral blood mononuclear cell	E_02_0690	PCR,RT-PCR	Intergenic SNP rs12789028 acts as allele-specific long-range enhancer for NEAT1 via chromatin interactions.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Intergenic SNP rs12789028 acts as allele-specific long-range enhancer for NEAT1 via chromatin interactions.		Intergenic SNP rs12789028 acts as allele-specific long-range enhancer for NEAT1 via chromatin interactions.	Immunohistochemical staining	Intergenic SNP rs12789028 acts as allele-specific long-range enhancer for NEAT1 via chromatin interactions.			PCR,RT-PCR				NEAT1
32352029	chr1	147538782	147540782	BCL9	BCL9/STAT3 regulation of transcriptional enhancer networks promote DCIS progression	human,mouse	epithelial tissue	High+Lowthroughput	BCL9/STAT3 regulation of transcriptional enhancer networks promote DCIS progression	不相关	无	ductal carcinoma in situ	epithelial cell	E_02_0691	QPCR,ChIP-qPCR,Western blot	BCL9/STAT3 regulation of transcriptional enhancer networks promote DCIS progression	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	BCL9/STAT3 regulation of transcriptional enhancer networks promote DCIS progression		BCL9/STAT3 regulation of transcriptional enhancer networks promote DCIS progression	Immunohistochemical staining	BCL9/STAT3 regulation of transcriptional enhancer networks promote DCIS progression			QPCR,ChIP-qPCR,Western blot				BCL9
32352029	chr17	42310458	42312458	STAT3	BCL9/STAT3 regulation of transcriptional enhancer networks promote DCIS progression	human,mouse	epithelial tissue	High+Lowthroughput	BCL9/STAT3 regulation of transcriptional enhancer networks promote DCIS progression	不相关	无	ductal carcinoma in situ	epithelial cell	E_02_0691	QPCR,ChIP-qPCR,Western blot	BCL9/STAT3 regulation of transcriptional enhancer networks promote DCIS progression	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	BCL9/STAT3 regulation of transcriptional enhancer networks promote DCIS progression		BCL9/STAT3 regulation of transcriptional enhancer networks promote DCIS progression	Immunohistochemical staining	BCL9/STAT3 regulation of transcriptional enhancer networks promote DCIS progression			QPCR,ChIP-qPCR,Western blot				STAT3
32349972	chr2	15937833	15939833	MYCN	We demonstrate this phenotype is mediated through de-repression of a distal PRC2-regulated MYCN enhancer.	human,mouse	Spleen tissue	High+Lowthroughput	EZH2-Deficient T-cell Acute Lymphoblastic Leukemia Is Sensitized to CHK1 Inhibition through Enhanced Replication Stress	相关	无	acute lymphoblastic leukemia	T cell	E_02_0692	Q-PCR,ChIP-qPCR,western blotting	We demonstrate this phenotype is mediated through de-repression of a distal PRC2-regulated MYCN enhancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We demonstrate this phenotype is mediated through de-repression of a distal PRC2-regulated MYCN enhancer.		We demonstrate this phenotype is mediated through de-repression of a distal PRC2-regulated MYCN enhancer.	Immunohistochemical staining	We demonstrate this phenotype is mediated through de-repression of a distal PRC2-regulated MYCN enhancer.			Q-PCR,ChIP-qPCR,western blotting				MYCN
32332097	chr7	148804478	148806478	EZH2	Inhibition of the epigenetic enzyme Enhancer of Zeste Homolog 2 (EZH2) is both bone-anabolic and osteo-protective.	human,mouse	mineralized tissue	High+Lowthroughput	Inhibition of the epigenetic suppressor EZH2 primes osteogenic differentiation mediated by BMP2	不相关	无		mesenchymal stem cell	E_02_0693	RT-qPCR,Western Blotting	Inhibition of the epigenetic enzyme Enhancer of Zeste Homolog 2 (EZH2) is both bone-anabolic and osteo-protective.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Inhibition of the epigenetic enzyme Enhancer of Zeste Homolog 2 (EZH2) is both bone-anabolic and osteo-protective.		Inhibition of the epigenetic enzyme Enhancer of Zeste Homolog 2 (EZH2) is both bone-anabolic and osteo-protective.	Immunohistochemical staining	Inhibition of the epigenetic enzyme Enhancer of Zeste Homolog 2 (EZH2) is both bone-anabolic and osteo-protective.			RT-qPCR,Western Blotting				EZH2
32330245	chr3	128476893	128478893	GATA2	The 3q rearrangements reposition a GATA2 enhancer near the EVI1 (or MECOM)locus, which results in both EVI1 overexpression and GATA2 haploinsufficiency.	human,mouse		High+Lowthroughput	EVI1 and GATA2 misexpression induced by inv(3)(q21q26) contribute to megakaryocyte-lineage skewing and leukemogenesis	不相关	无	megakaryocyte-lineage skewing and leukemogenesis	progenitor cell	E_02_0694	PCR,Flow cytometry,RT-PCR	The 3q rearrangements reposition a GATA2 enhancer near the EVI1 (or MECOM)locus, which results in both EVI1 overexpression and GATA2 haploinsufficiency.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The 3q rearrangements reposition a GATA2 enhancer near the EVI1 (or MECOM)locus, which results in both EVI1 overexpression and GATA2 haploinsufficiency.		The 3q rearrangements reposition a GATA2 enhancer near the EVI1 (or MECOM)locus, which results in both EVI1 overexpression and GATA2 haploinsufficiency.	Immunohistochemical staining	The 3q rearrangements reposition a GATA2 enhancer near the EVI1 (or MECOM)locus, which results in both EVI1 overexpression and GATA2 haploinsufficiency.			PCR,Flow cytometry,RT-PCR				GATA2
32325694	chr6	137864043	137866043	TNFAIP3	The intracellular-ubiquitin-ending-enzyme tumor necrosis factor alpha-induced protein 3(TNFAIP3) is a potent inhibitor of the pro-inflammatory nuclear factor kappa-light-chain-enhancer of activated B cell (NF-kB) pathway.	human,mouse		High+Lowthroughput	TNFAIP3 Deficiency Affects Monocytes, Monocytes-Derived Cells and Microglia in Mice	不相关	无	Inflammation	Monocytes-Derived Cell	E_02_0695	PCR，Flow-Cytometry	The intracellular-ubiquitin-ending-enzyme tumor necrosis factor alpha-induced protein 3(TNFAIP3) is a potent inhibitor of the pro-inflammatory nuclear factor kappa-light-chain-enhancer of activated B cell (NF-kB) pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The intracellular-ubiquitin-ending-enzyme tumor necrosis factor alpha-induced protein 3(TNFAIP3) is a potent inhibitor of the pro-inflammatory nuclear factor kappa-light-chain-enhancer of activated B cell (NF-kB) pathway.		The intracellular-ubiquitin-ending-enzyme tumor necrosis factor alpha-induced protein 3(TNFAIP3) is a potent inhibitor of the pro-inflammatory nuclear factor kappa-light-chain-enhancer of activated B cell (NF-kB) pathway.	Immunohistochemical staining	The intracellular-ubiquitin-ending-enzyme tumor necrosis factor alpha-induced protein 3(TNFAIP3) is a potent inhibitor of the pro-inflammatory nuclear factor kappa-light-chain-enhancer of activated B cell (NF-kB) pathway.			PCR，Flow-Cytometry				TNFAIP3
32321991	chr11	6562441	6564441	Tbrg4	The interdependence of mammary-specific super_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_enhancers and their native promoters facilitates gene activation during pregnancy	human,mouse	liver tissues	High+Lowthroughput	The interdependence of mammary-specific super-enhancers and their native promoters facilitates gene activation during pregnancy	不相关	无		T cell	E_02_0696	qRT-PCR，ChIP-seq	The interdependence of mammary-specific super_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_enhancers and their native promoters facilitates gene activation during pregnancy	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The interdependence of mammary-specific super_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_enhancers and their native promoters facilitates gene activation during pregnancy		The interdependence of mammary-specific super_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_enhancers and their native promoters facilitates gene activation during pregnancy	Immunohistochemical staining	The interdependence of mammary-specific super_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_enhancers and their native promoters facilitates gene activation during pregnancy			qRT-PCR，ChIP-seq				Tbrg4
32318569	chr5	175437606	175439606	DRD1	we report that cocaine-treated male mice showed alterations on specific histone post-translational modifications (PTMs) including increased silent chromatin marks H3K9me3 and H3K27me3 and decreased active enhancer and promoter marks H3K27ac and H3K4me3 in isolated germ cells	human,mouse		High+Lowthroughput	Dopamine Receptor D1 Contributes to Cocaine Epigenetic Reprogramming of Histone Modifications in Male Germ Cells	不相关	无		male germ cells	E_02_0697	RT-PCR，western blot	we report that cocaine-treated male mice showed alterations on specific histone post-translational modifications (PTMs) including increased silent chromatin marks H3K9me3 and H3K27me3 and decreased active enhancer and promoter marks H3K27ac and H3K4me3 in isolated germ cells	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	we report that cocaine-treated male mice showed alterations on specific histone post-translational modifications (PTMs) including increased silent chromatin marks H3K9me3 and H3K27me3 and decreased active enhancer and promoter marks H3K27ac and H3K4me3 in isolated germ cells		we report that cocaine-treated male mice showed alterations on specific histone post-translational modifications (PTMs) including increased silent chromatin marks H3K9me3 and H3K27me3 and decreased active enhancer and promoter marks H3K27ac and H3K4me3 in isolated germ cells	Immunohistochemical staining	we report that cocaine-treated male mice showed alterations on specific histone post-translational modifications (PTMs) including increased silent chromatin marks H3K9me3 and H3K27me3 and decreased active enhancer and promoter marks H3K27ac and H3K4me3 in isolated germ cells			RT-PCR，western blot				DRD1
32299090	chr22	39517359	39519359	ATF4	Notably, HRI-deficient mice display normal Bcl11a levels, suggesting species-selective regulation, which we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable.	human,mouse		High+Lowthroughput	The HRI-regulated transcription factor ATF4 activates BCL11A transcription to silence fetal hemoglobin expression	不相关	无	β-thalassemia	sickle cell	E_02_0698	RT-qPCR,ChIP-seq	Notably, HRI-deficient mice display normal Bcl11a levels, suggesting species-selective regulation, which we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Notably, HRI-deficient mice display normal Bcl11a levels, suggesting species-selective regulation, which we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable.		Notably, HRI-deficient mice display normal Bcl11a levels, suggesting species-selective regulation, which we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable.	Immunohistochemical staining	Notably, HRI-deficient mice display normal Bcl11a levels, suggesting species-selective regulation, which we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable.			RT-qPCR,ChIP-seq				ATF4
32299090	chr2	60448048	60450048	BCL11A	Notably, HRI-deficient mice display normal Bcl11a levels, suggesting species-selective regulation, which we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable.	human,mouse		High+Lowthroughput	The HRI-regulated transcription factor ATF4 activates BCL11A transcription to silence fetal hemoglobin expression	不相关	无	β-thalassemia	sickle cell	E_02_0698	RT-qPCR,ChIP-seq	Notably, HRI-deficient mice display normal Bcl11a levels, suggesting species-selective regulation, which we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Notably, HRI-deficient mice display normal Bcl11a levels, suggesting species-selective regulation, which we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable.		Notably, HRI-deficient mice display normal Bcl11a levels, suggesting species-selective regulation, which we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable.	Immunohistochemical staining	Notably, HRI-deficient mice display normal Bcl11a levels, suggesting species-selective regulation, which we explain here by demonstrating that the analogous ATF4 motif at the murine Bcl11a enhancer is largely dispensable.			RT-qPCR,ChIP-seq				BCL11A
32290615	chr15	97870866	97872866	Col2a1	To investigate the functions of Hck in chondrocytes,transgenic mice expressing a constitutively active form of Hck (HckCA) were generated using the Col2a1 promoter/enhancer.	human,mouse	cartilaginous tissues	High+Lowthroughput	Expression of a Constitutively Active Form of Hck in Chondrocytes Activates Wnt and Hedgehog Signaling Pathways, and Induces Chondrocyte Proliferation in Mice	不相关	无		mutant lymphoma cell	E_02_0699	Real-Time PCR，ChIP	To investigate the functions of Hck in chondrocytes,transgenic mice expressing a constitutively active form of Hck (HckCA) were generated using the Col2a1 promoter/enhancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	To investigate the functions of Hck in chondrocytes,transgenic mice expressing a constitutively active form of Hck (HckCA) were generated using the Col2a1 promoter/enhancer.		To investigate the functions of Hck in chondrocytes,transgenic mice expressing a constitutively active form of Hck (HckCA) were generated using the Col2a1 promoter/enhancer.	Immunohistochemical staining	To investigate the functions of Hck in chondrocytes,transgenic mice expressing a constitutively active form of Hck (HckCA) were generated using the Col2a1 promoter/enhancer.			Real-Time PCR，ChIP				Col2a1
32286279	chr9	14371056	14373056	Kdm4d	TADs are further removed until the 2-cell stage before being progressively reestablished.Obvious defects including stronger TAD boundaries, aberrant super-enhancer and promoter interactions are found in SCNT embryos.	human,mouse		High+Lowthroughput	Chromatin architecture reorganization in murine somatic cell nuclear transfer embryos	不相关	无		somatic cell	E_02_0700	Immunostaining，RNA-seq，ChIP-seq	TADs are further removed until the 2-cell stage before being progressively reestablished.Obvious defects including stronger TAD boundaries, aberrant super-enhancer and promoter interactions are found in SCNT embryos.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	TADs are further removed until the 2-cell stage before being progressively reestablished.Obvious defects including stronger TAD boundaries, aberrant super-enhancer and promoter interactions are found in SCNT embryos.		TADs are further removed until the 2-cell stage before being progressively reestablished.Obvious defects including stronger TAD boundaries, aberrant super-enhancer and promoter interactions are found in SCNT embryos.	Immunohistochemical staining	TADs are further removed until the 2-cell stage before being progressively reestablished.Obvious defects including stronger TAD boundaries, aberrant super-enhancer and promoter interactions are found in SCNT embryos.			Immunostaining，RNA-seq，ChIP-seq				Kdm4d
32286261	chr16	67559535	67561535	CTCF	In mammals, the CTCF protein defines the boundaries of most chromatin loops, and variations in CTCF occupancy are associated with looping divergence.	human,mouse		High+Lowthroughput	Transposable elements contribute to cell and species-specific chromatin looping and gene regulation in mammalian genomes	不相关	无			E_02_0701		In mammals, the CTCF protein defines the boundaries of most chromatin loops, and variations in CTCF occupancy are associated with looping divergence.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In mammals, the CTCF protein defines the boundaries of most chromatin loops, and variations in CTCF occupancy are associated with looping divergence.		In mammals, the CTCF protein defines the boundaries of most chromatin loops, and variations in CTCF occupancy are associated with looping divergence.	Immunohistochemical staining	In mammals, the CTCF protein defines the boundaries of most chromatin loops, and variations in CTCF occupancy are associated with looping divergence.							CTCF
32278722	chr5	75310474	75312474	Pdgfra	We established a con_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ditional knockout Mouse for the Pdgfra gene (N-PRa-KO) using a Nestin promoter/enhancer driven Cre recombi_x0002_nase and examined forebrain development. The expression of PDGFRa was efficiently suppressed in the Olig2+cells in N-PRa-KO mice.	human,mouse	brain tissues	High+Lowthroughput	Oligodendrogenesis and Myelin Formation in the Forebrain Require Platelet-derived Growth Factor Receptor-alpha	不相关	无		Olig2+	E_02_0702	PCR，Immunostainings	We established a con_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ditional knockout Mouse for the Pdgfra gene (N-PRa-KO) using a Nestin promoter/enhancer driven Cre recombi_x0002_nase and examined forebrain development. The expression of PDGFRa was efficiently suppressed in the Olig2+cells in N-PRa-KO mice.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We established a con_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ditional knockout Mouse for the Pdgfra gene (N-PRa-KO) using a Nestin promoter/enhancer driven Cre recombi_x0002_nase and examined forebrain development. The expression of PDGFRa was efficiently suppressed in the Olig2+cells in N-PRa-KO mice.		We established a con_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ditional knockout Mouse for the Pdgfra gene (N-PRa-KO) using a Nestin promoter/enhancer driven Cre recombi_x0002_nase and examined forebrain development. The expression of PDGFRa was efficiently suppressed in the Olig2+cells in N-PRa-KO mice.	Immunohistochemical staining	We established a con_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ditional knockout Mouse for the Pdgfra gene (N-PRa-KO) using a Nestin promoter/enhancer driven Cre recombi_x0002_nase and examined forebrain development. The expression of PDGFRa was efficiently suppressed in the Olig2+cells in N-PRa-KO mice.			PCR，Immunostainings				Pdgfra
32277945	chr5	51380781	51382781	ISL1	Dyslipidemia leads to decreased nitric oxide (NO) bioavailability, an early sign of endothelial failure. Low insulin gene enhancer protein (ISL1) levels decrease healthy NO bioavailability.	human,mouse	aortic tissue	High+Lowthroughput	Statin downregulation of miR-652-3p protects endothelium from dyslipidemia by promoting ISL1 expression	不相关	无	Dyslipidemia	endothelial cell	E_02_0703	qRT-PCR，Western blot	Dyslipidemia leads to decreased nitric oxide (NO) bioavailability, an early sign of endothelial failure. Low insulin gene enhancer protein (ISL1) levels decrease healthy NO bioavailability.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Dyslipidemia leads to decreased nitric oxide (NO) bioavailability, an early sign of endothelial failure. Low insulin gene enhancer protein (ISL1) levels decrease healthy NO bioavailability.		Dyslipidemia leads to decreased nitric oxide (NO) bioavailability, an early sign of endothelial failure. Low insulin gene enhancer protein (ISL1) levels decrease healthy NO bioavailability.	Immunohistochemical staining	Dyslipidemia leads to decreased nitric oxide (NO) bioavailability, an early sign of endothelial failure. Low insulin gene enhancer protein (ISL1) levels decrease healthy NO bioavailability.			qRT-PCR，Western blot				ISL1
32266943	chr18	69473409	69475409	Tcf4	Transcription factor Tcf4 is the preferred heterodimerization partner for Olig2 in oligodendrocytes and required for differentiation	human,mouse	brain tissue	High+Lowthroughput	Transcription factor Tcf4 is the preferred heterodimerization partner for Olig2 in oligodendrocytes and required for differentiation	不相关	无	syndromic and non-syndromic formsof intellectual disability, schizophrenia and autism	primary cell	E_02_0704	Immunocytochemistry，RT-PCR，Chromatin immunoprecipitation	Transcription factor Tcf4 is the preferred heterodimerization partner for Olig2 in oligodendrocytes and required for differentiation	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Transcription factor Tcf4 is the preferred heterodimerization partner for Olig2 in oligodendrocytes and required for differentiation		Transcription factor Tcf4 is the preferred heterodimerization partner for Olig2 in oligodendrocytes and required for differentiation	Immunohistochemical staining	Transcription factor Tcf4 is the preferred heterodimerization partner for Olig2 in oligodendrocytes and required for differentiation			Immunocytochemistry，RT-PCR，Chromatin immunoprecipitation				Tcf4
32257815	chr13	68705525	68707525	Mtrr	Mtrr hypomorphic mutation alters liver morphology, metabolism and fuel storage in mice	human,mouse	liver tissue	High+Lowthroughput	Mtrr hypomorphic mutation alters liver morphology, metabolism and fuel storage in mice	不相关	无	Nonalcoholic fatty liver disease	hepatocyte	E_02_0705	RT-qPCR	Mtrr hypomorphic mutation alters liver morphology, metabolism and fuel storage in mice	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mtrr hypomorphic mutation alters liver morphology, metabolism and fuel storage in mice		Mtrr hypomorphic mutation alters liver morphology, metabolism and fuel storage in mice	Immunohistochemical staining	Mtrr hypomorphic mutation alters liver morphology, metabolism and fuel storage in mice			RT-qPCR				Mtrr
32256588	chr16	72102792	72104792	Robo1	We have shown previously the enhanced cytotoxic effects of saporin-conjugated anti_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_Robo1 immunotoxin (IT-Robo1) on the HNSCC cell line HSQ-89 in combination with a photochemical internalization technique.	human,mouse		High+Lowthroughput	Saponin Facilitates Anti-Robo1 Immunotoxin Cytotoxic Effects on Maxillary Sinus Squamous Cell Carcinoma	不相关	无	Head and neck squamous cell carcinoma	Head and Neck Squamous Cell	E_02_0706	real-time PCR，Western blot， flow cytometry	We have shown previously the enhanced cytotoxic effects of saporin-conjugated anti_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_Robo1 immunotoxin (IT-Robo1) on the HNSCC cell line HSQ-89 in combination with a photochemical internalization technique.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We have shown previously the enhanced cytotoxic effects of saporin-conjugated anti_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_Robo1 immunotoxin (IT-Robo1) on the HNSCC cell line HSQ-89 in combination with a photochemical internalization technique.		We have shown previously the enhanced cytotoxic effects of saporin-conjugated anti_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_Robo1 immunotoxin (IT-Robo1) on the HNSCC cell line HSQ-89 in combination with a photochemical internalization technique.	Immunohistochemical staining	We have shown previously the enhanced cytotoxic effects of saporin-conjugated anti_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_Robo1 immunotoxin (IT-Robo1) on the HNSCC cell line HSQ-89 in combination with a photochemical internalization technique.			real-time PCR，Western blot， flow cytometry				Robo1
32245889	chr19	49672950	49674950	PRMT1	Protein arginine methyltransferase 1 (PRMT1) is a key regulator of hepatic immune responses. 	human,mouse	liver tissue	High+Lowthroughput	The polymorphism rs975484 in the protein arginine methyltransferase 1 gene modulates expression of immune checkpoint genes in hepatocellular carcinoma	相关	rs975484	hepatocellular carcinoma	programmed cell	E_02_0707	Real Time PCR，Immunohistochemistry，ChIP	Protein arginine methyltransferase 1 (PRMT1) is a key regulator of hepatic immune responses. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Protein arginine methyltransferase 1 (PRMT1) is a key regulator of hepatic immune responses. 		Protein arginine methyltransferase 1 (PRMT1) is a key regulator of hepatic immune responses. 	Immunohistochemical staining	Protein arginine methyltransferase 1 (PRMT1) is a key regulator of hepatic immune responses. 			Real Time PCR，Immunohistochemistry，ChIP				PRMT1
32245184	chr12	71935898	71937898	TPH2	For transduction of 5-HT neurons in wildtype mice, adeno-associated virus (AAV) bearing the Mouse tryptophan hydroxylase 2 (TPH2) gene promoter was used.	human,mouse		High+Lowthroughput	The Role of Dorsal Raphe Serotonin Neurons in the Balance between Reward and Aversion	不相关	无		positive cell	E_02_0708	PCR	For transduction of 5-HT neurons in wildtype mice, adeno-associated virus (AAV) bearing the Mouse tryptophan hydroxylase 2 (TPH2) gene promoter was used.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	For transduction of 5-HT neurons in wildtype mice, adeno-associated virus (AAV) bearing the Mouse tryptophan hydroxylase 2 (TPH2) gene promoter was used.		For transduction of 5-HT neurons in wildtype mice, adeno-associated virus (AAV) bearing the Mouse tryptophan hydroxylase 2 (TPH2) gene promoter was used.	Immunohistochemical staining	For transduction of 5-HT neurons in wildtype mice, adeno-associated virus (AAV) bearing the Mouse tryptophan hydroxylase 2 (TPH2) gene promoter was used.			PCR				TPH2
32243837	chr12	49016038	49018038	KMT2D	KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer	human,mouse	lung tumor tissues	High+Lowthroughput	KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer	不相关	无	Lung Cancer	Lung cancer cell	E_02_0709	RT-PCR，ChIP-seq，RNA-seq	KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer		KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer	Immunohistochemical staining	KMT2D Deficiency Impairs Super-Enhancers to Confer a Glycolytic Vulnerability in Lung Cancer			RT-PCR，ChIP-seq，RNA-seq				KMT2D
32241909	chr11	94897936	94899936	Samd14	Deletion of a Samd14 enhancer(Samd14–Enh), occupied by GATA2 and SCL/TAL1 transcrip_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_tion factors, reduces SAMD14 expression in bone marrow and spleen and is lethal in a hemolytic anemia Mouse model.	human,mouse		High+Lowthroughput	Sterile α-motif domain requirement for cellular signaling and survival	不相关	无		precursor cell	E_02_0710	Western blotting，flow cytometric	Deletion of a Samd14 enhancer(Samd14–Enh), occupied by GATA2 and SCL/TAL1 transcrip_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_tion factors, reduces SAMD14 expression in bone marrow and spleen and is lethal in a hemolytic anemia Mouse model.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Deletion of a Samd14 enhancer(Samd14–Enh), occupied by GATA2 and SCL/TAL1 transcrip_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_tion factors, reduces SAMD14 expression in bone marrow and spleen and is lethal in a hemolytic anemia Mouse model.		Deletion of a Samd14 enhancer(Samd14–Enh), occupied by GATA2 and SCL/TAL1 transcrip_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_tion factors, reduces SAMD14 expression in bone marrow and spleen and is lethal in a hemolytic anemia Mouse model.	Immunohistochemical staining	Deletion of a Samd14 enhancer(Samd14–Enh), occupied by GATA2 and SCL/TAL1 transcrip_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_tion factors, reduces SAMD14 expression in bone marrow and spleen and is lethal in a hemolytic anemia Mouse model.			Western blotting，flow cytometric				Samd14
32359406	chr22	41364688	41366688	TEF	We show that Lox interacts with, and directly oxidizes, vestigial-like 3 (Vgll3), a transcriptional co-activator acting with Mef2 and transcriptional enhancer factor (TEF) TFs.	human,mouse	parenchymal tissues	High+Lowthroughput	Intracellular Role for the Matrix-Modifying Enzyme Lox in Regulating Transcription Factor Subcellular Localization and Activity in Muscle Regeneration	不相关	无		progenitor cell	E_02_0711	Western Blot,Real-time Quantitative PCR,Immunofluorescent Staining	We show that Lox interacts with, and directly oxidizes, vestigial-like 3 (Vgll3), a transcriptional co-activator acting with Mef2 and transcriptional enhancer factor (TEF) TFs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We show that Lox interacts with, and directly oxidizes, vestigial-like 3 (Vgll3), a transcriptional co-activator acting with Mef2 and transcriptional enhancer factor (TEF) TFs.		We show that Lox interacts with, and directly oxidizes, vestigial-like 3 (Vgll3), a transcriptional co-activator acting with Mef2 and transcriptional enhancer factor (TEF) TFs.	Immunohistochemical staining	We show that Lox interacts with, and directly oxidizes, vestigial-like 3 (Vgll3), a transcriptional co-activator acting with Mef2 and transcriptional enhancer factor (TEF) TFs.			Western Blot,Real-time Quantitative PCR,Immunofluorescent Staining				TEF
32692439	chr14	95083486	95085486	DICER1	Loss of histone H3 trimethylation on lysine 27 and nuclear expression of transducin-like enhancer 1 in primary intracranial sarcoma, DICER1-mutant	human	brain tissue	High+Lowthroughput	Loss of histone H3 trimethylation on lysine 27 and nuclear expression of transducin-like enhancer 1 in primary intracranial sarcoma, DICER1-mutant	不相关	无	Primary intracranial sarcoma		E_01_0933	Immunohistochemistry	Loss of histone H3 trimethylation on lysine 27 and nuclear expression of transducin-like enhancer 1 in primary intracranial sarcoma, DICER1-mutant	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Loss of histone H3 trimethylation on lysine 27 and nuclear expression of transducin-like enhancer 1 in primary intracranial sarcoma, DICER1-mutant	Immunohistochemical staining	Loss of histone H3 trimethylation on lysine 27 and nuclear expression of transducin-like enhancer 1 in primary intracranial sarcoma, DICER1-mutant	DICER1		Immunohistochemistry	Loss of histone H3 trimethylation on lysine 27 and nuclear expression of transducin-like enhancer 1 in primary intracranial sarcoma, DICER1-mutant			
32691553	chr4	108045150	108047150	LEF1	The spatially and temporally different expression of bone morphogenetic proteins 4 (BMP4), fibroblast growth factor 8 (FGF8), sonic hedgehog (SHH), lymphoid enhancer factor 1 (LEF1) proteins and their genes expression in the early odontogenesis stage (embryo day 10.5 (E10.5)、E11.5、E14.5) in fetal mice were detected by immunohistochemistry staining and quantitative real-time PCR (RT-qPCR). According to the results,we screened the probable key odontogenic genes.	mouse	mesenchymal tissues	High+Lowthroughput	[Screen and Function Study of the Key Regulative Odontogenic Genes in Mice]	不相关	无		epithelial cell	E_02_0712	RT-qPCR, immunohistochemistry staining	The spatially and temporally different expression of bone morphogenetic proteins 4 (BMP4), fibroblast growth factor 8 (FGF8), sonic hedgehog (SHH), lymphoid enhancer factor 1 (LEF1) proteins and their genes expression in the early odontogenesis stage (embryo day 10.5 (E10.5)、E11.5、E14.5) in fetal mice were detected by immunohistochemistry staining and quantitative real-time PCR (RT-qPCR). According to the results,we screened the probable key odontogenic genes.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The spatially and temporally different expression of bone morphogenetic proteins 4 (BMP4), fibroblast growth factor 8 (FGF8), sonic hedgehog (SHH), lymphoid enhancer factor 1 (LEF1) proteins and their genes expression in the early odontogenesis stage (embryo day 10.5 (E10.5)、E11.5、E14.5) in fetal mice were detected by immunohistochemistry staining and quantitative real-time PCR (RT-qPCR). According to the results,we screened the probable key odontogenic genes.		The spatially and temporally different expression of bone morphogenetic proteins 4 (BMP4), fibroblast growth factor 8 (FGF8), sonic hedgehog (SHH), lymphoid enhancer factor 1 (LEF1) proteins and their genes expression in the early odontogenesis stage (embryo day 10.5 (E10.5)、E11.5、E14.5) in fetal mice were detected by immunohistochemistry staining and quantitative real-time PCR (RT-qPCR). According to the results,we screened the probable key odontogenic genes.	Immunohistochemical staining	The spatially and temporally different expression of bone morphogenetic proteins 4 (BMP4), fibroblast growth factor 8 (FGF8), sonic hedgehog (SHH), lymphoid enhancer factor 1 (LEF1) proteins and their genes expression in the early odontogenesis stage (embryo day 10.5 (E10.5)、E11.5、E14.5) in fetal mice were detected by immunohistochemistry staining and quantitative real-time PCR (RT-qPCR). According to the results,we screened the probable key odontogenic genes.			RT-qPCR, immunohistochemistry staining				LEF1
32680982	chr6	34534982	34536982	SPDEF	Enhancer with the risk allele gains response to androgen stimulation by recruiting the transcription factor SPDEF whereas, non-risk alleles remain non-responsive.	human	cancer tissues	High+Lowthroughput	A rare variant of African ancestry activates 8q24 lncRNA hub by modulating cancer associated enhancer	不相关	无	prostate cancer	prostate cancer cell	E_01_0934	q-RT PCR, ChIP-qPCRs	Enhancer with the risk allele gains response to androgen stimulation by recruiting the transcription factor SPDEF whereas, non-risk alleles remain non-responsive.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer with the risk allele gains response to androgen stimulation by recruiting the transcription factor SPDEF whereas, non-risk alleles remain non-responsive.	Immunohistochemical staining	Enhancer with the risk allele gains response to androgen stimulation by recruiting the transcription factor SPDEF whereas, non-risk alleles remain non-responsive.	SPDEF		q-RT PCR, ChIP-qPCRs	Enhancer with the risk allele gains response to androgen stimulation by recruiting the transcription factor SPDEF whereas, non-risk alleles remain non-responsive.			
32680543	chr16	67559370	67561370	CTCF	Sex-difer_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ential chromatin interactions involving sex-biased gene promoters, enhancers, and lncRNAs were associated with sex-biased binding of cohesin and/or CTCF.	mouse	 liver tissue	High+Lowthroughput	Impact of 3D genome organization, guided by cohesin and CTCF looping, on sex-biased chromatin interactions and gene expression in Mouse liver	不相关	无		embryonic stem cell	E_02_0713	PCR，ChIP‑seq	Sex-difer_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ential chromatin interactions involving sex-biased gene promoters, enhancers, and lncRNAs were associated with sex-biased binding of cohesin and/or CTCF.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Sex-difer_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ential chromatin interactions involving sex-biased gene promoters, enhancers, and lncRNAs were associated with sex-biased binding of cohesin and/or CTCF.		Sex-difer_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ential chromatin interactions involving sex-biased gene promoters, enhancers, and lncRNAs were associated with sex-biased binding of cohesin and/or CTCF.	Immunohistochemical staining	Sex-difer_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ential chromatin interactions involving sex-biased gene promoters, enhancers, and lncRNAs were associated with sex-biased binding of cohesin and/or CTCF.			PCR，ChIP‑seq				CTCF
32677466	chr12	7785139	7787139	NANOG	Intersecting NPC core enhancers with TFBSs predicted by Homer [25] revealed 13 transcription factors significantly enriched (q < 0.01 and >20% enhancers with motif ) (Supplementary Figure 2), including the master regulators of pluripotency NANOG and SOX3, as well as key regulators of brain development such as LHX3, a transcription factor involved in the specification of motor neurons and interneurons	human	brain tissue	High+Lowthroughput	Epigenomic programming in early fetal brain development	相关	无		neural progenitor cell	E_01_0935	MeDIP-seq,RNA-seq,miRNA-seq	Intersecting NPC core enhancers with TFBSs predicted by Homer [25] revealed 13 transcription factors significantly enriched (q < 0.01 and >20% enhancers with motif ) (Supplementary Figure 2), including the master regulators of pluripotency NANOG and SOX3, as well as key regulators of brain development such as LHX3, a transcription factor involved in the specification of motor neurons and interneurons	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Intersecting NPC core enhancers with TFBSs predicted by Homer [25] revealed 13 transcription factors significantly enriched (q < 0.01 and >20% enhancers with motif ) (Supplementary Figure 2), including the master regulators of pluripotency NANOG and SOX3, as well as key regulators of brain development such as LHX3, a transcription factor involved in the specification of motor neurons and interneurons		Intersecting NPC core enhancers with TFBSs predicted by Homer [25] revealed 13 transcription factors significantly enriched (q < 0.01 and >20% enhancers with motif ) (Supplementary Figure 2), including the master regulators of pluripotency NANOG and SOX3, as well as key regulators of brain development such as LHX3, a transcription factor involved in the specification of motor neurons and interneurons	Immunohistochemical staining	Intersecting NPC core enhancers with TFBSs predicted by Homer [25] revealed 13 transcription factors significantly enriched (q < 0.01 and >20% enhancers with motif ) (Supplementary Figure 2), including the master regulators of pluripotency NANOG and SOX3, as well as key regulators of brain development such as LHX3, a transcription factor involved in the specification of motor neurons and interneurons			MeDIP-seq,RNA-seq,miRNA-seq				NANOG
32677466	chrX	140500353	140502353	SOX3	Intersecting NPC core enhancers with TFBSs predicted by Homer [25] revealed 13 transcription factors significantly enriched (q < 0.01 and >20% enhancers with motif ) (Supplementary Figure 2), including the master regulators of pluripotency NANOG and SOX3, as well as key regulators of brain development such as LHX3, a transcription factor involved in the specification of motor neurons and interneurons	human	brain tissue	High+Lowthroughput	Epigenomic programming in early fetal brain development	相关	无		neural progenitor cell	E_01_0935	MeDIP-seq,RNA-seq,miRNA-seq	Intersecting NPC core enhancers with TFBSs predicted by Homer [25] revealed 13 transcription factors significantly enriched (q < 0.01 and >20% enhancers with motif ) (Supplementary Figure 2), including the master regulators of pluripotency NANOG and SOX3, as well as key regulators of brain development such as LHX3, a transcription factor involved in the specification of motor neurons and interneurons	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Intersecting NPC core enhancers with TFBSs predicted by Homer [25] revealed 13 transcription factors significantly enriched (q < 0.01 and >20% enhancers with motif ) (Supplementary Figure 2), including the master regulators of pluripotency NANOG and SOX3, as well as key regulators of brain development such as LHX3, a transcription factor involved in the specification of motor neurons and interneurons	Immunohistochemical staining	Intersecting NPC core enhancers with TFBSs predicted by Homer [25] revealed 13 transcription factors significantly enriched (q < 0.01 and >20% enhancers with motif ) (Supplementary Figure 2), including the master regulators of pluripotency NANOG and SOX3, as well as key regulators of brain development such as LHX3, a transcription factor involved in the specification of motor neurons and interneurons	SOX3		MeDIP-seq,RNA-seq,miRNA-seq	Intersecting NPC core enhancers with TFBSs predicted by Homer [25] revealed 13 transcription factors significantly enriched (q < 0.01 and >20% enhancers with motif ) (Supplementary Figure 2), including the master regulators of pluripotency NANOG and SOX3, as well as key regulators of brain development such as LHX3, a transcription factor involved in the specification of motor neurons and interneurons			
32674144	chr7	148804895	148806895	EZH2	Convection-Enhanced Delivery of Enhancer of Zeste Homolog-2 (EZH2) Inhibitor for the Treatment of Diffuse Intrinsic Pontine Glioma	human	brain tissues	High+Lowthroughput	Convection-Enhanced Delivery of Enhancer of Zeste Homolog-2 (EZH2) Inhibitor for the Treatment of Diffuse Intrinsic Pontine Glioma	不相关	无	Brainstem Tumor	stem cell	E_01_0936	Immunoblot,Immunohistochemistry	Convection-Enhanced Delivery of Enhancer of Zeste Homolog-2 (EZH2) Inhibitor for the Treatment of Diffuse Intrinsic Pontine Glioma	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Convection-Enhanced Delivery of Enhancer of Zeste Homolog-2 (EZH2) Inhibitor for the Treatment of Diffuse Intrinsic Pontine Glioma	Immunohistochemical staining	Convection-Enhanced Delivery of Enhancer of Zeste Homolog-2 (EZH2) Inhibitor for the Treatment of Diffuse Intrinsic Pontine Glioma	EZH2		Immunoblot,Immunohistochemistry	Convection-Enhanced Delivery of Enhancer of Zeste Homolog-2 (EZH2) Inhibitor for the Treatment of Diffuse Intrinsic Pontine Glioma			
32673938	chr5	143275121	143277121	NR3C1	DNA methylation standards (100 %; 75 %; 50 %; 25 % and 0 %) and DNA of a female and male donor were bisulfite treated in three independent trials and were used to generate sequencing libraries for 42 CpGs from the NR3C1 1 F promoter region, 84 CpGs of the SLC6A4 5′ regulatory region, 5 CpGs located in FKBP5 intron 7, andadditional 12 CpGs located in a potential enhancer element in intron 3 of the OXTR.	human	brain tissues	High+Lowthroughput	Targeted bisulfite sequencing: A novel tool for the assessment of DNA methylation with high sensitivity and increased coverage	相关	rs114435510,rs75975944,rs7636061		mucosal cell	E_01_0937	PCR	DNA methylation standards (100 %; 75 %; 50 %; 25 % and 0 %) and DNA of a female and male donor were bisulfite treated in three independent trials and were used to generate sequencing libraries for 42 CpGs from the NR3C1 1 F promoter region, 84 CpGs of the SLC6A4 5′ regulatory region, 5 CpGs located in FKBP5 intron 7, andadditional 12 CpGs located in a potential enhancer element in intron 3 of the OXTR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			DNA methylation standards (100 %; 75 %; 50 %; 25 % and 0 %) and DNA of a female and male donor were bisulfite treated in three independent trials and were used to generate sequencing libraries for 42 CpGs from the NR3C1 1 F promoter region, 84 CpGs of the SLC6A4 5′ regulatory region, 5 CpGs located in FKBP5 intron 7, andadditional 12 CpGs located in a potential enhancer element in intron 3 of the OXTR.	Immunohistochemical staining	DNA methylation standards (100 %; 75 %; 50 %; 25 % and 0 %) and DNA of a female and male donor were bisulfite treated in three independent trials and were used to generate sequencing libraries for 42 CpGs from the NR3C1 1 F promoter region, 84 CpGs of the SLC6A4 5′ regulatory region, 5 CpGs located in FKBP5 intron 7, andadditional 12 CpGs located in a potential enhancer element in intron 3 of the OXTR.	NR3C1		PCR	DNA methylation standards (100 %; 75 %; 50 %; 25 % and 0 %) and DNA of a female and male donor were bisulfite treated in three independent trials and were used to generate sequencing libraries for 42 CpGs from the NR3C1 1 F promoter region, 84 CpGs of the SLC6A4 5′ regulatory region, 5 CpGs located in FKBP5 intron 7, andadditional 12 CpGs located in a potential enhancer element in intron 3 of the OXTR.			
32673938	chr6	35571037	35573037	FKBP5	DNA methylation standards (100 %; 75 %; 50 %; 25 % and 0 %) and DNA of a female and male donor were bisulfite treated in three independent trials and were used to generate sequencing libraries for 42 CpGs from the NR3C1 1 F promoter region, 84 CpGs of the SLC6A4 5′ regulatory region, 5 CpGs located in FKBP5 intron 7, andadditional 12 CpGs located in a potential enhancer element in intron 3 of the OXTR.	human	brain tissues	High+Lowthroughput	Targeted bisulfite sequencing: A novel tool for the assessment of DNA methylation with high sensitivity and increased coverage	相关	rs114435510,rs75975944,rs7636061		mucosal cell	E_01_0937	PCR	DNA methylation standards (100 %; 75 %; 50 %; 25 % and 0 %) and DNA of a female and male donor were bisulfite treated in three independent trials and were used to generate sequencing libraries for 42 CpGs from the NR3C1 1 F promoter region, 84 CpGs of the SLC6A4 5′ regulatory region, 5 CpGs located in FKBP5 intron 7, andadditional 12 CpGs located in a potential enhancer element in intron 3 of the OXTR.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	DNA methylation standards (100 %; 75 %; 50 %; 25 % and 0 %) and DNA of a female and male donor were bisulfite treated in three independent trials and were used to generate sequencing libraries for 42 CpGs from the NR3C1 1 F promoter region, 84 CpGs of the SLC6A4 5′ regulatory region, 5 CpGs located in FKBP5 intron 7, andadditional 12 CpGs located in a potential enhancer element in intron 3 of the OXTR.		DNA methylation standards (100 %; 75 %; 50 %; 25 % and 0 %) and DNA of a female and male donor were bisulfite treated in three independent trials and were used to generate sequencing libraries for 42 CpGs from the NR3C1 1 F promoter region, 84 CpGs of the SLC6A4 5′ regulatory region, 5 CpGs located in FKBP5 intron 7, andadditional 12 CpGs located in a potential enhancer element in intron 3 of the OXTR.	Immunohistochemical staining	DNA methylation standards (100 %; 75 %; 50 %; 25 % and 0 %) and DNA of a female and male donor were bisulfite treated in three independent trials and were used to generate sequencing libraries for 42 CpGs from the NR3C1 1 F promoter region, 84 CpGs of the SLC6A4 5′ regulatory region, 5 CpGs located in FKBP5 intron 7, andadditional 12 CpGs located in a potential enhancer element in intron 3 of the OXTR.			PCR				FKBP5
32673756	chr12	57513827	57515827	DDIT3	Commonly associated with endoplasmic reticulum stress, the bZIP transcription factor CCAAT/enhancer-binding protein homologous protein (CHOP/DDIT3) mediates the cellular response to redox stress with effects on cellular growth, differentiation, and survival.	human		High+Lowthroughput	Phosphorylation within the bipartite NLS alters the localization and toxicity of the ER stress response factor DDIT3/CHOP	不相关	无			E_01_0938	Western blotting	Commonly associated with endoplasmic reticulum stress, the bZIP transcription factor CCAAT/enhancer-binding protein homologous protein (CHOP/DDIT3) mediates the cellular response to redox stress with effects on cellular growth, differentiation, and survival.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Commonly associated with endoplasmic reticulum stress, the bZIP transcription factor CCAAT/enhancer-binding protein homologous protein (CHOP/DDIT3) mediates the cellular response to redox stress with effects on cellular growth, differentiation, and survival.	Immunohistochemical staining	Commonly associated with endoplasmic reticulum stress, the bZIP transcription factor CCAAT/enhancer-binding protein homologous protein (CHOP/DDIT3) mediates the cellular response to redox stress with effects on cellular growth, differentiation, and survival.	DDIT3		Western blotting	Commonly associated with endoplasmic reticulum stress, the bZIP transcription factor CCAAT/enhancer-binding protein homologous protein (CHOP/DDIT3) mediates the cellular response to redox stress with effects on cellular growth, differentiation, and survival.			
32672536	chr12	114667169	114669169	TBX3	Trait-associated noncoding variant regions affect TBX3 regulation and cardiac conduction	mouse	cardiac conduction tissue	High+Lowthroughput	Trait-associated noncoding variant regions affect TBX3 regulation and cardiac conduction	不相关	无		stem cell，primary cultured cell	E_02_0714	STARR-seq,ATAC-seq	Trait-associated noncoding variant regions affect TBX3 regulation and cardiac conduction	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Trait-associated noncoding variant regions affect TBX3 regulation and cardiac conduction		Trait-associated noncoding variant regions affect TBX3 regulation and cardiac conduction	Immunohistochemical staining	Trait-associated noncoding variant regions affect TBX3 regulation and cardiac conduction			STARR-seq,ATAC-seq				TBX3
32671756	chr1	156460926	156462926	MEF2D	Myocyte enhancer factor 2D(MEF2D) is an important protein for neuron survival, and it can be degraded by CMA.	mouse	brain tissues	High+Lowthroughput	Autophagy and Tumour Stem Cells	相关	无		Cancer stem cell	E_02_0715		Myocyte enhancer factor 2D(MEF2D) is an important protein for neuron survival, and it can be degraded by CMA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Myocyte enhancer factor 2D(MEF2D) is an important protein for neuron survival, and it can be degraded by CMA.		Myocyte enhancer factor 2D(MEF2D) is an important protein for neuron survival, and it can be degraded by CMA.	Immunohistochemical staining	Myocyte enhancer factor 2D(MEF2D) is an important protein for neuron survival, and it can be degraded by CMA.							MEF2D
32670558	chr3	47411003	47413003	SCAP	3MC induces the expression of PSA, SCAP, and FKBP51 genes in LNCaP and T47D cells.	human		High+Lowthroughput	An androgen-independent mechanism underlying the androgenic effects of 3-methylcholanthrene, a potent aryl hydrocarbon receptor agonist	不相关	无		T47D cell	E_01_0939	RT-PCR,Western blotting,Chromatin immunoprecipitation	3MC induces the expression of PSA, SCAP, and FKBP51 genes in LNCaP and T47D cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	3MC induces the expression of PSA, SCAP, and FKBP51 genes in LNCaP and T47D cells.		3MC induces the expression of PSA, SCAP, and FKBP51 genes in LNCaP and T47D cells.	Immunohistochemical staining	3MC induces the expression of PSA, SCAP, and FKBP51 genes in LNCaP and T47D cells.			RT-PCR,Western blotting,Chromatin immunoprecipitation				SCAP
32669659	chr19	16322430	16324430	KLF2	Mechanistically, NMP increases the expression of the transcription factor Kruppel-like factor 2 (KLF2).	mouse	aortic tissue	High+Lowthroughput	The pharmaceutical solvent N-methyl-2-pyrollidone (NMP) attenuates inflammation through Krüppel-like factor 2 activation to reduce atherogenesis	不相关	无	atherosclerosis	endothelial cell	E_02_0716	Q-PCR,RT‑PCR,Immunohistochemical analysis	Mechanistically, NMP increases the expression of the transcription factor Kruppel-like factor 2 (KLF2).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Mechanistically, NMP increases the expression of the transcription factor Kruppel-like factor 2 (KLF2).		Mechanistically, NMP increases the expression of the transcription factor Kruppel-like factor 2 (KLF2).	Immunohistochemical staining	Mechanistically, NMP increases the expression of the transcription factor Kruppel-like factor 2 (KLF2).			Q-PCR,RT‑PCR,Immunohistochemical analysis				KLF2
32669118	chr18	33575219	33577219	ASXL3	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer	mouse	cancer tissue	High+Lowthroughput	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer	不相关	无	small cell lung cancer	SCLC  cell	E_02_0717	Immunoprecipitation,real-time PCR,ChIP-seq,RNA-seq	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer		ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer	Immunohistochemical staining	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer			Immunoprecipitation,real-time PCR,ChIP-seq,RNA-seq				ASXL3
32669118	chr19	15232539	15234539	BRD4	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer	mouse	cancer tissue	High+Lowthroughput	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer	不相关	无	small cell lung cancer	SCLC  cell	E_02_0717	Immunoprecipitation,real-time PCR,ChIP-seq,RNA-seq	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer		ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer	Immunohistochemical staining	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer			Immunoprecipitation,real-time PCR,ChIP-seq,RNA-seq				BRD4
32669118	chr3	52398485	52400485	BAP1	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer	mouse	cancer tissue	High+Lowthroughput	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer	不相关	无	small cell lung cancer	SCLC  cell	E_02_0717	Immunoprecipitation,real-time PCR,ChIP-seq,RNA-seq	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer		ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer	Immunohistochemical staining	ASXL3 bridges BRD4 to BAP1 complex and governs enhancer activity in small cell lung cancer			Immunoprecipitation,real-time PCR,ChIP-seq,RNA-seq				BAP1
32668391	chr1	153658780	153660780	ILF2	We found that AK085865 specifically in_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_teracts with interleukin enhancer-binding factor 2 (ILF2) and facilitates M2 macrophage polarization by functioning as a negative regulator in the ILF2-ILF3 complex-mediated micro_x0002_RNA (miRNA or miR) processing pathway.	human	heart tissues	High+Lowthroughput	lncRNA AK085865 Promotes Macrophage M2 Polarization in CVB3-Induced VM by Regulating ILF2-ILF3 Complex-Mediated miRNA-192 Biogenesis	不相关	无	myocarditis	inflammatory cell	E_01_0940	qRT-PCR，western blot	We found that AK085865 specifically in_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_teracts with interleukin enhancer-binding factor 2 (ILF2) and facilitates M2 macrophage polarization by functioning as a negative regulator in the ILF2-ILF3 complex-mediated micro_x0002_RNA (miRNA or miR) processing pathway.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We found that AK085865 specifically in_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_teracts with interleukin enhancer-binding factor 2 (ILF2) and facilitates M2 macrophage polarization by functioning as a negative regulator in the ILF2-ILF3 complex-mediated micro_x0002_RNA (miRNA or miR) processing pathway.		We found that AK085865 specifically in_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_teracts with interleukin enhancer-binding factor 2 (ILF2) and facilitates M2 macrophage polarization by functioning as a negative regulator in the ILF2-ILF3 complex-mediated micro_x0002_RNA (miRNA or miR) processing pathway.	Immunohistochemical staining	We found that AK085865 specifically in_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_teracts with interleukin enhancer-binding factor 2 (ILF2) and facilitates M2 macrophage polarization by functioning as a negative regulator in the ILF2-ILF3 complex-mediated micro_x0002_RNA (miRNA or miR) processing pathway.			qRT-PCR，western blot				ILF2
32667910	chr12	85517961	85519961	Fos	Our findings reveal that 533 genes, including known contractility-driving genes(Gap junction alpha 1 [Gja1], FBJ osteosarcoma oncogene [Fos], Fos-like antigen 2 [Fosl2],Oxytocin receptor [Oxtr], and Prostaglandin G/H synthase 2 (Ptgs2), for example), are up_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_regulated at day 19 during active labor because of an increase in transcription at gene bod_x0002_ies.	mouse	myometrial tissues	High+Lowthroughput	The pregnant myometrium is epigenetically activated at contractility-driving gene loci prior to the onset of labor in mice	不相关	无		smooth muscle cell	E_02_0718	RNA-seq,RT-qPCR	Our findings reveal that 533 genes, including known contractility-driving genes(Gap junction alpha 1 [Gja1], FBJ osteosarcoma oncogene [Fos], Fos-like antigen 2 [Fosl2],Oxytocin receptor [Oxtr], and Prostaglandin G/H synthase 2 (Ptgs2), for example), are up_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_regulated at day 19 during active labor because of an increase in transcription at gene bod_x0002_ies.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Our findings reveal that 533 genes, including known contractility-driving genes(Gap junction alpha 1 [Gja1], FBJ osteosarcoma oncogene [Fos], Fos-like antigen 2 [Fosl2],Oxytocin receptor [Oxtr], and Prostaglandin G/H synthase 2 (Ptgs2), for example), are up_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_regulated at day 19 during active labor because of an increase in transcription at gene bod_x0002_ies.		Our findings reveal that 533 genes, including known contractility-driving genes(Gap junction alpha 1 [Gja1], FBJ osteosarcoma oncogene [Fos], Fos-like antigen 2 [Fosl2],Oxytocin receptor [Oxtr], and Prostaglandin G/H synthase 2 (Ptgs2), for example), are up_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_regulated at day 19 during active labor because of an increase in transcription at gene bod_x0002_ies.	Immunohistochemical staining	Our findings reveal that 533 genes, including known contractility-driving genes(Gap junction alpha 1 [Gja1], FBJ osteosarcoma oncogene [Fos], Fos-like antigen 2 [Fosl2],Oxytocin receptor [Oxtr], and Prostaglandin G/H synthase 2 (Ptgs2), for example), are up_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_regulated at day 19 during active labor because of an increase in transcription at gene bod_x0002_ies.			RNA-seq,RT-qPCR				Fos
32664627	chr22	41364474	41366474	TEF	Chagas heart disease; heart endothelial cells; hippo signaling; transcriptional enhancer factor (TEF) family/TEA domain (TEAD) family.	mouse		High+Lowthroughput	Thrombospondin-1 Plays an Essential Role in Yes-Associated Protein Nuclear Translocation during the Early Phase of Trypanosoma cruzi Infection in Heart Endothelial Cells	不相关	无	Trypanosoma cruzi Infection	cardiac endothelial cell	E_02_0719	Immunoblotting, Immunofluorescence	Chagas heart disease; heart endothelial cells; hippo signaling; transcriptional enhancer factor (TEF) family/TEA domain (TEAD) family.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Chagas heart disease; heart endothelial cells; hippo signaling; transcriptional enhancer factor (TEF) family/TEA domain (TEAD) family.		Chagas heart disease; heart endothelial cells; hippo signaling; transcriptional enhancer factor (TEF) family/TEA domain (TEAD) family.	Immunohistochemical staining	Chagas heart disease; heart endothelial cells; hippo signaling; transcriptional enhancer factor (TEF) family/TEA domain (TEAD) family.			Immunoblotting, Immunofluorescence				TEF
32663239	chr10	73906377	73908377	PLAU	We show that the QPD duplication leads to ectopic interactions between PLAU and a conserved megakaryocyte enhancer found within the same topologically associating domain (TAD).	human	non-neuronal solid tissues	High+Lowthroughput	Enhancer-gene rewiring in the pathogenesis of Quebec platelet disorder	相关	rs1916341	Quebec Platelet Disorder	dendritic cell	E_01_0941	ChIP-seq	We show that the QPD duplication leads to ectopic interactions between PLAU and a conserved megakaryocyte enhancer found within the same topologically associating domain (TAD).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We show that the QPD duplication leads to ectopic interactions between PLAU and a conserved megakaryocyte enhancer found within the same topologically associating domain (TAD).		We show that the QPD duplication leads to ectopic interactions between PLAU and a conserved megakaryocyte enhancer found within the same topologically associating domain (TAD).	Immunohistochemical staining	We show that the QPD duplication leads to ectopic interactions between PLAU and a conserved megakaryocyte enhancer found within the same topologically associating domain (TAD).			ChIP-seq				PLAU
32661323	chr8	47734489	47736489	CEBPD	Inhibiting Importin 4-mediated nuclear import of CEBPD enhances chemosensitivity by repression of PRKDC-driven DNA damage repair in cervical cancer	human	sample tissues	High+Lowthroughput	Inhibiting Importin 4-mediated nuclear import of CEBPD enhances chemosensitivity by repression of PRKDC-driven DNA damage repair in cervical cancer	不相关	无	cervical cancer	cervical cancer cells	E_01_0942	qPCR,Immunohistochemistry,Western blotting	Inhibiting Importin 4-mediated nuclear import of CEBPD enhances chemosensitivity by repression of PRKDC-driven DNA damage repair in cervical cancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Inhibiting Importin 4-mediated nuclear import of CEBPD enhances chemosensitivity by repression of PRKDC-driven DNA damage repair in cervical cancer	Immunohistochemical staining	Inhibiting Importin 4-mediated nuclear import of CEBPD enhances chemosensitivity by repression of PRKDC-driven DNA damage repair in cervical cancer	CEBPD		qPCR,Immunohistochemistry,Western blotting	Inhibiting Importin 4-mediated nuclear import of CEBPD enhances chemosensitivity by repression of PRKDC-driven DNA damage repair in cervical cancer			
32661061	chr1	45337174	45339174	TOE1	We show that CRY2 represses TOE1 binding to the regulatory element within the Block E enhancer of FT.	mouse	vascular tissue	High+Lowthroughput	Photoexcited Cryptochrome2 Interacts Directly with TOE1 and TOE2 in Flowering Regulation	不相关	无			E_02_0720	Western Blotting,RT-qPCR,ChIP-qPCR	We show that CRY2 represses TOE1 binding to the regulatory element within the Block E enhancer of FT.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We show that CRY2 represses TOE1 binding to the regulatory element within the Block E enhancer of FT.		We show that CRY2 represses TOE1 binding to the regulatory element within the Block E enhancer of FT.	Immunohistochemical staining	We show that CRY2 represses TOE1 binding to the regulatory element within the Block E enhancer of FT.			Western Blotting,RT-qPCR,ChIP-qPCR				TOE1
32661061	chr11	45844693	45846693	CRY2	We show that CRY2 represses TOE1 binding to the regulatory element within the Block E enhancer of FT.	mouse	vascular tissue	High+Lowthroughput	Photoexcited Cryptochrome2 Interacts Directly with TOE1 and TOE2 in Flowering Regulation	不相关	无			E_02_0720	Western Blotting,RT-qPCR,ChIP-qPCR	We show that CRY2 represses TOE1 binding to the regulatory element within the Block E enhancer of FT.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We show that CRY2 represses TOE1 binding to the regulatory element within the Block E enhancer of FT.		We show that CRY2 represses TOE1 binding to the regulatory element within the Block E enhancer of FT.	Immunohistochemical staining	We show that CRY2 represses TOE1 binding to the regulatory element within the Block E enhancer of FT.			Western Blotting,RT-qPCR,ChIP-qPCR				CRY2
32661056	chr7	148804103	148806103	EZH2	EZH2 emerged as the predominant driver of the differentially downregulated genes. We suggest that functional gene alterations identified in metabolism, transcription and intercellular communication underlie critical microglial heterogeneity and sex differences in CNS regions that contribute to respiratory disorders categorized by dysfunction in neural control.	mouse		High+Lowthroughput	Sex- and Region-Specific Differences in the Transcriptomes of Rat Microglia from the Brainstem and Cervical Spinal Cord	不相关	无		Immune cell	E_02_0721	RNA Sequencing，	EZH2 emerged as the predominant driver of the differentially downregulated genes. We suggest that functional gene alterations identified in metabolism, transcription and intercellular communication underlie critical microglial heterogeneity and sex differences in CNS regions that contribute to respiratory disorders categorized by dysfunction in neural control.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	EZH2 emerged as the predominant driver of the differentially downregulated genes. We suggest that functional gene alterations identified in metabolism, transcription and intercellular communication underlie critical microglial heterogeneity and sex differences in CNS regions that contribute to respiratory disorders categorized by dysfunction in neural control.		EZH2 emerged as the predominant driver of the differentially downregulated genes. We suggest that functional gene alterations identified in metabolism, transcription and intercellular communication underlie critical microglial heterogeneity and sex differences in CNS regions that contribute to respiratory disorders categorized by dysfunction in neural control.	Immunohistochemical staining	EZH2 emerged as the predominant driver of the differentially downregulated genes. We suggest that functional gene alterations identified in metabolism, transcription and intercellular communication underlie critical microglial heterogeneity and sex differences in CNS regions that contribute to respiratory disorders categorized by dysfunction in neural control.			RNA Sequencing，				EZH2
32660626	chr8	101489497	101491497	GRHL2	Expression of miR-130b-3p and GRHL2 was quantified in 63 pairs of cancerous and noncancerous gastric tissues.	human	gastric tissues	High+Lowthroughput	M2 macrophage-derived extracellular vesicles promote gastric cancer progression via a microRNA-130b-3p/MLL3/GRHL2 signaling cascade	不相关	无	gastric cancer	vein endothelial cell	E_01_0943	 chromatin immunoprecipitation	Expression of miR-130b-3p and GRHL2 was quantified in 63 pairs of cancerous and noncancerous gastric tissues.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Expression of miR-130b-3p and GRHL2 was quantified in 63 pairs of cancerous and noncancerous gastric tissues.	Immunohistochemical staining	Expression of miR-130b-3p and GRHL2 was quantified in 63 pairs of cancerous and noncancerous gastric tissues.	GRHL2		 chromatin immunoprecipitation	Expression of miR-130b-3p and GRHL2 was quantified in 63 pairs of cancerous and noncancerous gastric tissues.			
32659776	chr2	135784821	135786821	LCT	Polymorphisms in the enhancer of the lactase gene (LCT) are strongly associated with lactase per_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_sistence, but not always predictive of the phenotype.	human		High+Lowthroughput	Lack of Association between LCT_rs140433552*CA>del Indel Polymorphism and Lactose Intolerance in a Southern Brazilian Population	不相关	rs4988235,rs140433552,rs140433552	Lactose Intolerance		E_01_0944	PCR	Polymorphisms in the enhancer of the lactase gene (LCT) are strongly associated with lactase per_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_sistence, but not always predictive of the phenotype.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Polymorphisms in the enhancer of the lactase gene (LCT) are strongly associated with lactase per_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_sistence, but not always predictive of the phenotype.		Polymorphisms in the enhancer of the lactase gene (LCT) are strongly associated with lactase per_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_sistence, but not always predictive of the phenotype.	Immunohistochemical staining	Polymorphisms in the enhancer of the lactase gene (LCT) are strongly associated with lactase per_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_sistence, but not always predictive of the phenotype.			PCR				LCT
32659720	chr4	38661436	38663436	KLF3	Over half of KLF3’s genomic binding sites occur at active enhancers.KLF3 binds to active enhancers proximal to differentiation genes that are depen_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_dent upon KLF3 for expression.	human	epithelial tissue	High+Lowthroughput	KLF3 Mediates Epidermal Differentiation through the Epigenomic Writer CBP	不相关	无	skin diseases	progenitor cell	E_01_0945	RT-qPCR,Western blot	Over half of KLF3’s genomic binding sites occur at active enhancers.KLF3 binds to active enhancers proximal to differentiation genes that are depen_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_dent upon KLF3 for expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Over half of KLF3’s genomic binding sites occur at active enhancers.KLF3 binds to active enhancers proximal to differentiation genes that are depen_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_dent upon KLF3 for expression.	Immunohistochemical staining	Over half of KLF3’s genomic binding sites occur at active enhancers.KLF3 binds to active enhancers proximal to differentiation genes that are depen_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_dent upon KLF3 for expression.	KLF3		RT-qPCR,Western blot	Over half of KLF3’s genomic binding sites occur at active enhancers.KLF3 binds to active enhancers proximal to differentiation genes that are depen_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_dent upon KLF3 for expression.			
32657761	chr7	148804541	148806541	EZH2	This study proposed a potential target, enhancer of zeste homolog 2 (EZH2) for facilitating hair growth, due to its function over HFSC activities by mediating the miR-22/serine/threonine kinase 40(STK40)/myocyte enhancer factor 2 (MEF2)/alkaline phosphatase (ALP) axis.	human	skin tissues	High+Lowthroughput	EZH2-mediated inhibition of microRNA-22 promotes differentiation of hair follicle stem cells by elevating STK40 expression	不相关	无		Hair Follicle Stem Cell	E_01_0946	Flow cytometry,Immunofluorescence,Western blot,RT-qPCR	This study proposed a potential target, enhancer of zeste homolog 2 (EZH2) for facilitating hair growth, due to its function over HFSC activities by mediating the miR-22/serine/threonine kinase 40(STK40)/myocyte enhancer factor 2 (MEF2)/alkaline phosphatase (ALP) axis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			This study proposed a potential target, enhancer of zeste homolog 2 (EZH2) for facilitating hair growth, due to its function over HFSC activities by mediating the miR-22/serine/threonine kinase 40(STK40)/myocyte enhancer factor 2 (MEF2)/alkaline phosphatase (ALP) axis.	Immunohistochemical staining	This study proposed a potential target, enhancer of zeste homolog 2 (EZH2) for facilitating hair growth, due to its function over HFSC activities by mediating the miR-22/serine/threonine kinase 40(STK40)/myocyte enhancer factor 2 (MEF2)/alkaline phosphatase (ALP) axis.	EZH2		Flow cytometry,Immunofluorescence,Western blot,RT-qPCR	This study proposed a potential target, enhancer of zeste homolog 2 (EZH2) for facilitating hair growth, due to its function over HFSC activities by mediating the miR-22/serine/threonine kinase 40(STK40)/myocyte enhancer factor 2 (MEF2)/alkaline phosphatase (ALP) axis.			
32657640	chr7	37903134	37905134	SFRP4	SFRP4 overexpression affected the expression of genes related to adipocyte differentiation, causing the upregulation of adiponectin and glucose transporter 4, and the downregulation of CCAAT/enhancer-binding protein-β, in both visceral and subcutaneous adipose tissue.	mouse	adipose tissue	High+Lowthroughput	Effects of SFRP4 overexpression on the production of adipokines in transgenic mice	不相关	无	obesity	mesenchymal stem cell	E_02_0722	qPCR,western blotting	SFRP4 overexpression affected the expression of genes related to adipocyte differentiation, causing the upregulation of adiponectin and glucose transporter 4, and the downregulation of CCAAT/enhancer-binding protein-β, in both visceral and subcutaneous adipose tissue.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	SFRP4 overexpression affected the expression of genes related to adipocyte differentiation, causing the upregulation of adiponectin and glucose transporter 4, and the downregulation of CCAAT/enhancer-binding protein-β, in both visceral and subcutaneous adipose tissue.		SFRP4 overexpression affected the expression of genes related to adipocyte differentiation, causing the upregulation of adiponectin and glucose transporter 4, and the downregulation of CCAAT/enhancer-binding protein-β, in both visceral and subcutaneous adipose tissue.	Immunohistochemical staining	SFRP4 overexpression affected the expression of genes related to adipocyte differentiation, causing the upregulation of adiponectin and glucose transporter 4, and the downregulation of CCAAT/enhancer-binding protein-β, in both visceral and subcutaneous adipose tissue.			qPCR,western blotting				SFRP4
32655542	chr7	148804032	148806032	EZH2	The enhancer of zeste homolog 2 (EZH2) promoter activity was evaluated in the presence of miR-200a by dual luciferase reporter gene assay.	human	aorta tissues	High+Lowthroughput	MicroRNA-200a Inhibits Inflammation and Atherosclerotic Lesion Formation by Disrupting EZH2-Mediated Methylation of STAT3	不相关	无	Inflammation and Atherosclerotic	monocyte cells	E_01_0947	Western Blot,Immunoprecipitation,Immunohistochemistry	The enhancer of zeste homolog 2 (EZH2) promoter activity was evaluated in the presence of miR-200a by dual luciferase reporter gene assay.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The enhancer of zeste homolog 2 (EZH2) promoter activity was evaluated in the presence of miR-200a by dual luciferase reporter gene assay.	Immunohistochemical staining	The enhancer of zeste homolog 2 (EZH2) promoter activity was evaluated in the presence of miR-200a by dual luciferase reporter gene assay.	EZH2		Western Blot,Immunoprecipitation,Immunohistochemistry	The enhancer of zeste homolog 2 (EZH2) promoter activity was evaluated in the presence of miR-200a by dual luciferase reporter gene assay.			
32655015	chr19	55425893	55427893	SHISA7	Enhancer Function of MicroRNA-3681 Derived from Long Terminal Repeats Represses the Activity of Variable Number Tandem Repeats in the 3’ UTR of SHISA7	human		High+Lowthroughput	Enhancer Function of MicroRNA-3681 Derived from Long Terminal Repeats Represses the Activity of Variable Number Tandem Repeats in the 3' UTR of SHISA7	不相关	无			E_01_0948	Q-PCR	Enhancer Function of MicroRNA-3681 Derived from Long Terminal Repeats Represses the Activity of Variable Number Tandem Repeats in the 3’ UTR of SHISA7	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer Function of MicroRNA-3681 Derived from Long Terminal Repeats Represses the Activity of Variable Number Tandem Repeats in the 3’ UTR of SHISA7		Enhancer Function of MicroRNA-3681 Derived from Long Terminal Repeats Represses the Activity of Variable Number Tandem Repeats in the 3’ UTR of SHISA7	Immunohistochemical staining	Enhancer Function of MicroRNA-3681 Derived from Long Terminal Repeats Represses the Activity of Variable Number Tandem Repeats in the 3’ UTR of SHISA7			Q-PCR				SHISA7
32654217	chr8	56158114	56160114	PLAG1	These findings indicate that PLAG1 and HMGA2, similar to MYB in adenoid cystic carcinoma, may be activated by enhancer-hijacking events, in which super-enhancers in NFIB are translocated upstream of PLAG1 or downstream of HMGA2.	human	tumor tissue	High+Lowthroughput	Activation of PLAG1 and HMGA2 by gene fusions involving the transcriptional regulator gene NFIB	不相关	无	pleomorphic adenoma	tumor cell	E_01_0949	RT-PCR	These findings indicate that PLAG1 and HMGA2, similar to MYB in adenoid cystic carcinoma, may be activated by enhancer-hijacking events, in which super-enhancers in NFIB are translocated upstream of PLAG1 or downstream of HMGA2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings indicate that PLAG1 and HMGA2, similar to MYB in adenoid cystic carcinoma, may be activated by enhancer-hijacking events, in which super-enhancers in NFIB are translocated upstream of PLAG1 or downstream of HMGA2.		These findings indicate that PLAG1 and HMGA2, similar to MYB in adenoid cystic carcinoma, may be activated by enhancer-hijacking events, in which super-enhancers in NFIB are translocated upstream of PLAG1 or downstream of HMGA2.	Immunohistochemical staining	These findings indicate that PLAG1 and HMGA2, similar to MYB in adenoid cystic carcinoma, may be activated by enhancer-hijacking events, in which super-enhancers in NFIB are translocated upstream of PLAG1 or downstream of HMGA2.			RT-PCR				PLAG1
32654217	chr12	65821787	65823787	HMGA2	These findings indicate that PLAG1 and HMGA2, similar to MYB in adenoid cystic carcinoma, may be activated by enhancer-hijacking events, in which super-enhancers in NFIB are translocated upstream of PLAG1 or downstream of HMGA2.	human	tumor tissue	High+Lowthroughput	Activation of PLAG1 and HMGA2 by gene fusions involving the transcriptional regulator gene NFIB	不相关	无	pleomorphic adenoma	tumor cell	E_01_0949	RT-PCR	These findings indicate that PLAG1 and HMGA2, similar to MYB in adenoid cystic carcinoma, may be activated by enhancer-hijacking events, in which super-enhancers in NFIB are translocated upstream of PLAG1 or downstream of HMGA2.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	These findings indicate that PLAG1 and HMGA2, similar to MYB in adenoid cystic carcinoma, may be activated by enhancer-hijacking events, in which super-enhancers in NFIB are translocated upstream of PLAG1 or downstream of HMGA2.		These findings indicate that PLAG1 and HMGA2, similar to MYB in adenoid cystic carcinoma, may be activated by enhancer-hijacking events, in which super-enhancers in NFIB are translocated upstream of PLAG1 or downstream of HMGA2.	Immunohistochemical staining	These findings indicate that PLAG1 and HMGA2, similar to MYB in adenoid cystic carcinoma, may be activated by enhancer-hijacking events, in which super-enhancers in NFIB are translocated upstream of PLAG1 or downstream of HMGA2.			RT-PCR				HMGA2
32654106	chr11	102108307	102110307	YAP1	Mechanically, immunoprecipitation (IP) was used to show that LATS2 interacted with YAP1 and subsequently limited nuclear translocation of YAP1; chromatin immunoprecipitation (ChIP) was used to confrm that YAP1 could bind to enhancer region of PD-L1 to enhance transcription activity of PD-L1.	human	ovarian cancer tissue	High+Lowthroughput	MiR-92 overexpression suppresses immune cell function in ovarian cancer via LATS2/YAP1/PD-L1 pathway	不相关	无	ovarian cancer	ovarian cancer cell	E_01_0950	RT-PCR,Western blot,Immunoprecipitation	Mechanically, immunoprecipitation (IP) was used to show that LATS2 interacted with YAP1 and subsequently limited nuclear translocation of YAP1; chromatin immunoprecipitation (ChIP) was used to confrm that YAP1 could bind to enhancer region of PD-L1 to enhance transcription activity of PD-L1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Mechanically, immunoprecipitation (IP) was used to show that LATS2 interacted with YAP1 and subsequently limited nuclear translocation of YAP1; chromatin immunoprecipitation (ChIP) was used to confrm that YAP1 could bind to enhancer region of PD-L1 to enhance transcription activity of PD-L1.	Immunohistochemical staining	Mechanically, immunoprecipitation (IP) was used to show that LATS2 interacted with YAP1 and subsequently limited nuclear translocation of YAP1; chromatin immunoprecipitation (ChIP) was used to confrm that YAP1 could bind to enhancer region of PD-L1 to enhance transcription activity of PD-L1.	YAP1		RT-PCR,Western blot,Immunoprecipitation	Mechanically, immunoprecipitation (IP) was used to show that LATS2 interacted with YAP1 and subsequently limited nuclear translocation of YAP1; chromatin immunoprecipitation (ChIP) was used to confrm that YAP1 could bind to enhancer region of PD-L1 to enhance transcription activity of PD-L1.			
32649979	chr7	27097694	27099694	HOXA2	Using dual luciferase reporter assays,we showed that both HOXA2 mutations have impaired activation of the long-range enhancer of HMX1.	human	BA2-derived tissue	High+Lowthroughput	Identification of loss-of-function HOXA2 mutations in Chinese families with dominant bilateral microtia	不相关	无	bilateral microtia	neural crest cell	E_01_0951	PCR	Using dual luciferase reporter assays,we showed that both HOXA2 mutations have impaired activation of the long-range enhancer of HMX1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Using dual luciferase reporter assays,we showed that both HOXA2 mutations have impaired activation of the long-range enhancer of HMX1.	Immunohistochemical staining	Using dual luciferase reporter assays,we showed that both HOXA2 mutations have impaired activation of the long-range enhancer of HMX1.	HOXA2		PCR	Using dual luciferase reporter assays,we showed that both HOXA2 mutations have impaired activation of the long-range enhancer of HMX1.			
32649979	chr4	8843675	8845675	HMX1	Using dual luciferase reporter assays,we showed that both HOXA2 mutations have impaired activation of the long-range enhancer of HMX1.	human	BA2-derived tissue	High+Lowthroughput	Identification of loss-of-function HOXA2 mutations in Chinese families with dominant bilateral microtia	不相关	无	bilateral microtia	neural crest cell	E_01_0951	PCR	Using dual luciferase reporter assays,we showed that both HOXA2 mutations have impaired activation of the long-range enhancer of HMX1.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Using dual luciferase reporter assays,we showed that both HOXA2 mutations have impaired activation of the long-range enhancer of HMX1.		Using dual luciferase reporter assays,we showed that both HOXA2 mutations have impaired activation of the long-range enhancer of HMX1.	Immunohistochemical staining	Using dual luciferase reporter assays,we showed that both HOXA2 mutations have impaired activation of the long-range enhancer of HMX1.			PCR				HMX1
32649856	chrX	48783413	48785413	GATA1	We identified a single sentinel variant in the GRK5 locus (rs10886430-G, p ¼ 3.0 3 10_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ 42) associated with increased thrombin induced platelet aggregation (b ¼ 0.70, SE ¼ 0.05). We show that disruption of platelet GRK5 expression by rs10886430-G is associated with enhanced platelet reactivity. The proposed mechanism of a GATA1-driven megakaryocyte enhancer is confirmed in allele-specific exper_x0002_iments.	human	Genotype-Tissue	High+Lowthroughput	A Platelet Function Modulator of Thrombin Activation Is Causally Linked to Cardiovascular Disease and Affects PAR4 Receptor Signaling	不相关	无	pulmonary embolism		E_01_0952	qRT-PCR	We identified a single sentinel variant in the GRK5 locus (rs10886430-G, p ¼ 3.0 3 10_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ 42) associated with increased thrombin induced platelet aggregation (b ¼ 0.70, SE ¼ 0.05). We show that disruption of platelet GRK5 expression by rs10886430-G is associated with enhanced platelet reactivity. The proposed mechanism of a GATA1-driven megakaryocyte enhancer is confirmed in allele-specific exper_x0002_iments.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We identified a single sentinel variant in the GRK5 locus (rs10886430-G, p ¼ 3.0 3 10_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ 42) associated with increased thrombin induced platelet aggregation (b ¼ 0.70, SE ¼ 0.05). We show that disruption of platelet GRK5 expression by rs10886430-G is associated with enhanced platelet reactivity. The proposed mechanism of a GATA1-driven megakaryocyte enhancer is confirmed in allele-specific exper_x0002_iments.	Immunohistochemical staining	We identified a single sentinel variant in the GRK5 locus (rs10886430-G, p ¼ 3.0 3 10_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ 42) associated with increased thrombin induced platelet aggregation (b ¼ 0.70, SE ¼ 0.05). We show that disruption of platelet GRK5 expression by rs10886430-G is associated with enhanced platelet reactivity. The proposed mechanism of a GATA1-driven megakaryocyte enhancer is confirmed in allele-specific exper_x0002_iments.	GATA1		qRT-PCR	We identified a single sentinel variant in the GRK5 locus (rs10886430-G, p ¼ 3.0 3 10_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ 42) associated with increased thrombin induced platelet aggregation (b ¼ 0.70, SE ¼ 0.05). We show that disruption of platelet GRK5 expression by rs10886430-G is associated with enhanced platelet reactivity. The proposed mechanism of a GATA1-driven megakaryocyte enhancer is confirmed in allele-specific exper_x0002_iments.			
32649856	chr10	119205367	119207367	GRK5	We identified a single sentinel variant in the GRK5 locus (rs10886430-G, p ¼ 3.0 3 10_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ 42) associated with increased thrombin induced platelet aggregation (b ¼ 0.70, SE ¼ 0.05). We show that disruption of platelet GRK5 expression by rs10886430-G is associated with enhanced platelet reactivity. The proposed mechanism of a GATA1-driven megakaryocyte enhancer is confirmed in allele-specific exper_x0002_iments.	human	Genotype-Tissue	High+Lowthroughput	A Platelet Function Modulator of Thrombin Activation Is Causally Linked to Cardiovascular Disease and Affects PAR4 Receptor Signaling	不相关	无	pulmonary embolism		E_01_0952	qRT-PCR	We identified a single sentinel variant in the GRK5 locus (rs10886430-G, p ¼ 3.0 3 10_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ 42) associated with increased thrombin induced platelet aggregation (b ¼ 0.70, SE ¼ 0.05). We show that disruption of platelet GRK5 expression by rs10886430-G is associated with enhanced platelet reactivity. The proposed mechanism of a GATA1-driven megakaryocyte enhancer is confirmed in allele-specific exper_x0002_iments.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identified a single sentinel variant in the GRK5 locus (rs10886430-G, p ¼ 3.0 3 10_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ 42) associated with increased thrombin induced platelet aggregation (b ¼ 0.70, SE ¼ 0.05). We show that disruption of platelet GRK5 expression by rs10886430-G is associated with enhanced platelet reactivity. The proposed mechanism of a GATA1-driven megakaryocyte enhancer is confirmed in allele-specific exper_x0002_iments.		We identified a single sentinel variant in the GRK5 locus (rs10886430-G, p ¼ 3.0 3 10_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ 42) associated with increased thrombin induced platelet aggregation (b ¼ 0.70, SE ¼ 0.05). We show that disruption of platelet GRK5 expression by rs10886430-G is associated with enhanced platelet reactivity. The proposed mechanism of a GATA1-driven megakaryocyte enhancer is confirmed in allele-specific exper_x0002_iments.	Immunohistochemical staining	We identified a single sentinel variant in the GRK5 locus (rs10886430-G, p ¼ 3.0 3 10_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ 42) associated with increased thrombin induced platelet aggregation (b ¼ 0.70, SE ¼ 0.05). We show that disruption of platelet GRK5 expression by rs10886430-G is associated with enhanced platelet reactivity. The proposed mechanism of a GATA1-driven megakaryocyte enhancer is confirmed in allele-specific exper_x0002_iments.			qRT-PCR				GRK5
32647123	chr6	125070535	125072535	Chd4	Conditional knockout of Chd4 promotes recruitment of the archi_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_tectural protein complex cohesin preferentially to gene enhancers in granule neurons in vivo.	mouse		High+Lowthroughput	The chromatin remodeling enzyme Chd4 regulates genome architecture in the Mouse brain	不相关	无		embryonic stem cell	E_02_0723	DNaseI-seq,ChIP-seq,RNA-seq	Conditional knockout of Chd4 promotes recruitment of the archi_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_tectural protein complex cohesin preferentially to gene enhancers in granule neurons in vivo.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Conditional knockout of Chd4 promotes recruitment of the archi_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_tectural protein complex cohesin preferentially to gene enhancers in granule neurons in vivo.		Conditional knockout of Chd4 promotes recruitment of the archi_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_tectural protein complex cohesin preferentially to gene enhancers in granule neurons in vivo.	Immunohistochemical staining	Conditional knockout of Chd4 promotes recruitment of the archi_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_tectural protein complex cohesin preferentially to gene enhancers in granule neurons in vivo.			DNaseI-seq,ChIP-seq,RNA-seq				Chd4
32641411	chr3	138941350	138943350	FOXL2	This binding induced an enhancer-like chromatin state, leading to transcription of nearby genes, many of which are characteristic of epithelial-to_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_mesenchymal transition. FOXL2C134W also bound hybrid loci in primary AGCT.	human	tumor tissue	High+Lowthroughput	Mutant FOXL2(C134W) Hijacks SMAD4 and SMAD2/3 to Drive Adult Granulosa Cell Tumors	不相关	无	Granulosa Cell Tumors	Ovarian granulosa cell	E_01_0953	ChIP-seq，RNA-seq	This binding induced an enhancer-like chromatin state, leading to transcription of nearby genes, many of which are characteristic of epithelial-to_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_mesenchymal transition. FOXL2C134W also bound hybrid loci in primary AGCT.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			This binding induced an enhancer-like chromatin state, leading to transcription of nearby genes, many of which are characteristic of epithelial-to_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_mesenchymal transition. FOXL2C134W also bound hybrid loci in primary AGCT.	Immunohistochemical staining	This binding induced an enhancer-like chromatin state, leading to transcription of nearby genes, many of which are characteristic of epithelial-to_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_mesenchymal transition. FOXL2C134W also bound hybrid loci in primary AGCT.	FOXL2		ChIP-seq，RNA-seq	This binding induced an enhancer-like chromatin state, leading to transcription of nearby genes, many of which are characteristic of epithelial-to_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_mesenchymal transition. FOXL2C134W also bound hybrid loci in primary AGCT.			
32636391	chr17	42310887	42312887	STAT3	We identify key transcription factors including HNF4A, GR,STAT3 and STAT5, which show specific binding at enhancer and super enhancer sites,revealing enhancer dynamics and transcriptional changes during kidney repair.	human	kidney tissue	High+Lowthroughput	Enhancer and super-enhancer dynamics in repair after ischemic acute kidney injury	不相关	无	kidney disease	tubular epithelial cell	E_01_0954	ChIP-seq,RNA-seq	We identify key transcription factors including HNF4A, GR,STAT3 and STAT5, which show specific binding at enhancer and super enhancer sites,revealing enhancer dynamics and transcriptional changes during kidney repair.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We identify key transcription factors including HNF4A, GR,STAT3 and STAT5, which show specific binding at enhancer and super enhancer sites,revealing enhancer dynamics and transcriptional changes during kidney repair.	Immunohistochemical staining	We identify key transcription factors including HNF4A, GR,STAT3 and STAT5, which show specific binding at enhancer and super enhancer sites,revealing enhancer dynamics and transcriptional changes during kidney repair.	STAT3		ChIP-seq,RNA-seq	We identify key transcription factors including HNF4A, GR,STAT3 and STAT5, which show specific binding at enhancer and super enhancer sites,revealing enhancer dynamics and transcriptional changes during kidney repair.			
32635336	chr7	148804321	148806321	EZH2	Enhancer of zeste homolog 2(EZH2) and C-X-C motif chemokine receptor 4 (CXCR4) have been determined to have important roles in the occurrence and development of tumors, but the specific relationship between EZH2 and CXCR4 expression in GBM is less well characterized.	human	Glioblastoma tissue	High+Lowthroughput	Epigenetic Silencing of miR-9 Promotes Migration and Invasion by EZH2 in Glioblastoma Cells	不相关	无	Glioblastoma	glioblastoma cell	E_01_0955	qRT-PCR,Chromatin Immunoprecipitation,Western Blot	Enhancer of zeste homolog 2(EZH2) and C-X-C motif chemokine receptor 4 (CXCR4) have been determined to have important roles in the occurrence and development of tumors, but the specific relationship between EZH2 and CXCR4 expression in GBM is less well characterized.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2(EZH2) and C-X-C motif chemokine receptor 4 (CXCR4) have been determined to have important roles in the occurrence and development of tumors, but the specific relationship between EZH2 and CXCR4 expression in GBM is less well characterized.	Immunohistochemical staining	Enhancer of zeste homolog 2(EZH2) and C-X-C motif chemokine receptor 4 (CXCR4) have been determined to have important roles in the occurrence and development of tumors, but the specific relationship between EZH2 and CXCR4 expression in GBM is less well characterized.	EZH2		qRT-PCR,Chromatin Immunoprecipitation,Western Blot	Enhancer of zeste homolog 2(EZH2) and C-X-C motif chemokine receptor 4 (CXCR4) have been determined to have important roles in the occurrence and development of tumors, but the specific relationship between EZH2 and CXCR4 expression in GBM is less well characterized.			
32635336	chr2	136111405	136113405	CXCR4	Enhancer of zeste homolog 2(EZH2) and C-X-C motif chemokine receptor 4 (CXCR4) have been determined to have important roles in the occurrence and development of tumors, but the specific relationship between EZH2 and CXCR4 expression in GBM is less well characterized.	human	Glioblastoma tissue	High+Lowthroughput	Epigenetic Silencing of miR-9 Promotes Migration and Invasion by EZH2 in Glioblastoma Cells	不相关	无	Glioblastoma	glioblastoma cell	E_01_0955	qRT-PCR,Chromatin Immunoprecipitation,Western Blot	Enhancer of zeste homolog 2(EZH2) and C-X-C motif chemokine receptor 4 (CXCR4) have been determined to have important roles in the occurrence and development of tumors, but the specific relationship between EZH2 and CXCR4 expression in GBM is less well characterized.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of zeste homolog 2(EZH2) and C-X-C motif chemokine receptor 4 (CXCR4) have been determined to have important roles in the occurrence and development of tumors, but the specific relationship between EZH2 and CXCR4 expression in GBM is less well characterized.	Immunohistochemical staining	Enhancer of zeste homolog 2(EZH2) and C-X-C motif chemokine receptor 4 (CXCR4) have been determined to have important roles in the occurrence and development of tumors, but the specific relationship between EZH2 and CXCR4 expression in GBM is less well characterized.	CXCR4		qRT-PCR,Chromatin Immunoprecipitation,Western Blot	Enhancer of zeste homolog 2(EZH2) and C-X-C motif chemokine receptor 4 (CXCR4) have been determined to have important roles in the occurrence and development of tumors, but the specific relationship between EZH2 and CXCR4 expression in GBM is less well characterized.			
32634265	chr7	148804399	148806399	EZH2	HOTTIP recruited enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1) to silence LATS2 and thus activated YAP/β-catenin signaling.	human	osteosarcoma tissue	High+Lowthroughput	The Sp1/FOXC1/HOTTIP/LATS2/YAP/β-catenin cascade promotes malignant and metastatic progression of osteosarcoma	不相关	无	osteosarcoma	mesenchymal stem cell	E_01_0956	RT-PCR,Western blot	HOTTIP recruited enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1) to silence LATS2 and thus activated YAP/β-catenin signaling.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			HOTTIP recruited enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1) to silence LATS2 and thus activated YAP/β-catenin signaling.	Immunohistochemical staining	HOTTIP recruited enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1) to silence LATS2 and thus activated YAP/β-catenin signaling.	EZH2		RT-PCR,Western blot	HOTTIP recruited enhancer of zeste homolog 2 (EZH2) and lysine specific demethylase 1 (LSD1) to silence LATS2 and thus activated YAP/β-catenin signaling.			
32633375	chr4	108045078	108047078	LEF1	The expression of miR-381 and LEF1 (lymphoid enhancer-bind_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ing factor-1) was quantified using quantitative Real Time-Polymerase Chain Reaction (qRT_x0002_PCR) and Western blot analysis.	human		High+Lowthroughput	MicroRNA-381 inhibits metastasis and epithelial-mesenchymal transition of glioblastoma cells through targeting LEF1	不相关	无	Glioblastoma	glioblastoma cell	E_01_0957	qRT-PCR,Western blot	The expression of miR-381 and LEF1 (lymphoid enhancer-bind_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ing factor-1) was quantified using quantitative Real Time-Polymerase Chain Reaction (qRT_x0002_PCR) and Western blot analysis.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The expression of miR-381 and LEF1 (lymphoid enhancer-bind_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ing factor-1) was quantified using quantitative Real Time-Polymerase Chain Reaction (qRT_x0002_PCR) and Western blot analysis.	Immunohistochemical staining	The expression of miR-381 and LEF1 (lymphoid enhancer-bind_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ing factor-1) was quantified using quantitative Real Time-Polymerase Chain Reaction (qRT_x0002_PCR) and Western blot analysis.	LEF1		qRT-PCR,Western blot	The expression of miR-381 and LEF1 (lymphoid enhancer-bind_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_ing factor-1) was quantified using quantitative Real Time-Polymerase Chain Reaction (qRT_x0002_PCR) and Western blot analysis.			
32633341	chr7	148804242	148806242	EZH2	Correlations of circ100284 with lysine-specific histone demethylase 1A (LSD1) and enhancer of zeste homolog 2 (EZH2) target pro_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_teins were analyzed by RNA co-precipitation exper_x0002_iments.	human	osteosarcoma tissue	High+Lowthroughput	Circ100284 promotes invasion and migration of osteosarcoma cells by down-regulating PTEN and EMP1	不相关	无	osteosarcoma	osteosarcoma cell	E_01_0958	qRT-PCR,Western Blotting	Correlations of circ100284 with lysine-specific histone demethylase 1A (LSD1) and enhancer of zeste homolog 2 (EZH2) target pro_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_teins were analyzed by RNA co-precipitation exper_x0002_iments.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Correlations of circ100284 with lysine-specific histone demethylase 1A (LSD1) and enhancer of zeste homolog 2 (EZH2) target pro_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_teins were analyzed by RNA co-precipitation exper_x0002_iments.	Immunohistochemical staining	Correlations of circ100284 with lysine-specific histone demethylase 1A (LSD1) and enhancer of zeste homolog 2 (EZH2) target pro_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_teins were analyzed by RNA co-precipitation exper_x0002_iments.	EZH2		qRT-PCR,Western Blotting	Correlations of circ100284 with lysine-specific histone demethylase 1A (LSD1) and enhancer of zeste homolog 2 (EZH2) target pro_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_teins were analyzed by RNA co-precipitation exper_x0002_iments.			
32632701	chr6	45325376	45327376	RUNX2	The signifcant loss of chondrocytes in grades 2 and 3 of LFJs was observed. The expression levels of CCAAT enhancer binding protein β (C/EBPβ), Runt-related transcription factor 2 (RUNX2), and matrix metalloproteinase 13 (MMP13) also increased with the aggravation of degeneration (4.89, 5.77, and 6.3 times by Western blot).	human	cartilage tissues	High+Lowthroughput	Interaction between C/EBPβ and RUNX2 promotes apoptosis of chondrocytes during Human lumbar facet joint degeneration	不相关	无	arthritis	neuroblast	E_01_0959	Flow cytometry,Western blot	The signifcant loss of chondrocytes in grades 2 and 3 of LFJs was observed. The expression levels of CCAAT enhancer binding protein β (C/EBPβ), Runt-related transcription factor 2 (RUNX2), and matrix metalloproteinase 13 (MMP13) also increased with the aggravation of degeneration (4.89, 5.77, and 6.3 times by Western blot).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The signifcant loss of chondrocytes in grades 2 and 3 of LFJs was observed. The expression levels of CCAAT enhancer binding protein β (C/EBPβ), Runt-related transcription factor 2 (RUNX2), and matrix metalloproteinase 13 (MMP13) also increased with the aggravation of degeneration (4.89, 5.77, and 6.3 times by Western blot).	Immunohistochemical staining	The signifcant loss of chondrocytes in grades 2 and 3 of LFJs was observed. The expression levels of CCAAT enhancer binding protein β (C/EBPβ), Runt-related transcription factor 2 (RUNX2), and matrix metalloproteinase 13 (MMP13) also increased with the aggravation of degeneration (4.89, 5.77, and 6.3 times by Western blot).	RUNX2		Flow cytometry,Western blot	The signifcant loss of chondrocytes in grades 2 and 3 of LFJs was observed. The expression levels of CCAAT enhancer binding protein β (C/EBPβ), Runt-related transcription factor 2 (RUNX2), and matrix metalloproteinase 13 (MMP13) also increased with the aggravation of degeneration (4.89, 5.77, and 6.3 times by Western blot).			
32632335	chr11	33856049	33858049	LMO2	For example, cis-X identified both ABTB2 and TMEM38B as cis-activated by structural variants; however, both genes were adjacent to known proto-oncogenes in the same TAD (LMO2 and TAL2, respectively); thus, they were potentially coregu_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_lated by an aberrant enhancer.	human		High+Lowthroughput	Discovery of regulatory noncoding variants in individual cancer genomes by using cis-X	不相关	无	leukemia	tumor cell	E_01_0960	RNA-seq,ChIP–seq	For example, cis-X identified both ABTB2 and TMEM38B as cis-activated by structural variants; however, both genes were adjacent to known proto-oncogenes in the same TAD (LMO2 and TAL2, respectively); thus, they were potentially coregu_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_lated by an aberrant enhancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	For example, cis-X identified both ABTB2 and TMEM38B as cis-activated by structural variants; however, both genes were adjacent to known proto-oncogenes in the same TAD (LMO2 and TAL2, respectively); thus, they were potentially coregu_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_lated by an aberrant enhancer.		For example, cis-X identified both ABTB2 and TMEM38B as cis-activated by structural variants; however, both genes were adjacent to known proto-oncogenes in the same TAD (LMO2 and TAL2, respectively); thus, they were potentially coregu_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_lated by an aberrant enhancer.	Immunohistochemical staining	For example, cis-X identified both ABTB2 and TMEM38B as cis-activated by structural variants; however, both genes were adjacent to known proto-oncogenes in the same TAD (LMO2 and TAL2, respectively); thus, they were potentially coregu_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_lated by an aberrant enhancer.			RNA-seq,ChIP–seq				LMO2
32632335	chr9	105660121	105662121	TAL2	For example, cis-X identified both ABTB2 and TMEM38B as cis-activated by structural variants; however, both genes were adjacent to known proto-oncogenes in the same TAD (LMO2 and TAL2, respectively); thus, they were potentially coregu_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_lated by an aberrant enhancer.	human		High+Lowthroughput	Discovery of regulatory noncoding variants in individual cancer genomes by using cis-X	不相关	无	leukemia	tumor cell	E_01_0960	RNA-seq,ChIP–seq	For example, cis-X identified both ABTB2 and TMEM38B as cis-activated by structural variants; however, both genes were adjacent to known proto-oncogenes in the same TAD (LMO2 and TAL2, respectively); thus, they were potentially coregu_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_lated by an aberrant enhancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	For example, cis-X identified both ABTB2 and TMEM38B as cis-activated by structural variants; however, both genes were adjacent to known proto-oncogenes in the same TAD (LMO2 and TAL2, respectively); thus, they were potentially coregu_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_lated by an aberrant enhancer.		For example, cis-X identified both ABTB2 and TMEM38B as cis-activated by structural variants; however, both genes were adjacent to known proto-oncogenes in the same TAD (LMO2 and TAL2, respectively); thus, they were potentially coregu_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_lated by an aberrant enhancer.	Immunohistochemical staining	For example, cis-X identified both ABTB2 and TMEM38B as cis-activated by structural variants; however, both genes were adjacent to known proto-oncogenes in the same TAD (LMO2 and TAL2, respectively); thus, they were potentially coregu_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x005f_x0002_lated by an aberrant enhancer.			RNA-seq,ChIP–seq				TAL2
32631994	chr7	148804082	148806082	EZH2	Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb Repressive Complex 2 (PRC2), which minimally requires two other subunits, EED and SUZ12, for enzymatic activity.	human		High+Lowthroughput	A partially disordered region connects gene repression and activation functions of EZH2	不相关	无		cancer cell	E_01_0961	RT-PCR	Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb Repressive Complex 2 (PRC2), which minimally requires two other subunits, EED and SUZ12, for enzymatic activity.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb Repressive Complex 2 (PRC2), which minimally requires two other subunits, EED and SUZ12, for enzymatic activity.	Immunohistochemical staining	Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb Repressive Complex 2 (PRC2), which minimally requires two other subunits, EED and SUZ12, for enzymatic activity.	EZH2		RT-PCR	Enhancer of Zeste Homolog 2 (EZH2) is the catalytic subunit of Polycomb Repressive Complex 2 (PRC2), which minimally requires two other subunits, EED and SUZ12, for enzymatic activity.			
33084574	chr4	133403903	133405903	Arid1a	In mice genetically-invalidated in 27 hepatocytes for the chromatin remodeler Arid1a, and for Apc, the major silencer of Wnt 28 pathway, chromatin was more accessible and histone marks turned into active ones at the 29 Epo downstream enhancer.	mouse	liver tissue	High+Lowthroughput	ARID1A loss in adult hepatocytes activates β-catenin-mediated erythropoietin transcription	不相关	无			E_02_0600	Immunohistochemistry,RT-PCR,Western blotting	In mice genetically-invalidated in 27 hepatocytes for the chromatin remodeler Arid1a, and for Apc, the major silencer of Wnt 28 pathway, chromatin was more accessible and histone marks turned into active ones at the 29 Epo downstream enhancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In mice genetically-invalidated in 27 hepatocytes for the chromatin remodeler Arid1a, and for Apc, the major silencer of Wnt 28 pathway, chromatin was more accessible and histone marks turned into active ones at the 29 Epo downstream enhancer.		In mice genetically-invalidated in 27 hepatocytes for the chromatin remodeler Arid1a, and for Apc, the major silencer of Wnt 28 pathway, chromatin was more accessible and histone marks turned into active ones at the 29 Epo downstream enhancer.	Immunohistochemical staining	In mice genetically-invalidated in 27 hepatocytes for the chromatin remodeler Arid1a, and for Apc, the major silencer of Wnt 28 pathway, chromatin was more accessible and histone marks turned into active ones at the 29 Epo downstream enhancer.			Immunohistochemistry,RT-PCR,Western blotting				Arid1a
33084547	chr14	100235938	100237938	YY1	We also confirmed that cellular transcription factor Yin-Yang 1 (YY1) and viral protein HBx mediated the spatial regulation of HBV cccDNA transcription by 19p13.11 enhancer.	human	liver tissues	High+Lowthroughput	Yin-Yang 1 and HBx protein activate HBV transcription by mediating the spatial interaction of cccDNA minichromosome with cellular chromosome 19p13.11	不相关	无	liver cancer	HCC cell	E_01_0962	PCR,western blots	We also confirmed that cellular transcription factor Yin-Yang 1 (YY1) and viral protein HBx mediated the spatial regulation of HBV cccDNA transcription by 19p13.11 enhancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			We also confirmed that cellular transcription factor Yin-Yang 1 (YY1) and viral protein HBx mediated the spatial regulation of HBV cccDNA transcription by 19p13.11 enhancer.	Immunohistochemical staining	We also confirmed that cellular transcription factor Yin-Yang 1 (YY1) and viral protein HBx mediated the spatial regulation of HBV cccDNA transcription by 19p13.11 enhancer.	YY1		PCR,western blots	We also confirmed that cellular transcription factor Yin-Yang 1 (YY1) and viral protein HBx mediated the spatial regulation of HBV cccDNA transcription by 19p13.11 enhancer.			
33084203	chr2	147881950	147883950	Foxa2	We established a Foxa2 notochord_x005f_x0002_specific enhancer-driven Cre transgenic Mouse model (Foxa2mNE-Cre) that acts only in the embryonic to foetal period up to E14.5, to genetically label notochord cells with enhanced green fluorescent protein (EGFP).	mouse		High+Lowthroughput	Transformation of resident notochord-descendent nucleus pulposus cells in Mouse injury-induced fibrotic intervertebral discs	不相关	无			E_02_0724		We established a Foxa2 notochord_x005f_x0002_specific enhancer-driven Cre transgenic Mouse model (Foxa2mNE-Cre) that acts only in the embryonic to foetal period up to E14.5, to genetically label notochord cells with enhanced green fluorescent protein (EGFP).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We established a Foxa2 notochord_x005f_x0002_specific enhancer-driven Cre transgenic Mouse model (Foxa2mNE-Cre) that acts only in the embryonic to foetal period up to E14.5, to genetically label notochord cells with enhanced green fluorescent protein (EGFP).		We established a Foxa2 notochord_x005f_x0002_specific enhancer-driven Cre transgenic Mouse model (Foxa2mNE-Cre) that acts only in the embryonic to foetal period up to E14.5, to genetically label notochord cells with enhanced green fluorescent protein (EGFP).	Immunohistochemical staining	We established a Foxa2 notochord_x005f_x0002_specific enhancer-driven Cre transgenic Mouse model (Foxa2mNE-Cre) that acts only in the embryonic to foetal period up to E14.5, to genetically label notochord cells with enhanced green fluorescent protein (EGFP).							Foxa2
33078455	chr8	27594345	27596345	CLU	CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).	mouse	adipose tissue	High+Lowthroughput	Regulation of adipocyte differentiation by clusterin-mediated Krüppel-like factor 5 stabilization	不相关	无		mesenchymal stem cell	E_02_0602	qRT-PCR,Immunoprecipitation,Immunoblot	CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).		CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).	Immunohistochemical staining	CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).			qRT-PCR,Immunoprecipitation,Immunoblot				CLU
33078455	chr7	34815809	34817809	Cebpa	CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).	mouse	adipose tissue	High+Lowthroughput	Regulation of adipocyte differentiation by clusterin-mediated Krüppel-like factor 5 stabilization	不相关	无		mesenchymal stem cell	E_02_0602	qRT-PCR,Immunoprecipitation,Immunoblot	CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).		CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).	Immunohistochemical staining	CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).			qRT-PCR,Immunoprecipitation,Immunoblot				Cebpa
33078455	chr6	115334436	115336436	Pparg	CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).	mouse	adipose tissue	High+Lowthroughput	Regulation of adipocyte differentiation by clusterin-mediated Krüppel-like factor 5 stabilization	不相关	无		mesenchymal stem cell	E_02_0602	qRT-PCR,Immunoprecipitation,Immunoblot	CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).		CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).	Immunohistochemical staining	CLU overexpression promoted adipogenic differentiation of preadipocytes and increased the mRNA levels of adipogenic markers including peroxisome proliferator-activated  receptor γ (Pparg) and CCAAT enhancer-binding protein α (Cebpa).			qRT-PCR,Immunoprecipitation,Immunoblot				Pparg
33070167	chr1	202005474	202007474	ELF3		human		High+Lowthroughput	Aberrant super-enhancer landscape reveals core transcriptional regulatory circuitry in lung adenocarcinoma	不相关	无	Lung adenocarcinoma		E_01_0963	ChIP-qPCR,western blot		Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq				Immunohistochemical staining		ELF3		ChIP-qPCR,western blot				
33070167	chr11	34618195	34620195	EHF		human		High+Lowthroughput	Aberrant super-enhancer landscape reveals core transcriptional regulatory circuitry in lung adenocarcinoma	不相关	无	Lung adenocarcinoma		E_01_0963	ChIP-qPCR,western blot		Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq				Immunohistochemical staining		EHF		ChIP-qPCR,western blot				
33070167	chr18	3409014	3411014	TGIF1		human		High+Lowthroughput	Aberrant super-enhancer landscape reveals core transcriptional regulatory circuitry in lung adenocarcinoma	不相关	无	Lung adenocarcinoma		E_01_0963	ChIP-qPCR,western blot		Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq				Immunohistochemical staining		TGIF1		ChIP-qPCR,western blot				
33065764	chr15	38485286	38487286	RASGRP1	By analyzing H3K27 acetylation profiles in Human T cells, we identified a RASGRP1 enhancer that harbors autoimmunity_x005f_x0002_associated SNPs. CRISPR-Cas9 disruption of this enhancer caused lower RasGRP1 expression, and decreased binding of RUNX1 and CBFB transcription factors.	mouse		High+Lowthroughput	Dysregulated RASGRP1 expression through RUNX1 mediated transcription promotes autoimmunity	不相关	无	inflammatory disease	T cell	E_02_0725	Flow cytometry	By analyzing H3K27 acetylation profiles in Human T cells, we identified a RASGRP1 enhancer that harbors autoimmunity_x005f_x0002_associated SNPs. CRISPR-Cas9 disruption of this enhancer caused lower RasGRP1 expression, and decreased binding of RUNX1 and CBFB transcription factors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	By analyzing H3K27 acetylation profiles in Human T cells, we identified a RASGRP1 enhancer that harbors autoimmunity_x005f_x0002_associated SNPs. CRISPR-Cas9 disruption of this enhancer caused lower RasGRP1 expression, and decreased binding of RUNX1 and CBFB transcription factors.		By analyzing H3K27 acetylation profiles in Human T cells, we identified a RASGRP1 enhancer that harbors autoimmunity_x005f_x0002_associated SNPs. CRISPR-Cas9 disruption of this enhancer caused lower RasGRP1 expression, and decreased binding of RUNX1 and CBFB transcription factors.	Immunohistochemical staining	By analyzing H3K27 acetylation profiles in Human T cells, we identified a RASGRP1 enhancer that harbors autoimmunity_x005f_x0002_associated SNPs. CRISPR-Cas9 disruption of this enhancer caused lower RasGRP1 expression, and decreased binding of RUNX1 and CBFB transcription factors.			Flow cytometry				RASGRP1
33062456	chr1	91677376	91679376	TGFBR3	Further study showed that SB431542, an inhibitor of the TGF-β/BMP signaling,significantly suppressed the mRNA expression of TGFBR3, BMP4, BMP7, BMPR1B,SMAD3, SMAD4, and the pro-proliferative effect of HA on hAECs.	human		High+Lowthroughput	Hyaluronic acid ameliorates the proliferative ability of Human amniotic epithelial cells through activation of TGF-β/BMP signaling	不相关	无			E_01_0964	RT-qPCR	Further study showed that SB431542, an inhibitor of the TGF-β/BMP signaling,significantly suppressed the mRNA expression of TGFBR3, BMP4, BMP7, BMPR1B,SMAD3, SMAD4, and the pro-proliferative effect of HA on hAECs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Further study showed that SB431542, an inhibitor of the TGF-β/BMP signaling,significantly suppressed the mRNA expression of TGFBR3, BMP4, BMP7, BMPR1B,SMAD3, SMAD4, and the pro-proliferative effect of HA on hAECs.		Further study showed that SB431542, an inhibitor of the TGF-β/BMP signaling,significantly suppressed the mRNA expression of TGFBR3, BMP4, BMP7, BMPR1B,SMAD3, SMAD4, and the pro-proliferative effect of HA on hAECs.	Immunohistochemical staining	Further study showed that SB431542, an inhibitor of the TGF-β/BMP signaling,significantly suppressed the mRNA expression of TGFBR3, BMP4, BMP7, BMPR1B,SMAD3, SMAD4, and the pro-proliferative effect of HA on hAECs.			RT-qPCR				TGFBR3
33062456	chr15	67060659	67062659	SMAD3	Further study showed that SB431542, an inhibitor of the TGF-β/BMP signaling,significantly suppressed the mRNA expression of TGFBR3, BMP4, BMP7, BMPR1B,SMAD3, SMAD4, and the pro-proliferative effect of HA on hAECs.	human		High+Lowthroughput	Hyaluronic acid ameliorates the proliferative ability of Human amniotic epithelial cells through activation of TGF-β/BMP signaling	不相关	无			E_01_0964	RT-qPCR	Further study showed that SB431542, an inhibitor of the TGF-β/BMP signaling,significantly suppressed the mRNA expression of TGFBR3, BMP4, BMP7, BMPR1B,SMAD3, SMAD4, and the pro-proliferative effect of HA on hAECs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Further study showed that SB431542, an inhibitor of the TGF-β/BMP signaling,significantly suppressed the mRNA expression of TGFBR3, BMP4, BMP7, BMPR1B,SMAD3, SMAD4, and the pro-proliferative effect of HA on hAECs.	Immunohistochemical staining	Further study showed that SB431542, an inhibitor of the TGF-β/BMP signaling,significantly suppressed the mRNA expression of TGFBR3, BMP4, BMP7, BMPR1B,SMAD3, SMAD4, and the pro-proliferative effect of HA on hAECs.	SMAD3		RT-qPCR	Further study showed that SB431542, an inhibitor of the TGF-β/BMP signaling,significantly suppressed the mRNA expression of TGFBR3, BMP4, BMP7, BMPR1B,SMAD3, SMAD4, and the pro-proliferative effect of HA on hAECs.			
33061937	chr13	48301408	48303408	RB1	The present study analyses the regulatory activity of a Human Alu sequence from the AluSx family located in the second intron of the long intergenic non-coding RNA Linc00441, found in divergent orientation to the RB1 gene.	human		High+Lowthroughput	An Intronic Alu Element Attenuates the Transcription of a Long Non-coding RNA in Human Cell Lines	不相关	无		K562 cell	E_01_0965	PCR	The present study analyses the regulatory activity of a Human Alu sequence from the AluSx family located in the second intron of the long intergenic non-coding RNA Linc00441, found in divergent orientation to the RB1 gene.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			The present study analyses the regulatory activity of a Human Alu sequence from the AluSx family located in the second intron of the long intergenic non-coding RNA Linc00441, found in divergent orientation to the RB1 gene.	Immunohistochemical staining	The present study analyses the regulatory activity of a Human Alu sequence from the AluSx family located in the second intron of the long intergenic non-coding RNA Linc00441, found in divergent orientation to the RB1 gene.	RB1		PCR	The present study analyses the regulatory activity of a Human Alu sequence from the AluSx family located in the second intron of the long intergenic non-coding RNA Linc00441, found in divergent orientation to the RB1 gene.			
33060580	chr3	181709320	181711320	SOX2	We further show that DOT1L inhibition affects accessibility of SOX2-bound enhancers and impairs SOX2 binding in neural pro_x005f_x0002_genitors.	mouse		High+Lowthroughput	DOT1L-mediated murine neuronal differentiation associates with H3K79me2 accumulation and preserves SOX2-enhancer accessibility	不相关	无		embryonic stem cell	E_02_0726	ChIP-seq,RNA-seq,ATAC-seq,Immunoblotting	We further show that DOT1L inhibition affects accessibility of SOX2-bound enhancers and impairs SOX2 binding in neural pro_x005f_x0002_genitors.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We further show that DOT1L inhibition affects accessibility of SOX2-bound enhancers and impairs SOX2 binding in neural pro_x005f_x0002_genitors.		We further show that DOT1L inhibition affects accessibility of SOX2-bound enhancers and impairs SOX2 binding in neural pro_x005f_x0002_genitors.	Immunohistochemical staining	We further show that DOT1L inhibition affects accessibility of SOX2-bound enhancers and impairs SOX2 binding in neural pro_x005f_x0002_genitors.			ChIP-seq,RNA-seq,ATAC-seq,Immunoblotting				SOX2
33060578	chr13	27917232	27919232	PDX1	NFaT transcription factors, rather than the cano_x005f_x0002_nical PDX1 enhancer complex, are predicted to drive INS transactivation.	human		High+Lowthroughput	Aberrant methylation underlies insulin gene expression in Human insulinoma	不相关	无	insulinoma	Beta cell	E_01_0966	PCR	NFaT transcription factors, rather than the cano_x005f_x0002_nical PDX1 enhancer complex, are predicted to drive INS transactivation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			NFaT transcription factors, rather than the cano_x005f_x0002_nical PDX1 enhancer complex, are predicted to drive INS transactivation.	Immunohistochemical staining	NFaT transcription factors, rather than the cano_x005f_x0002_nical PDX1 enhancer complex, are predicted to drive INS transactivation.	PDX1		PCR	NFaT transcription factors, rather than the cano_x005f_x0002_nical PDX1 enhancer complex, are predicted to drive INS transactivation.			
33057201	chr4	105142814	105144814	TET2	In silico-informed in vitro evaluation of the TET2 germline locus enabled the identifcation of a causal variant that disrupts a TET2 distal enhancer, resulting in increased self-renewal of haematopoietic stem cells.	human		High+Lowthroughput	Inherited causes of clonal haematopoiesis in 97,691 whole genomes	相关	rs13167280,rs1210060191		hematopoietic stem cell	E_01_0967	PCR,RNA-seq	In silico-informed in vitro evaluation of the TET2 germline locus enabled the identifcation of a causal variant that disrupts a TET2 distal enhancer, resulting in increased self-renewal of haematopoietic stem cells.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	In silico-informed in vitro evaluation of the TET2 germline locus enabled the identifcation of a causal variant that disrupts a TET2 distal enhancer, resulting in increased self-renewal of haematopoietic stem cells.		In silico-informed in vitro evaluation of the TET2 germline locus enabled the identifcation of a causal variant that disrupts a TET2 distal enhancer, resulting in increased self-renewal of haematopoietic stem cells.	Immunohistochemical staining	In silico-informed in vitro evaluation of the TET2 germline locus enabled the identifcation of a causal variant that disrupts a TET2 distal enhancer, resulting in increased self-renewal of haematopoietic stem cells.			PCR,RNA-seq				TET2
33054858	chr16	67870026	67872026	EDC4	Enhancer of mRNA decapping protein 4 (EDC4) is a known regulator of mRNA decapping, which was related with genome stability and sensitivity of drugs.	human		High+Lowthroughput	Enhancer of mRNA Decapping protein 4 (EDC4) interacts with replication protein a (RPA) and contributes to Cisplatin resistance in cervical Cancer by alleviating DNA damage	不相关	无	Cervical cancer	cervical cancer cells	E_01_0968	RT-PCR	Enhancer of mRNA decapping protein 4 (EDC4) is a known regulator of mRNA decapping, which was related with genome stability and sensitivity of drugs.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Enhancer of mRNA decapping protein 4 (EDC4) is a known regulator of mRNA decapping, which was related with genome stability and sensitivity of drugs.		Enhancer of mRNA decapping protein 4 (EDC4) is a known regulator of mRNA decapping, which was related with genome stability and sensitivity of drugs.	Immunohistochemical staining	Enhancer of mRNA decapping protein 4 (EDC4) is a known regulator of mRNA decapping, which was related with genome stability and sensitivity of drugs.			RT-PCR				EDC4
33054540	chr20	52048868	52050868	ZFP64	Expressions of notch intracellular domain (NICD) and hairy and enhancer of split 1 (Hes-1) in H1975 cell were determined by western blot. Epithelial-mesenchymal transition (EMT)-related pro_x005f_x0002_teins (E-Cadherin and Vimentin) expressions were identified through qRT-PCR and western blot.	human	cancer tissue	High+Lowthroughput	Function and mechanism exploration of zinc finger protein 64 in lung adenocarcinoma cell growth and metastasis	不相关	无	lung adenocarcinoma	 Lung adenocarcinoma cell	E_01_0969	qRT-PCR,western blot	Expressions of notch intracellular domain (NICD) and hairy and enhancer of split 1 (Hes-1) in H1975 cell were determined by western blot. Epithelial-mesenchymal transition (EMT)-related pro_x005f_x0002_teins (E-Cadherin and Vimentin) expressions were identified through qRT-PCR and western blot.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Expressions of notch intracellular domain (NICD) and hairy and enhancer of split 1 (Hes-1) in H1975 cell were determined by western blot. Epithelial-mesenchymal transition (EMT)-related pro_x005f_x0002_teins (E-Cadherin and Vimentin) expressions were identified through qRT-PCR and western blot.		Expressions of notch intracellular domain (NICD) and hairy and enhancer of split 1 (Hes-1) in H1975 cell were determined by western blot. Epithelial-mesenchymal transition (EMT)-related pro_x005f_x0002_teins (E-Cadherin and Vimentin) expressions were identified through qRT-PCR and western blot.	Immunohistochemical staining	Expressions of notch intracellular domain (NICD) and hairy and enhancer of split 1 (Hes-1) in H1975 cell were determined by western blot. Epithelial-mesenchymal transition (EMT)-related pro_x005f_x0002_teins (E-Cadherin and Vimentin) expressions were identified through qRT-PCR and western blot.			qRT-PCR,western blot				ZFP64
33054489	chr8	11674063	11676063	GATA4	Expressions of cell apoptotic proteins Bax, Cleaved(C) caspase-3 and Bcl-2, and expressions of cardiomyocyte differentiation markers GATA4, troponin T (cTnT) and myocyte enhancer factor2C (MEF2C) in hCMPCs were identified by qRT-PCR and western blot.	human	heart tissue	High+Lowthroughput	MiR-33a-5p targets NOMO1 to modulate Human cardiomyocyte progenitor cells proliferation and differentiation and apoptosis	不相关	无	congenital heart disease	neural progenitor cell	E_01_0970	qRT-PCR,Western blot	Expressions of cell apoptotic proteins Bax, Cleaved(C) caspase-3 and Bcl-2, and expressions of cardiomyocyte differentiation markers GATA4, troponin T (cTnT) and myocyte enhancer factor2C (MEF2C) in hCMPCs were identified by qRT-PCR and western blot.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Expressions of cell apoptotic proteins Bax, Cleaved(C) caspase-3 and Bcl-2, and expressions of cardiomyocyte differentiation markers GATA4, troponin T (cTnT) and myocyte enhancer factor2C (MEF2C) in hCMPCs were identified by qRT-PCR and western blot.	Immunohistochemical staining	Expressions of cell apoptotic proteins Bax, Cleaved(C) caspase-3 and Bcl-2, and expressions of cardiomyocyte differentiation markers GATA4, troponin T (cTnT) and myocyte enhancer factor2C (MEF2C) in hCMPCs were identified by qRT-PCR and western blot.	GATA4		qRT-PCR,Western blot	Expressions of cell apoptotic proteins Bax, Cleaved(C) caspase-3 and Bcl-2, and expressions of cardiomyocyte differentiation markers GATA4, troponin T (cTnT) and myocyte enhancer factor2C (MEF2C) in hCMPCs were identified by qRT-PCR and western blot.			
33054400	chr2	150520026	150522026	Vsx1	We identify the enhancers that are sufficient to drive the spatially restricted expression of the Vsx1 and Rx genes in the OPC.	mouse		High+Lowthroughput	Identification of enhancers that drive the spatially restricted expression of Vsx1 and Rx in the outer proliferation center of the developing Drosophila optic lobe	不相关	无		stem cell	E_02_0727	PCR,Immunohistochemistry	We identify the enhancers that are sufficient to drive the spatially restricted expression of the Vsx1 and Rx genes in the OPC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	We identify the enhancers that are sufficient to drive the spatially restricted expression of the Vsx1 and Rx genes in the OPC.		We identify the enhancers that are sufficient to drive the spatially restricted expression of the Vsx1 and Rx genes in the OPC.	Immunohistochemical staining	We identify the enhancers that are sufficient to drive the spatially restricted expression of the Vsx1 and Rx genes in the OPC.			PCR,Immunohistochemistry				Vsx1
33044128	chr13	116432461	116434461	Isl1	ATAC-seq Reveals an Isl1 Enhancer that Regulates Sinoatrial Node Development and Function	mouse		High+Lowthroughput	ATAC-Seq Reveals an Isl1 Enhancer That Regulates Sinoatrial Node Development and Function	不相关	无		Cardiac pacemaker cell	E_02_0728	ATAC-seq	ATAC-seq Reveals an Isl1 Enhancer that Regulates Sinoatrial Node Development and Function	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	ATAC-seq Reveals an Isl1 Enhancer that Regulates Sinoatrial Node Development and Function		ATAC-seq Reveals an Isl1 Enhancer that Regulates Sinoatrial Node Development and Function	Immunohistochemical staining	ATAC-seq Reveals an Isl1 Enhancer that Regulates Sinoatrial Node Development and Function			ATAC-seq				Isl1
33043448	chr22	42123656	42125656	CYP2D6	The rs5758550A>G SNP apparently turns the region into an enhancer that interacts with the CYP2D6 promoter and increases  transcription.	human		High+Lowthroughput	Tri-Allelic Haplotypes Determine and Differentiate Functionally Normal Allele CYP2D6*2 and Impaired Allele CYP2D6*41	相关	rs5758550		HCC cell	E_01_0971	pcr,Western blotting	The rs5758550A>G SNP apparently turns the region into an enhancer that interacts with the CYP2D6 promoter and increases  transcription.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	The rs5758550A>G SNP apparently turns the region into an enhancer that interacts with the CYP2D6 promoter and increases  transcription.		The rs5758550A>G SNP apparently turns the region into an enhancer that interacts with the CYP2D6 promoter and increases  transcription.	Immunohistochemical staining	The rs5758550A>G SNP apparently turns the region into an enhancer that interacts with the CYP2D6 promoter and increases  transcription.			pcr,Western blotting				CYP2D6
33040635	chr12	114667368	114669368	TBX3	Genome-Wide Analysis Identifies an Essential Human TBX3 Pacemaker Enhancer	mouse	atrial tissue	High+Lowthroughput	Genome-Wide Analysis Identifies an Essential Human TBX3 Pacemaker Enhancer	相关	rs61928421		pacemaker cell	E_02_0729	qPCR	Genome-Wide Analysis Identifies an Essential Human TBX3 Pacemaker Enhancer	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Genome-Wide Analysis Identifies an Essential Human TBX3 Pacemaker Enhancer		Genome-Wide Analysis Identifies an Essential Human TBX3 Pacemaker Enhancer	Immunohistochemical staining	Genome-Wide Analysis Identifies an Essential Human TBX3 Pacemaker Enhancer			qPCR				TBX3
33035348	chr22	20077488	20079488	DGCR8	Here,we identify Enhancer of Rudimentary Homolog (ERH) as a new component of Microprocessor.	human		High+Lowthroughput	ERH facilitates microRNA maturation through the interaction with the N-terminus of DGCR8	不相关	无		embryonic kidney 293E cell	E_01_0972	PCR,Immunoprecipitation	Here,we identify Enhancer of Rudimentary Homolog (ERH) as a new component of Microprocessor.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Here,we identify Enhancer of Rudimentary Homolog (ERH) as a new component of Microprocessor.		Here,we identify Enhancer of Rudimentary Homolog (ERH) as a new component of Microprocessor.	Immunohistochemical staining	Here,we identify Enhancer of Rudimentary Homolog (ERH) as a new component of Microprocessor.			PCR,Immunoprecipitation				DGCR8
33033262	chr3	181708937	181710937	SOX2	JMJD3 also promotes enhancer-promoter looping through the cohesin loading factor NIPBL and ultimately transcriptional elongation.	mouse	brain tissues	High+Lowthroughput	JMJD3 acts in tandem with KLF4 to facilitate reprogramming to pluripotency	不相关	无		somatic cell	E_02_0603	RT-qPCR,Western blotting	JMJD3 also promotes enhancer-promoter looping through the cohesin loading factor NIPBL and ultimately transcriptional elongation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	JMJD3 also promotes enhancer-promoter looping through the cohesin loading factor NIPBL and ultimately transcriptional elongation.		JMJD3 also promotes enhancer-promoter looping through the cohesin loading factor NIPBL and ultimately transcriptional elongation.	Immunohistochemical staining	JMJD3 also promotes enhancer-promoter looping through the cohesin loading factor NIPBL and ultimately transcriptional elongation.			RT-qPCR,Western blotting				SOX2
33033216	chr10	102827537	102829537	CYP17A1	Transgenic mice with a knock-in mole CYP17A1 enhancer or overexpressing FGF9 showed phenotypes recapitulating mole sexual features.	mouse	ovarian tissue	High+Lowthroughput	The mole genome reveals regulatory rearrangements associated with adaptive intersexuality	不相关	无		germ line cell	E_02_0730		Transgenic mice with a knock-in mole CYP17A1 enhancer or overexpressing FGF9 showed phenotypes recapitulating mole sexual features.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Transgenic mice with a knock-in mole CYP17A1 enhancer or overexpressing FGF9 showed phenotypes recapitulating mole sexual features.		Transgenic mice with a knock-in mole CYP17A1 enhancer or overexpressing FGF9 showed phenotypes recapitulating mole sexual features.	Immunohistochemical staining	Transgenic mice with a knock-in mole CYP17A1 enhancer or overexpressing FGF9 showed phenotypes recapitulating mole sexual features.							CYP17A1
33033055	chr12	49016308	49018308	KMT2D	Trithorax-related (trr), MLL3 (KMT2C), and MLL4 (KMT2D) represent the “branch” of COMPASS family ly_x005f_x0002_sine methyltransferases responsible for catalyzing histone 3 lysine 4 monomethylation (H3K4me1) at enhancer chro_x0002_matin in Drosophila and mammals, respectively (Herzet al. 2012; Hu et al. 2013).	mouse		High+Lowthroughput	A small UTX stabilization domain of Trr is conserved within mammalian MLL3-4/COMPASS and is sufficient to rescue loss of viability in null animals	不相关	无		embryonic stem cell	E_02_0731	Western blots,chip-seq	Trithorax-related (trr), MLL3 (KMT2C), and MLL4 (KMT2D) represent the “branch” of COMPASS family ly_x005f_x0002_sine methyltransferases responsible for catalyzing histone 3 lysine 4 monomethylation (H3K4me1) at enhancer chro_x0002_matin in Drosophila and mammals, respectively (Herzet al. 2012; Hu et al. 2013).	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Trithorax-related (trr), MLL3 (KMT2C), and MLL4 (KMT2D) represent the “branch” of COMPASS family ly_x005f_x0002_sine methyltransferases responsible for catalyzing histone 3 lysine 4 monomethylation (H3K4me1) at enhancer chro_x0002_matin in Drosophila and mammals, respectively (Herzet al. 2012; Hu et al. 2013).		Trithorax-related (trr), MLL3 (KMT2C), and MLL4 (KMT2D) represent the “branch” of COMPASS family ly_x005f_x0002_sine methyltransferases responsible for catalyzing histone 3 lysine 4 monomethylation (H3K4me1) at enhancer chro_x0002_matin in Drosophila and mammals, respectively (Herzet al. 2012; Hu et al. 2013).	Immunohistochemical staining	Trithorax-related (trr), MLL3 (KMT2C), and MLL4 (KMT2D) represent the “branch” of COMPASS family ly_x005f_x0002_sine methyltransferases responsible for catalyzing histone 3 lysine 4 monomethylation (H3K4me1) at enhancer chro_x0002_matin in Drosophila and mammals, respectively (Herzet al. 2012; Hu et al. 2013).			Western blots,chip-seq				KMT2D
33028869	chr6	31572563	31574563	TNF	Further bioinformatic analysis, employing Ingenuity Pathway Analysis identifed signifcant enrichment in XAV-939-treated cells of functional categories and networks involved in TNF, NFκB, and STAT signaling. We identifed a Tankyrase inhibitor (XAV-939) as a powerful enhancer of osteoblastic diferentiation of hBMSC that may be useful as a therapeutic option for treating conditions associated with low bone formation.	mouse		High+Lowthroughput	Tankyrase inhibitor XAV-939 enhances osteoblastogenesis and mineralization of Human skeletal (mesenchymal) stem cells	不相关	无		stem cell	E_02_0732	qRT-PCR	Further bioinformatic analysis, employing Ingenuity Pathway Analysis identifed signifcant enrichment in XAV-939-treated cells of functional categories and networks involved in TNF, NFκB, and STAT signaling. We identifed a Tankyrase inhibitor (XAV-939) as a powerful enhancer of osteoblastic diferentiation of hBMSC that may be useful as a therapeutic option for treating conditions associated with low bone formation.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Further bioinformatic analysis, employing Ingenuity Pathway Analysis identifed signifcant enrichment in XAV-939-treated cells of functional categories and networks involved in TNF, NFκB, and STAT signaling. We identifed a Tankyrase inhibitor (XAV-939) as a powerful enhancer of osteoblastic diferentiation of hBMSC that may be useful as a therapeutic option for treating conditions associated with low bone formation.		Further bioinformatic analysis, employing Ingenuity Pathway Analysis identifed signifcant enrichment in XAV-939-treated cells of functional categories and networks involved in TNF, NFκB, and STAT signaling. We identifed a Tankyrase inhibitor (XAV-939) as a powerful enhancer of osteoblastic diferentiation of hBMSC that may be useful as a therapeutic option for treating conditions associated with low bone formation.	Immunohistochemical staining	Further bioinformatic analysis, employing Ingenuity Pathway Analysis identifed signifcant enrichment in XAV-939-treated cells of functional categories and networks involved in TNF, NFκB, and STAT signaling. We identifed a Tankyrase inhibitor (XAV-939) as a powerful enhancer of osteoblastic diferentiation of hBMSC that may be useful as a therapeutic option for treating conditions associated with low bone formation.			qRT-PCR				TNF
33026112	chr7	148804775	148806775	EZH2	Chromatin immunoprecipitation and dual_x005f_x0002_luciferase assays validated that enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) inhibited transcription of miR-22 promoter	mouse		High+Lowthroughput	Inhibition of EZH2 attenuates coronary heart disease by interacting with microRNA-22 to regulate the TXNIP/nuclear factor-κB pathway	不相关	无	coronary heart disease	blood vessel smooth muscle cell	E_02_0733	Flow cytometry,RT-PCR	Chromatin immunoprecipitation and dual_x005f_x0002_luciferase assays validated that enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) inhibited transcription of miR-22 promoter	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Chromatin immunoprecipitation and dual_x005f_x0002_luciferase assays validated that enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) inhibited transcription of miR-22 promoter		Chromatin immunoprecipitation and dual_x005f_x0002_luciferase assays validated that enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) inhibited transcription of miR-22 promoter	Immunohistochemical staining	Chromatin immunoprecipitation and dual_x005f_x0002_luciferase assays validated that enhancer of zeste 2 polycomb repressive complex 2 subunit (EZH2) inhibited transcription of miR-22 promoter			Flow cytometry,RT-PCR				EZH2
32206101	chr19	10868773	10870773	CARM1	": CARM1 was found to be predominantly and specifically recruited to ERα-bound active 
enhancers and essential for the transcriptional activation of cognate estrogen-induced genes in response 
to estrogen treatment"	human,mouse	mammary cancer	High+Lowthroughput	A hypermethylation strategy utilized by enhancer-bound CARM1 to promote estrogen receptor α-dependent transcriptional activation and breast carcinogenesis	否		mammary cancer	breast cancer cell	E_02_0734	Transfection, RT qPCR, Western blot	": CARM1 was found to be predominantly and specifically recruited to ERα-bound active 
enhancers and essential for the transcriptional activation of cognate estrogen-induced genes in response 
to estrogen treatment"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	": CARM1 was found to be predominantly and specifically recruited to ERα-bound active 
enhancers and essential for the transcriptional activation of cognate estrogen-induced genes in response 
to estrogen treatment"		": CARM1 was found to be predominantly and specifically recruited to ERα-bound active 
enhancers and essential for the transcriptional activation of cognate estrogen-induced genes in response 
to estrogen treatment"	Immunohistochemical staining	": CARM1 was found to be predominantly and specifically recruited to ERα-bound active 
enhancers and essential for the transcriptional activation of cognate estrogen-induced genes in response 
to estrogen treatment"			转染，RT-qPCR，Western blot				CARM1
32204915	chr16	67559503	67561503	CTCF	"TAD boundaries are enriched in binding of structural proteins 
(CTCF and cohesin)11."	human	blood	High+Lowthroughput	Three-dimensional chromatin landscapes in T cell acute lymphoblastic leukemia	否		acute lymphoblastic leukemia		E_01_0973	4C-seq，HiChIP，GRO-seq	"TAD boundaries are enriched in binding of structural proteins 
(CTCF and cohesin)11."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"TAD boundaries are enriched in binding of structural proteins 
(CTCF and cohesin)11."	Immunohistochemical staining	"TAD boundaries are enriched in binding of structural proteins 
(CTCF and cohesin)11."	CTCF		4C-seq，HiChIP，GRO-seq	"TAD boundaries are enriched in binding of structural proteins 
(CTCF and cohesin)11."			
32199616	chr19	15232997	15234997	BRD4	"Bromodomain and extra terminal domain (BET) protein BRD4
binds to super-enhancers (SEs) that drive high expression of oncogenes in many cancers."	human	Human prostate cancer	High+Lowthroughput	Long non-coding RNA MANCR is a target of BET bromodomain protein BRD4 and plays a critical role in cellular migration and invasion abilities of prostate cancer	否		prostatic cancer	prostate cancer cell	E_01_0974	Transfection, migration invasion assay, RT qPCR	"Bromodomain and extra terminal domain (BET) protein BRD4
binds to super-enhancers (SEs) that drive high expression of oncogenes in many cancers."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Bromodomain and extra terminal domain (BET) protein BRD4
binds to super-enhancers (SEs) that drive high expression of oncogenes in many cancers."	Immunohistochemical staining	"Bromodomain and extra terminal domain (BET) protein BRD4
binds to super-enhancers (SEs) that drive high expression of oncogenes in many cancers."	BRD4		转染，迁移侵袭测定，RT-qPCR	"Bromodomain and extra terminal domain (BET) protein BRD4
binds to super-enhancers (SEs) that drive high expression of oncogenes in many cancers."			
32194712	chr19	10651426	10653426	ILF3	"Interleukin-enhancer binding factor 3 (ILF3) 
is a double-stranded RNA-binding protein that has been 
reported to contribute to the occurrence and progression of 
various malignant tumors."	human		High+Lowthroughput	High expression of interleukin-enhancer binding factor 3 predicts poor prognosis in patients with lung adenocarcinoma	否		Lung adenocarcinoma		E_01_0975	TMA, immunohistochemistry	"Interleukin-enhancer binding factor 3 (ILF3) 
is a double-stranded RNA-binding protein that has been 
reported to contribute to the occurrence and progression of 
various malignant tumors."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Interleukin-enhancer binding factor 3 (ILF3) 
is a double-stranded RNA-binding protein that has been 
reported to contribute to the occurrence and progression of 
various malignant tumors."	Immunohistochemical staining	"Interleukin-enhancer binding factor 3 (ILF3) 
is a double-stranded RNA-binding protein that has been 
reported to contribute to the occurrence and progression of 
various malignant tumors."	ILF3		TMA,免疫组化	"Interleukin-enhancer binding factor 3 (ILF3) 
is a double-stranded RNA-binding protein that has been 
reported to contribute to the occurrence and progression of 
various malignant tumors."			
32194081	chr7	148804808	148806808	EZH2	"Enhancer of zeste homolog 2 (EZH2) is associated with ulcerative colitis development. 
However, the mechanism of EZH2 in ulcerative colitis progression remains unclear."	human,mouse	Colon adenocarcinoma	High+Lowthroughput	EZH2 inhibition promotes ANGPTL4/CREB1 to suppress the progression of ulcerative colitis			Ulcerative colitis		E_02_0735	Flow cytometry, RT qPCR, Western blot, ELISA	"Enhancer of zeste homolog 2 (EZH2) is associated with ulcerative colitis development. 
However, the mechanism of EZH2 in ulcerative colitis progression remains unclear."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Enhancer of zeste homolog 2 (EZH2) is associated with ulcerative colitis development. 
However, the mechanism of EZH2 in ulcerative colitis progression remains unclear."		"Enhancer of zeste homolog 2 (EZH2) is associated with ulcerative colitis development. 
However, the mechanism of EZH2 in ulcerative colitis progression remains unclear."	Immunohistochemical staining	"Enhancer of zeste homolog 2 (EZH2) is associated with ulcerative colitis development. 
However, the mechanism of EZH2 in ulcerative colitis progression remains unclear."			流式细胞术，RT-qPCR,western blot,酶联免疫吸附				EZH2
32219447	chr3	128476870	128478870	GATA2	the translocation of a GATA2 enhancer (3q21) to MECOM (3q26) results in overexpression of the MECOM isoform EVI1 and monoallelic expression of GATA2 from the unaffected allele. 	human	blood	High+Lowthroughput	Atypical 3q26/MECOM rearrangements genocopy inv(3)/t(3;3) in acute myeloid leukemia	是		Acute myeloid leukemia	Leukemic blast cell	E_01_0976	RNA sequencing, exon sequencing	the translocation of a GATA2 enhancer (3q21) to MECOM (3q26) results in overexpression of the MECOM isoform EVI1 and monoallelic expression of GATA2 from the unaffected allele. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			the translocation of a GATA2 enhancer (3q21) to MECOM (3q26) results in overexpression of the MECOM isoform EVI1 and monoallelic expression of GATA2 from the unaffected allele. 	Immunohistochemical staining	the translocation of a GATA2 enhancer (3q21) to MECOM (3q26) results in overexpression of the MECOM isoform EVI1 and monoallelic expression of GATA2 from the unaffected allele. 	GATA2		RNA测序，外显子测序	the translocation of a GATA2 enhancer (3q21) to MECOM (3q26) results in overexpression of the MECOM isoform EVI1 and monoallelic expression of GATA2 from the unaffected allele. 			
32218434	chr17	35869035	35871035	CCL5	" the prox_x0002_imal enhancer mediates the constitutive CCL5 expression during the steady state, while the
distal enhancer located 1.35 Mb from the promoter induces CCL5 expression in activated
cells. "	mouse	Spleen, lymph nodes	High+Lowthroughput	"Runx-mediated regulation of CCL5 via antagonizing
two enhancers influences immune cell function
and anti-tumor immunity"	否		antitumor immunity	T cell	E_02_0736	NK cytotoxicity assay, mouse modeling, chromatin immunoprecipitation assay	" the prox_x0002_imal enhancer mediates the constitutive CCL5 expression during the steady state, while the
distal enhancer located 1.35 Mb from the promoter induces CCL5 expression in activated
cells. "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	" the prox_x0002_imal enhancer mediates the constitutive CCL5 expression during the steady state, while the
distal enhancer located 1.35 Mb from the promoter induces CCL5 expression in activated
cells. "		" the prox_x0002_imal enhancer mediates the constitutive CCL5 expression during the steady state, while the
distal enhancer located 1.35 Mb from the promoter induces CCL5 expression in activated
cells. "	Immunohistochemical staining	" the prox_x0002_imal enhancer mediates the constitutive CCL5 expression during the steady state, while the
distal enhancer located 1.35 Mb from the promoter induces CCL5 expression in activated
cells. "			NK 细胞毒性测定，小鼠造模，染色质免疫沉淀测定				CCL5
32209973	chr15	99562591	99564591	MEF2A	"we identify the transcription factor myocyte enhancer factor 2A (MEF2A) as the common
link between OT and cellular changes symptomatic for ASD, encompassing neuronal morphology,
connectivity, and mitochondrial function"	mouse	hypothalamus	High+Lowthroughput	Myocyte Enhancer Factor 2A (MEF2A) Defines Oxytocin-Induced Morphological Effects and Regulates Mitochondrial Function in Neurons	否		mitochondrial disorder		E_02_0737	Transfection, Western blot, immunofluorescence, cell viability assays	"we identify the transcription factor myocyte enhancer factor 2A (MEF2A) as the common
link between OT and cellular changes symptomatic for ASD, encompassing neuronal morphology,
connectivity, and mitochondrial function"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"we identify the transcription factor myocyte enhancer factor 2A (MEF2A) as the common
link between OT and cellular changes symptomatic for ASD, encompassing neuronal morphology,
connectivity, and mitochondrial function"		"we identify the transcription factor myocyte enhancer factor 2A (MEF2A) as the common
link between OT and cellular changes symptomatic for ASD, encompassing neuronal morphology,
connectivity, and mitochondrial function"	Immunohistochemical staining	"we identify the transcription factor myocyte enhancer factor 2A (MEF2A) as the common
link between OT and cellular changes symptomatic for ASD, encompassing neuronal morphology,
connectivity, and mitochondrial function"			转染，Western blot，免疫荧光，细胞活力检测				MEF2A
32209656	chr21	34785474	34787474	RUNX1	" involving the formation 
of a transcriptional enhancer complex consisting 
of proto-oncogene c-Jun (c-Jun), RELA proto_x0002_oncogene NF-κB subunit (RelA), RUNX family 
transcription factor 1 (RUNX1), a"	human	colorectal 	High+Lowthroughput	"Inflammatory and mitogenic signals drive interleukin 23 subunit alpha (IL23A) secretion 
independent of IL12B in intestinal epithelial cells"	否		Inflammatory diseases		E_01_0977	RT qPCR, Western blot, ELISA	" involving the formation 
of a transcriptional enhancer complex consisting 
of proto-oncogene c-Jun (c-Jun), RELA proto_x0002_oncogene NF-κB subunit (RelA), RUNX family 
transcription factor 1 (RUNX1), a"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			" involving the formation 
of a transcriptional enhancer complex consisting 
of proto-oncogene c-Jun (c-Jun), RELA proto_x0002_oncogene NF-κB subunit (RelA), RUNX family 
transcription factor 1 (RUNX1), a"	Immunohistochemical staining	" involving the formation 
of a transcriptional enhancer complex consisting 
of proto-oncogene c-Jun (c-Jun), RELA proto_x0002_oncogene NF-κB subunit (RelA), RUNX family 
transcription factor 1 (RUNX1), a"	RUNX1		RT-qPCR,western blot，酶联吸附反应	" involving the formation 
of a transcriptional enhancer complex consisting 
of proto-oncogene c-Jun (c-Jun), RELA proto_x0002_oncogene NF-κB subunit (RelA), RUNX family 
transcription factor 1 (RUNX1), a"			
32183903	chr5	37810291	37812291	GDNF	"GDNF is a dual promoter gene, and the promoter II
with two enhancers and two silencers plays a major role in transcription initiation."	human	Glioblastoma	High+Lowthroughput	Crosstalk between DNA methylation and histone acetylation triggers GDNF high transcription in glioblastoma cells	否		Glioblastoma		E_01_0978	RT-qPCR, Western blot, transfection, chip SEQ, chip PCR, re chip PCR, immunofluorescence	"GDNF is a dual promoter gene, and the promoter II
with two enhancers and two silencers plays a major role in transcription initiation."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"GDNF is a dual promoter gene, and the promoter II
with two enhancers and two silencers plays a major role in transcription initiation."	Immunohistochemical staining	"GDNF is a dual promoter gene, and the promoter II
with two enhancers and two silencers plays a major role in transcription initiation."	GDNF		RT-QPCR，Western blot，转染，ChIP-seq、ChIP-PCR ， re-ChIP-PCR，免疫荧光	"GDNF is a dual promoter gene, and the promoter II
with two enhancers and two silencers plays a major role in transcription initiation."			
32165301	chr16	69561943	69563943	NFAT5	"The nuclear factor of activated T-cells 5 (NFAT5), also known as tonicity-responsive enhancer-binding protein
(TonEBP), is a transcription factor that regulates osmoadaptive response in multiple tissues and is highly ex_x0002_pressed in the developing central nervous system. "	mouse	adrenal gland	High+Lowthroughput	"DDC expression is not regulated by NFAT5 (TonEBP) in dopaminergic neural
cell lines"	否		Psychiatric disorders		E_02_0738	Trt-qpcr, immunohistochemistry, transfection	"The nuclear factor of activated T-cells 5 (NFAT5), also known as tonicity-responsive enhancer-binding protein
(TonEBP), is a transcription factor that regulates osmoadaptive response in multiple tissues and is highly ex_x0002_pressed in the developing central nervous system. "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"The nuclear factor of activated T-cells 5 (NFAT5), also known as tonicity-responsive enhancer-binding protein
(TonEBP), is a transcription factor that regulates osmoadaptive response in multiple tissues and is highly ex_x0002_pressed in the developing central nervous system. "		"The nuclear factor of activated T-cells 5 (NFAT5), also known as tonicity-responsive enhancer-binding protein
(TonEBP), is a transcription factor that regulates osmoadaptive response in multiple tissues and is highly ex_x0002_pressed in the developing central nervous system. "	Immunohistochemical staining	"The nuclear factor of activated T-cells 5 (NFAT5), also known as tonicity-responsive enhancer-binding protein
(TonEBP), is a transcription factor that regulates osmoadaptive response in multiple tissues and is highly ex_x0002_pressed in the developing central nervous system. "			TRT-QPCR，免疫组化，转染				NFAT5
32158256	chr9	117701191	117703191	TLR4	" The pathway
components were measured to evaluate the involvement of toll-like receptor 4/nuclear factor
kappa-light-chain-enhancer of activated B cells (TLR4/NF-κB) pathway."	human	cervical carcinoma	High+Lowthroughput	"Procyanidin Compound (PC) Suppresses
Lipopolysaccharide-Induced Cervical Cancer Cell
Proliferation Through Blocking the TLR4/NF-κB
Pathway"	否		cervical carcinoma		E_01_0979	CCK8, flow cytometry Western blot, RT-qPCR, scratch assay	" The pathway
components were measured to evaluate the involvement of toll-like receptor 4/nuclear factor
kappa-light-chain-enhancer of activated B cells (TLR4/NF-κB) pathway."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			" The pathway
components were measured to evaluate the involvement of toll-like receptor 4/nuclear factor
kappa-light-chain-enhancer of activated B cells (TLR4/NF-κB) pathway."	Immunohistochemical staining	" The pathway
components were measured to evaluate the involvement of toll-like receptor 4/nuclear factor
kappa-light-chain-enhancer of activated B cells (TLR4/NF-κB) pathway."	TLR4		CCK8，流式细胞术Western blot，RT-QPCR，划痕实验	" The pathway
components were measured to evaluate the involvement of toll-like receptor 4/nuclear factor
kappa-light-chain-enhancer of activated B cells (TLR4/NF-κB) pathway."			
32157157	chr13	20970532	20972532	LATS2	" RNA immunoprecipitation and chromatin immunoprecipitation assays
demonstrated that lncRNA NEAT1 recruited enhancer of zeste homolog 2 (EZH2) to the LATS2 promoter and
repressed LATS2 expression"	human	liver	High+Lowthroughput	Long noncoding RNA NEAT1 suppresses hepatocyte proliferation in fulminant hepatic failure through increased recruitment of EZH2 to the LATS2 promoter region and promotion of H3K27me3 methylation	否		Hepatic failure		E_01_0980	Transfection, Western blot, chip SEQ, ELISA, TUNEL staining, he staining, immunohistochemistry	" RNA immunoprecipitation and chromatin immunoprecipitation assays
demonstrated that lncRNA NEAT1 recruited enhancer of zeste homolog 2 (EZH2) to the LATS2 promoter and
repressed LATS2 expression"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	" RNA immunoprecipitation and chromatin immunoprecipitation assays
demonstrated that lncRNA NEAT1 recruited enhancer of zeste homolog 2 (EZH2) to the LATS2 promoter and
repressed LATS2 expression"		" RNA immunoprecipitation and chromatin immunoprecipitation assays
demonstrated that lncRNA NEAT1 recruited enhancer of zeste homolog 2 (EZH2) to the LATS2 promoter and
repressed LATS2 expression"	Immunohistochemical staining	" RNA immunoprecipitation and chromatin immunoprecipitation assays
demonstrated that lncRNA NEAT1 recruited enhancer of zeste homolog 2 (EZH2) to the LATS2 promoter and
repressed LATS2 expression"			转染，Western blot，ChIP-seq，酶联免疫吸附，tunel染色，HE染色，免疫组化				LATS2
32153739	chr10	31315838	31317838	ZEB1	"Zinc-finger Enhancer Binding protein (ZEB1) acts as a transcription fac_x0002_tor to promote cancer progression through regulating Epithelial to Mesenchymal 
Transition (EMT)."	human	gastric cancer	High+Lowthroughput	"Investigation of the Correlation between Androgen Receptor and ZEB1 and its Value 
in Progression of Gastric Cancer"	否		gastric cancer		E_01_0981	Cytotoxicity assay, RT-qPCR, reverse transcription	"Zinc-finger Enhancer Binding protein (ZEB1) acts as a transcription fac_x0002_tor to promote cancer progression through regulating Epithelial to Mesenchymal 
Transition (EMT)."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Zinc-finger Enhancer Binding protein (ZEB1) acts as a transcription fac_x0002_tor to promote cancer progression through regulating Epithelial to Mesenchymal 
Transition (EMT)."	Immunohistochemical staining	"Zinc-finger Enhancer Binding protein (ZEB1) acts as a transcription fac_x0002_tor to promote cancer progression through regulating Epithelial to Mesenchymal 
Transition (EMT)."	ZEB1		细胞毒性检测，RT-QPCR，逆转录	"Zinc-finger Enhancer Binding protein (ZEB1) acts as a transcription fac_x0002_tor to promote cancer progression through regulating Epithelial to Mesenchymal 
Transition (EMT)."			
32153563	chr18	79393019	79395019	NFATC1	"We also found binding sites
for nuclear factor of activated T-cells (NFATC1), nuclear factor kappa-light-chain_x0002_enhancer of activated B cells (NF-κB), early growth response factor (EGR1), and
the estrogen receptor 1 (ESR1)."	human	lymph	High+Lowthroughput	Estrogen Receptor, Inflammatory, and FOXO Transcription Factors Regulate Expression of Myasthenia Gravis-Associated Circulating microRNAs	否		myasthenia gravis		E_01_0982	ELISAs	"We also found binding sites
for nuclear factor of activated T-cells (NFATC1), nuclear factor kappa-light-chain_x0002_enhancer of activated B cells (NF-κB), early growth response factor (EGR1), and
the estrogen receptor 1 (ESR1)."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"We also found binding sites
for nuclear factor of activated T-cells (NFATC1), nuclear factor kappa-light-chain_x0002_enhancer of activated B cells (NF-κB), early growth response factor (EGR1), and
the estrogen receptor 1 (ESR1)."	Immunohistochemical staining	"We also found binding sites
for nuclear factor of activated T-cells (NFATC1), nuclear factor kappa-light-chain_x0002_enhancer of activated B cells (NF-κB), early growth response factor (EGR1), and
the estrogen receptor 1 (ESR1)."	NFATC1		酶联免疫吸附	"We also found binding sites
for nuclear factor of activated T-cells (NFATC1), nuclear factor kappa-light-chain_x0002_enhancer of activated B cells (NF-κB), early growth response factor (EGR1), and
the estrogen receptor 1 (ESR1)."			
32151973	chr4	88723288	88725288	FAM13A	"Member A (FAM13A) has been associated with lipid levels and fat mass
by genome-wide association studies (GWAS). "	mouse	Fat	High+Lowthroughput	"FAM13A Represses AMPK Activity and Regulates
Hepatic Glucose and Lipid Metabolism"	是	rs2276936	Obesity		E_02_0739	Western blot，RT-QPCR	"Member A (FAM13A) has been associated with lipid levels and fat mass
by genome-wide association studies (GWAS). "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Member A (FAM13A) has been associated with lipid levels and fat mass
by genome-wide association studies (GWAS). "		"Member A (FAM13A) has been associated with lipid levels and fat mass
by genome-wide association studies (GWAS). "	Immunohistochemical staining	"Member A (FAM13A) has been associated with lipid levels and fat mass
by genome-wide association studies (GWAS). "			Western blot，RT-QPCR				FAM13A
32151175	chr8	47734528	47736528	CEBPD	" CCAAT enhancer-binding protein delta
(CEBPD) is important in immune and inflammatory responses."	human	Thyroid cancer	High+Lowthroughput	MiR-324-5p/PTPRD/CEBPD axis promotes papillary thyroid carcinoma progression via microenvironment alteration	否		Thyroid cancer		E_01_0983	RT-qPCR, transfection, CCK8, scratch assay, flow cytometry, Western blot	" CCAAT enhancer-binding protein delta
(CEBPD) is important in immune and inflammatory responses."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			" CCAAT enhancer-binding protein delta
(CEBPD) is important in immune and inflammatory responses."	Immunohistochemical staining	" CCAAT enhancer-binding protein delta
(CEBPD) is important in immune and inflammatory responses."	CEBPD		RT-QPCR，转染，CCK8，划痕实验，流式细胞术，Western blot	" CCAAT enhancer-binding protein delta
(CEBPD) is important in immune and inflammatory responses."			
32132110	chr5	88714434	88716434	MEF2C	"g. Further, we identified the Myocyte enhancer factor 2 C (MEF2C) transcription factor as 
a key upstream activator of Myoc whose gain-of-function significantly deterred cancer-induced 
muscle wasting and dysfunction in a pre-clinical model of pancreatic ductal adenocarcinoma 
(PDAC)."	mouse	colon	High+Lowthroughput	"MEF2c-dependent downregulation of Myocilin mediates cancer-induced muscle wasting and 
associates with cachexia in cancer patients "	否		Muscle wasting		E_02_0740	Immunohistochemistry, oil red O staining, Western blot, RT-qPCR	"g. Further, we identified the Myocyte enhancer factor 2 C (MEF2C) transcription factor as 
a key upstream activator of Myoc whose gain-of-function significantly deterred cancer-induced 
muscle wasting and dysfunction in a pre-clinical model of pancreatic ductal adenocarcinoma 
(PDAC)."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"g. Further, we identified the Myocyte enhancer factor 2 C (MEF2C) transcription factor as 
a key upstream activator of Myoc whose gain-of-function significantly deterred cancer-induced 
muscle wasting and dysfunction in a pre-clinical model of pancreatic ductal adenocarcinoma 
(PDAC)."		"g. Further, we identified the Myocyte enhancer factor 2 C (MEF2C) transcription factor as 
a key upstream activator of Myoc whose gain-of-function significantly deterred cancer-induced 
muscle wasting and dysfunction in a pre-clinical model of pancreatic ductal adenocarcinoma 
(PDAC)."	Immunohistochemical staining	"g. Further, we identified the Myocyte enhancer factor 2 C (MEF2C) transcription factor as 
a key upstream activator of Myoc whose gain-of-function significantly deterred cancer-induced 
muscle wasting and dysfunction in a pre-clinical model of pancreatic ductal adenocarcinoma 
(PDAC)."			免疫组化，油红O染色，Western blot，RT-QPCR				MEF2C
32130892	chr5	158693087	158695087	EBF1	"Enhancer profiling and genetic
assays identified EBF1 as a candidate regulator of
the cold response in BAT."	mouse	Fat	High+Lowthroughput	Early B Cell Factor Activity Controls Developmental and Adaptive Thermogenic Gene Programming in Adipocytes	否		Obesity		E_02_0741	He staining, Western blot, RT-qPCR, chip seq	"Enhancer profiling and genetic
assays identified EBF1 as a candidate regulator of
the cold response in BAT."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Enhancer profiling and genetic
assays identified EBF1 as a candidate regulator of
the cold response in BAT."		"Enhancer profiling and genetic
assays identified EBF1 as a candidate regulator of
the cold response in BAT."	Immunohistochemical staining	"Enhancer profiling and genetic
assays identified EBF1 as a candidate regulator of
the cold response in BAT."			HE染色，Western blot，RT-QPCR，ChIP-seq				EBF1
32114505	chr13	49953816	49955816	DLEU2	"We show that HBx binds the promoter region, 
enhances the transcription and induces the accumulation 
of DLEU2 in infected hepatocytes. We found that 
nuclear DLEU2 directly binds HBx and the histone 
methyltransferase enhancer of zeste homolog 2 (EZH2), "	human	liver cancer	High+Lowthroughput	Hepatitis B protein HBx binds the DLEU2 lncRNA to sustain cccDNA and host cancer-related gene transcription	否		Hepatocellular carcinoma		E_01_0984	ChIP-seq，Western blot，RIP，ChIRP，ddPCR	"We show that HBx binds the promoter region, 
enhances the transcription and induces the accumulation 
of DLEU2 in infected hepatocytes. We found that 
nuclear DLEU2 directly binds HBx and the histone 
methyltransferase enhancer of zeste homolog 2 (EZH2), "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"We show that HBx binds the promoter region, 
enhances the transcription and induces the accumulation 
of DLEU2 in infected hepatocytes. We found that 
nuclear DLEU2 directly binds HBx and the histone 
methyltransferase enhancer of zeste homolog 2 (EZH2), "		"We show that HBx binds the promoter region, 
enhances the transcription and induces the accumulation 
of DLEU2 in infected hepatocytes. We found that 
nuclear DLEU2 directly binds HBx and the histone 
methyltransferase enhancer of zeste homolog 2 (EZH2), "	Immunohistochemical staining	"We show that HBx binds the promoter region, 
enhances the transcription and induces the accumulation 
of DLEU2 in infected hepatocytes. We found that 
nuclear DLEU2 directly binds HBx and the histone 
methyltransferase enhancer of zeste homolog 2 (EZH2), "			ChIP-seq，Western blot，RIP，ChIRP，ddPCR				DLEU2
32113834	chr11	65495092	65497092	MALAT1	"With luciferase reporter assays, a STAT3-binding sequence in the 
enhancer region of MALAT1 gene was demonstrated to be crucial for the IL-6- or 
STAT3-induced MALAT1 promoter activation."	human	cervical carcinoma	High+Lowthroughput	IL-6/STAT3 mediates the HPV18 E6/E7 stimulated upregulation of MALAT1 gene in cervical cancer HeLa cells	否		cervical carcinoma		E_01_0985	RNA isolation, RT-qPCR, Western blot, luciferase reporter assay	"With luciferase reporter assays, a STAT3-binding sequence in the 
enhancer region of MALAT1 gene was demonstrated to be crucial for the IL-6- or 
STAT3-induced MALAT1 promoter activation."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"With luciferase reporter assays, a STAT3-binding sequence in the 
enhancer region of MALAT1 gene was demonstrated to be crucial for the IL-6- or 
STAT3-induced MALAT1 promoter activation."	Immunohistochemical staining	"With luciferase reporter assays, a STAT3-binding sequence in the 
enhancer region of MALAT1 gene was demonstrated to be crucial for the IL-6- or 
STAT3-induced MALAT1 promoter activation."	MALAT1		RNA分离，RT-QPCR，Western blot，荧光素酶报告测定	"With luciferase reporter assays, a STAT3-binding sequence in the 
enhancer region of MALAT1 gene was demonstrated to be crucial for the IL-6- or 
STAT3-induced MALAT1 promoter activation."			
32103293	chr17	42310440	42312440	STAT3	"Interleukin 6 (IL-6)-induced phosphorylated STAT3-regulated programmed cell death ligand 1, CCAAT/enhancer-binding 
proteins alpha and beta and Interleukin 10 expression in MDSCs. "	human	tumour	High+Lowthroughput	"Myeloid‑derived suppressor cells impede T cell functionality 
and promote Th17 differentiation in oral squamous cell carcinoma"	否		OSCC		E_01_0986	Flow cytometry, Western blot, RT-qPCR, ELISA	"Interleukin 6 (IL-6)-induced phosphorylated STAT3-regulated programmed cell death ligand 1, CCAAT/enhancer-binding 
proteins alpha and beta and Interleukin 10 expression in MDSCs. "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Interleukin 6 (IL-6)-induced phosphorylated STAT3-regulated programmed cell death ligand 1, CCAAT/enhancer-binding 
proteins alpha and beta and Interleukin 10 expression in MDSCs. "	Immunohistochemical staining	"Interleukin 6 (IL-6)-induced phosphorylated STAT3-regulated programmed cell death ligand 1, CCAAT/enhancer-binding 
proteins alpha and beta and Interleukin 10 expression in MDSCs. "	STAT3		流式细胞术，Western blot，RT-QPCR，Elisa	"Interleukin 6 (IL-6)-induced phosphorylated STAT3-regulated programmed cell death ligand 1, CCAAT/enhancer-binding 
proteins alpha and beta and Interleukin 10 expression in MDSCs. "			
32098781	chr11	1980587	1982587	MRPL23-AS1	"MRPL23-AS1 increased the binding of EZH2 and H3K27me3 on the E-cadherin 
promoter region. Moreover, MRPL23-AS1 levels were higher in exosomes isolated 
from the blood plasma of SACC patients, and exosomal MRPL23-AS1 affected 
pulmonary microvascular endothelial cells in an 'exosomecrine' manner. "	human	oral cavity	High+Lowthroughput	Long Noncoding RNA MRPL23-AS1 Promotes Adenoid Cystic Carcinoma Lung Metastasis	否		Initiating cystic carcinoma lung metastases		E_01_0987	RT-qPCR, invasion migration assay of transfected cells, Western blot, rip SEQ, chip SEQ, rna-fish and immunofluorescence, flow cytometry	"MRPL23-AS1 increased the binding of EZH2 and H3K27me3 on the E-cadherin 
promoter region. Moreover, MRPL23-AS1 levels were higher in exosomes isolated 
from the blood plasma of SACC patients, and exosomal MRPL23-AS1 affected 
pulmonary microvascular endothelial cells in an 'exosomecrine' manner. "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"MRPL23-AS1 increased the binding of EZH2 and H3K27me3 on the E-cadherin 
promoter region. Moreover, MRPL23-AS1 levels were higher in exosomes isolated 
from the blood plasma of SACC patients, and exosomal MRPL23-AS1 affected 
pulmonary microvascular endothelial cells in an 'exosomecrine' manner. "		"MRPL23-AS1 increased the binding of EZH2 and H3K27me3 on the E-cadherin 
promoter region. Moreover, MRPL23-AS1 levels were higher in exosomes isolated 
from the blood plasma of SACC patients, and exosomal MRPL23-AS1 affected 
pulmonary microvascular endothelial cells in an 'exosomecrine' manner. "	Immunohistochemical staining	"MRPL23-AS1 increased the binding of EZH2 and H3K27me3 on the E-cadherin 
promoter region. Moreover, MRPL23-AS1 levels were higher in exosomes isolated 
from the blood plasma of SACC patients, and exosomal MRPL23-AS1 affected 
pulmonary microvascular endothelial cells in an 'exosomecrine' manner. "			RT-QPCR，转染细胞侵袭迁移检测，Western blot，RIP-seq，CHIP-seq，RNA-FISH和免疫荧光，流式细胞术				MRPL23-AS1
32095812	chr7	117284492	117286492	CFTR	"Within this TAD specific
cis-regulatory elements (CREs) play critical roles in the reg_x0002_ulation of CFTR expression, either by acting as enhancers
or as structural features that facilitate the recruitment of ac_x0002_tive elements to the gene promoter (6)."	human	Lung adenocarcinoma	High+Lowthroughput	"Looping of upstream cis-regulatory elements is
required for CFTR expression in human airway
epithelial cells"	否		lung disease		E_01_0988	RT qPCR, Erna detection, chip qPCR, chip SEQ, luciferase detection,	"Within this TAD specific
cis-regulatory elements (CREs) play critical roles in the reg_x0002_ulation of CFTR expression, either by acting as enhancers
or as structural features that facilitate the recruitment of ac_x0002_tive elements to the gene promoter (6)."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Within this TAD specific
cis-regulatory elements (CREs) play critical roles in the reg_x0002_ulation of CFTR expression, either by acting as enhancers
or as structural features that facilitate the recruitment of ac_x0002_tive elements to the gene promoter (6)."	Immunohistochemical staining	"Within this TAD specific
cis-regulatory elements (CREs) play critical roles in the reg_x0002_ulation of CFTR expression, either by acting as enhancers
or as structural features that facilitate the recruitment of ac_x0002_tive elements to the gene promoter (6)."	CFTR		RT-qPCR，eRNA检测，ChIP-qPCR，ChIP-seq，荧光素酶检测，	"Within this TAD specific
cis-regulatory elements (CREs) play critical roles in the reg_x0002_ulation of CFTR expression, either by acting as enhancers
or as structural features that facilitate the recruitment of ac_x0002_tive elements to the gene promoter (6)."			
32093567	chr3	52542758	52544758	PBRM1	"The inhibition of enhancer of zeste homolog 2 (EZH2) has been suggested to be synthetic lethal
with polybromo-1 (PBRM1) deficiency,"	human	Renal clear cell carcinoma	High+Lowthroughput	"A novel EZH2 inhibitor induces synthetic lethality and apoptosis in PBRM1-deficient
cancer cells"	否		renal carcinoma		E_01_0989	Transfection, Western blot, RNAi, flow cytometry	"The inhibition of enhancer of zeste homolog 2 (EZH2) has been suggested to be synthetic lethal
with polybromo-1 (PBRM1) deficiency,"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"The inhibition of enhancer of zeste homolog 2 (EZH2) has been suggested to be synthetic lethal
with polybromo-1 (PBRM1) deficiency,"	Immunohistochemical staining	"The inhibition of enhancer of zeste homolog 2 (EZH2) has been suggested to be synthetic lethal
with polybromo-1 (PBRM1) deficiency,"	PBRM1		转染，Western blot，RNAi，流式细胞术	"The inhibition of enhancer of zeste homolog 2 (EZH2) has been suggested to be synthetic lethal
with polybromo-1 (PBRM1) deficiency,"			
32093281	chr10	58382379	58384379	TFAM	Besides, downregulation of PISD with siRNA reduced the level of LC3-II, indicating that depletion of TFAM retarded autophagy via inhibiting PISD expression.	human	tumour	High+Lowthroughput	Knockdown of TFAM in Tumor Cells Retarded Autophagic Flux through Regulating p53 Acetylation and PISD Expression	否		tumour		E_01_0990	Transfection, Western blot, immunofluorescence, RT-qPCR,	Besides, downregulation of PISD with siRNA reduced the level of LC3-II, indicating that depletion of TFAM retarded autophagy via inhibiting PISD expression.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Besides, downregulation of PISD with siRNA reduced the level of LC3-II, indicating that depletion of TFAM retarded autophagy via inhibiting PISD expression.	Immunohistochemical staining	Besides, downregulation of PISD with siRNA reduced the level of LC3-II, indicating that depletion of TFAM retarded autophagy via inhibiting PISD expression.	TFAM		转染，Western blot，免疫荧光，RT-QPCR，	Besides, downregulation of PISD with siRNA reduced the level of LC3-II, indicating that depletion of TFAM retarded autophagy via inhibiting PISD expression.			
32067207	chr6	50815520	50817520	TFAP2B	"In a word, our results suggest that the TP73-AS1/ miRNA-874-3p / TFAP2B (transcription
factor activating enhancer-binding protein 2B) pathway contributes to the progression of RB, which may provide novel insights
into the function of lncRNA-driven retinoblastogenesis."	human	Retinoblastoma	High+Lowthroughput	Long non-coding RNA TP73-AS1 promotes TFAP2B-mediated proliferation, metastasis and invasion in retinoblastoma via decoying of miRNA-874-3p	否		Retinoblastoma		E_01_0991	RT-qPCR, MTT, transfection, flow cytometry, Western blot	"In a word, our results suggest that the TP73-AS1/ miRNA-874-3p / TFAP2B (transcription
factor activating enhancer-binding protein 2B) pathway contributes to the progression of RB, which may provide novel insights
into the function of lncRNA-driven retinoblastogenesis."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"In a word, our results suggest that the TP73-AS1/ miRNA-874-3p / TFAP2B (transcription
factor activating enhancer-binding protein 2B) pathway contributes to the progression of RB, which may provide novel insights
into the function of lncRNA-driven retinoblastogenesis."	Immunohistochemical staining	"In a word, our results suggest that the TP73-AS1/ miRNA-874-3p / TFAP2B (transcription
factor activating enhancer-binding protein 2B) pathway contributes to the progression of RB, which may provide novel insights
into the function of lncRNA-driven retinoblastogenesis."	TFAP2B		RT-QPCR，MTT，转染，流式细胞术，Western blot	"In a word, our results suggest that the TP73-AS1/ miRNA-874-3p / TFAP2B (transcription
factor activating enhancer-binding protein 2B) pathway contributes to the progression of RB, which may provide novel insights
into the function of lncRNA-driven retinoblastogenesis."			
32068311	chr8	11674018	11676018	GATA4	"We have also used the G2 enhancer of the GATA4 gene 
as a driver due to its activation in the proepicardium."	human,mouse	heart	High+Lowthroughput	"Epicardial cell lineages and the origin of the coronary 
endothelium"	否		coronary artery disease 		E_02_0742	Immunohistochemistry, flow cytometry, confocal,	"We have also used the G2 enhancer of the GATA4 gene 
as a driver due to its activation in the proepicardium."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"We have also used the G2 enhancer of the GATA4 gene 
as a driver due to its activation in the proepicardium."		"We have also used the G2 enhancer of the GATA4 gene 
as a driver due to its activation in the proepicardium."	Immunohistochemical staining	"We have also used the G2 enhancer of the GATA4 gene 
as a driver due to its activation in the proepicardium."			免疫组化，流式细胞术，共聚焦，				GATA4
32054946	chr3	60377473	60379473	Mbnl1	" We previously reported that a nonsteroidal anti_x0002_infammatory drug (NSAID), phenylbutazone, upregulates MBNL1 expression in DM1 mouse model 
by demethylation of MeR2, an enhancer element in Mbnl1 intron 1. "	human	Myoblasts	High+Lowthroughput	"Inhibition of cyclooxygenase-1 by 
nonsteroidal anti-infammatory 
drugs demethylates MeR2 
enhancer and promotes Mbnl1
transcription in myogenic cells"	否		Inflammatory diseases		E_01_0992	Western blot, transfection, immunofluorescence, luciferase assay	" We previously reported that a nonsteroidal anti_x0002_infammatory drug (NSAID), phenylbutazone, upregulates MBNL1 expression in DM1 mouse model 
by demethylation of MeR2, an enhancer element in Mbnl1 intron 1. "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	" We previously reported that a nonsteroidal anti_x0002_infammatory drug (NSAID), phenylbutazone, upregulates MBNL1 expression in DM1 mouse model 
by demethylation of MeR2, an enhancer element in Mbnl1 intron 1. "		" We previously reported that a nonsteroidal anti_x0002_infammatory drug (NSAID), phenylbutazone, upregulates MBNL1 expression in DM1 mouse model 
by demethylation of MeR2, an enhancer element in Mbnl1 intron 1. "	Immunohistochemical staining	" We previously reported that a nonsteroidal anti_x0002_infammatory drug (NSAID), phenylbutazone, upregulates MBNL1 expression in DM1 mouse model 
by demethylation of MeR2, an enhancer element in Mbnl1 intron 1. "			Western blot，转染，免疫荧光，荧光素酶检测				Mbnl1
32035085	chr10	30705715	30707715	Hey2	A basic helix-loop-helix transcription factor Hey2 is specifically expressed in the embryonic mouse ventricles and is indispensable for ventricular myocyte differentiation, compartment identity and morphogenesis of the heart	mouse	heart	High+Lowthroughput	"Expression of Hey2 transcription factor in the early embryonic ventricles is
controlled through a distal enhancer by Tbx20 and Gata
transcription factors"	否		Heart disease 		E_02_0743	Chip SEQ, transfection, immunohistochemistry, in situ hybridization, RT-qPCR, luciferase reporter assay	A basic helix-loop-helix transcription factor Hey2 is specifically expressed in the embryonic mouse ventricles and is indispensable for ventricular myocyte differentiation, compartment identity and morphogenesis of the heart	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A basic helix-loop-helix transcription factor Hey2 is specifically expressed in the embryonic mouse ventricles and is indispensable for ventricular myocyte differentiation, compartment identity and morphogenesis of the heart		A basic helix-loop-helix transcription factor Hey2 is specifically expressed in the embryonic mouse ventricles and is indispensable for ventricular myocyte differentiation, compartment identity and morphogenesis of the heart	Immunohistochemical staining	A basic helix-loop-helix transcription factor Hey2 is specifically expressed in the embryonic mouse ventricles and is indispensable for ventricular myocyte differentiation, compartment identity and morphogenesis of the heart			ChIP-seq，转染，免疫组化，原位杂交，RT-QPCR，荧光素酶报告测定				Hey2
32029739	chr8	127791613	127793613	PVT1	" However, the function of PVT1
intragenic enhancers in BETi-resistant leukemia cells remains lar_x0002_gely unexplored."	human,mouse	blood	High+Lowthroughput	"A combination strategy targeting enhancer
plasticity exerts synergistic lethality against
BETi-resistant leukemia cells"	否		leukemia		E_02_0744	Western blot, transfection, RT-qPCR, chip, ALT assay, flow cytometry	" However, the function of PVT1
intragenic enhancers in BETi-resistant leukemia cells remains lar_x0002_gely unexplored."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	" However, the function of PVT1
intragenic enhancers in BETi-resistant leukemia cells remains lar_x0002_gely unexplored."		" However, the function of PVT1
intragenic enhancers in BETi-resistant leukemia cells remains lar_x0002_gely unexplored."	Immunohistochemical staining	" However, the function of PVT1
intragenic enhancers in BETi-resistant leukemia cells remains lar_x0002_gely unexplored."			Western blot，转染，RT-QPCR，ChIP，ALT检测，流式细胞术				PVT1
32028069	chr2	105355146	105357146	FHL2	"Increased FHL2 and androgen receptor (AR) expression and decreased CCAAT/enhancer-binding
protein b (C/EBPb) expression were observed in hGCs from patients with PCOS."	human	granular cell 	High+Lowthroughput	"Up-regulated FHL2 inhibits ovulation through interacting with androgen
receptor and ERK1/2 in polycystic ovary syndrome"	否		PCOS		E_01_0993	Immunofluorescence, transfection, RT-qPCR, Western blot, chip,	"Increased FHL2 and androgen receptor (AR) expression and decreased CCAAT/enhancer-binding
protein b (C/EBPb) expression were observed in hGCs from patients with PCOS."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Increased FHL2 and androgen receptor (AR) expression and decreased CCAAT/enhancer-binding
protein b (C/EBPb) expression were observed in hGCs from patients with PCOS."		"Increased FHL2 and androgen receptor (AR) expression and decreased CCAAT/enhancer-binding
protein b (C/EBPb) expression were observed in hGCs from patients with PCOS."	Immunohistochemical staining	"Increased FHL2 and androgen receptor (AR) expression and decreased CCAAT/enhancer-binding
protein b (C/EBPb) expression were observed in hGCs from patients with PCOS."			免疫荧光，转染，RT-QPCR，Western blot，CHIP，				FHL2
32025238	chr11	89321560	89323560	NOX4	 NADPH oxidase 4 (NOX4)-associated oxidative stress has been shown to induce pre_x0002_mature NP cell senescence. Enhancer of zeste homolog 2 (EZH2) is a crucial gene regulating cell senescence	mouse	bone marrow	High+Lowthroughput	"A positive feedback loop between EZH2 
and NOX4 regulates nucleus pulposus cell 
senescence in age-related intervertebral disc 
degeneration"	否		Disc pathologies		E_02_0745	SA- β- Gal staining, edu staining, transfection, Western blot, immunofluorescence, immunohistochemistry, RT-qPCR, ROS measurement, flow cytometry, chip	 NADPH oxidase 4 (NOX4)-associated oxidative stress has been shown to induce pre_x0002_mature NP cell senescence. Enhancer of zeste homolog 2 (EZH2) is a crucial gene regulating cell senescence	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 NADPH oxidase 4 (NOX4)-associated oxidative stress has been shown to induce pre_x0002_mature NP cell senescence. Enhancer of zeste homolog 2 (EZH2) is a crucial gene regulating cell senescence		 NADPH oxidase 4 (NOX4)-associated oxidative stress has been shown to induce pre_x0002_mature NP cell senescence. Enhancer of zeste homolog 2 (EZH2) is a crucial gene regulating cell senescence	Immunohistochemical staining	 NADPH oxidase 4 (NOX4)-associated oxidative stress has been shown to induce pre_x0002_mature NP cell senescence. Enhancer of zeste homolog 2 (EZH2) is a crucial gene regulating cell senescence			SA-β-gal 染色，EDU染色，转染，Western blot，免疫荧光，免疫组化，RT-QPCR,ROS 测量,流式细胞术，ChIP				NOX4
32022326	chr7	148804929	148806929	EZH2	"Chip-seq demonstrated binding of β-catenin to the promoter of EZH2, a key 
component of the PRC2 complex that catalyzes histone methylation."	mouse	bone marrow	High+Lowthroughput	β-Catenin Preserves the Stem State of Murine Bone Marrow Stromal Cells Through Activation of EZH2	否		Bone marrow disorders	mesenchymal stem cell of the bone marrow	E_02_0746	Immunofluorescence, oil red O staining, RT-qPCR, Western blot, chip	"Chip-seq demonstrated binding of β-catenin to the promoter of EZH2, a key 
component of the PRC2 complex that catalyzes histone methylation."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"Chip-seq demonstrated binding of β-catenin to the promoter of EZH2, a key 
component of the PRC2 complex that catalyzes histone methylation."		"Chip-seq demonstrated binding of β-catenin to the promoter of EZH2, a key 
component of the PRC2 complex that catalyzes histone methylation."	Immunohistochemical staining	"Chip-seq demonstrated binding of β-catenin to the promoter of EZH2, a key 
component of the PRC2 complex that catalyzes histone methylation."			免疫荧光，油红O染色，RT-QPCR，Western blot，CHIP				EZH2
32021450	chr4	1868747	1870747	NSD2	"Nuclear receptor suppressor of variegation, enhancer of zeste, and trithorax
(SET) domain-containing 2 (NSD2), is a well-known histone lysine methyltransferase
(HMTase)"	human	kidney	High+Lowthroughput	"NSD2 Promotes Renal Cancer Progression
Through Stimulating Akt/Erk Signaling"	否		renal carcinoma		E_01_0994	Immunofluorescence, immunohistochemistry, transfection. RT-qPCR, flow cytometry, Western blot	"Nuclear receptor suppressor of variegation, enhancer of zeste, and trithorax
(SET) domain-containing 2 (NSD2), is a well-known histone lysine methyltransferase
(HMTase)"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Nuclear receptor suppressor of variegation, enhancer of zeste, and trithorax
(SET) domain-containing 2 (NSD2), is a well-known histone lysine methyltransferase
(HMTase)"	Immunohistochemical staining	"Nuclear receptor suppressor of variegation, enhancer of zeste, and trithorax
(SET) domain-containing 2 (NSD2), is a well-known histone lysine methyltransferase
(HMTase)"	NSD2		免疫荧光，免疫组化，转染。RT-QPCR，流式细胞术，Western blot	"Nuclear receptor suppressor of variegation, enhancer of zeste, and trithorax
(SET) domain-containing 2 (NSD2), is a well-known histone lysine methyltransferase
(HMTase)"			
32187157	chr22	42123841	42125841	CYP2D6	"in a critical enhancer region downstream of 
the CYP2D6 promoter was proposed to modulate CYP2D6 
activity, depending on its linkage disequilibrium (LD) 
with the common CYP2D6 SNP, rs16947."	human		High+Lowthroughput	Distribution and linkage disequilibrium of the enhancer SNP rs5758550 among Latin American populations: influence of continental ancestry	是	rs5758550 rs16947 rs5030656 rs35742688	Ethnic origin effects		E_01_0995		"in a critical enhancer region downstream of 
the CYP2D6 promoter was proposed to modulate CYP2D6 
activity, depending on its linkage disequilibrium (LD) 
with the common CYP2D6 SNP, rs16947."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"in a critical enhancer region downstream of 
the CYP2D6 promoter was proposed to modulate CYP2D6 
activity, depending on its linkage disequilibrium (LD) 
with the common CYP2D6 SNP, rs16947."		"in a critical enhancer region downstream of 
the CYP2D6 promoter was proposed to modulate CYP2D6 
activity, depending on its linkage disequilibrium (LD) 
with the common CYP2D6 SNP, rs16947."	Immunohistochemical staining	"in a critical enhancer region downstream of 
the CYP2D6 promoter was proposed to modulate CYP2D6 
activity, depending on its linkage disequilibrium (LD) 
with the common CYP2D6 SNP, rs16947."							CYP2D6
32186750	chr5	88714648	88716648	MEF2C	"EC cell lines 
transfected with vectors overexpressing miR‑638, its target 
gene myocyte enhancer factor 2C (MEF2C) or both, were 
constructed. "	human	endometrium	High+Lowthroughput	"Methylation‑associated silencing of miR‑638 promotes 
endometrial carcinoma progression by targeting MEF2C"	否		Endometrial cancer		E_01_0996	RT-qPCR, DNA methylation analysis, cell viability assay, Western blot	"EC cell lines 
transfected with vectors overexpressing miR‑638, its target 
gene myocyte enhancer factor 2C (MEF2C) or both, were 
constructed. "	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"EC cell lines 
transfected with vectors overexpressing miR‑638, its target 
gene myocyte enhancer factor 2C (MEF2C) or both, were 
constructed. "	Immunohistochemical staining	"EC cell lines 
transfected with vectors overexpressing miR‑638, its target 
gene myocyte enhancer factor 2C (MEF2C) or both, were 
constructed. "	MEF2C		RT-QPCR，DNA甲基化分析，细胞活力检测，Western blot	"EC cell lines 
transfected with vectors overexpressing miR‑638, its target 
gene myocyte enhancer factor 2C (MEF2C) or both, were 
constructed. "			
32017069	chr5	88714258	88716258	MEF2C	"The myocyte enhancer factor 2C
gene (MEF2C), located at chromosome 5q14.3, encodes a
transcription factor from the MCM1-agamous-deficiens_x0002_serum response factor family (Potthoff & Olson, 2007)"	human		High+Lowthroughput	"High expression of myocyte enhancer factor 2C predicts poor
prognosis for adult acute myeloid leukaemia with normal
karyotype"	否		Acute myeloid leukemia		E_01_0997	RT-QPCR	"The myocyte enhancer factor 2C
gene (MEF2C), located at chromosome 5q14.3, encodes a
transcription factor from the MCM1-agamous-deficiens_x0002_serum response factor family (Potthoff & Olson, 2007)"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"The myocyte enhancer factor 2C
gene (MEF2C), located at chromosome 5q14.3, encodes a
transcription factor from the MCM1-agamous-deficiens_x0002_serum response factor family (Potthoff & Olson, 2007)"	Immunohistochemical staining	"The myocyte enhancer factor 2C
gene (MEF2C), located at chromosome 5q14.3, encodes a
transcription factor from the MCM1-agamous-deficiens_x0002_serum response factor family (Potthoff & Olson, 2007)"	MEF2C		RT-QPCR	"The myocyte enhancer factor 2C
gene (MEF2C), located at chromosome 5q14.3, encodes a
transcription factor from the MCM1-agamous-deficiens_x0002_serum response factor family (Potthoff & Olson, 2007)"			
32012382	chr15	99562302	99564302	MEF2A	"TargetScan and MicroT-CDS predict
myocyte enhancer factor-2A (MEF2A), a transcription factor that regulates peroxi_x0002_some proliferator-activated receptor-gamma coactivator (PGC1α) transcription"	human	Peripheral blood	High+Lowthroughput	"MiRNA-137-mediated modulation of mitochondrial dynamics
regulates human neural stem cell fate"	否		Neurological disorders		E_01_0998	Transfection, RT-qPCR, Western blot, flow cytometry	"TargetScan and MicroT-CDS predict
myocyte enhancer factor-2A (MEF2A), a transcription factor that regulates peroxi_x0002_some proliferator-activated receptor-gamma coactivator (PGC1α) transcription"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"TargetScan and MicroT-CDS predict
myocyte enhancer factor-2A (MEF2A), a transcription factor that regulates peroxi_x0002_some proliferator-activated receptor-gamma coactivator (PGC1α) transcription"	Immunohistochemical staining	"TargetScan and MicroT-CDS predict
myocyte enhancer factor-2A (MEF2A), a transcription factor that regulates peroxi_x0002_some proliferator-activated receptor-gamma coactivator (PGC1α) transcription"	MEF2A		转染，RT-QPCR，Western blot，流式细胞数	"TargetScan and MicroT-CDS predict
myocyte enhancer factor-2A (MEF2A), a transcription factor that regulates peroxi_x0002_some proliferator-activated receptor-gamma coactivator (PGC1α) transcription"			
32009938	chr1	247412961	247414961	NLRP3	"leucine rich repeat and pyrin domain
containing 3 (NLRP3) and nuclear factor kappa-light-chain-enhancer of activated B
cells (NF-κB) are the major neuroinflammatory pathways that intensify AD pathogenesis"	human	Neuroblastoma	High+Lowthroughput	Inhibition of Amyloid-Beta Production, Associated Neuroinflammation, and Histone Deacetylase 2-Mediated Epigenetic Modifications Prevent Neuropathology in Alzheimer's Disease in vitro Model	否		Alzheimer disease		E_01_0999	Congo red staining, Western blot	"leucine rich repeat and pyrin domain
containing 3 (NLRP3) and nuclear factor kappa-light-chain-enhancer of activated B
cells (NF-κB) are the major neuroinflammatory pathways that intensify AD pathogenesis"	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	"leucine rich repeat and pyrin domain
containing 3 (NLRP3) and nuclear factor kappa-light-chain-enhancer of activated B
cells (NF-κB) are the major neuroinflammatory pathways that intensify AD pathogenesis"		"leucine rich repeat and pyrin domain
containing 3 (NLRP3) and nuclear factor kappa-light-chain-enhancer of activated B
cells (NF-κB) are the major neuroinflammatory pathways that intensify AD pathogenesis"	Immunohistochemical staining	"leucine rich repeat and pyrin domain
containing 3 (NLRP3) and nuclear factor kappa-light-chain-enhancer of activated B
cells (NF-κB) are the major neuroinflammatory pathways that intensify AD pathogenesis"			刚果红染色，Western blot				NLRP3
32009798	chr7	148804280	148806280	EZH2	"Emerging evidence reveals the vital role of enhancer of zeste homolog 2
(EZH2) in cancer chemoresistance."	human	breast	High+Lowthroughput	"EZH2 Contributes To Cisplatin Resistance In
Breast Cancer By Epigenetically Suppressing
miR-381 Expression"	否		mammary cancer		E_01_1000	Transfection, RT-qPCR, Western blot, flow cytometry, chip,	"Emerging evidence reveals the vital role of enhancer of zeste homolog 2
(EZH2) in cancer chemoresistance."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"Emerging evidence reveals the vital role of enhancer of zeste homolog 2
(EZH2) in cancer chemoresistance."	Immunohistochemical staining	"Emerging evidence reveals the vital role of enhancer of zeste homolog 2
(EZH2) in cancer chemoresistance."	EZH2		转染，RT-QPCR，Western blot，流式细胞术，CHIP，	"Emerging evidence reveals the vital role of enhancer of zeste homolog 2
(EZH2) in cancer chemoresistance."			
32005028	chr7	148805071	148807071	EZH2	"PSMA3-AS1 and miR-101 expression were explored using qRT-PCR in ESCC tissues and cell lines.
Immunohistochemistry assays were carried out to analyze EZH2 (enhancer of zeste homolog) protein expression."	human	esophagus	High+Lowthroughput	"Long non-coding RNA PSMA3-AS1 promotes malignant phenotypes 
of esophageal cancer by modulating the miR-101/EZH2 axis as a 
ceRNA"	否		ESCC		E_01_1001	RT qPCR, rip, luciferase reporter, Western blot, scratch assay, transfection	"PSMA3-AS1 and miR-101 expression were explored using qRT-PCR in ESCC tissues and cell lines.
Immunohistochemistry assays were carried out to analyze EZH2 (enhancer of zeste homolog) protein expression."	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			"PSMA3-AS1 and miR-101 expression were explored using qRT-PCR in ESCC tissues and cell lines.
Immunohistochemistry assays were carried out to analyze EZH2 (enhancer of zeste homolog) protein expression."	Immunohistochemical staining	"PSMA3-AS1 and miR-101 expression were explored using qRT-PCR in ESCC tissues and cell lines.
Immunohistochemistry assays were carried out to analyze EZH2 (enhancer of zeste homolog) protein expression."	EZH2		RT-qPCR，RIP，荧光素酶报告，Western blot，划痕实验，转染	"PSMA3-AS1 and miR-101 expression were explored using qRT-PCR in ESCC tissues and cell lines.
Immunohistochemistry assays were carried out to analyze EZH2 (enhancer of zeste homolog) protein expression."			
30945310	chr19	2508640	2510640	GNG7	Taken together, our findings suggest that GNG7 is a tumor suppressor gene in ccRCC progression and represents a novel candidate for ccRCC treatment.	human		High+Lowthroughput	G Protein γ subunit 7 loss contributes to progression of clear cell renal cell carcinoma	否		 clear cell renal cell carcinoma		E_01_1002	Western blot, cell transfection	Taken together, our findings suggest that GNG7 is a tumor suppressor gene in ccRCC progression and represents a novel candidate for ccRCC treatment.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, our findings suggest that GNG7 is a tumor suppressor gene in ccRCC progression and represents a novel candidate for ccRCC treatment.		Taken together, our findings suggest that GNG7 is a tumor suppressor gene in ccRCC progression and represents a novel candidate for ccRCC treatment.	Immunohistochemical staining	Taken together, our findings suggest that GNG7 is a tumor suppressor gene in ccRCC progression and represents a novel candidate for ccRCC treatment.			Western blot、细胞转染技术				GNG7
30945310	chr19	46631007	46633007	GNG8	Taken together, our findings suggest that GNG8 is a tumor suppressor gene in ccRCC progression and represents a novel candidate for ccRCC treatment.	human		High+Lowthroughput	G Protein γ subunit 8 loss contributes to progression of clear cell renal cell carcinoma	否		 clear cell renal cell carcinoma		E_01_1002	Western blot, cell transfection	Taken together, our findings suggest that GNG8 is a tumor suppressor gene in ccRCC progression and represents a novel candidate for ccRCC treatment.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Taken together, our findings suggest that GNG8 is a tumor suppressor gene in ccRCC progression and represents a novel candidate for ccRCC treatment.		Taken together, our findings suggest that GNG8 is a tumor suppressor gene in ccRCC progression and represents a novel candidate for ccRCC treatment.	Immunohistochemical staining	Taken together, our findings suggest that GNG8 is a tumor suppressor gene in ccRCC progression and represents a novel candidate for ccRCC treatment.			Western blot、细胞转染技术				GNG8
30944316	chr16	67559734	67561734	CTCF	Remarkably, these compartments are characterized by active chromatin states, and enhanced ERα binding but decreased transcription factor CCCTC-binding factor (CTCF) binding. 	human		High+Lowthroughput	Temporal dynamic reorganization of 3D chromatin architecture in hormone-induced breast cancer and endocrine resistance	否		 hormone-induced breast cancer		E_01_1003	ChIP-seq、3C-qPCR、RNA-seq、	Remarkably, these compartments are characterized by active chromatin states, and enhanced ERα binding but decreased transcription factor CCCTC-binding factor (CTCF) binding. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Remarkably, these compartments are characterized by active chromatin states, and enhanced ERα binding but decreased transcription factor CCCTC-binding factor (CTCF) binding. 	Immunohistochemical staining	Remarkably, these compartments are characterized by active chromatin states, and enhanced ERα binding but decreased transcription factor CCCTC-binding factor (CTCF) binding. 	CTCF		ChIP-seq、3C-qPCR、RNA-seq、	Remarkably, these compartments are characterized by active chromatin states, and enhanced ERα binding but decreased transcription factor CCCTC-binding factor (CTCF) binding. 			
30942441	chr2	136111440	136113440	CXCR4	Osteoarthritis (OA) is an aseptic inflammatory disease which is associated with the stromal cell-derived factor 1/C-X-C chemokine receptor type 4 (SDF-1/CXCR4) axis. 	human	lymphoid tissue	High+Lowthroughput	miR‑146a‑5p expression is upregulated by the CXCR4 antagonist TN14003 and attenuates SDF‑1‑induced cartilage degradation	否		Osteoarthritis	B cell	E_01_1004	RT-qPCR、western blot	Osteoarthritis (OA) is an aseptic inflammatory disease which is associated with the stromal cell-derived factor 1/C-X-C chemokine receptor type 4 (SDF-1/CXCR4) axis. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Osteoarthritis (OA) is an aseptic inflammatory disease which is associated with the stromal cell-derived factor 1/C-X-C chemokine receptor type 4 (SDF-1/CXCR4) axis. 	Immunohistochemical staining	Osteoarthritis (OA) is an aseptic inflammatory disease which is associated with the stromal cell-derived factor 1/C-X-C chemokine receptor type 4 (SDF-1/CXCR4) axis. 	CXCR4		RT-qPCR、western blot	Osteoarthritis (OA) is an aseptic inflammatory disease which is associated with the stromal cell-derived factor 1/C-X-C chemokine receptor type 4 (SDF-1/CXCR4) axis. 			
30942422	chr1	159915486	159917486	TAGLN2	Cervical cancer is a malignancy that threatens female health. The present study aimed to investigate the role of transgelin 2 (TAGLN2) in cervical cancer.	human		High+Lowthroughput	Transgelin 2 overexpression inhibits cervical cancer cell invasion and migration	否		cervical cancer		E_01_1005	Cell transfection techniques, RT qPCR, Western blot	Cervical cancer is a malignancy that threatens female health. The present study aimed to investigate the role of transgelin 2 (TAGLN2) in cervical cancer.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Cervical cancer is a malignancy that threatens female health. The present study aimed to investigate the role of transgelin 2 (TAGLN2) in cervical cancer.		Cervical cancer is a malignancy that threatens female health. The present study aimed to investigate the role of transgelin 2 (TAGLN2) in cervical cancer.	Immunohistochemical staining	Cervical cancer is a malignancy that threatens female health. The present study aimed to investigate the role of transgelin 2 (TAGLN2) in cervical cancer.			细胞转染技术、RT-qPCR、Western blot				TAGLN2
30942411	chr5	171384232	171386232	NPM1	A total of 11 frequent mutations were identified, including nucleophosmin 1 (NPM1), Fms related tyrosine kinase 3 (FLT3), DNA methyltransferase 3α (DNMT3A) and Notch 2 (NOTCH2), with a mutation rate of ≥10%.	human		High+Lowthroughput	Mutational spectrum and associations with clinical features in patients with acute myeloid leukaemia based on next?generation sequencing	是		 acute myeloid leukaemia		E_01_1006	sequence	A total of 11 frequent mutations were identified, including nucleophosmin 1 (NPM1), Fms related tyrosine kinase 3 (FLT3), DNA methyltransferase 3α (DNMT3A) and Notch 2 (NOTCH2), with a mutation rate of ≥10%.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	A total of 11 frequent mutations were identified, including nucleophosmin 1 (NPM1), Fms related tyrosine kinase 3 (FLT3), DNA methyltransferase 3α (DNMT3A) and Notch 2 (NOTCH2), with a mutation rate of ≥10%.		A total of 11 frequent mutations were identified, including nucleophosmin 1 (NPM1), Fms related tyrosine kinase 3 (FLT3), DNA methyltransferase 3α (DNMT3A) and Notch 2 (NOTCH2), with a mutation rate of ≥10%.	Immunohistochemical staining	A total of 11 frequent mutations were identified, including nucleophosmin 1 (NPM1), Fms related tyrosine kinase 3 (FLT3), DNA methyltransferase 3α (DNMT3A) and Notch 2 (NOTCH2), with a mutation rate of ≥10%.			测序				NPM1
30941855	chr18	76976150	76978150	MBP	 Though there is one-amino-acid difference in the linker between maltose-binding protein (MBP) tag and DR3 DD, according to our self-interaction analysis, the hydrophobic interface discovered in MBP-hDR3 DD crystal structure is responsible for both hDR3 DD and mDR3 DD homotypic interaction.	human		High+Lowthroughput	Crystal structure and activation mechanism of DR3 death domain	否				E_01_1007	Western blot, sequencing	 Though there is one-amino-acid difference in the linker between maltose-binding protein (MBP) tag and DR3 DD, according to our self-interaction analysis, the hydrophobic interface discovered in MBP-hDR3 DD crystal structure is responsible for both hDR3 DD and mDR3 DD homotypic interaction.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	 Though there is one-amino-acid difference in the linker between maltose-binding protein (MBP) tag and DR3 DD, according to our self-interaction analysis, the hydrophobic interface discovered in MBP-hDR3 DD crystal structure is responsible for both hDR3 DD and mDR3 DD homotypic interaction.		 Though there is one-amino-acid difference in the linker between maltose-binding protein (MBP) tag and DR3 DD, according to our self-interaction analysis, the hydrophobic interface discovered in MBP-hDR3 DD crystal structure is responsible for both hDR3 DD and mDR3 DD homotypic interaction.	Immunohistochemical staining	 Though there is one-amino-acid difference in the linker between maltose-binding protein (MBP) tag and DR3 DD, according to our self-interaction analysis, the hydrophobic interface discovered in MBP-hDR3 DD crystal structure is responsible for both hDR3 DD and mDR3 DD homotypic interaction.			western blot、测序				MBP
30940821	chr11	35135644	35137644	CD44	For example, the splicing factor class that consists of heterogeneous nuclear ribonucleoproteins (hnRNPs) is known to control metastasis formation by regulating alternative splicing of the small GTPase Rac17, but also by affecting CD44 isoform expression which increases TGFβ signaling8.	human	Tumor tissues	High+Lowthroughput	Co-regulated gene expression of splicing factors as drivers of cancer progression	否		cancer	tumor cell	E_01_1008	Bioinformatic prediction	For example, the splicing factor class that consists of heterogeneous nuclear ribonucleoproteins (hnRNPs) is known to control metastasis formation by regulating alternative splicing of the small GTPase Rac17, but also by affecting CD44 isoform expression which increases TGFβ signaling8.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	For example, the splicing factor class that consists of heterogeneous nuclear ribonucleoproteins (hnRNPs) is known to control metastasis formation by regulating alternative splicing of the small GTPase Rac17, but also by affecting CD44 isoform expression which increases TGFβ signaling8.		For example, the splicing factor class that consists of heterogeneous nuclear ribonucleoproteins (hnRNPs) is known to control metastasis formation by regulating alternative splicing of the small GTPase Rac17, but also by affecting CD44 isoform expression which increases TGFβ signaling8.	Immunohistochemical staining	For example, the splicing factor class that consists of heterogeneous nuclear ribonucleoproteins (hnRNPs) is known to control metastasis formation by regulating alternative splicing of the small GTPase Rac17, but also by affecting CD44 isoform expression which increases TGFβ signaling8.			生物信息学预测				CD44
30940675	chr4	155042794	155044794	Hes5	DNA methylation array analysis identified hairy and enhancer of split 5 (Hes5) as having a CpG island with hyper-methylation in the promoter region, and the Hes5 expression was strongly silenced in SBMA.	human		High+Lowthroughput	DNA methylation inhibitor attenuates polyglutamine-induced neurodegeneration by regulating Hes5	否				E_01_1009	Immunoblotting	DNA methylation array analysis identified hairy and enhancer of split 5 (Hes5) as having a CpG island with hyper-methylation in the promoter region, and the Hes5 expression was strongly silenced in SBMA.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	DNA methylation array analysis identified hairy and enhancer of split 5 (Hes5) as having a CpG island with hyper-methylation in the promoter region, and the Hes5 expression was strongly silenced in SBMA.		DNA methylation array analysis identified hairy and enhancer of split 5 (Hes5) as having a CpG island with hyper-methylation in the promoter region, and the Hes5 expression was strongly silenced in SBMA.	Immunohistochemical staining	DNA methylation array analysis identified hairy and enhancer of split 5 (Hes5) as having a CpG island with hyper-methylation in the promoter region, and the Hes5 expression was strongly silenced in SBMA.			免疫印迹				Hes5
30933372	chr20	44352856	44354856	HNF4A	Hepatocyte nuclear factor 4 alpha (HNF4A), a liver-enriched TF, acts as a master controller in specification of hepatic progenitor cells by regulating a network of TFs to control the onset of hepatocyte cell fate. 	human		High+Lowthroughput	Hepatocyte Nuclear Factor 4-Alpha Is Essential for the Active Epigenetic State at Enhancers in Mouse Liver	否				E_01_1010	co-IP	Hepatocyte nuclear factor 4 alpha (HNF4A), a liver-enriched TF, acts as a master controller in specification of hepatic progenitor cells by regulating a network of TFs to control the onset of hepatocyte cell fate. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Hepatocyte nuclear factor 4 alpha (HNF4A), a liver-enriched TF, acts as a master controller in specification of hepatic progenitor cells by regulating a network of TFs to control the onset of hepatocyte cell fate. 	Immunohistochemical staining	Hepatocyte nuclear factor 4 alpha (HNF4A), a liver-enriched TF, acts as a master controller in specification of hepatic progenitor cells by regulating a network of TFs to control the onset of hepatocyte cell fate. 	HNF1A		co-IP	Hepatocyte nuclear factor 4 alpha (HNF4A), a liver-enriched TF, acts as a master controller in specification of hepatic progenitor cells by regulating a network of TFs to control the onset of hepatocyte cell fate. 			
30930987	chr17	1776712	1778712	SMYD4	Additionally, SMYD2 and SMYD4 may be potential prognostic indicators of patients with BC.	human	Tumor tissues	High+Lowthroughput	Expression patterns and the prognostic value of the SMYD family members in human breast carcinoma using integrative bioinformatics analysis	否		human breast carcinoma	tumor cell	E_01_1011	Bioinformatic prediction	Additionally, SMYD2 and SMYD4 may be potential prognostic indicators of patients with BC.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Additionally, SMYD2 and SMYD4 may be potential prognostic indicators of patients with BC.		Additionally, SMYD2 and SMYD4 may be potential prognostic indicators of patients with BC.	Immunohistochemical staining	Additionally, SMYD2 and SMYD4 may be potential prognostic indicators of patients with BC.			生物信息学预测				SMYD4
30926878	chr16	67559655	67561655	CTCF	Genomic studies also suggest that curaxins induce partial depletion of CTCF from its binding sites, which contributes to the observed changes in genome topology. 	human	Tumor tissues	High+Lowthroughput	The anti-cancer drugs curaxins target spatial genome organization	否			tumor cell	E_01_1012	RT qPCR, immunoblot analysis	Genomic studies also suggest that curaxins induce partial depletion of CTCF from its binding sites, which contributes to the observed changes in genome topology. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Genomic studies also suggest that curaxins induce partial depletion of CTCF from its binding sites, which contributes to the observed changes in genome topology. 	Immunohistochemical staining	Genomic studies also suggest that curaxins induce partial depletion of CTCF from its binding sites, which contributes to the observed changes in genome topology. 	CTCF		RT-qPCR、免疫印迹分析	Genomic studies also suggest that curaxins induce partial depletion of CTCF from its binding sites, which contributes to the observed changes in genome topology. 			
30923826	chr7	148804824	148806824	EZH2	Recently, we reported overexpression of chromosome X open reading frame 67 (CXorf67) as a hallmark of PFA ependymoma and showed that CXorf67 can interact with enhancer of zeste homolog 2 (EZH2), thereby inhibiting polycomb repressive complex 2 (PRC2), but the mechanism of action remained unclear.	human		High+Lowthroughput	EZHIP/CXorf67 mimics K27M mutated oncohistones and functions as an intrinsic inhibitor of PRC2 function in aggressive posterior fossa ependymoma	否				E_01_1013	Immunohistochemistry, Western blot	Recently, we reported overexpression of chromosome X open reading frame 67 (CXorf67) as a hallmark of PFA ependymoma and showed that CXorf67 can interact with enhancer of zeste homolog 2 (EZH2), thereby inhibiting polycomb repressive complex 2 (PRC2), but the mechanism of action remained unclear.	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq			Recently, we reported overexpression of chromosome X open reading frame 67 (CXorf67) as a hallmark of PFA ependymoma and showed that CXorf67 can interact with enhancer of zeste homolog 2 (EZH2), thereby inhibiting polycomb repressive complex 2 (PRC2), but the mechanism of action remained unclear.	Immunohistochemical staining	Recently, we reported overexpression of chromosome X open reading frame 67 (CXorf67) as a hallmark of PFA ependymoma and showed that CXorf67 can interact with enhancer of zeste homolog 2 (EZH2), thereby inhibiting polycomb repressive complex 2 (PRC2), but the mechanism of action remained unclear.	EZH2		免疫组化、Western Blot 	Recently, we reported overexpression of chromosome X open reading frame 67 (CXorf67) as a hallmark of PFA ependymoma and showed that CXorf67 can interact with enhancer of zeste homolog 2 (EZH2), thereby inhibiting polycomb repressive complex 2 (PRC2), but the mechanism of action remained unclear.			
30922078	chr16	18801868	18803868	SMG1	Consequently, a substrate of SMG1, ATP-dependent RNA helicase upframeshift 1, is hyperphoshorylated in a HERNA1- and SMG1-dependent manner. 	human	epithelial cells	High+Lowthroughput	Inhibition of the Hypoxia-Inducible Factor 1α-Induced Cardiospecific HERNA1 Enhance-Templated RNA Protects From Heart Disease	否		 Heart Disease		E_01_1014	Immunohistochemistry, gel electrophoresis, qPCR	Consequently, a substrate of SMG1, ATP-dependent RNA helicase upframeshift 1, is hyperphoshorylated in a HERNA1- and SMG1-dependent manner. 	Enhancer	qRT-PCR,qPCR,ChIP,3C	RNA-Seq	Consequently, a substrate of SMG1, ATP-dependent RNA helicase upframeshift 1, is hyperphoshorylated in a HERNA1- and SMG1-dependent manner. 		Consequently, a substrate of SMG1, ATP-dependent RNA helicase upframeshift 1, is hyperphoshorylated in a HERNA1- and SMG1-dependent manner. 	Immunohistochemical staining	Consequently, a substrate of SMG1, ATP-dependent RNA helicase upframeshift 1, is hyperphoshorylated in a HERNA1- and SMG1-dependent manner. 			免疫组化、凝胶电泳、 qPCR				SMG1
30590035	chr6	31139519	31140167	TFAP2C	From this screen, we used CRISPR/Cas9 approaches to determine that re-opening of a large fraction of TFAP2C-bound ground-state naive enhancers (NEs) combined with a shift in the global transcriptional program toward ground-state naive pluripotency is a major milestone in the regeneration of human germline cells from primed pluripotent stem cells.	human	embryonic	Low+High throughput	The TFAP2C-Regulated OCT4 Naive Enhancer Is Involved in Human Germline Formation		--	--	primordial germ cell	E_02_0747	ATAC-seq,ChIP-seq	These data show that the PE, DE, and NE are all open in hPGCLCs at day 4 of aggregate differentiation, with the NE being more open in hPGCs than the DE and PE. This observation raises the possibility that restriction of OCT4 expression between days 2 and 3 of aggregate differentiation may be due to NE and/or the DE enhancer activation at the OCT4 locus. Given that the NE is bound by TFAP2C in groundstate naive pluripotent stem cells, whereas the DE is not , we next confirmed that the OCT4 NE is also a target of TFAP2C during hPGCLC differentiation.	Enhancer	--	ChIP-qPCR	Screenshot of ATAC-seq and TFAP2C ChIP-seq signals showing three Enhancers at the POU5F1 locus (encoding OCT4). Shaded boxes highlight the naive Enhancer(NE),proximalEnhancer(PE),anddistalEnhancer(DE)atthePOU5F1locus.DEdeletion andNEdeletion indicategenomicregionsthatweredeleted by CRISPR/Cas9-mediated genome editing. Primers for ChIP-qPCR (P1-2,P3-4,P5-6) of NE and control regions are shown.	OCT3, OCT4, OTF-3, OTF3, OTF4, Oct-3, Oct-4	TFAP2C regulates human germline cell formation is opening naive-specific Enhancers, with one of these Enhancers corresponding to the NE at the OCT4 locus.	CRISPR/Cas9	Using CRISPR/Cas9, we show that deleting the TFAP2C-bound naive enhancer at the OCT4 locus (also called POU5F1) results in impaired OCT4 expression and a negative effect on hPGCLC identity.	TFAP2C	AP2-GAMMA,ERF1,TFAP2G,hAP-2g	CRISPR/Cas9	Using CRISPR/Cas9, we show that deleting the TFAP2C-bound naive Enhancer at the OCT4 locus (also called POU5F1) results in impaired OCT4 expression and a negative effect on hPGCLC identity.	--	--	POU5F1
30568279	chr14	106327635	106328903	IGHE	As proof-of-concept that HiDRA is capable of identifying true enhancer elements, we examined the well-studied immunoglobulin heavy-chain enhancer within the intron of the immunoglobulin heavy constant epsilon (IGHE) gene	human	lymph	Low+High throughput	High-resolution genome-wide functional dissection of transcriptional regulatory regions and nucleotides in human		--	--	GM12878 cell	E_02_0748	Luciferase Reporter Assay,ChIP-seq	Surprisingly, this enrichment stayed constant thereafter for promoter regions, and increased modestly for enhancer regions, ultimately surpassing the enrichment seen for promoters. In fact, even though promoter chromatin states were more enriched at intermediate HiDRA activity levels,enhancer chromatin states were the most enriched at the highest HiDRA activity levels , suggesting that enhancer elements have a greater dynamic range of regulatory activity potential, which has implications for the regulatory architecture of genes.	Enhancer	--	Luciferase Reporter Assay	We observed that the peak of HiDRA activity is centered precisely within the region previously identi?ed as driving Enhancer activity in low-throughput luciferase assays (Fig. 2c).	IgE	--	--	--	--	--	--	--	--	--	IGHE
30566872	chr10	33492690	33519530	TF	The transcription factor (TF) p63 is an ancient member of the p53 gene family.	human	skin	Low+High throughput	Mutant p63 Affects Epidermal Cell Identity through Rewiring the Enhancer Landscape		--	EEC syndrome	Epidermal cell	E_02_0749	siRNA,ChIP-seq	Two clusters of active enhancers were bound by p63 . Regions in C3 showed higher p63-binding signals.nearby genes were involved in apoptosis and epidermis development. Regions in C4 had relatively lower p63-binding signals, and nearby genes were involved in keratinocyte differentiation.	Enhancer	--	siRNA	Indeed, we observed a clear decrease of H3K27ac signals at Enhancers that had higher H3K27ac signals and bound by RUNX1 in p63 mutant keratinocytes (Figure 6B; n = 6,035) in two biological replicas, such as Enhancers near NRP1, which is involved in angiogenesis .	BDCA4,CD304,NP1,NRP,VEGF165R	--	--	--	TP63,RUNX1	AIS,B(p51A),B(p51B),EEC3,KET,LMS,NBP,OFC8,RHS,SHFM4,TP53CP,TP53L,TP73L,p40,p51,p53CP,p63,p73H,p73L,AML1, AML1-EVI-1, AMLCR1, CBF2alpha, CBFA2, EVI-1, PEBP2aB, PEBP2alpha	siRNA,qRT-PCR	Gene expression analysis by qRT-PCR of TP63 and RUNX1 expression in TP63 knockdown (siTP63) compared to non-targeting siRNA (siNT) in control keratinocytes.	--	--	NRP1
30545847	chr10	50623698	50625698	Mc4r	Using obesity as a model, we tested in mice whether CRISPR-mediated activation of the existing normal copy of two different genes, Sim1 or Mc4r, where loss-of-function mutations that lead to haploinsufficiency are a major cause of human obesity, can rescue their obesity phenotype.	mouse		Low+High throughput	CRISPR-mediated activation of a promoter or enhancer rescues obesity caused by haploinsufficiency.	否	--	Haploinsufficiency	Hypothalamus cell	E_02_0750	ChIP-seq,ATAC-seq	CRISPRa targeting of the Sim1 promoter or its hypothalamusspecific enhancer, which is 270 kilobases away from the gene, in Sim1 haploinsufficient mice increased the expression of the normal copy of Sim1. 	Enhancer	--	ChIP-seq,PCR,Transgenic mice	We also carried out ChIP-seq using an antibody against S. pyogenes Cas9 in both CRISPRa-promoter and CRISPRa-Enhancer transfected cells and found on-target binding for the promoter and Enhancer,respectively.	bHLHe14, mSIM1	Transgenic-based CRISPRa targeting of the Sim1 promoter or its distant hypothalamic enhancer up-regulated its expression from the endogenous functional allele in a tissue-specific manner, rescuing the obesity phenotype in Sim1 heterozygous mice.	CRISPR/Cas9,ChIP-seq	Transgenic-based CRISPRa targeting of the Sim1 promoter or its distant hypothalamic enhancer up-regulated its expression from the endogenous functional allele in a tissue-specific manner, rescuing the obesity phenotype in Sim1 heterozygous mice.	Sim1	bHLHe14,mSIM1	CRISPR/Cas9,qPCR	CRISPRa targeting of the Sim1 promoter or its hypothalamusspecific enhancer, which is 270 kilobases away from the gene, in Sim1 haploinsufficient mice increased the expression of the normal copy of Sim1. This up-regulation was sufficient to rescue the obesity phenotype of Sim1 heterozygous mice and led to significantly reduced food intake and body fat content in thesemice.	--	--	Sim1
30545847	chr10	50623698	50625698	Sim1	Using obesity as a model, we tested in mice whether CRISPR-mediated activation of the existing normal copy of two different genes, Sim1 or Mc4r, where loss-of-function mutations that lead to haploinsufficiency are a major cause of human obesity, can rescue their obesity phenotype.	mouse		Low+High throughput	CRISPR-mediated activation of a promoter or enhancer rescues obesity caused by haploinsufficiency.	否	--	Haploinsufficiency	Hypothalamus cell	E_02_0750	ChIP-seq,ATAC-seq	CRISPRa targeting of the Sim1 promoter or its hypothalamusspecific enhancer, which is 270 kilobases away from the gene, in Sim1 haploinsufficient mice increased the expression of the normal copy of Sim1. 	Enhancer	--	ChIP-seq,PCR,Transgenic mice	We also carried out ChIP-seq using an antibody against S. pyogenes Cas9 in both CRISPRa-promoter and CRISPRa-Enhancer transfected cells and found on-target binding for the promoter and Enhancer,respectively.	bHLHe14, mSIM1	Transgenic-based CRISPRa targeting of the Sim1 promoter or its distant hypothalamic enhancer up-regulated its expression from the endogenous functional allele in a tissue-specific manner, rescuing the obesity phenotype in Sim1 heterozygous mice.	CRISPR/Cas9,ChIP-seq	Transgenic-based CRISPRa targeting of the Sim1 promoter or its distant hypothalamic enhancer up-regulated its expression from the endogenous functional allele in a tissue-specific manner, rescuing the obesity phenotype in Sim1 heterozygous mice.	Sim1	bHLHe14,mSIM1	CRISPR/Cas9,qPCR	CRISPRa targeting of the Sim1 promoter or its hypothalamusspecific enhancer, which is 270 kilobases away from the gene, in Sim1 haploinsufficient mice increased the expression of the normal copy of Sim1. This up-regulation was sufficient to rescue the obesity phenotype of Sim1 heterozygous mice and led to significantly reduced food intake and body fat content in thesemice.	--	--	Sim1
30527662	chr17	30249928	30278499	CTCF	 Deletion of CTCF sites at the boundary of select insulated neighborhoods results in ectopic transcription stimulation of one or more flanking genes via formation of an enhancer-promoter loop across the region encompassing the deleted boundary (Dowen et al., 2014). 	mouse		Low+High throughput	Promoter-Enhancer Communication Occurs Primarily within Insulated Neighborhoods	否	--	--	embryonic stem cell	E_02_0751	ChIP-seq,ChIA-PET	The data show that the promoters are located within Smc1 ChIA-PET loops,the anchors of which align with strong cohesin and CTCF ChIP-seq peaks lacking H3K27ac ( These insulated neighborhoods encompass the TSS(arrow),promoters (vertical gray bars),and potential Enhancers of Mitf and Sik1 (vertical green bar). View of a genomic region around Mitf integrating Smc1 ChIA-PET,and Smc1,Smc3,Rad21,CTCF,Med1,and H3K27ac ChIP-seq with 4C data and promoter capture Hi-C data.	Enhancer	4C	Hi-C,ChIP-seq,ChIA-PET	"High-resolution 4C was employed using promoter viewpoints to determine whether individual genes fit into the framework described in Figure 1.Figures 2A and 2B compare the Mitf and Sik1 genes expressed at low(RPKM = 2.2) and modest (RPKM = 21) levels, respectively, as
measured by mRNA-seq and nascent RNA-seq (RPKM 0.53 and 4.2 for Mitf and Sik1). The data show that the promoters are located within Smc1 ChIA-PET loops, the anchors of which align with strong cohesin and CTCF ChIP-seq peaks (vertical red bars) lacking H3K27ac."	Hrt-20,Msk,Sik,Sik-1,Snf1lk	--	--	--	Esrrb,Med1	Err2,Errb,Estrrb,Nr3b2,AI480703,CRSP210,DRIP205,PBP,Pparbp,TRAP220,TRIP-2,l11Jus15	ChIP,Immobilized Template Assay,siRNA,Western blot	Consistent with the biochemical data, knockdown of Esrrb by small interfering RNA (siRNA) (Esrrb KD) in cells causes diminished recruitment of Mediator (Med1 and Med12) to Esrrb binding sites genome-wide.For example, upon Esrrb KD, Med1 and Med12 binding decreases at Esrrb sites within the enhancer (Enh) of the divergently transcribed Slc13a5 and Xaf1 genes.In sum, on select genes, Esrrb KD can be used to deplete the Mediator and inactivate Enhancers, either partially or near fully, to downregulate transcription of their target genes.	--	--	Sik1
30518632	chr1	47704791	47705107	NOTCH3	The two compounds induced apoptosis in TCP-resistant T-ALL cells in vitro and in vivo by repressing transcription of the NOTCH3 and TAL1 genes through increased H3K9 methylation and reciprocal H3K27 deacetylation at superenhancer regions.	human	nerve	Low throughput	Eradication of Central Nervous System Leukemia of T-Cell Origin with a Brain-Permeable LSD1 Inhibitor		--	Central Nervous System Leukemia	T-acute lymphoblastic leukemia (T-ALL)	E_02_0752	ChIP-qPCR,qRT-PCR,ChIP,Transgenic mice	We found robust cytotoxicity against T-ALL cells, but not normal bone marrow progenitors, for two N-alkylated TCP derivatives, S2116 and S2157. The two compounds induced apoptosis in TCP-resistant T-ALL cells in vitro and in vivo by repressing transcription of the NOTCH3 and TAL1 genes through increased H3K9 methylation and reciprocal H3K27 deacetylation at super-enhancer regions.	Super-Enhancer	--	qRT-PCR,ChIP	we found that both S2116 and S2157 readily increased the methylation level of H3K9 and reciprocally reduced the acetylation level of H3K27 at Super-Enhancer regions of the NOTCH3 and TAL1 genes (GRCh38/hg38: 15,198,031-15,197,862 and GRCh38/hg38: 47,239,435-47,239,119,respectively) using ChIP assays.In addition,global ChIP-seq analyses revealed that the acetylation level of H3K27 was readily decreased by LSD1 inhibition through the entire range of NOTCH3 and TAL1 Enhancers.	SCL,TCL5,bHLHa17,tal-1	--	--	--	ZEB2	HSPC082,SIP-1,SIP1,SMADIP1,ZFHX1B	RT-PCR	We used the Expression Assays(Hs01097987 for TAL1, Hs01128537 for NOTCH3, Hs00207691 for ZEB2, and Hs01922876 forGAPDH) and TaqMan Universal PCR Master Mix (Applied Biosystems, Waltham, MA) for real-time quantitative RT-PCR (RQ-PCR).	--	--	TAL1
30518632	chr1	47704791	47705107	TAL1	The two compounds induced apoptosis in TCP-resistant T-ALL cells in vitro and in vivo by repressing transcription of the NOTCH3 and TAL1 genes through increased H3K9 methylation and reciprocal H3K27 deacetylation at superenhancer regions.	human	nerve	Low throughput	Eradication of Central Nervous System Leukemia of T-Cell Origin with a Brain-Permeable LSD1 Inhibitor		--	Central Nervous System Leukemia	T-acute lymphoblastic leukemia (T-ALL)	E_02_0752	ChIP-qPCR,qRT-PCR,ChIP,Transgenic mice	We found robust cytotoxicity against T-ALL cells, but not normal bone marrow progenitors, for two N-alkylated TCP derivatives, S2116 and S2157. The two compounds induced apoptosis in TCP-resistant T-ALL cells in vitro and in vivo by repressing transcription of the NOTCH3 and TAL1 genes through increased H3K9 methylation and reciprocal H3K27 deacetylation at super-enhancer regions.	Super-Enhancer	--	qRT-PCR,ChIP	we found that both S2116 and S2157 readily increased the methylation level of H3K9 and reciprocally reduced the acetylation level of H3K27 at Super-Enhancer regions of the NOTCH3 and TAL1 genes (GRCh38/hg38: 15,198,031-15,197,862 and GRCh38/hg38: 47,239,435-47,239,119,respectively) using ChIP assays.In addition,global ChIP-seq analyses revealed that the acetylation level of H3K27 was readily decreased by LSD1 inhibition through the entire range of NOTCH3 and TAL1 Enhancers.	SCL,TCL5,bHLHa17,tal-1	--	--	--	ZEB2	HSPC082,SIP-1,SIP1,SMADIP1,ZFHX1B	RT-PCR	We used the Expression Assays(Hs01097987 for TAL1, Hs01128537 for NOTCH3, Hs00207691 for ZEB2, and Hs01922876 forGAPDH) and TaqMan Universal PCR Master Mix (Applied Biosystems, Waltham, MA) for real-time quantitative RT-PCR (RQ-PCR).	--	--	TAL1
30518632	chr1	47704791	47705107	TAL2	The two compounds induced apoptosis in TCP-resistant T-ALL cells in vitro and in vivo by repressing transcription of the NOTCH3 and TAL1 genes through increased H3K9 methylation and reciprocal H3K28 deacetylation at superenhancer regions.	human	nerve	Low throughput	Eradication of Central Nervous System Leukemia of T-Cell Origin with a Brain-Permeable LSD2 Inhibitor		--	Central Nervous System Leukemia	T-acute lymphoblastic leukemia (T-ALL)	E_02_0752	ChIP-qPCR,qRT-PCR,ChIP,Transgenic mice	We found robust cytotoxicity against T-ALL cells, but not normal bone marrow progenitors, for two N-alkylated TCP derivatives, S2116 and S2157. The two compounds induced apoptosis in TCP-resistant T-ALL cells in vitro and in vivo by repressing transcription of the NOTCH3 and TAL1 genes through increased H3K9 methylation and reciprocal H3K27 deacetylation at super-enhancer regions.	Super-Enhancer	--	qRT-PCR,ChIP	we found that both S2116 and S2157 readily increased the methylation level of H3K9 and reciprocally reduced the acetylation level of H3K27 at Super-Enhancer regions of the NOTCH3 and TAL1 genes (GRCh38/hg38: 15,198,031-15,197,862 and GRCh38/hg38: 47,239,435-47,239,119,respectively) using ChIP assays.In addition,global ChIP-seq analyses revealed that the acetylation level of H3K27 was readily decreased by LSD1 inhibition through the entire range of NOTCH3 and TAL1 Enhancers.	SCL,TCL5,bHLHa17,tal-1	--	--	--	ZEB2	HSPC082,SIP-1,SIP1,SMADIP1,ZFHX1B	RT-PCR	We used the Expression Assays(Hs01097987 for TAL1, Hs01128537 for NOTCH3, Hs00207691 for ZEB2, and Hs01922876 forGAPDH) and TaqMan Universal PCR Master Mix (Applied Biosystems, Waltham, MA) for real-time quantitative RT-PCR (RQ-PCR).	--	--	TAL1
30511964	chr14	76419740	76421740	TGFB3	Mechanistically, this is due to genomic occupancy of FOXA1 on an upstream enhancer of the TGFB3 gene to directly inhibit its transcription.	human	prostate	Low+High throughput	Targeting FOXA1-mediated repression of TGF-β signaling suppresses castration-resistant prostate cancer progression		--	Prostate Cancer	LNCaP	E_02_0753	ChIP-seq,ChIP-qPCR	Analysis of FOXA1 ChIP-seq previously performed in LNCaP cells identified strong FOXA1 binding at an enhancer of approximately 3.7 kb upstream of the TGFB3 gene promoter.	Enhancer	--	ChIP-qPCR	Analysis of FOXA1 ChIP-seq previously performed in LNCaP cells identified strong FOXA1 binding at an Enhancer of approximately 3.7 kb upstream of the TGFB3 gene promoter.Importantly, qRT-PCR analysis demonstrated that CRISPR-mediated Enhancer deletion in only one-fourth of the cell population was able to substantially restore the transcription of TGFB3 gene, comparing cells transfected with TGFB3-targeting gRNAs to those with control gRNAs.	ARVD,ARVD1,LDS5,RNHF,TGF-beta3	--	--	--	FOXA1	HNF3A,TCF3A	CRISPR/Cas9	To demonstrate that FOXA1 binding at the upstream Enhancer indeed inhibits TGFB3 gene transcription in vivo, we used a lentiviral CRISPR/Cas9 editing system to delete the Enhancer elements with small guide RNAs.Taken together, these results strongly support that FOXA1 binds to an upstream Enhancer to directly repress TGFB3 transcription.	--	--	TGFB3
30397001	chr2	234665349	234665739	CCAR1	We demonstrated that CCAR1 can act as an enhancer-dependent coactivator of CAR.	human	liver	Low throughput	Cell Cycle and Apoptosis Regulator 1, CCAR1, Regulates Enhancer-Dependent Nuclear Receptor CAR Transactivation.		--	Hepatocellular Carcinoma	Hep G2 cell	E_02_0754	Luciferase Reporter Assay,qRT-PCR	These observations suggested that a specific enhancer region, such as neighboring transcriptional factors, is required for CAR/CCAR1 interaction.	Enhancer	--	ChIP	The phenobarbital-responsive Enhancer module of UGT1A1 (gtPBREM)-driven Luciferaseplasmid (gtPBREM-Luc.) containing a 290-bp distal Enhancer module (23570/23180) was constructed based on pGL3-promoter (Promega).	BILIQTL1,GNT1,HUG-BR1,UDPGT,UDPGT1-1,UGT1,UGT1A	CCAR1 enhances transcriptional activity of CAR and acts as an Enhancer-dependent selective cofactor of CAR for UGT1A1 expression.	Luciferase Reporter Assay	The phenobarbital-responsive Enhancer module of UGT1A1 (gtPBREM)-driven luciferase reporter plasmid (gtPBREM-Luc.) containing a 290-bp distal Enhancer module (-23570/-23180) was constructed based on pGL3-promoter (Promega).	CCAR1	CCAR1	ChIP	CCAR1 regulates CAR-mediated mRNA expression (Figs. 4 and 5) and reporter activity (Figs. 2 and 3) of UGT1A1 but not CYP2B6.We speculated that CCAR1 is differentially recruited to CAR-responsive Enhancer regions. To investigate this hypothesis,we carried out ChIP experiments in HepTR/CAR cells.	--	--	UGT1A1
30146478	chr11	111838889	111839334	Stat3	Stat3 as a trans-acting factor, regulating carti_x0002_lage-specific Sox9 expression and subsequent skel_x0002_etal development.	mouse		Low+High throughput	Combinatorial CRISPR/Cas9 Approach to Elucidate a Far-Upstream Enhancer Complex for Tissue-Specific Sox9 Expression	是	--	--	chondroblast	E_02_0456	ChIP-qPCR	We next performed the ChIP-qPCR using anti-H3K4me1 and H3K27ac antibody in all five regions and found that RCSE regions were significantly enriched in both H3K4me1 and H3K27ac ChIP, suggesting the potential enhancer.	Enhancer	3C	PCR	These data suggest that there is a long-range interaction between the Sox9 promoter and RCSE region in primary chondrocytes.	2010306G03Rik,AV220920,mKIAA4243	TG mice with the Sox9 promoter and 43 RCSE region.These data suggest that the RCSE region functions as a costal- and sternum cartilage-specific Enhancer.	Transgenic mice	TG mice with the Sox9 promoter and 43 RCSE region.These data suggest that the RCSE region functions as a costal- and sternum cartilage-specific Enhancer.	Stat3	1110034C02Rik,AW109958,Aprf	Luciferase Reporter Assay,Immunostaining	Furthermore, transcription factors that regulate Sox9 expres sion were screened using a CRISPR/Cas9-chromatin immuno precipitation (ChIP)-mass spectrometry (MS) system targeting the RCSE region in chondrocytes; signal transducer and acti vator of transcription 3 (Stat3) was identified as a transacting fac tor for the Sox9 Enhancer.	--	--	Sox9
30146478	chr11	111838889	111839334	Sox9	Stat3 as a trans-acting factor, regulating carti_x0002_lage-specific Sox9 expression and subsequent skel_x0002_etal development.	mouse		Low+High throughput	Combinatorial CRISPR/Cas9 Approach to Elucidate a Far-Upstream Enhancer Complex for Tissue-Specific Sox9 Expression	是	--	--	chondroblast	E_02_0456	ChIP-qPCR	We next performed the ChIP-qPCR using anti-H3K4me1 and H3K27ac antibody in all five regions and found that RCSE regions were significantly enriched in both H3K4me1 and H3K27ac ChIP, suggesting the potential enhancer.	Enhancer	3C	PCR	These data suggest that there is a long-range interaction between the Sox9 promoter and RCSE region in primary chondrocytes.	2010306G03Rik,AV220920,mKIAA4243	TG mice with the Sox9 promoter and 43 RCSE region.These data suggest that the RCSE region functions as a costal- and sternum cartilage-specific Enhancer.	Transgenic mice	TG mice with the Sox9 promoter and 43 RCSE region.These data suggest that the RCSE region functions as a costal- and sternum cartilage-specific Enhancer.	Stat3	1110034C02Rik,AW109958,Aprf	Luciferase Reporter Assay,Immunostaining	Furthermore, transcription factors that regulate Sox9 expres sion were screened using a CRISPR/Cas9-chromatin immuno precipitation (ChIP)-mass spectrometry (MS) system targeting the RCSE region in chondrocytes; signal transducer and acti vator of transcription 3 (Stat3) was identified as a transacting fac tor for the Sox9 Enhancer.	--	--	Sox9
30008200	chr13	56243248	56243833	CTCF	Furthermore, reduced Neurog1 gene expression by CTCF knockdown was found to be associated with changes in histone modification at the gene’s promoter, as well as its upstream enhancer	mouse		Low throughput	CTCF Regulates Otic Neurogenesis via Histone Modification in the Neurog1Locus	否	--	--	P19	E_02_0755	ChIP	In control cells, the enrichment of H3K27Ac, an active Enhancer marker, was significantly increased at the Neurog1 promoter, as well as other Enhancers, upon RA treatment.	Enhancer	--	ChIP-qPCR	"Genome-wide CTCF occupancy patterns, which have been mapped across more than 100 mammalian cell types, re_x0002_vealed prominent CTCF binding to the -14.4 kb and -7.6 kb transcription start sites of Neurog1.We performed ChIP-qPCR analysis to validate the in vivo binding of CTCF in 
P19 cells, and observed strong occupancy of CTCF to these binding sites."	AKA,Math4C,Neurod3,bHLHa6,ngn1	--	--	--	Ctcf	AW108038	ChIP-qPCR	Genome-wide CTCF occupancy patterns, which have been mapped across more than 100 mammalian cell types, re_x0002_vealed prominent CTCF binding to the -14.4 kb and -7.6 kb transcription start sites of Neurog1.We performed ChIP-qPCR analysis to validate the in vivo binding of CTCF in P19 cells, and observed strong occupancy of CTCF to these binding sites.	--	--	Neurog1
29967281	chr17	85527960	85530660	Six4	Dopamine receptor DRD1-expressing medium spiny neurons (D1 MSNs) and dopamine receptor DRD2-expressing medium spiny neurons (D2 MSNs) are the principal projection neurons in the striatum, which is divided into dorsal striatum (caudate nucleus and putamen) and ventral striatum (nucleus accumbens and olfactory tubercle).                                                                                                                                                                                                                                    SP8 and SP9 together drive expression of the transcription factor Six4 in a spatially restricted domain of the LGE subventricular zone.	mouse		Low+High throughput	SP8 and SP9 coordinately promote D2-type medium spiny neuron production by activating Six4 expression.	否	--	--		E_02_0543	Luciferase Reporter Assay,ChIP-seq	We found an SP9 ChIP-Seq peak at the Six3 promoter region (?5 to +411 of the TSS) (Fig. 9C), and several additional peaks upstream of the Six3 gene (regions 1, 2 and 3) (Fig. 9C);Thus, these noncoding domains are strong candidates for the Six3 promoter and three Six3 enhancers.	Enhancer	--	ChIP-seq,Luciferase Reporter Assay	Together,the results of ChIP-seq and Dual-Luciferase assay provide evidence that SP9 promotes Six3 expression in the LGE SVZ through its direct binding to the promoter and possibly through binding to regulatory elements within the Six3 locus.	E130112M24Rika,Six3alpha,Six3b,Six3beta,?Six3	--	--	--	Six3	E130112M24Rika，Six3alpha，Six3b，Six3beta	RNA-seq,ChIP-seq	SP8 and SP9 together drive expression of the transcription factor Six3 in a spatially restricted domain of the LGE subventricular zone. Conditional deletion of Six3 also prevents the formation of most D2 MSNs, phenocopying the Sp8/9 mutants.This implies that there are additional mechanisms that regulate the generation of D2 MSNs in Sp9-KO mice, one of which was suggested by the LGE RNA-Seq analysis. We identified that expression of the TF Six3 was decreased ?5-fold in E16.5 Sp8/9-DCKO mice compared with control mice.	--	--	Six3
29967281	chr17	85527960	85530660	Six5	Dopamine receptor DRD1-expressing medium spiny neurons (D1 MSNs) and dopamine receptor DRD2-expressing medium spiny neurons (D2 MSNs) are the principal projection neurons in the striatum, which is divided into dorsal striatum (caudate nucleus and putamen) and ventral striatum (nucleus accumbens and olfactory tubercle).                                                                                                                                                                                                                                    SP8 and SP9 together drive expression of the transcription factor Six5 in a spatially restricted domain of the LGE subventricular zone.	mouse		Low+High throughput	SP8 and SP9 coordinately promote D2-type medium spiny neuron production by activating Six5 expression.	否	--	--		E_02_0543	Luciferase Reporter Assay,ChIP-seq	We found an SP9 ChIP-Seq peak at the Six3 promoter region (?5 to +411 of the TSS) (Fig. 9C), and several additional peaks upstream of the Six3 gene (regions 1, 2 and 3) (Fig. 9C);Thus, these noncoding domains are strong candidates for the Six3 promoter and three Six3 enhancers.	Enhancer	--	ChIP-seq,Luciferase Reporter Assay	Together,the results of ChIP-seq and Dual-Luciferase assay provide evidence that SP9 promotes Six3 expression in the LGE SVZ through its direct binding to the promoter and possibly through binding to regulatory elements within the Six3 locus.	E130112M24Rika,Six3alpha,Six3b,Six3beta,?Six3	--	--	--	Six3	E130112M24Rika，Six3alpha，Six3b，Six3beta	RNA-seq,ChIP-seq	SP8 and SP9 together drive expression of the transcription factor Six3 in a spatially restricted domain of the LGE subventricular zone. Conditional deletion of Six3 also prevents the formation of most D2 MSNs, phenocopying the Sp8/9 mutants.This implies that there are additional mechanisms that regulate the generation of D2 MSNs in Sp9-KO mice, one of which was suggested by the LGE RNA-Seq analysis. We identified that expression of the TF Six3 was decreased ?5-fold in E16.5 Sp8/9-DCKO mice compared with control mice.	--	--	Six3
29912188	chr12	132285987	132290767	CTCF	This set of genes should include housekeeping genes, such as CTCF or GAPDH.	human	tumour	Low+High throughput	Dissection of Enhancer Function Using Multiplex CRISPR-based Enhancer Interference in Cell Lines	否	--	--	Ishikawa cell	E_02_0756	ChIP-seq	Ensure that each regulatory element to be targeted with Enhancer-i has at least 4 unique oligonucleotides designed for it. Order these sequences along with the “U6_internal” primers	Enhancer	CRISPR/Cas9	--	To determine the contributions of ER-bound Enhancers near the estrogen_x0002_regulated gene MMP17,which has 3 binding sites nearby as defined by ChIP-seq.Figure 2D shows results from an Enhancer dissection experiment, where multiple Enhancers nearby MMP17 are targeted alone and in combination using Enhancer-i.	MMP-17,MT4-MMP,MT4MMP,MTMMP4	--	--	--	--	--	--	--	--	--	MMP17
29912188	chr12	132285987	132290767	GAPDH	This set of genes should include housekeeping genes, such as CTCF or GAPDH.	human	tumour	Low+High throughput	Dissection of Enhancer Function Using Multiplex CRISPR-based Enhancer Interference in Cell Lines	否	--	--	Ishikawa cell	E_02_0756	ChIP-seq	Ensure that each regulatory element to be targeted with Enhancer-i has at least 4 unique oligonucleotides designed for it. Order these sequences along with the “U6_internal” primers	Enhancer	CRISPR/Cas9	--	To determine the contributions of ER-bound Enhancers near the estrogen_x0002_regulated gene MMP17,which has 3 binding sites nearby as defined by ChIP-seq.Figure 2D shows results from an Enhancer dissection experiment, where multiple Enhancers nearby MMP17 are targeted alone and in combination using Enhancer-i.	MMP-17,MT4-MMP,MT4MMP,MTMMP4	--	--	--	--	--	--	--	--	--	MMP17
29903739	chr15	96725740	96737960	TBX20	Tbx20 Is Required in Mid-Gestation Cardiomyocytes and Plays a Central Role in Atrial Development.	human	heart	Low+High throughput	Tbx20 Is Required in Mid-Gestation Cardiomyocytes and Plays a Central Role in Atrial Development	否	--	Congenital Heart Disease	E11.5 Heart	E_02_0283	ChIP-seq,Hi-C	we made use of our TBX20 ChIP-Seq analysis in E11.5 hearts and attributed TBX20 bound sites to the nearest expressed gene in E11.5 control or Tbx20 cKO cardiomyocytes. Next, we overlaid our RNA-Seq data with that of our TBX20 ChIP-Seq analysis in E11.5 hearts and identified 548 genes that were differentially expressed in Tbx20 cKO cardiomyocytes and were marked by one or more TBX20 binding events in the vicinity of the gene.	Enhancer	--	Hi-C	We next established that this Enhancer was functionally connected with COUP-TFII. We performed a promoter-based Capture Hi-C in iPSC-derived human cardiomyocytes to identify long-range physical interactions between genes and Enhancers. We observed that this Enhancer directly loops and contacts the COUP-TFII promoter,140-Kb away,confirming that this is a COUP-TFII Enhancer.	ARP-1,ARP1,CHTD4,COUPTF2,COUPTFB,COUPTFII,NF-E3,SVP40,TFCOUP2	This Enhancer interacted with the NR2F2 promoter in human cardiomyocytes and conferred atrial specific gene expression in a transgenic mouse in a TBX20 dependent manner.	Hi-C	Taken together, these results linked TBX20 binding to an evolutionary conserved Enhancer that regulates COUP-TFII expression in developing atrial cardiomyocytes, uncovering a mechanism by which COUP-TFII expression is TBX20 dependent.	TBX20	ASD4	X-Gal Staining Assay 	Section analysis of COUP-TFII enh1::lacZ transgenic embryo demonstrates X-gal staining in developing atrial myocardium (arrows) and caval vein (arrowheads). 	--	--	NR2F2
29628309	chr3	150450617	150456921	JMJD6	JMJD6 Licenses ERa-Dependent Enhancer and Coding Gene Activation by Modulating the Recruitment of the CARM1/MED12 Co-activator Complex.	human	breast	Low+High throughput	JMJD6 Licenses ERa-Dependent Enhancer and Coding Gene Activation by Modulating the Recruitment of the CARM1/MED12 Co-activator Complex	否	--	Breast Cancer	MCF-7 cell	E_02_0757	ChIP-seq,ChIP-qPCR	We next assessed whether those estrogen-induced JMJD6 binding sites shared enhancer characteristics, including highly enriched H3K4me1/2 but low levels of H3K4me3. Heatmap and tag density plots confirmed they were, indeed, ERa-bound enhancers . Furthermore, it was reported recently that a group of enhancers, namely active enhancers, were essential for the transcriptional activation of estrogeninduced coding target genes	Enhancer	--	ChIP-qPCR,qRT-PCR	To validate JMJD6 effects on eRNA production, total RNA extracted from MCF7 cells transfected with control siRNA or two independent siRNAs pecifically against JMJD6 in the presence or absence of strogen treatment were subjected to qRT-PCR analysis using primers specifically targeting several ERa and JMJD6 co-bound active enhancers nearby estrogen-induced coding genes, such as FOXC1, SIAH2, GREB1, NRIP1, and SMAD7.	hSiah2	--	--	--	JMJD6,ESR1	PSR,PTDSR,PTDSR1,ER,ESR,ESRA,ESTRR,Era,NR3A1	siRNA,RT-qPCR	To validate JMJD6 effects on eRNA production, total RNA extracted from MCF7 cells transfected with control siRNA or two independent siRNAs specifically against JMJD6 in the presence or absence of estrogen treatment were subjected to RT-qPCR analysis using primers specifically targeting several ERα and JMJD6 co-bound active enhancers nearby estrogen-induced coding genes.	--	--	SIAH2
29628309	chr3	150450617	150456921	CARM1	JMJD6 Licenses ERa-Dependent Enhancer and Coding Gene Activation by Modulating the Recruitment of the CARM1/MED12 Co-activator Complex.	human	breast	Low+High throughput	JMJD6 Licenses ERa-Dependent Enhancer and Coding Gene Activation by Modulating the Recruitment of the CARM1/MED12 Co-activator Complex	否	--	Breast Cancer	MCF-7 cell	E_02_0757	ChIP-seq,ChIP-qPCR	We next assessed whether those estrogen-induced JMJD6 binding sites shared enhancer characteristics, including highly enriched H3K4me1/2 but low levels of H3K4me3. Heatmap and tag density plots confirmed they were, indeed, ERa-bound enhancers . Furthermore, it was reported recently that a group of enhancers, namely active enhancers, were essential for the transcriptional activation of estrogeninduced coding target genes	Enhancer	--	ChIP-qPCR,qRT-PCR	To validate JMJD6 effects on eRNA production, total RNA extracted from MCF7 cells transfected with control siRNA or two independent siRNAs pecifically against JMJD6 in the presence or absence of strogen treatment were subjected to qRT-PCR analysis using primers specifically targeting several ERa and JMJD6 co-bound active enhancers nearby estrogen-induced coding genes, such as FOXC1, SIAH2, GREB1, NRIP1, and SMAD7.	hSiah2	--	--	--	JMJD6,ESR1	PSR,PTDSR,PTDSR1,ER,ESR,ESRA,ESTRR,Era,NR3A1	siRNA,RT-qPCR	To validate JMJD6 effects on eRNA production, total RNA extracted from MCF7 cells transfected with control siRNA or two independent siRNAs specifically against JMJD6 in the presence or absence of estrogen treatment were subjected to RT-qPCR analysis using primers specifically targeting several ERα and JMJD6 co-bound active enhancers nearby estrogen-induced coding genes.	--	--	SIAH2
29628309	chr3	150450617	150456921	MED12	JMJD6 Licenses ERa-Dependent Enhancer and Coding Gene Activation by Modulating the Recruitment of the CARM1/MED12 Co-activator Complex.	human	breast	Low+High throughput	JMJD6 Licenses ERa-Dependent Enhancer and Coding Gene Activation by Modulating the Recruitment of the CARM1/MED12 Co-activator Complex	否	--	Breast Cancer	MCF-7 cell	E_02_0757	ChIP-seq,ChIP-qPCR	We next assessed whether those estrogen-induced JMJD6 binding sites shared enhancer characteristics, including highly enriched H3K4me1/2 but low levels of H3K4me3. Heatmap and tag density plots confirmed they were, indeed, ERa-bound enhancers . Furthermore, it was reported recently that a group of enhancers, namely active enhancers, were essential for the transcriptional activation of estrogeninduced coding target genes	Enhancer	--	ChIP-qPCR,qRT-PCR	To validate JMJD6 effects on eRNA production, total RNA extracted from MCF7 cells transfected with control siRNA or two independent siRNAs pecifically against JMJD6 in the presence or absence of strogen treatment were subjected to qRT-PCR analysis using primers specifically targeting several ERa and JMJD6 co-bound active enhancers nearby estrogen-induced coding genes, such as FOXC1, SIAH2, GREB1, NRIP1, and SMAD7.	hSiah2	--	--	--	JMJD6,ESR1	PSR,PTDSR,PTDSR1,ER,ESR,ESRA,ESTRR,Era,NR3A1	siRNA,RT-qPCR	To validate JMJD6 effects on eRNA production, total RNA extracted from MCF7 cells transfected with control siRNA or two independent siRNAs specifically against JMJD6 in the presence or absence of estrogen treatment were subjected to RT-qPCR analysis using primers specifically targeting several ERα and JMJD6 co-bound active enhancers nearby estrogen-induced coding genes.	--	--	SIAH2
29527594	chr6	127033997	127036097	FGF23	Fibroblast growth factor 23 (FGF23) production is regulated by both calciotropic hormones and inflammation. Consistent with this, elevated FGF23 levels are associated with inflammatory markers as well as parathyroid hormone (PTH) in various disease states, including chronic kidney disease (CKD). 	mouse		Low+High throughput	A Novel Distal Enhancer Mediates Inflammation-, PTH-, and Early Onset Murine Kidney Disease-Induced Expression of the Mouse Fgf23 Gene.	否	--	Chronic Kidney Disease	Osteocyte Cell Lines	E_02_0758	ChIP-seq,CRISPR/Cas9	"We therefore utilized chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) data from an osteocyte cell line to identify potential regulatory regions of the Fgf23 gene. Based on ChIP-seq analysis of enhancer_x0002_associated histone modifications, including H3K4 methylation and H3K9 acetylation, we discovered several potential enhancers for
Fgf23, one of which was located 16kb upstream of the gene’s transcriptional start site."	Enhancer	CRISPR/Cas9	ChIP-seq,RT-PCR	Nevertheless, lack of the _x0003_16kb enhancer blunted FGF23 upregulation in a tissue-specific manner by the acute inflammatory inducers lipopolysaccharide (LPS), interleukin-1-beta (IL-1b), and tumor necrosis factor-alpha (TNFa) in bone, non-osseous tissues,and in circulation. Lack of the _x0003_16kb enhancer also inhibited PTH-induced bone Fgf23 mRNA. Moreover, the absence of this Fgf23 enhancer in an oxalate diet-induced murine CKD model prevented the early onset induction of osseous, renal, and thymic Fgf23 mRNA levels and led to a significant blunting of elevated circulating intact FGF23 levels. These results suggest that _x0003_16kb enhancer mediates the induction of Fgf23 by inflammation and PTH and facilitates the increase in FGF23 expression in a murine model of CKD.	Fgf23	16kb Enhancer mediates the induction of Fgf23 by inflammation and PTH and facilitates the increase in FGF23 expression in a murine model of CKD	ChIP-seq	These results suggest that 16kb Enhancer mediates the induction of Fgf23 by inflammation and PTH and facilitates the increase in FGF23 expression in a murine model of CKD.	Nfkb1,Hif1a	NF-KB1,NF-kappaB,NF-kappaB1,p105,p50,p50/p105;AA959795,HIF-1-alpha,HIF1-alpha,HIF1alpha,MOP1,bHLHe78	ChIP-seq	Advances in genome‐wide techniques such as chromatin immunoprecipitation followed by DNA sequencing (ChIP‐seq) have revealed that the transcriptional regulation of many genes, including receptor activator of NF‐κB ligand (Tnfsf11), vitamin D receptor (Vdr), or matrix metallopeptidase 13 (Mmp13), are mediated through a complex network of Enhancers each providing distinct factor‐ and cell‐type specificity.	--	--	Fgf23
29527594	chr6	127033997	127036097	PTH	Fibroblast growth factor 23 (FGF23) production is regulated by both calciotropic hormones and inflammation. Consistent with this, elevated FGF23 levels are associated with inflammatory markers as well as parathyroid hormone (PTH) in various disease states, including chronic kidney disease (CKD). 	mouse		Low+High throughput	A Novel Distal Enhancer Mediates Inflammation-, PTH-, and Early Onset Murine Kidney Disease-Induced Expression of the Mouse Fgf23 Gene.	否	--	Chronic Kidney Disease	Osteocyte Cell Lines	E_02_0758	ChIP-seq,CRISPR/Cas9	"We therefore utilized chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) data from an osteocyte cell line to identify potential regulatory regions of the Fgf23 gene. Based on ChIP-seq analysis of enhancer_x0002_associated histone modifications, including H3K4 methylation and H3K9 acetylation, we discovered several potential enhancers for
Fgf23, one of which was located 16kb upstream of the gene’s transcriptional start site."	Enhancer	CRISPR/Cas9	ChIP-seq,RT-PCR	Nevertheless, lack of the _x0003_16kb enhancer blunted FGF23 upregulation in a tissue-specific manner by the acute inflammatory inducers lipopolysaccharide (LPS), interleukin-1-beta (IL-1b), and tumor necrosis factor-alpha (TNFa) in bone, non-osseous tissues,and in circulation. Lack of the _x0003_16kb enhancer also inhibited PTH-induced bone Fgf23 mRNA. Moreover, the absence of this Fgf23 enhancer in an oxalate diet-induced murine CKD model prevented the early onset induction of osseous, renal, and thymic Fgf23 mRNA levels and led to a significant blunting of elevated circulating intact FGF23 levels. These results suggest that _x0003_16kb enhancer mediates the induction of Fgf23 by inflammation and PTH and facilitates the increase in FGF23 expression in a murine model of CKD.	Fgf23	16kb Enhancer mediates the induction of Fgf23 by inflammation and PTH and facilitates the increase in FGF23 expression in a murine model of CKD	ChIP-seq	These results suggest that 16kb Enhancer mediates the induction of Fgf23 by inflammation and PTH and facilitates the increase in FGF23 expression in a murine model of CKD.	Nfkb1,Hif1a	NF-KB1,NF-kappaB,NF-kappaB1,p105,p50,p50/p105;AA959795,HIF-1-alpha,HIF1-alpha,HIF1alpha,MOP1,bHLHe78	ChIP-seq	Advances in genome‐wide techniques such as chromatin immunoprecipitation followed by DNA sequencing (ChIP‐seq) have revealed that the transcriptional regulation of many genes, including receptor activator of NF‐κB ligand (Tnfsf11), vitamin D receptor (Vdr), or matrix metallopeptidase 13 (Mmp13), are mediated through a complex network of Enhancers each providing distinct factor‐ and cell‐type specificity.	--	--	Fgf23
29514092	chr19	61151074	61161722	IRF8	Of the transcription factors pre- dicted to bind to these enhancers, IRF8, essential for monocyte and DC development, was found to be required for the establishment of these en- hancers, particularly those common to both mono- cyte and DC lineages.                                                                                                                                                                                                                                                                                                                                                                                                               CBFb, which heterodimerizes with RUNX family transcription factors to bind target genes, is needed for MDP and CDP devel- opment, and its deficiency causes a loss of monocytes, cDCs, and pDCs (Satpathy et al., 2014).	mouse		Low+High throughput	Transcription Factor IRF8 Governs Enhancer Landscape Dynamics in Mononuclear Phagocyte Progenitors.	否	--	--	Mononuclear cell,dendritic cell	E_02_0759	ChIP-seq	"Active enhancers shared by monocytes and DCs (but not neutrophils) and those specific
for monocytes were primed and activated with similar kinetics(Figure 2A, left and center). H3K4me1 and H3K27ac ChIP-seq tag densities in these enhancer regions initially increased at
the MDP stage.Notably, the expression of genes with primed but not active (often called poised) enhancers was barely induced in monocytes and DCs (Figure S2). We found
that the kinetics of DC-specific active enhancers were slower(Figure 2A, right);"	Super-Enhancer	--	ChIP-seq,Transgenic mice,RT-qPCR	Representative genome browser images of monocyte- or DC-specific en_x0002_hancers, associated with the Bfsp1 and Ehf genes, respec_x0002_tively, are depicted in Figures 2B and 2C.Thus, monocyte_x0002_and/or DC-specific active enhancers are gradually established at progenitor stages prior to the expression of associated genes.	CD116,Csfgmra,GM-CSFR,GM-CSF-Ra	--	--	--	Irf8	AI893568,ICSBP,IRF-8,Icsbp1,Myls	ChIP-seq,Transgenic mice	Analysis of Enhancer landscapes in Irf8–/– mononuclear phagocyte progenitors and ChIP-seq of IRF8 binding sites in wild-type (WT) cells uncovered a critical role for IRF8.Using an in vitro monocyte differentiation system, we additionally showed that IRF8 binds to promoter-distal enhancers and promotes H3K4me1 enrichment at its binding sites.Consistent with these data, the correlation coefficient of H3K4me1 ChIP-seq tag densities between WT MDPs and Irf8–/– MDPs was lower than that of the microarray data.	--	--	Csf2ra
29511351	chr4	84277627	84281723	HPSE	HPSE enhancer RNA promotes cancer progression through driving chromatin looping and regulating hnRNPU/p300/EGR1/HPSE axis.	human	Nervous tissue	Low+High throughput	HPSE enhancer RNA promotes cancer progression through driving chromatin looping and regulating hnRNPU/p300/EGR1/HPSE axis	否	--	Gastric Cancer	AGS	E_02_0760	3C,ChIP-seq,qPCR	"Overlapping analysis of FANTOM5 expression atlas and chromatin interaction dataset derived from 4DGenome revealed one potential enhancer region (chr4:84277627–84281723) adjacent to human HPSE promoter(chr4: 84255915–84256935).
Chromosome conformation capture (3C) and nucleic acid sequencing revealed the endogenous chromatin looping between HPSE promoter and super enhancer in AGS cells"	Super-Enhancer	--	Luciferase Reporter Assay,qPCR	Dual-luciferase assay revealed that this super enhancer increased the activity of HPSE promoter in gastric cancer cell lines SGC-7901 and AGS, independent of the orientation or location.	HPA,HPA1,HPR1,HPSE1,HSE1	HPSE eRNA promotes cancer progression through driving chromatin looping and regulating hnRNPU/p300/EGR1/HPSE axis.	ChIP,qPCR	ChIP and qPCR assay revealed that knockdown or ectopic expression of hnRNPU prevented the increased or decreased binding of hnRNPU or p300 to super Enhancer region following stable ectopic expression or knockdown of HPSE eRNA	EGR1	AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225	ChIP-seq,qPCR	ChIP and qPCR assay revealed that ectopic expression or knockdown of HPSE eRNA increased and decreased the enrichment of EGR1 on HPSE promoter,which was attenuated by knockdown or overexpression of hnRNPU or p300, respectively.	--	--	HPSE
29511351	chr4	84277627	84281723	EGR1	HPSE enhancer RNA promotes cancer progression through driving chromatin looping and regulating hnRNPU/p300/EGR1/HPSE axis.	human	Nervous tissue	Low+High throughput	HPSE enhancer RNA promotes cancer progression through driving chromatin looping and regulating hnRNPU/p300/EGR1/HPSE axis	否	--	Gastric Cancer	AGS	E_02_0760	3C,ChIP-seq,qPCR	"Overlapping analysis of FANTOM5 expression atlas and chromatin interaction dataset derived from 4DGenome revealed one potential enhancer region (chr4:84277627–84281723) adjacent to human HPSE promoter(chr4: 84255915–84256935).
Chromosome conformation capture (3C) and nucleic acid sequencing revealed the endogenous chromatin looping between HPSE promoter and super enhancer in AGS cells"	Super-Enhancer	--	Luciferase Reporter Assay,qPCR	Dual-luciferase assay revealed that this super enhancer increased the activity of HPSE promoter in gastric cancer cell lines SGC-7901 and AGS, independent of the orientation or location.	HPA,HPA1,HPR1,HPSE1,HSE1	HPSE eRNA promotes cancer progression through driving chromatin looping and regulating hnRNPU/p300/EGR1/HPSE axis.	ChIP,qPCR	ChIP and qPCR assay revealed that knockdown or ectopic expression of hnRNPU prevented the increased or decreased binding of hnRNPU or p300 to super Enhancer region following stable ectopic expression or knockdown of HPSE eRNA	EGR1	AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225	ChIP-seq,qPCR	ChIP and qPCR assay revealed that ectopic expression or knockdown of HPSE eRNA increased and decreased the enrichment of EGR1 on HPSE promoter,which was attenuated by knockdown or overexpression of hnRNPU or p300, respectively.	--	--	HPSE
29507293	chr15	66074477	66098025	CTCF	Hub enhancers share similar histone marks with non-hub enhancers, but are distinctly associated with cohesin and CTCF binding sites and disease-associated genetic variants.	human	bone marrow	Low+High throughput	Dissecting super-enhancer hierarchy based on chromatin interactions	是	--	--	Erythroleukemia Cell Lines	E_02_0761	Hi-C,ChIP-seq	Finally, if an enhancer element within hierarchical SEs overlaps with a bin associated with a z-score greater than the threshold H-score, the element is referred to a hub enhancer, whereas the remaining enhancers at the same SE are termed non-hub enhancers	Super-Enhancer	CRISPR/Cas9	--	we employed CRISPR-Cas9-mediated genome engineering to delete individual hub or non-hub enhancers with paired sgRNAs flanking the enhancer elements at the MYO1D SE.We observed that 3 of the 5 genes within the SE-containing TAD domain MYO1D,TMEM98 and SPACA3)displayed significant downregulation in mRNA expression, whereas the other two genes (PSMD11 and CDK5R1) remained unaffected , suggesting that the MYO1D SE may regulate only a subset of genes within the same TAD domain.	PPP1R108,myr4,KMT3E,ZMYND1,ZNFN3A1,bA74P14.1	Hub enhancers are the major constituents responsible for SE functional and structural organization.	ChIP-seq,CRISPR/Cas9	The signals for H3K27ac and DNase I hypersensitivity are slightly higher at hub than other types of Enhancers. 	GATA1,TAL1,PAX5,EBF1	ERYF1,GATA-1,GF-1,GF1,NF-E1,NFE1,XLANP,XLTDA,XLTT,SCL,ALL3,BSAPTCL5,bHLHa17,tal-1,ALL3,BSAP,COE1,EBF,O/E-1,OLF1	ChIP-seq	Hub Enhancers contain significantly higher ChIP-seq binding signals for lineage-regulating master regulators than non-hub Enhancers, such as GATA1 and TAL1 in K562 cells, and PAX5 and EBF1 in GM12878 cells.	--	--	MYO1D
29507293	chr15	66074477	66098025	CTCF	Hub enhancers share similar histone marks with non-hub enhancers, but are distinctly associated with cohesin and CTCF binding sites and disease-associated genetic variants.	human	bone marrow	Low+High throughput	Dissecting super-enhancer hierarchy based on chromatin interactions	是	--	--	Erythroleukemia Cell Lines	E_02_0761	Hi-C,ChIP-seq	Finally, if an enhancer element within hierarchical SEs overlaps with a bin associated with a z-score greater than the threshold H-score, the element is referred to a hub enhancer, whereas the remaining enhancers at the same SE are termed non-hub enhancers	Super-Enhancer	CRISPR/Cas9	--	we employed CRISPR-Cas9-mediated genome engineering to delete individual hub or non-hub enhancers with paired sgRNAs flanking the enhancer elements at the MYO1D SE.We observed that 3 of the 5 genes within the SE-containing TAD domain MYO1D,TMEM98 and SPACA3)displayed significant downregulation in mRNA expression, whereas the other two genes (PSMD11 and CDK5R1) remained unaffected , suggesting that the MYO1D SE may regulate only a subset of genes within the same TAD domain.	PPP1R108,myr4,KMT3E,ZMYND1,ZNFN3A1,bA74P14.1	Hub enhancers are the major constituents responsible for SE functional and structural organization.	ChIP-seq,CRISPR/Cas9	The signals for H3K27ac and DNase I hypersensitivity are slightly higher at hub than other types of Enhancers. 	GATA1,TAL1,PAX5,EBF1	ERYF1,GATA-1,GF-1,GF1,NF-E1,NFE1,XLANP,XLTDA,XLTT,SCL,ALL3,BSAPTCL5,bHLHa17,tal-1,ALL3,BSAP,COE1,EBF,O/E-1,OLF1	ChIP-seq	Hub Enhancers contain significantly higher ChIP-seq binding signals for lineage-regulating master regulators than non-hub Enhancers, such as GATA1 and TAL1 in K562 cells, and PAX5 and EBF1 in GM12878 cells.	--	--	SMYD3 
29440643	chr6	138226720	138233280	TNFAIP3	While the widely used immunohistochemical biomarker CD99 shows high sensitivity for Ewing sarcoma.	human	lymph	Low+High throughput	Dissection and function of autoimmunity-associated TNFAIP3 (A20) gene enhancers in humanized mouse models	否	--	Autoimmune Diseases	B cell,mononuclear cell	E_02_0762	CRISPR/Cas9,Hi-C,ChIP-seq	Recent studies have begun to address mammalian enhancer function using CRISPR-mediated genome editing, including in vivo analysis of mouse genes.To identify enhancers activated by inflammatory stimuli,we analyzed ATAC-seq and ChIP-seq data sets generated in our laboratory (GSE43036, GSE9836926, and GSE104638) for chromatin accessibility, binding of PU.1 and C/EBP (which bind to regulatory elements and help define enhancers in myeloid cells), and induction of acetylation of histone 3 lysine 27 (H3K27-Ac), which indicates enhancer activation, at enhancer peaks after LPS stimulation of primary monocytes.	Enhancer	--	Hi-C,ChIP-seq	To guide selection of BACs for generation of humanized transgenic mice, we analyzed chromatin conformation, accessibility, and enhancer-related histone marks at the TNFAIP3 locus using our laboratory’s (GSE4303620, GSE10038321 and previously unpublished data, GSE104628) and ENCODE and NIH Roadmap ChIP-seq data (available at genome.ucsc.edu and roadmapepigenomics.org) and Hi-C data.Analysis of pre-existing high-resolution Hi-C (chromatin conformation) data in GM12878 B cells identified a 305?kb topologically associating domain (TAD) flanked by CTCF sites roughly centered around the TNFAIP3 gene body.	A20,AISBL,OTUD7C,TNFA1P2	These findings provide insights into enhancers that regulate human A20 expression to prevent inflammatory pathology and autoimmunity.	PCR,CRISPR/Cas9	Collectively, the results show that deletion of the TT>A Enhancer at the TNFAIP3 locus results in an autoimmune/inflammatory phenotype most clearly evident as athritis.	--	--	--	--	--	--	TNFAIP3
29416716	chr14	99770698	99782638	ATP1A1	Collectively, we show that ATP1A1, BCL11B, and GLG1 are EWSR1-FLI1 targets.	human	Musculature	Low throughput 	Robust diagnosis of Ewing sarcoma by immunohistochemical detection of super-enhancer-driven EWSR1-ETS targets	否	--	Ewing Sarcoma	A673 cell	E_02_0763	Luciferase Reporter Assay,qRT-PCR	 Expression of these genes appeared to be induced by EWSR1-FLI1-bound super-enhancers, which showed high activity in reporter assays.In fact, EWSR1-FLI1 is known to convert non-functional GGAA-microsatellites into potent enhancers to steer a large proportion of its target genes [24–26]. Strong EWSR1-FLI1-dependent enhancer activity of these GGAA-microsatellites in luciferase reporter assays was consistently observed. 	Super-Enhancer	--	qRT-PCR,ChIP-seq	These data in cell lines suggested that ATP1A1, BCL11B, and GLG1 may be direct EWSR1-FLI1 target genes. Testing this hypothesis involved analyzing available ChIP-Seq and DNase-Seq data generated in Ewing sarcoma cell lines, which showed strong EWSR1-FLI1-binding to GGAA-microsatellites close to these genes.	ATL1,ATL1-alpha,ATL1-beta,ATL1-delta,ATL1-gamma,CTIP-2,CTIP2,IDDFSTA,IMD49,RIT1,ZNF856B,hRIT1-alpha	--	--	--	--	--	--	--	--	--	BCL11B
29416716	chr14	99770698	99782638	BCL11B	Collectively, we show that ATP1A1, BCL11B, and GLG1 are EWSR1-FLI1 targets.	human	Musculature	Low throughput 	Robust diagnosis of Ewing sarcoma by immunohistochemical detection of super-enhancer-driven EWSR1-ETS targets	否	--	Ewing Sarcoma	A673 cell	E_02_0763	Luciferase Reporter Assay,qRT-PCR	 Expression of these genes appeared to be induced by EWSR1-FLI1-bound super-enhancers, which showed high activity in reporter assays.In fact, EWSR1-FLI1 is known to convert non-functional GGAA-microsatellites into potent enhancers to steer a large proportion of its target genes [24–26]. Strong EWSR1-FLI1-dependent enhancer activity of these GGAA-microsatellites in luciferase reporter assays was consistently observed. 	Super-Enhancer	--	qRT-PCR,ChIP-seq	These data in cell lines suggested that ATP1A1, BCL11B, and GLG1 may be direct EWSR1-FLI1 target genes. Testing this hypothesis involved analyzing available ChIP-Seq and DNase-Seq data generated in Ewing sarcoma cell lines, which showed strong EWSR1-FLI1-binding to GGAA-microsatellites close to these genes.	ATL1,ATL1-alpha,ATL1-beta,ATL1-delta,ATL1-gamma,CTIP-2,CTIP2,IDDFSTA,IMD49,RIT1,ZNF856B,hRIT1-alpha	--	--	--	--	--	--	--	--	--	BCL11B
29416716	chr14	99770698	99782638	GLG1	Collectively, we show that ATP1A1, BCL11B, and GLG1 are EWSR1-FLI1 targets.	human	Musculature	Low throughput 	Robust diagnosis of Ewing sarcoma by immunohistochemical detection of super-enhancer-driven EWSR1-ETS targets	否	--	Ewing Sarcoma	A673 cell	E_02_0763	Luciferase Reporter Assay,qRT-PCR	 Expression of these genes appeared to be induced by EWSR1-FLI1-bound super-enhancers, which showed high activity in reporter assays.In fact, EWSR1-FLI1 is known to convert non-functional GGAA-microsatellites into potent enhancers to steer a large proportion of its target genes [24–26]. Strong EWSR1-FLI1-dependent enhancer activity of these GGAA-microsatellites in luciferase reporter assays was consistently observed. 	Super-Enhancer	--	qRT-PCR,ChIP-seq	These data in cell lines suggested that ATP1A1, BCL11B, and GLG1 may be direct EWSR1-FLI1 target genes. Testing this hypothesis involved analyzing available ChIP-Seq and DNase-Seq data generated in Ewing sarcoma cell lines, which showed strong EWSR1-FLI1-binding to GGAA-microsatellites close to these genes.	ATL1,ATL1-alpha,ATL1-beta,ATL1-delta,ATL1-gamma,CTIP-2,CTIP2,IDDFSTA,IMD49,RIT1,ZNF856B,hRIT1-alpha	--	--	--	--	--	--	--	--	--	BCL11B
29408204	chr3	69863244	70187654	CDK7	High MITF Expression Is Associated with Super-Enhancers and Suppressed by CDK7 Inhibition in Melanoma.	human	tumour	Low+High throughput	High MITF Expression Is Associated with Super-Enhancers and Suppressed by CDK7 Inhibition in Melanoma	否	--	Melanoma	melanoma cells	E_02_0764	ChIP-seq,Western blot,siRNA,qPCR	H3K27ac chromatin immunoprecipitation sequencing (ChIP-seq) profiling, which marks active enhancers, indicated the presence of SEs at the MITF gene locus in MITF-hi cells and substantially less enhancer signal at the same location in an MITF-lo cell line (LOXIMVI) and a normal human dermal fibroblast line.	Super-Enhancer	--	qPCR,ChIP-seq	To identify a set of MITF high- and low-expressing cells, we performed quantitative real-time reverse transcriptase-PCR analysis on 18 melanoma lines and found 8 lines with high MITF (MITF-hi) (>2-fold mean normalized MITF levels) and 5 lines with low MITF (MITF-lo) (<?-fold mean normalized MITF levels) expression levels (Figure 1b). Analysis of MITF copy number in these lines showed only two lines with evidence of MITF gene amplification.	CMM8,COMMAD,MI,WS2,WS2A,bHLHe32	--	--	--	CDK7	CAK,CAK1,CDKN7,HCAK,MO15,STK1,p39MO15	siRNA	To verify that CDK7 blockade can lead to growth suppression, we subjected SK-MEL-5, SK-MEL-30, and UACC257 cells to small interfering RNA (siRNA) against CDK7 and observed consistent decreases in cell growth (see Supplementary Figure S6 online) compared with siRNA nontargeting controls. Cell lines with lower MITF levels (LOXIMVI, A375, SK-MEL-63) (see Supplementary Figure S7 online) were also sensitive to THZ1, exhibited appropriate CDK7 targeting, and showed an apoptotic response when exposed to the agent.	--	--	MITF
29385519	chrx	106959618	106962917	CTCF	The CCCTC-binding factor (CTCF) plays a key role in the organization of chromatin architecture and the formation of chromatin loops to facilitate long_x0002_range interactions.	human	tumour	Low+High throughput	Genomic dissection of enhancers uncovers principles of combinatorial regulation and cell type-specific wiring of enhancer–promoter contacts	否	--	--	U-2 OS cell	E_02_0765	ChIP-qPCR,4C	However, in contrast to the effects on the hormone-induced levels, these effects do not consistently correlate with deletions at the GILZ GBS1–4 enhancer and might reflect difficulties to quantify these transcripts by qPCR due to low expression levels in the absence of hormone treatment.To test if deletion of an individual GBS influences GR occupancy at the edited enhancer, we analyzed GR binding by ChIP-qPCR in a representative clonal cell line in which we deleted the GILZ GBS1. 	Enhancer	CRISPR/Cas9	--	To experimentally test the contribution of the smallest regulatory units of gene regulation, individual GR binding sequences (GBSs), we used the CRISPR/Cas9-system (25) to delete selected GBSs in their endogenous genomic context. We chose a GBS located 1.5 kb upstream of the GR target gene GILZ (glucocorticoid induced leucine zipper, alias TSC22D3) and one GBS 1.5 kb upstream of the target gene DUSP1.	SOM,TFCP2L4,VWS2	--	--	--	NR3C1	GCCR,GCR,GCRST,GR,GRL	ChIP-seq	To study the global connection between GR binding and GR-dependent gene regulation, we combined data from genome-wide GR binding experiments (Chromatin Immunoprecipitation followed by sequencing (ChIP-seq)) with RNA-seq data regarding gene expression changes upon GR-activation in A549 cells (3).	--	--	TSC22D3
29379199	chr4	174441057	174442400	MYC	The MYC family of transcription factors, comprising MYC, MYCN, and MYCL, includes the most commonly altered onco_x0002_genes in cancer1,2	human	Nervous tissue	Low+High throughput	Enhancer invasion shapes MYCN-dependent transcriptional amplification in neuroblastoma	否	--	Neuroblastoma	neuroblastoma cell lines	E_02_0766	ChIP-seq,Western blot	We observe that two hours after shutdown, MYCN is significantly depleted from promoters and enhancers (Fig. 1f; Supplementary Fig. 2c,e,f) - a result revealed by ChIP-Rx cell-count normalization.Although both traditional ChIP-seq and ChIP-Rx reveal global loss of MYCN at promoters and enhancers, we do observe global loss of additional marks (H3K4me3, CTCF, H3K27ac, and RNA Pol II) at 24 hours post MYCN shutdown only in ChIP-Rx data. In contrast, induction of MYCN in parental SHEP neuroblastoma cells (Fig. 1c,d) results in loading of MYCN at active promoters and enhancers, and is coincident with increases in global H3K27ac. 	Enhancer	--	ChIP-seq	ChIP-seq tracks of MYCN and H3K27ac at 0, 2 and 6hrs post MYCN induction at RPL22, HAND2 and the upstream ID2 enhancer.Visual inspection of MYCN load at highly occupied genes revealed a diversity of binding profiles with some genes exhibiting promoter MYCN binding (RPL22) and others a more mixed array of promoter and enhancer binding (HAND2 & ID2). 	DHAND2,Hed,Thing2,bHLHa26,dHand	--	--	--	MYCN	MODED,N-myc,NMYC,ODED,bHLHe37	Western blot,ChIP-seq	Across MYCN-amplified neuroblastoma lines, we used chromatin immunoprecipitation coupled to high-throughput sequencing (ChIP-seq) to generate a consensus genome-wide map of ~10,000 regions that exhibit strong and consistent MYCN occupancy.	--	--	HAND2
29379199	chr4	174441057	174442400	MYCN	Enhancer invasion shapes MYCN-dependent transcriptional amplification in neuroblastoma.	human	Nervous tissue	Low+High throughput	Enhancer invasion shapes MYCN-dependent transcriptional amplification in neuroblastoma	否	--	Neuroblastoma	neuroblastoma cell lines	E_02_0766	ChIP-seq,Western blot	We observe that two hours after shutdown, MYCN is significantly depleted from promoters and enhancers (Fig. 1f; Supplementary Fig. 2c,e,f) - a result revealed by ChIP-Rx cell-count normalization.Although both traditional ChIP-seq and ChIP-Rx reveal global loss of MYCN at promoters and enhancers, we do observe global loss of additional marks (H3K4me3, CTCF, H3K27ac, and RNA Pol II) at 24 hours post MYCN shutdown only in ChIP-Rx data. In contrast, induction of MYCN in parental SHEP neuroblastoma cells (Fig. 1c,d) results in loading of MYCN at active promoters and enhancers, and is coincident with increases in global H3K27ac. 	Enhancer	--	ChIP-seq	ChIP-seq tracks of MYCN and H3K27ac at 0, 2 and 6hrs post MYCN induction at RPL22, HAND2 and the upstream ID2 enhancer.Visual inspection of MYCN load at highly occupied genes revealed a diversity of binding profiles with some genes exhibiting promoter MYCN binding (RPL22) and others a more mixed array of promoter and enhancer binding (HAND2 & ID2). 	DHAND2,Hed,Thing2,bHLHa26,dHand	--	--	--	MYCN	MODED,N-myc,NMYC,ODED,bHLHe37	Western blot,ChIP-seq	Across MYCN-amplified neuroblastoma lines, we used chromatin immunoprecipitation coupled to high-throughput sequencing (ChIP-seq) to generate a consensus genome-wide map of ~10,000 regions that exhibit strong and consistent MYCN occupancy.	--	--	HAND2
29378668	chr2	11633299	11641134	TDG	Genome-wide analysis reveals a role for TDG in estrogen receptor-mediated enhancer RNA transcription and 3-dimensional reorganization.	human	breast	Low+High throughput	Genome-wide analysis reveals a role for TDG in estrogen receptor-mediated enhancer RNA transcription and 3-dimensional reorganization	否	--	Breast Cancer	MCF-7 cell	E_02_0767	ChIP-seq,3C,ChIP-qPCR	Additionally, overlap with datasets containing histone ChIP-Seq data reveals the enrichment of histone marks corresponding to active/poised enhancers and depleted of those markings found at repressed/silenced enhancers.Validations were performed using conventional ChIP-qPCR.Compared to genomic background, global analysis of the high-confidence TDG peaks revealed that E2-dependent TDG binding was enriched at promoters as well as distal to promoters with approximately 60% occurring intergenically.However, overlapping TDG peaks with sites of E2-dependent ERα localization revealed that 45% of TDG peaks occur at the same sites where ERα localizes in response to E2.	Enhancer	3C	--	ChIP using ER in the presence and absence of TDG as well as ? or + E2, showing that ER binding is unaltered during depletion of TDG. e Loss of TDG prevents enhancer–promoter looping at the GREB1 locus. MCF7 cells were treated with siControl or siTDG, and then treated with 100 nM E2 for 1 h. 3C, semiquantitative method of measuring the looping between the GREB1 enhancer and promoter, revealed that E2-driven looping of the enhancer and promoter is disrupted upon TDG knockdown.	GREB1	--	--	--	TDG	hTDG	CRISPR/Cas9	Remarkably, at a subset of enhancers that E2 targets, we found that TDG depletion abrogates E2-mediated eRNA, disrupts 3-dimensional reorganization at ER-targets such as GREB1 and disrupts E2-mediated transcription of corresponding ER-target genes. To investigate whether TDG plays a functional role in E2 signaling in breast cancer, we engineered an MCF7 TDG knockout cell line using CRISPR technology and found that TDG knockout and depletion leads to defects in E2-mediated proliferation and sensitizes MCF7 cells to the anti-estrogen. 	--	--	GREB1
29348663	chr14	56245000	56285000	LINC00520	The RNA level of LEENE (gene name LINC00520, aka C14orf34)	human	blood	Low+High throughput	Enhancer-associated long non-coding RNA LEENE regulates endothelial nitric oxide synthase and endothelial function		--	--	Endothelial cell	E_02_0768	ChIP-seq,qPCR,Hi-C	To test this possibility, we first attempted to identify the promoter/enhancer region of LEENE. In evaluating the genomic region surrounding LEENE, i.e., 20?kb up- and down-stream of the transcription start site (TSS) on chr14: 56,245,000–56,285,000, we observed the enrichments of H3K27ac and H3K4me1 in the HUVEC chromatin immunoprecipitation (ChIP)-seq data available in the ENCODE Database, indicating an “enhancer” state of this DNA region.We did find that PS led to significant increase in the H3K27ac in the LEENE region as measured by ChIP-qPCR, indicating the activation of LEENE as an enhancer in ECs subjected to PS vs. 	Enhancer	--	ChIP-qPCR,qPCR,Hi-C	As shown in Fig. 1f, quantitative PCR (qPCR) with LEENE RNA-specific primers also revealed the significantly higher level of LEENE in ECs subjected to PS than to OS. To confirm the flow regulation of LEENE in ECs and explore its relevance to endothelial function, we tested whether LEENE is differentially regulated by tumor necrosis factor alpha (TNFα), which exerts pro-inflammatory effects similar to OS, and atorvastatin (ATV), which confers endothelial protective effects similar to PS. Resembling the opposite effects of OS and PS, TNFα decreased, while ATV increased the level of LEENE.These findings are in line with the differential levels of KLF2/KLF4-eNOS signaling.	C14orf34	LEENE-associated Enhancer plays a role in positive regulation of eNOS transcription	CRISPR/Cas9	As a result of the Enhancer ablation, the transcription of LEENE and eNOS was significantly suppressed, in both DMSO (a control vehicle) and ATV-treated ECs	KLF2,KLF4	LKLF,EZF,GKLF	ChIP-qPCR	To confirm the association of such TFs on the promoter of LEENE, we performed ChIP-qPCR, which detected a robust binding between KLF4 and multiple regions within the promoter region of LEENE (marked by H3K4me3 peaks, Fig. 2a); these interactions were significantly increased by Ad-KLF4, which mimics the effect of PS and ATV.	--	--	LINC00520
29348663	chr14	56245000	56285000	KLF2	It has been established that eNOS transcription is largely regulated by Krüppel-like factors 2 (KLF2) and 4 (KLF4), two key TFs in endothelial identity and vascular homeostasis5.	human	Epithelial tissues	Low+High throughput	Enhancer-associated long non-coding RNA LEENE regulates endothelial nitric oxide synthase and endothelial function	否	--	--	Endothelial cell	E_02_0768	ChIP-seq,qPCR,Hi-C	To test this possibility, we first attempted to identify the promoter/enhancer region of LEENE. In evaluating the genomic region surrounding LEENE, i.e., 20?kb up- and down-stream of the transcription start site (TSS) on chr14: 56,245,000–56,285,000, we observed the enrichments of H3K27ac and H3K4me1 in the HUVEC chromatin immunoprecipitation (ChIP)-seq data available in the ENCODE Database, indicating an “enhancer” state of this DNA region.We did find that PS led to significant increase in the H3K27ac in the LEENE region as measured by ChIP-qPCR, indicating the activation of LEENE as an enhancer in ECs subjected to PS vs. 	Enhancer	--	ChIP-qPCR,qPCR,Hi-C	As shown in Fig. 1f, quantitative PCR (qPCR) with LEENE RNA-specific primers also revealed the significantly higher level of LEENE in ECs subjected to PS than to OS. To confirm the flow regulation of LEENE in ECs and explore its relevance to endothelial function, we tested whether LEENE is differentially regulated by tumor necrosis factor alpha (TNFα), which exerts pro-inflammatory effects similar to OS, and atorvastatin (ATV), which confers endothelial protective effects similar to PS. Resembling the opposite effects of OS and PS, TNFα decreased, while ATV increased the level of LEENE.These findings are in line with the differential levels of KLF2/KLF4-eNOS signaling.	C14orf34	LEENE-associated Enhancer plays a role in positive regulation of eNOS transcription	CRISPR/Cas9	As a result of the Enhancer ablation, the transcription of LEENE and eNOS was significantly suppressed, in both DMSO (a control vehicle) and ATV-treated ECs	KLF2,KLF4	LKLF,EZF,GKLF	ChIP-qPCR	To confirm the association of such TFs on the promoter of LEENE, we performed ChIP-qPCR, which detected a robust binding between KLF4 and multiple regions within the promoter region of LEENE (marked by H3K4me3 peaks, Fig. 2a); these interactions were significantly increased by Ad-KLF4, which mimics the effect of PS and ATV.	--	--	LINC00520
29348663	chr14	56245000	56285000	KLF4	It has been established that eNOS transcription is largely regulated by Krüppel-like factors 2 (KLF2) and 4 (KLF4), two key TFs in endothelial identity and vascular homeostasis5.	human	Epithelial tissues	Low+High throughput	Enhancer-associated long non-coding RNA LEENE regulates endothelial nitric oxide synthase and endothelial function	否	--	--	Endothelial cell	E_02_0768	ChIP-seq,qPCR,Hi-C	To test this possibility, we first attempted to identify the promoter/enhancer region of LEENE. In evaluating the genomic region surrounding LEENE, i.e., 20?kb up- and down-stream of the transcription start site (TSS) on chr14: 56,245,000–56,285,000, we observed the enrichments of H3K27ac and H3K4me1 in the HUVEC chromatin immunoprecipitation (ChIP)-seq data available in the ENCODE Database, indicating an “enhancer” state of this DNA region.We did find that PS led to significant increase in the H3K27ac in the LEENE region as measured by ChIP-qPCR, indicating the activation of LEENE as an enhancer in ECs subjected to PS vs. 	Enhancer	--	ChIP-qPCR,qPCR,Hi-C	As shown in Fig. 1f, quantitative PCR (qPCR) with LEENE RNA-specific primers also revealed the significantly higher level of LEENE in ECs subjected to PS than to OS. To confirm the flow regulation of LEENE in ECs and explore its relevance to endothelial function, we tested whether LEENE is differentially regulated by tumor necrosis factor alpha (TNFα), which exerts pro-inflammatory effects similar to OS, and atorvastatin (ATV), which confers endothelial protective effects similar to PS. Resembling the opposite effects of OS and PS, TNFα decreased, while ATV increased the level of LEENE.These findings are in line with the differential levels of KLF2/KLF4-eNOS signaling.	C14orf34	LEENE-associated Enhancer plays a role in positive regulation of eNOS transcription	CRISPR/Cas9	As a result of the Enhancer ablation, the transcription of LEENE and eNOS was significantly suppressed, in both DMSO (a control vehicle) and ATV-treated ECs	KLF2,KLF4	LKLF,EZF,GKLF	ChIP-qPCR	To confirm the association of such TFs on the promoter of LEENE, we performed ChIP-qPCR, which detected a robust binding between KLF4 and multiple regions within the promoter region of LEENE (marked by H3K4me3 peaks, Fig. 2a); these interactions were significantly increased by Ad-KLF4, which mimics the effect of PS and ATV.	--	--	LINC00520
29326336	chr10	63525013	63527013	ARID5B	ARID5B as a critical downstream target of the TAL1 complex that activates the oncogenic transcriptional program and promotes T-cell leukemogenesis.	human	bone marrow	Low+High throughput	ARID5B as a critical downstream target of the TAL1 complex that activates the oncogenic transcriptional program and promotes T-cell leukemogenesis	是	--	T-Cell Acute Lymphoblastic Leukemia	T-acute lymphoblastic leukemia (T-ALL)	E_02_0769	ChIA-PET,CRISPR/Cas9	A ChIP-seq analysis of the ARID5B protein showed that ARID5B binds directly to the NOTCH-driven MYC enhancer (N-Me), which has been reported previously to be activated by NOTCH1 in T-ALL cells.Analysis of transcriptional activity using a luciferase reporter assay with the N-Me sequence also demonstrated that ARID5B knockdown significantly inhibited the enhancer activity.Hence, these results indicated that ARID5B directly activates the expression of MYC in T-ALL.	Enhancer	CRISPR/Cas9	ChIA-PET	Importantly, a chromatin–chromatin interaction analysis by paired-end tag sequencing (ChIA-PET) for the cohesin protein demonstrated a cis-regulatory interaction between the ?135-kb element and the ARID5B transcriptional start site (TSS).In fact, genetic knockout of the ?135-kb element by the CRISPR/Cas9 method resulted in a marked down-regulation of ARID5B gene expression.Thus, these results indicate that the TAL1-bound region at ?135 kb is the enhancer controlling ARID5B expression in T-ALL cells.	DESRT, MRF-2, MRF2	The TAL1-bound region at ?135 kb is the Enhancer controlling ARID5B expression in T-ALL cells.	CRISPR/Cas9	In fact, genetic knockout of the -135-kb element by the CRISPR/Cas9 method resulted in a marked down-regulation of ARID5B gene expression	TAL1	SCL,TCL5,bHLHa17,tal-1	CRISPR/Cas9	In fact, genetic knockout of the ?135- kb element by the CRISPR/Cas9 method resulted in a marked down-regulation of ARID5B gene expression (Fig. 1G; Supplemental Fig. S1B–E). Thus, these results indicate that the TAL1-bound region at ?135 kb is the enhancer controlling ARID5B expression in T-ALL cells. 	--	--	ARID5B
29284139	chr7	143459172	143459787	Shh	Sonic Hedgehog (Shh) signaling plays key regulatory roles in embryonic development and postnatal homeostasis and repair.                                                                                                                                                                                              We show that Foxd1 deletion abrogates the proliferative response to SHH ligand while FOXD1 overexpression alone is sufficient to induce cellular proliferation.	mouse		Low throughput	Coordinated d-cyclin/Foxd1 activation drives mitogenic activity of the Sonic Hedgehog signaling pathway.	否	--	Malignancies	mouse embryonic fibroblast cell	E_02_0770	Luciferase Reporter Assay	As shown in Fig 5A, enh1 is in the second intron of Cdkn1c while enh2 is located in the 3’ UTR. Luciferase reporter constructs were transfected into iMEFs stably overexpressing FOXD1 or a negative control vector.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,RT-PCR	We tested whether FOXD1 directly binds these enhancer sequences using established luciferase reporter constructs. As shown in Fig. 5A, enh1 is in the second intron of Cdkn1c while enh2 is located in the 3′ UTR. Luciferase reporter constructs were transfected into iMEFs stably overexpressing FOXD1 or a negative control vector. FOXD1-expressing cells exhibited higher activity of enh1-driven luciferase than negative controls while no difference was observed in luciferase activity driven by enh2(Fig. 5B).	AL024410,CDKI,Kip2,p57(kip2),p57Kip2	--	--	--	Foxd1	AI385632,BF-2,FREAC4,Hfh10,Hfhbf2	Luciferase Reporter Assay	Firefly luciferase reporter assay driven by Cdkn1c enhancer elements, enh1 and enh2, in iMEFs overexpressing empty pLenti construct or FOXD1.	--	--	Cdkn1c
29284139	chr7	143459172	143459787	Foxd1	Sonic Hedgehog (Shh) signaling plays key regulatory roles in embryonic development and postnatal homeostasis and repair.                                                                                                                                                                                              We show that Foxd1 deletion abrogates the proliferative response to SHH ligand while FOXD1 overexpression alone is sufficient to induce cellular proliferation.	mouse		Low throughput	Coordinated d-cyclin/Foxd1 activation drives mitogenic activity of the Sonic Hedgehog signaling pathway.	否	--	Malignancies	mouse embryonic fibroblast cell	E_02_0770	Luciferase Reporter Assay	As shown in Fig 5A, enh1 is in the second intron of Cdkn1c while enh2 is located in the 3’ UTR. Luciferase reporter constructs were transfected into iMEFs stably overexpressing FOXD1 or a negative control vector.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,RT-PCR	We tested whether FOXD1 directly binds these enhancer sequences using established luciferase reporter constructs. As shown in Fig. 5A, enh1 is in the second intron of Cdkn1c while enh2 is located in the 3′ UTR. Luciferase reporter constructs were transfected into iMEFs stably overexpressing FOXD1 or a negative control vector. FOXD1-expressing cells exhibited higher activity of enh1-driven luciferase than negative controls while no difference was observed in luciferase activity driven by enh2(Fig. 5B).	AL024410,CDKI,Kip2,p57(kip2),p57Kip2	--	--	--	Foxd1	AI385632,BF-2,FREAC4,Hfh10,Hfhbf2	Luciferase Reporter Assay	Firefly luciferase reporter assay driven by Cdkn1c enhancer elements, enh1 and enh2, in iMEFs overexpressing empty pLenti construct or FOXD1.	--	--	Cdkn1c
29277702	chr2	126601468	126603468	Hdc	Luciferase reporter transcription assay confirmed enhancer activities of putative enhancers in the Hdc gene.                                                                                                                                                                                                                                        GATA2 induced the expression of Mitf, Ahr, Ahrr and Bhlhe40 in mast cells.                                                           	mouse		Low+High throughput	The transcription factors GATA2 and microphthalmia-associated transcription factor regulate Hdc gene expression in mast cells and are required for IgE/mast cell-mediated anaphylaxis.	否	--	IgE/mast cell-mediated anaphylaxis	Mast cell	E_02_0771	ChIP-seq,Luciferase Reporter Assay	Chromatin immunoprecipitation sequencing analysis identified putative Hdc enhancers.Luciferase reporter transcription assay confirmed enhancer activities of putative enhancers in the Hdc gene.MITF bound to an enhancer located 8.8 kb upstream of the transcription start site of the Hdc gene and directed enhancer activity.To determine whether the putative Hdc Enhancers function in Hdc gene transcription, we constructed a luciferase reporter gene in which luciferase expression is under the control of the Hdc minimal promoter (-44 to +1 relative to the TSS) and the -8.8 or +0.3 Hdc Enhancer. We found that the -8.8 Hdc Enhancer dramatically increased the activity of the Hdc minimal promoter (13.4-fold increase) , whereas the +0.3 Hdc Enhancer failed to show significant Enhancer activity.	Enhancer	--	ChIP-qPCR,Luciferase Reporter Assay	Chromatin immunoprecipitation sequencing analysis identified putative Hdc enhancers.Luciferase reporter transcription assay confirmed enhancer activities of putative enhancers in the Hdc gene.MITF bound to an enhancer located 8.8 kb upstream of the transcription start site of the Hdc gene and directed enhancer activity.	AW108189-a,?Hdc-c,Hdc-e,?Hdc-s,?Hdc	--	--	--	Gata2,Mitf	Gata-2,BCC2,Bhlhe32,Gsfbcc2,Vitiligo,Wh,bw,mi,vit	ChIP-qPCR,shRNA,Luciferase Reporter Assay	Our ChIP-qPCR analysis of MITF binding in BMMCs revealed that among five predicted MITF-binding sites located within the -8.8 and +0.3 Hdc Enhancers.We found that Hdc mRNA expression was significantly diminished (70% reduction) in TBMMCs with knocked down Mitf mRNA expression.Conversely, overexpression of MITF in a non-mast cell line greatly 383 increased the activity of the -8.8 Hdc Enhancer.	--	--	Hdc
29277702	chr2	126601468	126603468	Gata2	Luciferase reporter transcription assay confirmed enhancer activities of putative enhancers in the Hdc gene.                                                                                                                                                                                                                                        GATA2 induced the expression of Mitf, Ahr, Ahrr and Bhlhe40 in mast cells.                                                           	mouse		Low+High throughput	The transcription factors GATA2 and microphthalmia-associated transcription factor regulate Hdc gene expression in mast cells and are required for IgE/mast cell-mediated anaphylaxis.	否	--	IgE/mast cell-mediated anaphylaxis	Mast cell	E_02_0771	ChIP-seq,Luciferase Reporter Assay	Chromatin immunoprecipitation sequencing analysis identified putative Hdc enhancers.Luciferase reporter transcription assay confirmed enhancer activities of putative enhancers in the Hdc gene.MITF bound to an enhancer located 8.8 kb upstream of the transcription start site of the Hdc gene and directed enhancer activity.To determine whether the putative Hdc Enhancers function in Hdc gene transcription, we constructed a luciferase reporter gene in which luciferase expression is under the control of the Hdc minimal promoter (-44 to +1 relative to the TSS) and the -8.8 or +0.3 Hdc Enhancer. We found that the -8.8 Hdc Enhancer dramatically increased the activity of the Hdc minimal promoter (13.4-fold increase) , whereas the +0.3 Hdc Enhancer failed to show significant Enhancer activity.	Enhancer	--	ChIP-qPCR,Luciferase Reporter Assay	Chromatin immunoprecipitation sequencing analysis identified putative Hdc enhancers.Luciferase reporter transcription assay confirmed enhancer activities of putative enhancers in the Hdc gene.MITF bound to an enhancer located 8.8 kb upstream of the transcription start site of the Hdc gene and directed enhancer activity.	AW108189-a,?Hdc-c,Hdc-e,?Hdc-s,?Hdc	--	--	--	Gata2,Mitf	Gata-2,BCC2,Bhlhe32,Gsfbcc2,Vitiligo,Wh,bw,mi,vit	ChIP-qPCR,shRNA,Luciferase Reporter Assay	Our ChIP-qPCR analysis of MITF binding in BMMCs revealed that among five predicted MITF-binding sites located within the -8.8 and +0.3 Hdc Enhancers.We found that Hdc mRNA expression was significantly diminished (70% reduction) in TBMMCs with knocked down Mitf mRNA expression.Conversely, overexpression of MITF in a non-mast cell line greatly 383 increased the activity of the -8.8 Hdc Enhancer.	--	--	Hdc
29277702	chr2	126601468	126603468	MITF	Luciferase reporter transcription assay confirmed enhancer activities of putative enhancers in the Hdc gene.                                                                                                                                                                                                                                        GATA2 induced the expression of Mitf, Ahr, Ahrr and Bhlhe40 in mast cells.                                                           	mouse		Low+High throughput	The transcription factors GATA2 and microphthalmia-associated transcription factor regulate Hdc gene expression in mast cells and are required for IgE/mast cell-mediated anaphylaxis.	否	--	IgE/mast cell-mediated anaphylaxis	Mast cell	E_02_0771	ChIP-seq,Luciferase Reporter Assay	Chromatin immunoprecipitation sequencing analysis identified putative Hdc enhancers.Luciferase reporter transcription assay confirmed enhancer activities of putative enhancers in the Hdc gene.MITF bound to an enhancer located 8.8 kb upstream of the transcription start site of the Hdc gene and directed enhancer activity.To determine whether the putative Hdc Enhancers function in Hdc gene transcription, we constructed a luciferase reporter gene in which luciferase expression is under the control of the Hdc minimal promoter (-44 to +1 relative to the TSS) and the -8.8 or +0.3 Hdc Enhancer. We found that the -8.8 Hdc Enhancer dramatically increased the activity of the Hdc minimal promoter (13.4-fold increase) , whereas the +0.3 Hdc Enhancer failed to show significant Enhancer activity.	Enhancer	--	ChIP-qPCR,Luciferase Reporter Assay	Chromatin immunoprecipitation sequencing analysis identified putative Hdc enhancers.Luciferase reporter transcription assay confirmed enhancer activities of putative enhancers in the Hdc gene.MITF bound to an enhancer located 8.8 kb upstream of the transcription start site of the Hdc gene and directed enhancer activity.	AW108189-a,?Hdc-c,Hdc-e,?Hdc-s,?Hdc	--	--	--	Gata2,Mitf	Gata-2,BCC2,Bhlhe32,Gsfbcc2,Vitiligo,Wh,bw,mi,vit	ChIP-qPCR,shRNA,Luciferase Reporter Assay	Our ChIP-qPCR analysis of MITF binding in BMMCs revealed that among five predicted MITF-binding sites located within the -8.8 and +0.3 Hdc Enhancers.We found that Hdc mRNA expression was significantly diminished (70% reduction) in TBMMCs with knocked down Mitf mRNA expression.Conversely, overexpression of MITF in a non-mast cell line greatly 383 increased the activity of the -8.8 Hdc Enhancer.	--	--	Hdc
29273679	chr2	75120051	75165771	CTCF	While all four gene clusters are activated early on during embryogenesis (Deschamps and van Nes 2005), both HoxA and HoxD clusters are subsequently reactivated during the development of the appendicular skeleton, where they also participate in the building of the limbs (Dolle et al. 1989; Zakany and Duboule 2007).	mouse		Low+High throughput	The HoxD cluster is a dynamic and resilient TAD boundary controlling the segregation of antagonistic regulatory landscapes.	否	--	--	Murine Limb Bud cell	E_02_0772	Hi-C,4C,ChIP-seq	In order to gain insights into TAD organization around the HoxD locus during limb bud development, we performed Hi-C (chromosome capture followed by high-throughput sequencing) on microdissected distal and proximal limb bud cells isolated from embryonic day 12.5 (E12.5) embryos. At this stage, T-DOM enhancers regulate Hoxd gene expression in proximal cells and are silent in distal cells, whereas C-DOM enhancers control Hoxd gene targets in future digit cells and are silent in proximal cells. Therefore, the two TADs are either transcriptionally active or inactive in an exclusive manner in the two tissue samples (Fig. 1A,B, top schemes).	Enhancer	4C	Hi-C,qPCR	Consequently,under wild-type conditions, Hoxd4 is expressed only in proximal limb cells under the control of the T-DOM,while C-DOM Enhancers control Evx2 transcripts in dis_x0002_tal cells exclusively.	Hox-4,Hox-5,Ul,ulnaless	--	--	--	--	--	--	--	--	--	Hoxd
29236325	chr4	55859107	55860311	RAD21	Cohesin complex which contains four conserved subunits, RAD21, SMC1A, SMC3, and STAG, is implicated in the formation of a looping structure within chromosomes and is important for a variety of biological processes, such as chromosome segregation and DNA damage2,4-6.	human	bone marrow	Low throughput	AML1/ETO trans-activates c-KIT expression through the long range interaction between promoter and intronic enhancer	否	--	--	Kasumi-1 cells	E_02_0773	PCR,Luciferase Reporter Assay,ChIP-qPCR,ChIP-3C	Intriguingly, we also identified a DHS site located at 30 kb downstream of TSS, which was also enriched by p300 (GSE6284728) and thus defined as the intronic enhancer (Figure 2a).To verify whether these co-factors binding to the promoter and intron regions of cKIT, we performed ChIP-qPCR assays with a series of primers for these regions using t(8;21) positive Kasumi-1 cells (Figure 2c).	Enhancer	ChIP-3C	Luciferase Reporter Assay,ChIP-qPCR	"We firstly detected the luciferase activity of c-KIT promoter or promoter plus intronic enhancer in Kasumi-1 cells.As shown in Figure 4c, the activity of c-KIT promoter plus intronic enhancer (pGL3-c-KIT-P+I) was significantly higher than that of the c-KIT promoter (pGL3-c-KIT-P).The motif analysis (Figure 2b) as well as
the finding that the intronic enhance region increased the activity of c-KIT promoter prompt us to ask whether there exists an interaction between the promoter and intronic enhancer region of c-KIT. To demonstrate our speculation, we firstly performed ChIPqPCR experiments using antibodies of CTCF and a cohesion complex member, RAD21, in Kasumi-1 cell line.Secondly, to provide further evidence that looping occurs in vivo between promoter and enhancer, we performed ChIP combined chromosome conformation capture (ChIP-3C) assays in Kasumi-1 cells. 
"	C-Kit,CD117,MASTC,PBT,SCFR	The intronic Enhancer region of c-KIT prompts the transactivation of AML1/ETO to c-KIT.	Luciferase Reporter Assay,siRNA	We firstly detected the luciferase activity of c-KIT promoter or promoter plus intronic Enhancer in Kasumi-1 cells. As shown in Figure 4c, the activity of c-KIT promoter plus intronic Enhancer (pGL3-c-KIT-P+I) was significantly higher than that of the c-KIT promoter (pGL3-c-KIT-P). Further knockdown of AML1/ETO (Figure 4c) led to a dramatic decrease of the activity of both reporter plasmids (Figure 4b). Secondly, we induced AML1/ETO expression using PA in U937-AE cell line (Figure 4d) and measured the luciferase activity of the aforementioned plasmids before and after AML1/ETO induction. As shown in Figure 4e, the luciferase activity of all the reporter plasmids was increased after 48 hours of AML1/ETO induction. The activity of reporter plasmid that contained both c-KIT promoter and intronic Enhancer regions was significantly higher than that contain only c-KIT promoter region.	RUNX1	AML1,AML1-EVI-1,AMLCR1,CBF2alpha,CBFA2,EVI-1,PEBP2aB,PEBP2alpha	ChIP-3C	Knockdown of AML1/ETO led to a dramatic decrease of the activity of both reporter plasmids.Secondly, to provide further evidence that looping occurs in vivo between promoter and Enhancer, we performed ChIP combined chromosome conformation capture (ChIP-3C) assays in Kasumi-1 cells. Collectively, these findings suggest that AML1/ETO prompts the formation of DNA looping between the c-KIT promoter and intronic Enhancer. 	--	--	KIT
29236325	chr4	55859107	55860311	SMC1A	Cohesin complex which contains four conserved subunits, RAD21, SMC1A, SMC3, and STAG, is implicated in the formation of a looping structure within chromosomes and is important for a variety of biological processes, such as chromosome segregation and DNA damage2,4-6.	human	bone marrow	Low throughput	AML1/ETO trans-activates c-KIT expression through the long range interaction between promoter and intronic enhancer	否	--	--	Kasumi-1 cells	E_02_0773	PCR,Luciferase Reporter Assay,ChIP-qPCR,ChIP-3C	Intriguingly, we also identified a DHS site located at 30 kb downstream of TSS, which was also enriched by p300 (GSE6284728) and thus defined as the intronic enhancer (Figure 2a).To verify whether these co-factors binding to the promoter and intron regions of cKIT, we performed ChIP-qPCR assays with a series of primers for these regions using t(8;21) positive Kasumi-1 cells (Figure 2c).	Enhancer	ChIP-3C	Luciferase Reporter Assay,ChIP-qPCR	"We firstly detected the luciferase activity of c-KIT promoter or promoter plus intronic enhancer in Kasumi-1 cells.As shown in Figure 4c, the activity of c-KIT promoter plus intronic enhancer (pGL3-c-KIT-P+I) was significantly higher than that of the c-KIT promoter (pGL3-c-KIT-P).The motif analysis (Figure 2b) as well as
the finding that the intronic enhance region increased the activity of c-KIT promoter prompt us to ask whether there exists an interaction between the promoter and intronic enhancer region of c-KIT. To demonstrate our speculation, we firstly performed ChIPqPCR experiments using antibodies of CTCF and a cohesion complex member, RAD21, in Kasumi-1 cell line.Secondly, to provide further evidence that looping occurs in vivo between promoter and enhancer, we performed ChIP combined chromosome conformation capture (ChIP-3C) assays in Kasumi-1 cells. 
"	C-Kit,CD117,MASTC,PBT,SCFR	The intronic Enhancer region of c-KIT prompts the transactivation of AML1/ETO to c-KIT.	Luciferase Reporter Assay,siRNA	We firstly detected the luciferase activity of c-KIT promoter or promoter plus intronic Enhancer in Kasumi-1 cells. As shown in Figure 4c, the activity of c-KIT promoter plus intronic Enhancer (pGL3-c-KIT-P+I) was significantly higher than that of the c-KIT promoter (pGL3-c-KIT-P). Further knockdown of AML1/ETO (Figure 4c) led to a dramatic decrease of the activity of both reporter plasmids (Figure 4b). Secondly, we induced AML1/ETO expression using PA in U937-AE cell line (Figure 4d) and measured the luciferase activity of the aforementioned plasmids before and after AML1/ETO induction. As shown in Figure 4e, the luciferase activity of all the reporter plasmids was increased after 48 hours of AML1/ETO induction. The activity of reporter plasmid that contained both c-KIT promoter and intronic Enhancer regions was significantly higher than that contain only c-KIT promoter region.	RUNX1	AML1,AML1-EVI-1,AMLCR1,CBF2alpha,CBFA2,EVI-1,PEBP2aB,PEBP2alpha	ChIP-3C	Knockdown of AML1/ETO led to a dramatic decrease of the activity of both reporter plasmids.Secondly, to provide further evidence that looping occurs in vivo between promoter and Enhancer, we performed ChIP combined chromosome conformation capture (ChIP-3C) assays in Kasumi-1 cells. Collectively, these findings suggest that AML1/ETO prompts the formation of DNA looping between the c-KIT promoter and intronic Enhancer. 	--	--	KIT
29155818	chr13	28545205	28547205	CDX2	To validate the significance of this association, we investigated the impact of FOXA factors on structure and function of enhancers at the CDH1, CDX2 and EPHB3 genes.	human	colon	Low+High throughput	SNAIL1-mediated downregulation of FOXA proteins facilitates the inactivation of transcriptional enhancer elements at key epithelial genes in colorectal cancer cells	否	--	--	Human colorectal carcinoma cell	E_02_0774	ChIP-seq,ChIP,EMSA,Luciferase Reporter Assay	To identify candidate cis-regulatory elements targeted by FOXA factors, we performed literature search, interrogated the ECR browser for evolutionary conserved regions (ECRs), and integrated this information with the results of the FOXA1 and FOXA2 ChIP-seq analysis.Moreover, the ENCODE data base lists several FOXA1 ChIP-seq peaks at the CDH1 locus in different cell lines, especially in the second intron. Notably, at the +7.8 kb enhancer region a FOXA1 ChIP-seq signal overlapped with an ECR (Fig 5A). To find out if FOXA factors could be involved in the function of the intronic CDH1 enhancer in CRC cells, we performed ChIP analyses.	Enhancer	--	ChIP,Luciferase Reporter Assay	To test for binding of FOXA proteins at this site of the CDX2 locus in CRC cells we performed ChIP analyses. Indeed, this region was occupied by FOXA1 in LS174T and HT29 cells. Furthermore, FOXA3 was bound at the CDX2 +10.0 kb region in LS174T, SW480 and HT29 cells (Fig 5D). Even though binding did not correlate with CDX2 expression in the CRC cells (S10 Fig, panel B), this result suggests that FOXA proteins act upon a transcriptional enhancer at the CDX2 locus in CRC cells.To test the importance of the FOXA binding sites for CDH1, CDX2 and EPHB3 enhancer activity, we performed luciferase reporter assays in LS174T cells.	CDX-3,CDX2/AS,CDX3	--	--	--	FOXA1	HNF3A,TCF3A	EMSA,Luciferase Reporter Assay	EMSA to test for in vitro binding of FOXA1 and FOXA3 to the CDX2 +10.0 kb enhancer. (C) (Top) Scheme of the EPHB3 ?2.3 kb enhancer with its known transcription factor binding sites. TBE: TCF/LEF-binding element. (Bottom) EMSA to test for in vitro binding of FOXA1 and FOXA3 to the EPHB3 ?2.3 kb enhancer. (D, E, F) Luciferase reporter assay in LS174T cells with constructs covering the CDH1 (D), the CDX2 (E), and the EPHB3 (F) enhancer. Mutations of the respective FOX binding motifs are indicated by red crosses. Shown is the mean and SEM; n_x0015_3. RLA: relative luciferase activity. Statistical significance was calculated relative to the wild-type luciferase reporter constructs. 	--	--	CDX2
29155818	chr13	28545205	28547205	EPHB3	To validate the significance of this association, we investigated the impact of FOXA factors on structure and function of enhancers at the CDH1, CDX2 and EPHB3 genes.	human	colon	Low+High throughput	SNAIL1-mediated downregulation of FOXA proteins facilitates the inactivation of transcriptional enhancer elements at key epithelial genes in colorectal cancer cells	否	--	--	Human colorectal carcinoma cell	E_02_0774	ChIP-seq,ChIP,EMSA,Luciferase Reporter Assay	To identify candidate cis-regulatory elements targeted by FOXA factors, we performed literature search, interrogated the ECR browser for evolutionary conserved regions (ECRs), and integrated this information with the results of the FOXA1 and FOXA2 ChIP-seq analysis.Moreover, the ENCODE data base lists several FOXA1 ChIP-seq peaks at the CDH1 locus in different cell lines, especially in the second intron. Notably, at the +7.8 kb enhancer region a FOXA1 ChIP-seq signal overlapped with an ECR (Fig 5A). To find out if FOXA factors could be involved in the function of the intronic CDH1 enhancer in CRC cells, we performed ChIP analyses.	Enhancer	--	ChIP,Luciferase Reporter Assay	To test for binding of FOXA proteins at this site of the CDX2 locus in CRC cells we performed ChIP analyses. Indeed, this region was occupied by FOXA1 in LS174T and HT29 cells. Furthermore, FOXA3 was bound at the CDX2 +10.0 kb region in LS174T, SW480 and HT29 cells (Fig 5D). Even though binding did not correlate with CDX2 expression in the CRC cells (S10 Fig, panel B), this result suggests that FOXA proteins act upon a transcriptional enhancer at the CDX2 locus in CRC cells.To test the importance of the FOXA binding sites for CDH1, CDX2 and EPHB3 enhancer activity, we performed luciferase reporter assays in LS174T cells.	CDX-3,CDX2/AS,CDX3	--	--	--	FOXA1	HNF3A,TCF3A	EMSA,Luciferase Reporter Assay	EMSA to test for in vitro binding of FOXA1 and FOXA3 to the CDX2 +10.0 kb enhancer. (C) (Top) Scheme of the EPHB3 ?2.3 kb enhancer with its known transcription factor binding sites. TBE: TCF/LEF-binding element. (Bottom) EMSA to test for in vitro binding of FOXA1 and FOXA3 to the EPHB3 ?2.3 kb enhancer. (D, E, F) Luciferase reporter assay in LS174T cells with constructs covering the CDH1 (D), the CDX2 (E), and the EPHB3 (F) enhancer. Mutations of the respective FOX binding motifs are indicated by red crosses. Shown is the mean and SEM; n_x0015_3. RLA: relative luciferase activity. Statistical significance was calculated relative to the wild-type luciferase reporter constructs. 	--	--	CDX2
29151363	chr19	34845032	34847032	FOXA1	Motif enrichment analysis using HOMER [25] revealed that these enhancers are enriched for transcription fac_x0002_tor binding sites such as FOXA1, NKX3.1, and STAT3 (Additional file 4: Table S3).	human	prostate	Low+High throughput	Functional assessment of human enhancer activities using whole-genome STARR_x0002_sequencing	否	--	--	prostate cancer cell lines	E_02_0775	WHG-STARR-seq,ChIP-seq,Luciferase Reporter Assay,ATAC-seq,RNA-seq	In the current study, we use a human prostate cancer cell line, LNCaP as a model to perform whole human genome STARR-seq (WHG-STARR-seq) to reliably obtain an assessment of enhancer activity.Furthermore, these datasets can only identify putative enhancers based on TF and histone chromatin immunoprecipitation (ChIP-seq) data and therefore do not necessarily exhaustively define functional enhancers, leading to false negatives. In order to validate the function of the active enhancers determined by WHG-STARR-seq, we selected 15 regions for all activity measurements and measured their activity using traditional Renilla luciferase reporter assays.	Enhancer	--	ATAC-seq,mRNA-seq,WHG-STARR-seq	Following treatment with TSA, we performed assay for transposase accessible chromatin sequencing (ATAC-seq) and messenger RNA-sequencing (mRNA-seq) experiments to measure the genome-wide chromatic accessibility and gene expression levels, respectively.Genomic snapshot displaying the GPI locus region as detected by WHG-STARR-seq. There is a strong enhancer region approximately 10 kb upstream of GPI transcriptional start site and another weaker enhancer region in the 3’UTR of GPI. 	AMF,GNPI,NLK,PGI,PHI,SA-36,SA36	--	--	--	--	--	--	--	--	--	GPI
29149598	chr12	47471429	47487762	AMIGO2	Here we interrogated the transcrip_x0002_tional effects of BETi and identified AMIGO2, a trans_x0002_membrane molecule, as a BET target gene essential for melanoma cell survival.	human	connective tissue	Low+High throughput	Harnessing BET Inhibitor Sensitivity Reveals AMIGO2 as a Melanoma Survival Gene	否	--	--	SK-MEL-1 Cell	E_02_0776	ATAC-seq,ChIP-seq,Luciferase Reporter Assay,Transfection,CRISPR/Cas9	Using Assay for Transposase-Accessible Chromatin (ATAC)-seq (Buenrostro et al., 2013) and ChIP-seq for H3K4me1 and H3K27ac (Creyghton et al., 2010), we identified ~1,400 constituent enhancers within the SEs of melanoma cells (Table S5) and found them largely devoid of open chromatin, H3K27ac, and H3K4me1 in NHMs (Figures 5F and ?and5G).To test the functionality of the predicted enhancers (Figures 6B and ?and7A), we cloned E1–E5 upstream of a minimal promoter driving luciferase expression (Prescott et al., 2015) and trans-fected these constructs into SKmel147 cells. We next used CRISPR/Cas9 editing to individually delete the genomic regions containing E2–E3 and E4–E5.	Super-Enhancer	CRISPR/Cas9	Luciferase Reporter Assay	Schematic of AMIGO2 SE showing enhancers E1–E5 (B), deleted sequences for CRISPR-Cas9 editing (C), and DNA segments used for E3 luciferase assay (D). Luciferase reporter assays performed in SKmel147 cells for AMIGO2 enhancer elements E3A–C and E3A deleted for TF motifs (E3A-Del) 	ALI1,AMIGO-2,DEGA	--	--	--	FOSL2,TEAD4	FRA2，EFTR-2, RTEF1, TCF13L1, TEF-3, TEF3, TEFR-1, hRTEF-1B	Immunoblot	FOSL2 (left), TEAD4 (right), and AMIGO2 immunoblots of SKmel147 cells 96 hr post-transduction with shSCR or shFOSL2 (shF2 #1 and #2) and shSCR or shTEAD4+TEAD1 (shT4 #1+shT1 #1 and shT4 #2+shT1 #1). HSP90 and GAPDH were used as loading controls.	--	--	AMIGO2
29149598	chr12	47471429	47487762	ZBTB38	Silencing of HMGA2 showed the most significant prolif_x0002_eration defect. Four additional genes, AMIGO2, MED25, ZIC1, and ZBTB38, scored significantly (Figure 1E), functionally iden_x0002_tifying them as regulators of melanoma cell growth.	human	connective tissue	Low+High throughput	Harnessing BET Inhibitor Sensitivity Reveals AMIGO2 as a Melanoma Survival Gene	否	--	--	SK-MEL-1 Cell	E_02_0776	ATAC-seq,ChIP-seq,Luciferase Reporter Assay,Transfection,CRISPR/Cas9	Using Assay for Transposase-Accessible Chromatin (ATAC)-seq (Buenrostro et al., 2013) and ChIP-seq for H3K4me1 and H3K27ac (Creyghton et al., 2010), we identified ~1,400 constituent enhancers within the SEs of melanoma cells (Table S5) and found them largely devoid of open chromatin, H3K27ac, and H3K4me1 in NHMs (Figures 5F and ?and5G).To test the functionality of the predicted enhancers (Figures 6B and ?and7A), we cloned E1–E5 upstream of a minimal promoter driving luciferase expression (Prescott et al., 2015) and trans-fected these constructs into SKmel147 cells. We next used CRISPR/Cas9 editing to individually delete the genomic regions containing E2–E3 and E4–E5.	Super-Enhancer	CRISPR/Cas9	Luciferase Reporter Assay	Schematic of AMIGO2 SE showing enhancers E1–E5 (B), deleted sequences for CRISPR-Cas9 editing (C), and DNA segments used for E3 luciferase assay (D). Luciferase reporter assays performed in SKmel147 cells for AMIGO2 enhancer elements E3A–C and E3A deleted for TF motifs (E3A-Del) 	ALI1,AMIGO-2,DEGA	--	--	--	FOSL2,TEAD4	FRA2，EFTR-2, RTEF1, TCF13L1, TEF-3, TEF3, TEFR-1, hRTEF-1B	Immunoblot	FOSL2 (left), TEAD4 (right), and AMIGO2 immunoblots of SKmel147 cells 96 hr post-transduction with shSCR or shFOSL2 (shF2 #1 and #2) and shSCR or shTEAD4+TEAD1 (shT4 #1+shT1 #1 and shT4 #2+shT1 #1). HSP90 and GAPDH were used as loading controls.	--	--	AMIGO2
29141987	chr2	103887795	103888195	TBX21	Studies performed in T lymphocytes using the T box factor T BET (TBX21) demonstrated that amino acid residues in conserved binding pockets, which reside within the T box but face away from the DNA binding domain, are important for binding to RBBP5 (retinoblastoma binding protein 5), a protein within the TrxG/MLL (Trithorax group/MLL protein complexes) H3K4 methyltransferase complex, and for association with H3K27 demethylase activity, which is carried out by either KDM6A (UTX) or KDM6B (JMJD3) in vertebrates 7.	mouse		Low+High throughput	BRACHYURY directs histone acetylation to target loci during mesoderm development.	否	--	--	embryonic cell 	E_02_0033	ChIP-seq	We overlapped TBS with genome‐wide H3K4me1 peaks from T WT mesodermal cells and found the same trend of decreased H3K27ac within ±1 kb of TBS/H3K4me1 sites (Fig EV4E), suggesting that T functions to coordinate H3K27ac at putative enhancer regions throughout the genome, and may regulate the switch between poised H3K4me1(+) enhancers and active H3K27ac/H3K4me1(+) enhancer regions.	Enhancer	--	RT-qPCR,ChIP-qPCR,ChIP-seq	Both the ?70 enhancer and the TSS of Lmo2 display a decrease in H3K27ac in T Y88A mutant mesodermal cells, in the ChIP‐Seq data and confirmed by ChIP‐qPCR (Figs ?(Figs5A5A and B, and EV5A). We reasoned that T binding to the ?70 enhancer of Lmo2 may recruit permissive chromatin marks to the TSS to regulate expression, and that this regulation is disrupted in T Y88A mutant mesodermal cells.	Rbtn-2,Rbtn2,Rhom-2,Ttg2	--	--	--	T	Bra,D17Mit170,Low,Lr1,Tbxt,Tl2,Tl3,cou,me75,T	ChIP-seq,ChIP-qPCR	We performed a co-immunoprecipitation analysis from in vitrodifferentiated mesodermal cells and found an interaction between endogenous T and p300.Strikingly, loss of H3K27ac was found at TBS upstream of the T genomic locus itself by ChIP-Seq . We validated this decrease in H3K27ac at the T genomic locus by ChIP-qPCR in TY88A and TWT mesodermal cells differentiated in vitro.	--	--	Lmo2
29141987	chr2	103887795	103888195	RBBP5	Studies performed in T lymphocytes using the T box factor T BET (TBX21) demonstrated that amino acid residues in conserved binding pockets, which reside within the T box but face away from the DNA binding domain, are important for binding to RBBP5 (retinoblastoma binding protein 5), a protein within the TrxG/MLL (Trithorax group/MLL protein complexes) H3K4 methyltransferase complex, and for association with H3K27 demethylase activity, which is carried out by either KDM6A (UTX) or KDM6B (JMJD3) in vertebrates 7.	mouse		Low+High throughput	BRACHYURY directs histone acetylation to target loci during mesoderm development.	否	--	--	embryonic cell 	E_02_0033	ChIP-seq	We overlapped TBS with genome‐wide H3K4me1 peaks from T WT mesodermal cells and found the same trend of decreased H3K27ac within ±1 kb of TBS/H3K4me1 sites (Fig EV4E), suggesting that T functions to coordinate H3K27ac at putative enhancer regions throughout the genome, and may regulate the switch between poised H3K4me1(+) enhancers and active H3K27ac/H3K4me1(+) enhancer regions.	Enhancer	--	RT-qPCR,ChIP-qPCR,ChIP-seq	Both the ?70 enhancer and the TSS of Lmo2 display a decrease in H3K27ac in T Y88A mutant mesodermal cells, in the ChIP‐Seq data and confirmed by ChIP‐qPCR (Figs ?(Figs5A5A and B, and EV5A). We reasoned that T binding to the ?70 enhancer of Lmo2 may recruit permissive chromatin marks to the TSS to regulate expression, and that this regulation is disrupted in T Y88A mutant mesodermal cells.	Rbtn-2,Rbtn2,Rhom-2,Ttg2	--	--	--	T	Bra,D17Mit170,Low,Lr1,Tbxt,Tl2,Tl3,cou,me75,T	ChIP-seq,ChIP-qPCR	We performed a co-immunoprecipitation analysis from in vitrodifferentiated mesodermal cells and found an interaction between endogenous T and p300.Strikingly, loss of H3K27ac was found at TBS upstream of the T genomic locus itself by ChIP-Seq . We validated this decrease in H3K27ac at the T genomic locus by ChIP-qPCR in TY88A and TWT mesodermal cells differentiated in vitro.	--	--	Lmo2
29129929	chr6	91004796	91006944	ELK1	An active regulatory region within the BACH2 super-enhancer, under ELK1 control and differentially regulated upon B-cell activation and cellular divisions, helps integrate IL-2 signal.	human	blood	low throughput	IL-2 imprints human naive B cell fate towards plasma cell through ERK/ELK1-mediated BACH2 repression	否	--	--	B cell	E_02_0777	RT-PCR,ChIP-qPCR,Luciferase Reporter Assay	DNA immunoprecipitated by total ELK1 antibody or immunoglobulin G (IgG CTL) was amplified by real-time PCR using primers flanking the putative ELK1 binding site in BACH2 intron 1 (predicted BACH2 enhancer position), known ELK1 binding regions in MCL1, MYD88 and FOS genes, and negative control primers as a reference (negative site). ChIP analysis of histone modifications and p300 binding in IL-2-primed D3 B cells. We demonstrated an in vivo binding of ELK1 to this putative enhancer by chromatin immunoprecipitation followed by QPCR (ChIP-QPCR) in IL2-primed B cells collected at D3.	Enhancer	--	Luciferase Reporter Assay	We decided to detail the functional DNA regulatory sequence by luciferase reporter assay in the context of primary human naive B cell activation. The BACH2 proximal promoter41 (minPBACH2, ?725; +146) ligated upstream from the nano-luciferase coding sequence (NanoLuc) demonstrated a 4.2?±?0.2 (n?=?15) fold more transcriptional activity than the promoterless NanoLuc vector (pNL1.1), whatever the time point of B-cell electroporation (from D0 to D3). The enhancer region (+1265; +1493) was inserted in the native and reverse orientation downstream from the minPBACH2. 	BTBD25,IMD60	--	--	--	ELK1	ELK1	ChIP-qPCR	ChIP assay of the in vivo binding of ELK1 in IL-2-primed D3 B cells. DNA immunoprecipitated by total ELK1 antibody or immunoglobulin G (IgG CTL) was amplified by real-time PCR using primers flanking the putative ELK1 binding site in BACH2 intron 1 (predicted BACH2 enhancer position), known ELK1 binding regions in MCL1, MYD88 and FOS genes, and negative control primers as a reference (negative site). Means ± s.e.m. of four independent experiments.	--	--	BACH2
29091765	chr3	180728712	180730712	SOX2	In a human neural stem cell model of low_x0002_grade astrocytoma, Modrek et al. show that mutant IDH1 and loss of P53 and ATRX together block differentiation via disassociation of SOX2 from putative enhancers.	human	Nervous tissue	Low+High throughput	Low-Grade Astrocytoma Mutations in IDH1, P53, and ATRX Cooperate to Block Differentiation of Human Neural Stem Cells via Repression of SOX2	否	--	Low-grade astrocytomas	neuronal stem cell	E_02_0778	ChIP-seq,ChIP-qPCR,4C-seq,Hi-C	"To understand if loss of CTCF binding affects chromatin contacts at the SOX2 locus, we performed circularized chromosome conformation capture (4C-Seq)
using the SOX2 promoter as bait to identify genomic interactions that may regulate its expression (Figure 6B, S6B)."	Enhancer	4C-seq	Hi-C	"To understand if loss of CTCF binding affects chromatin contacts at the SOX2 locus, we performed circularized chromosome conformation capture (4C-Seq)
using the SOX2 promoter as bait to identify genomic interactions that may regulate its expression (Figure 6B, S6B).To see if this same pattern of chromatin contacts is maintained in other cell types, we examined the HiC profiles of hESCs, which express high levels of SOX2 , and IMR90 lung fibroblasts, which are low for SOX2These findings suggest that in LGA SOX2 downregulation is due to aberrant chromatin looping that results in disassociation of the SOX2 promoter from a downstream enhancer."	ANOP3,MCOPS	--	--	--	CTCF	MRD21	ChIP-qPCR	"To assess whether CTCF occupancy at these motifs had changed, we performed ChIP-qPCR for CTCF. Every site assayed had an 2-fold decrease in CTCF occupancy, supporting the hypothesis that DNA hypermethylation in 3-hit NSCs leads to reduced CTCF occupancy around.
the SOX2 locus."	--	--	SOX2
29091765	chr3	180728712	180730712	ATRX	Using in vitro growth assays, we found that two conditions, 1-hit and mutant IDH1 with ATRX knockdown, grew more slowly than the others (Figure 3A).	human	Nervous tissue	Low+High throughput	Low-Grade Astrocytoma Mutations in IDH1, P53, and ATRX Cooperate to Block Differentiation of Human Neural Stem Cells via Repression of SOX2	否	--	Low-grade astrocytomas	neuronal stem cell	E_02_0778	ChIP-seq,ChIP-qPCR,4C-seq,Hi-C	"To understand if loss of CTCF binding affects chromatin contacts at the SOX2 locus, we performed circularized chromosome conformation capture (4C-Seq)
using the SOX2 promoter as bait to identify genomic interactions that may regulate its expression (Figure 6B, S6B)."	Enhancer	4C-seq	Hi-C	"To understand if loss of CTCF binding affects chromatin contacts at the SOX2 locus, we performed circularized chromosome conformation capture (4C-Seq)
using the SOX2 promoter as bait to identify genomic interactions that may regulate its expression (Figure 6B, S6B).To see if this same pattern of chromatin contacts is maintained in other cell types, we examined the HiC profiles of hESCs, which express high levels of SOX2 , and IMR90 lung fibroblasts, which are low for SOX2These findings suggest that in LGA SOX2 downregulation is due to aberrant chromatin looping that results in disassociation of the SOX2 promoter from a downstream enhancer."	ANOP3,MCOPS	--	--	--	CTCF	MRD21	ChIP-qPCR	"To assess whether CTCF occupancy at these motifs had changed, we performed ChIP-qPCR for CTCF. Every site assayed had an 2-fold decrease in CTCF occupancy, supporting the hypothesis that DNA hypermethylation in 3-hit NSCs leads to reduced CTCF occupancy around.
the SOX2 locus."	--	--	SOX2
29091765	chr3	180728712	180730712	IDH1	To test how mutant IDH1 and loss of P53 and ATRX work together to promote gliomagenesis, we serially introduced an IDH1-mCherry fusion gene (R132H or wild-type or mCherry alone) into NSCs via a lentivirus (Figures 1B and 1C), generated a pure population by fluorescence-activated cell sorting (FACS) isolation, and added lentiviral shRNA against P53, followed by shRNA against ATRX (Figures 1B and 1C).	human	Nervous tissue	Low+High throughput	Low-Grade Astrocytoma Mutations in IDH1, P53, and ATRX Cooperate to Block Differentiation of Human Neural Stem Cells via Repression of SOX2	否	--	Low-grade astrocytomas	neuronal stem cell	E_02_0778	ChIP-seq,ChIP-qPCR,4C-seq,Hi-C	"To understand if loss of CTCF binding affects chromatin contacts at the SOX2 locus, we performed circularized chromosome conformation capture (4C-Seq)
using the SOX2 promoter as bait to identify genomic interactions that may regulate its expression (Figure 6B, S6B)."	Enhancer	4C-seq	Hi-C	"To understand if loss of CTCF binding affects chromatin contacts at the SOX2 locus, we performed circularized chromosome conformation capture (4C-Seq)
using the SOX2 promoter as bait to identify genomic interactions that may regulate its expression (Figure 6B, S6B).To see if this same pattern of chromatin contacts is maintained in other cell types, we examined the HiC profiles of hESCs, which express high levels of SOX2 , and IMR90 lung fibroblasts, which are low for SOX2These findings suggest that in LGA SOX2 downregulation is due to aberrant chromatin looping that results in disassociation of the SOX2 promoter from a downstream enhancer."	ANOP3,MCOPS	--	--	--	CTCF	MRD21	ChIP-qPCR	"To assess whether CTCF occupancy at these motifs had changed, we performed ChIP-qPCR for CTCF. Every site assayed had an 2-fold decrease in CTCF occupancy, supporting the hypothesis that DNA hypermethylation in 3-hit NSCs leads to reduced CTCF occupancy around.
the SOX2 locus."	--	--	SOX2
29078395	chr8	11564419	11614821	Il2ra	By deleting three STAT5 binding sites that mediate IL-2 induced chromatin looping at the Il2ra locus, we demonstrate that superenhancer elements cooperatively control gene expression. 	mouse		Low+High throughput	STAT5-mediated chromatin interactions in superenhancers activate IL-2 highly inducible genes: Functional dissection of the Il2ra gene locus.	否	--	--	T cell	E_02_0779	ChIP-seq,ChIA-PET	To clarify how distal enhancer elements within superenhancer loci form enhancer-promoter loops and chromatin interactions, we performed RNA Pol II-based chromatin interaction analysis by paired-end tag (ChIA-PET) sequencing (24, 25) using mouse CD4+ T cells that were preactivated by TCR stimulation (anti-CD3 plus anti-CD28) and then not treated or treated with IL-2 for 4 h.Interestingly, both H3K4me3 (blue peaks in Fig. 3, primarily at the promoter) and H3K27Ac (green peaks in Fig. 3, spanning the Il2ra superenhancer region; also shown in Fig. 1E) were strong after TCR preactivation and only modestly affected by stimulation with IL-2, in marked contrast to the changes in STAT5 binding and chromatin looping. 	Super-Enhancer	--	ChIP-seq,RNA-seq	As noted above, STAT5 and H3K27Ac are highly enriched at a subset of superenhancers, including at the Il2ra superenhancer (Fig. 1 A, B, and E), correlating with IL-2–induced gene expression (Fig. 2B and Fig. S1C). We also found extensive H3K27Ac and STAT5 binding at the human IL2RA locus (Fig. S2), analogous to the mouse Il2ra superenhancer, with significant conservation of some of the enhancer elements (Fig. S2).	CD25,Il2r,Ly-43	--	--	--	Stat5a,Stat3	AA959963,STAT5,1110034C02Rik,AW109958,Aprf	ChIP-seq,CRISPR/Cas9	Based on our genome-wide analysis of chromatin immunoprecipitation coupled to DNA sequencing (ChIP-Seq) profiles, we observed that STAT5-enriched Super-Enhancers spanned large genomic regions (average size of ～19 kb) and indeed were associated with high levels of H3K27Ac.	--	--	Il2ra
29042628	chr16	92625802	92627802	CTCF	ChIP-seq data of Rad21 (blue) and CTCF (pink) in MEL and CH12 cells were obtained from ENCODE51 and in HPC-7 cells from18,19.	mouse		Low+High throughput	A DNA Contact Map for the Mouse Runx1 Gene Identifies Novel Haematopoietic Enhancers.	否	--	Leukaemia	HPC-7 cell	E_02_0780	4C-seq,ChIP	4C-seq in HPC-7 cells using the P1 and P2 promoters and the +24 enhancer as ‘baits’ identified genomic interactions at Runx1 (Fig. 1a)	Enhancer	4C-seq	--	Strikingly, the +24 enhancer in particular forms many significant interactions outside the Runx1 domain (Fig. 1b,d). Many of these long-range interactions are with other genes or gene promoters on mouse chromosome 16 (Fig. 2). 	AML1,CBF-alpha-2,Cbfa2,Pebp2a2,Pebpa2b	known haematopoietic enhancers that are likely to be involved in regulating?Runx1?expression in haematopoietic progenitor cells.	DNase I Hypersensitivity Assay,4C-seq,Hi-C	These regions not only drive haematopoietic expression, but also physically connect with the Runx1-P1 promoter, lending confidence to the concept that they are bona fide regulators of Runx1 transcription.	--	--	--	--	--	--	Runx1
28991225	chr4	23811733	23994829	PPARGC1A	Energy produc_x0002_tion by mitochondria is partially controlled by the melanocyte_x0002_specific microphthalmia-associated transcription factor (MITF) and the transcriptional cofactor peroxisome proliferator-activated receptor-gamma coactivator-1α (PGC-1α, encoded by the PPARGC1A gene), which drive metabolic reprogramming in melanocytes.	human	tumour	Low+High throughput	Super-enhancers define a proliferative PGC-1α-expressing melanoma subgroup sensitive to BET inhibition	否	--	Melanoma	CHL-1 cell	E_02_0781	ChIP-seq	We performed chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) using antibodies against H3K27ac and BRD4. 	Super-Enhancer	--	ChIP-seq	We performed chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) using antibodies against H3K27ac and BRD4.	LEM6,PGC-1(alpha),PGC-1alpha,PGC-1v,PGC1,PGC1A,PPARGC1	BRD4 binding at super-enhancers that drive the expression of PGC-1α and SOX10	ChIP-seq,ChIP-qPCR	We provide evidence for a direct role of BRD4 binding at super-enhancers that drive the expression of PGC-1α and SOX10, a transcription factor involved in melanocyte development. 	--	--	--	--	--	--	PPARGC1A
28991225	chr4	23811733	23994829	BRD4	The bromodomain and extra-terminal domain (BET) family protein BRD4 promotes transcription elongation of a number of oncogenes and is essential in numerous tumor types.	human	tumour	Low+High throughput	Super-enhancers define a proliferative PGC-1α-expressing melanoma subgroup sensitive to BET inhibition	否	--	Melanoma	CHL-1 cell	E_02_0781	ChIP-seq	We performed chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) using antibodies against H3K27ac and BRD4. 	Super-Enhancer	--	ChIP-seq	We performed chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq) using antibodies against H3K27ac and BRD4.	LEM6,PGC-1(alpha),PGC-1alpha,PGC-1v,PGC1,PGC1A,PPARGC1	BRD4 binding at super-enhancers that drive the expression of PGC-1α and SOX10	ChIP-seq,ChIP-qPCR	We provide evidence for a direct role of BRD4 binding at super-enhancers that drive the expression of PGC-1α and SOX10, a transcription factor involved in melanocyte development. 	--	--	--	--	--	--	PPARGC1A
28982762	chr4	55449628	55461828	SOX2	Here, combining genetic, genomic, and imaging approaches, we characterize a complex long-range enhancer cluster governing Krüppel-like factor 4 (Klf4) expression in naïve pluripotency.Genome editing by CRISPR/Cas9 revealed that OCT4 and SOX2 safeguard an accessible chromatin neighborhood to assist the binding of other TFs/cofactors to the enhancer. 	mouse		low throughput	A dynamic interplay of enhancer elements regulates Klf4 expression in naïve pluripotency.	否	--	--	embryonic stem cell	E_02_0782	Luciferase Reporter Assay,3C	DNA fragments containing E1 and E2 specifically exhibited high transcriptional activity in na?ve state mESCs relative to primed EpiSCs as determined by transgene-driven luciferase assays, consistent with the Klf4 expression pattern in these two pluripotent cell types (Fig. 1B,C).To probe whether the putative enhancers E1 and E2 communicate with the Klf4 promoter ?55 kb away, we performed chromosome conformation capture (3C) assays to detect long-range interactions. For both E1 and E2, there was a significantly higher frequency of cross-linking to the Klf4 promoter in mESCs compared with EpiSCs (Fig. 1F), indicating that E1 and E2 spatially juxtapose the promoter in mESCs.	Enhancer	CRISPR/Cas9,3C	--	Additionally, biallelic deletion of either E1 or E2 by CRISPR/Cas9-mediated genome editing reduced Klf4 expression by ?70% and 85%, respectively, without significantly affecting the expression of an adjacent gene (Rad23b) or another pluripotency gene (Pou5f1) (Fig. 1E).Nevertheless, for the remainder of this report, we primarily discuss our findings regarding E1 and E2, as these two enhancers clearly represent dominant elements that regulate Klf4 expression in na?ve state mESCs.	EZF,Gklf,Zie	--	--	--	Oct4,Sox2,Stat3 	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,1110034C02Rik,AW109958,Aprf	ChIP-exo,CRISPR/Cas9,ChIP-qPCR	To validate the direct binding of these candidate TFs to the Klf4 Enhancers, we performed genome-wide high-resolution ChIP-exo experiments for SOX2, STAT3, and ESRRB in mESCs.Here, we probed whether the binding activities of OCT4, SOX2, ESRRB, and STAT3 at E2 are interdependent through ChIP-qPCR (ChIP combined with quantitative PCR) analysis following endogenous deletion of individual TF-binding sites.Peaks identified by ChIP-exo were consistent with peaks from previous ChIP-seq (ChIP combined with high-throughput sequcing) protocols (Supplemental Fig. S2B,C). As expected, we observed significant enrichment of all three TFs at the Klf4 enhancer cluster, particularly at E2 (Fig. 2D).	--	--	Klf4
28982762	chr4	55449628	55461828	Klf4	Here, combining genetic, genomic, and imaging approaches, we characterize a complex long-range enhancer cluster governing Krüppel-like factor 4 (Klf4) expression in naïve pluripotency.Genome editing by CRISPR/Cas9 revealed that OCT4 and SOX2 safeguard an accessible chromatin neighborhood to assist the binding of other TFs/cofactors to the enhancer. 	mouse		low throughput	A dynamic interplay of enhancer elements regulates Klf4 expression in naïve pluripotency.	否	--	--	embryonic stem cell	E_02_0782	Luciferase Reporter Assay,3C	DNA fragments containing E1 and E2 specifically exhibited high transcriptional activity in na?ve state mESCs relative to primed EpiSCs as determined by transgene-driven luciferase assays, consistent with the Klf4 expression pattern in these two pluripotent cell types (Fig. 1B,C).To probe whether the putative enhancers E1 and E2 communicate with the Klf4 promoter ?55 kb away, we performed chromosome conformation capture (3C) assays to detect long-range interactions. For both E1 and E2, there was a significantly higher frequency of cross-linking to the Klf4 promoter in mESCs compared with EpiSCs (Fig. 1F), indicating that E1 and E2 spatially juxtapose the promoter in mESCs.	Enhancer	CRISPR/Cas9,3C	--	Additionally, biallelic deletion of either E1 or E2 by CRISPR/Cas9-mediated genome editing reduced Klf4 expression by ?70% and 85%, respectively, without significantly affecting the expression of an adjacent gene (Rad23b) or another pluripotency gene (Pou5f1) (Fig. 1E).Nevertheless, for the remainder of this report, we primarily discuss our findings regarding E1 and E2, as these two enhancers clearly represent dominant elements that regulate Klf4 expression in na?ve state mESCs.	EZF,Gklf,Zie	--	--	--	Oct4,Sox2,Stat3 	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,1110034C02Rik,AW109958,Aprf	ChIP-exo,CRISPR/Cas9,ChIP-qPCR	To validate the direct binding of these candidate TFs to the Klf4 Enhancers, we performed genome-wide high-resolution ChIP-exo experiments for SOX2, STAT3, and ESRRB in mESCs.Here, we probed whether the binding activities of OCT4, SOX2, ESRRB, and STAT3 at E2 are interdependent through ChIP-qPCR (ChIP combined with quantitative PCR) analysis following endogenous deletion of individual TF-binding sites.Peaks identified by ChIP-exo were consistent with peaks from previous ChIP-seq (ChIP combined with high-throughput sequcing) protocols (Supplemental Fig. S2B,C). As expected, we observed significant enrichment of all three TFs at the Klf4 enhancer cluster, particularly at E2 (Fig. 2D).	--	--	Klf4
28973302	chr8	27455903	27456103	CLU	In this study, we aimed to investigate the functional significance of a clusterin intronic SNP, rs2279590 that has been associated with pseudoexfoliation (PEX), Alzheimer’s disease (AD), and diabetes.	human	kidney	Low throughput	Pseudoexfoliation and Alzheimer’s associated CLU risk variant, rs2279590 lies within an enhancer element and regulates CLU, EPHX2 and PTK2B gene expression.	是	rs2279590	Alzheimer's Disease	HEK-293 cells	E_02_0783	Luciferase Reporter Assay,CRISPR/Cas9,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	AAG4,APO-J,APOJ,CLI,CLU1,CLU2,KUB1,NA1/NA2,SGP-2,SGP2,SP-40,TRPM-2,TRPM2,CADTK,CAKB,FADK2,FAK2,PKB,PTK,PYK2,RAFTK	--	--	--	HSF1	HSTF1	EMSA,ChIP	"Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele ""A""constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.By binding to allele “A”, HSF1 abrogates the Enhancer effect of the locus as validated by reporter assays."	27456253	EMSA,ChIP	CLU
28973302	chr8	27455903	27456103	CLU	In this study, we aimed to investigate the functional significance of a clusterin intronic SNP, rs2279590 that has been associated with pseudoexfoliation (PEX), Alzheimer’s disease (AD), and diabetes.	human	kidney	Low throughput	Pseudoexfoliation and Alzheimer’s associated CLU risk variant, rs2279590 lies within an enhancer element and regulates CLU, EPHX2 and PTK2B gene expression.	是	rs2279590	Alzheimer's Disease	HEK-293 cells	E_02_0783	Luciferase Reporter Assay,CRISPR/Cas9,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	AAG4,APO-J,APOJ,CLI,CLU1,CLU2,KUB1,NA1/NA2,SGP-2,SGP2,SP-40,TRPM-2,TRPM2,CADTK,CAKB,FADK2,FAK2,PKB,PTK,PYK2,RAFTK	--	--	--	HSF1	HSTF1	EMSA,ChIP	"Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele ""A""constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.By binding to allele “A”, HSF1 abrogates the Enhancer effect of the locus as validated by reporter assays."	27456253	EMSA,ChIP	EPHX2
28973302	chr8	27455903	27456103	CLU	In this study, we aimed to investigate the functional significance of a clusterin intronic SNP, rs2279590 that has been associated with pseudoexfoliation (PEX), Alzheimer’s disease (AD), and diabetes.	human	kidney	Low throughput	Pseudoexfoliation and Alzheimer’s associated CLU risk variant, rs2279590 lies within an enhancer element and regulates CLU, EPHX2 and PTK2B gene expression.	是	rs2279590	Alzheimer's Disease	HEK-293 cells	E_02_0783	Luciferase Reporter Assay,CRISPR/Cas9,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	AAG4,APO-J,APOJ,CLI,CLU1,CLU2,KUB1,NA1/NA2,SGP-2,SGP2,SP-40,TRPM-2,TRPM2,CADTK,CAKB,FADK2,FAK2,PKB,PTK,PYK2,RAFTK	--	--	--	HSF1	HSTF1	EMSA,ChIP	"Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele ""A""constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.By binding to allele “A”, HSF1 abrogates the Enhancer effect of the locus as validated by reporter assays."	27456253	EMSA,ChIP	PTK2B
28973302	chr8	27455903	27456103	HSF1	Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.	human	kidney	Low throughput	Pseudoexfoliation and Alzheimer’s associated CLU risk variant, rs2279590 lies within an enhancer element and regulates CLU, EPHX2 and PTK2B gene expression.	是	rs2279590	Alzheimer's Disease	HEK-293 cells	E_02_0783	Luciferase Reporter Assay,CRISPR/Cas9,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	AAG4,APO-J,APOJ,CLI,CLU1,CLU2,KUB1,NA1/NA2,SGP-2,SGP2,SP-40,TRPM-2,TRPM2,CADTK,CAKB,FADK2,FAK2,PKB,PTK,PYK2,RAFTK	--	--	--	HSF1	HSTF1	EMSA,ChIP	"Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele ""A""constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.By binding to allele “A”, HSF1 abrogates the Enhancer effect of the locus as validated by reporter assays."	27456253	EMSA,ChIP	CLU
28973302	chr8	27455903	27456103	HSF1	Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.	human	kidney	Low throughput	Pseudoexfoliation and Alzheimer’s associated CLU risk variant, rs2279590 lies within an enhancer element and regulates CLU, EPHX2 and PTK2B gene expression.	是	rs2279590	Alzheimer's Disease	HEK-293 cells	E_02_0783	Luciferase Reporter Assay,CRISPR/Cas9,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	AAG4,APO-J,APOJ,CLI,CLU1,CLU2,KUB1,NA1/NA2,SGP-2,SGP2,SP-40,TRPM-2,TRPM2,CADTK,CAKB,FADK2,FAK2,PKB,PTK,PYK2,RAFTK	--	--	--	HSF1	HSTF1	EMSA,ChIP	"Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele ""A""constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.By binding to allele “A”, HSF1 abrogates the Enhancer effect of the locus as validated by reporter assays."	27456253	EMSA,ChIP	EPHX2
28973302	chr8	27455903	27456103	HSF1	Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.	human	kidney	Low throughput	Pseudoexfoliation and Alzheimer’s associated CLU risk variant, rs2279590 lies within an enhancer element and regulates CLU, EPHX2 and PTK2B gene expression.	是	rs2279590	Alzheimer's Disease	HEK-293 cells	E_02_0783	Luciferase Reporter Assay,CRISPR/Cas9,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	AAG4,APO-J,APOJ,CLI,CLU1,CLU2,KUB1,NA1/NA2,SGP-2,SGP2,SP-40,TRPM-2,TRPM2,CADTK,CAKB,FADK2,FAK2,PKB,PTK,PYK2,RAFTK	--	--	--	HSF1	HSTF1	EMSA,ChIP	"Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele ""A""constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.By binding to allele “A”, HSF1 abrogates the Enhancer effect of the locus as validated by reporter assays."	27456253	EMSA,ChIP	PTK2B
28973302	chr8	27455903	27456103	PTK2B	Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolase-2 (EPHX2); both of which have been previously associated with AD as risk factors.	human	kidney	Low throughput	Pseudoexfoliation and Alzheimer’s associated CLU risk variant, rs2279590 lies within an enhancer element and regulates CLU, EPHX2 and PTK2B gene expression.	是	rs2279590	Alzheimer's Disease	HEK-293 cells	E_02_0783	Luciferase Reporter Assay,CRISPR/Cas9,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	AAG4,APO-J,APOJ,CLI,CLU1,CLU2,KUB1,NA1/NA2,SGP-2,SGP2,SP-40,TRPM-2,TRPM2,CADTK,CAKB,FADK2,FAK2,PKB,PTK,PYK2,RAFTK	--	--	--	HSF1	HSTF1	EMSA,ChIP	"Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele ""A""constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.By binding to allele “A”, HSF1 abrogates the Enhancer effect of the locus as validated by reporter assays."	27456253	EMSA,ChIP	CLU
28973302	chr8	27455903	27456103	PTK2B	Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolase-2 (EPHX2); both of which have been previously associated with AD as risk factors.	human	kidney	Low throughput	Pseudoexfoliation and Alzheimer’s associated CLU risk variant, rs2279590 lies within an enhancer element and regulates CLU, EPHX2 and PTK2B gene expression.	是	rs2279590	Alzheimer's Disease	HEK-293 cells	E_02_0783	Luciferase Reporter Assay,CRISPR/Cas9,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	AAG4,APO-J,APOJ,CLI,CLU1,CLU2,KUB1,NA1/NA2,SGP-2,SGP2,SP-40,TRPM-2,TRPM2,CADTK,CAKB,FADK2,FAK2,PKB,PTK,PYK2,RAFTK	--	--	--	HSF1	HSTF1	EMSA,ChIP	"Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele ""A""constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.By binding to allele “A”, HSF1 abrogates the Enhancer effect of the locus as validated by reporter assays."	27456253	EMSA,ChIP	EPHX2
28973302	chr8	27455903	27456103	PTK2B	Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolase-2 (EPHX2); both of which have been previously associated with AD as risk factors.	human	kidney	Low throughput	Pseudoexfoliation and Alzheimer’s associated CLU risk variant, rs2279590 lies within an enhancer element and regulates CLU, EPHX2 and PTK2B gene expression.	是	rs2279590	Alzheimer's Disease	HEK-293 cells	E_02_0783	Luciferase Reporter Assay,CRISPR/Cas9,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	AAG4,APO-J,APOJ,CLI,CLU1,CLU2,KUB1,NA1/NA2,SGP-2,SGP2,SP-40,TRPM-2,TRPM2,CADTK,CAKB,FADK2,FAK2,PKB,PTK,PYK2,RAFTK	--	--	--	HSF1	HSTF1	EMSA,ChIP	"Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele ""A""constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.By binding to allele “A”, HSF1 abrogates the Enhancer effect of the locus as validated by reporter assays."	27456253	EMSA,ChIP	PTK2B
28973302	chr8	27455903	27456103	EPHX2	Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolase-2 (EPHX2); both of which have been previously associated with AD as risk factors.	human	kidney	Low throughput	Pseudoexfoliation and Alzheimer’s associated CLU risk variant, rs2279590 lies within an enhancer element and regulates CLU, EPHX2 and PTK2B gene expression.	是	rs2279590	Alzheimer's Disease	HEK-293 cells	E_02_0783	Luciferase Reporter Assay,CRISPR/Cas9,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	AAG4,APO-J,APOJ,CLI,CLU1,CLU2,KUB1,NA1/NA2,SGP-2,SGP2,SP-40,TRPM-2,TRPM2,CADTK,CAKB,FADK2,FAK2,PKB,PTK,PYK2,RAFTK	--	--	--	HSF1	HSTF1	EMSA,ChIP	"Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele ""A""constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.By binding to allele “A”, HSF1 abrogates the Enhancer effect of the locus as validated by reporter assays."	27456253	EMSA,ChIP	CLU
28973302	chr8	27455903	27456103	EPHX2	Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolase-2 (EPHX2); both of which have been previously associated with AD as risk factors.	human	kidney	Low throughput	Pseudoexfoliation and Alzheimer’s associated CLU risk variant, rs2279590 lies within an enhancer element and regulates CLU, EPHX2 and PTK2B gene expression.	是	rs2279590	Alzheimer's Disease	HEK-293 cells	E_02_0783	Luciferase Reporter Assay,CRISPR/Cas9,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	AAG4,APO-J,APOJ,CLI,CLU1,CLU2,KUB1,NA1/NA2,SGP-2,SGP2,SP-40,TRPM-2,TRPM2,CADTK,CAKB,FADK2,FAK2,PKB,PTK,PYK2,RAFTK	--	--	--	HSF1	HSTF1	EMSA,ChIP	"Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele ""A""constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.By binding to allele “A”, HSF1 abrogates the Enhancer effect of the locus as validated by reporter assays."	27456253	EMSA,ChIP	EPHX2
28973302	chr8	27455903	27456103	EPHX2	Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolase-2 (EPHX2); both of which have been previously associated with AD as risk factors.	human	kidney	Low throughput	Pseudoexfoliation and Alzheimer’s associated CLU risk variant, rs2279590 lies within an enhancer element and regulates CLU, EPHX2 and PTK2B gene expression.	是	rs2279590	Alzheimer's Disease	HEK-293 cells	E_02_0783	Luciferase Reporter Assay,CRISPR/Cas9,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,EMSA,ChIP	We have previously shown that the alleles at rs2279590 differentially regulate clusterin (CLU) gene expression in lens capsule tissues. This polymorphism resides in an active regulatory region marked by H3K27Ac and DNase I hypersensitive site and is an eQTL for CLU expression. Here, we report the presence of an enhancer element in surrounding region of rs2279590. Deletion of a 115 base pair intronic region flanking the rs2279590 variant through CRISPRB Cas9 genome editing in HEK293 cells demonstrated a decreased clusterin gene expression. Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele “A” constitutes a transcription factor binding site for heat shock factorB1 (HSF1) but not with allele “G”. By binding to allele “A”, HSF1 abrogates the enhancer effect of the locus as validated by reporter assays. Interestingly, rs2279590 locus have a widespread enhancer effect on two nearby genes, Protein tyrosine kinase 2 beta (PTK2B) and epoxide hydrolaseB2 (EPHX2); both of which have been previously associated with AD as risk factors.	AAG4,APO-J,APOJ,CLI,CLU1,CLU2,KUB1,NA1/NA2,SGP-2,SGP2,SP-40,TRPM-2,TRPM2,CADTK,CAKB,FADK2,FAK2,PKB,PTK,PYK2,RAFTK	--	--	--	HSF1	HSTF1	EMSA,ChIP	"Electrophoretic mobility shift and chromatin immunoprecipitation assays show that rs2279590 with allele ""A""constitutes a transcription factor binding site for heat shock factor-1 (HSF1) but not with allele “G”.By binding to allele “A”, HSF1 abrogates the Enhancer effect of the locus as validated by reporter assays."	27456253	EMSA,ChIP	PTK2B
28916725	chr2	226998914	227004586	KLF4	Kruppel-like factor (KLF) motifs were enriched in corneal epithelial enhancers, consistent with the important roles of KLF4 and KLF5 in promoting corneal epithelial differentiation.	human	Epithelial tissues	Low+High throughput	Characterization of enhancers and the role of the transcription factor KLF7 in regulating corneal epithelial differentiation	是	rs6758183	--	Corneal epithelial cell	E_02_0784	Luciferase Reporter Assay,ChIP-seq	"Because of their importance in controlling cell type–specific gene expression, we also defined SEs, using the strength of the H3K27ac mark as described previously (5, 6). We identified 1154 SEs and 12,424 TEs in corneal epithelial cells as well as 76,205 distal regulatory regions, marked by H3K4me1 alone (Fig. 1A).
As expected, the majority of enhancers was found at distal sites in the genome rather than in proximal promoters (Fig. 1B). Although TEs showed a trend toward being localized near genes, SEs were even more strongly enriched near genes; most SEs were found within 50 kb of a transcriptional start site.Together, these data indicate that most epithelial distal regulatory regions are common to multiple epithelial cell types, differing only in the type of enhancer and/or the level of enhancer activity, as indicated by the activation mark H3K27Ac (Fig. 2C)."	Enhancer	--	ChIA-PET	As insulin signaling is important for growth and development of both the corneal epithelium and the stroma, IRS1 is a candidate target for the enhancer containing rs6758183. Consistent with this possibility, in previously published siRNA data for EHF in corneal epithelial cells, we found that knockdown of EHF caused a small but significant increase in IRS1 gene expression (Figure 7G) (18). Together, these data suggest EHF regulates IRS1 through binding to the rs6758183 enhancer and that disruption of the EHF motif causes reduced affinity of EHF for this site, resulting in aberrant IRS1 expression during corneal development. 	HIRS-1	--	--	--	EHF	ESE3, ESE3B, ESEJ	ChIP,siRNA	"We hypothesized that these SNP variants could disrupt transcription factor binding, altering enhancer activity for each allele. At rs6758183, the disease associated A allele increased the strength of a SMAD motif, and decreased the strength of an ETS motif (Figure 7D).
Using ChIP, we found that EHF bound to the WT allele of rs6758183, suggesting disruption of EHF binding by the SNP could result in the observed differences in enhancer activity (Figure 7F). Intriguingly, the WT version of the SNP showed less enhancer activity than the mutant, suggesting EHF binding acts to repress the enhancer region. When this binding is lost, the enhancer becomes overactive, a change that could result in growth imbalances that cause alterations in the curvature and refractive power of the cornea. 
Consistent with this possibility, in previously published siRNA data for EHF in corneal epithelial cells, we found that knockdown of EHF caused a small but significant increase in IRS1 gene expression (Figure 7G) (18). Together, these data suggest EHF regulates IRS1 through binding to the rs6758183 enhancer and that disruption of the EHF motif causes reduced affinity of EHF for this site, resulting in aberrant IRS1 expression during corneal development. "	226136270	Luciferase Reporter Assay	IRS1
28916725	chr2	226998914	227004586	KLF5	Kruppel-like factor (KLF) motifs were enriched in corneal epithelial enhancers, consistent with the important roles of KLF4 and KLF5 in promoting corneal epithelial differentiation.	human	Epithelial tissues	Low+High throughput	Characterization of enhancers and the role of the transcription factor KLF7 in regulating corneal epithelial differentiation	是	rs6758183	--	Corneal epithelial cell	E_02_0784	Luciferase Reporter Assay,ChIP-seq	"Because of their importance in controlling cell type–specific gene expression, we also defined SEs, using the strength of the H3K27ac mark as described previously (5, 6). We identified 1154 SEs and 12,424 TEs in corneal epithelial cells as well as 76,205 distal regulatory regions, marked by H3K4me1 alone (Fig. 1A).
As expected, the majority of enhancers was found at distal sites in the genome rather than in proximal promoters (Fig. 1B). Although TEs showed a trend toward being localized near genes, SEs were even more strongly enriched near genes; most SEs were found within 50 kb of a transcriptional start site.Together, these data indicate that most epithelial distal regulatory regions are common to multiple epithelial cell types, differing only in the type of enhancer and/or the level of enhancer activity, as indicated by the activation mark H3K27Ac (Fig. 2C)."	Enhancer	--	ChIA-PET	As insulin signaling is important for growth and development of both the corneal epithelium and the stroma, IRS1 is a candidate target for the enhancer containing rs6758183. Consistent with this possibility, in previously published siRNA data for EHF in corneal epithelial cells, we found that knockdown of EHF caused a small but significant increase in IRS1 gene expression (Figure 7G) (18). Together, these data suggest EHF regulates IRS1 through binding to the rs6758183 enhancer and that disruption of the EHF motif causes reduced affinity of EHF for this site, resulting in aberrant IRS1 expression during corneal development. 	HIRS-1	--	--	--	EHF	ESE3, ESE3B, ESEJ	ChIP,siRNA	"We hypothesized that these SNP variants could disrupt transcription factor binding, altering enhancer activity for each allele. At rs6758183, the disease associated A allele increased the strength of a SMAD motif, and decreased the strength of an ETS motif (Figure 7D).
Using ChIP, we found that EHF bound to the WT allele of rs6758183, suggesting disruption of EHF binding by the SNP could result in the observed differences in enhancer activity (Figure 7F). Intriguingly, the WT version of the SNP showed less enhancer activity than the mutant, suggesting EHF binding acts to repress the enhancer region. When this binding is lost, the enhancer becomes overactive, a change that could result in growth imbalances that cause alterations in the curvature and refractive power of the cornea. 
Consistent with this possibility, in previously published siRNA data for EHF in corneal epithelial cells, we found that knockdown of EHF caused a small but significant increase in IRS1 gene expression (Figure 7G) (18). Together, these data suggest EHF regulates IRS1 through binding to the rs6758183 enhancer and that disruption of the EHF motif causes reduced affinity of EHF for this site, resulting in aberrant IRS1 expression during corneal development. "	226136270	Luciferase Reporter Assay	IRS1
28916725	chr2	226998914	227004586	PAX6	An SE is located directly over the PAX6 gene body and three TEs are found upstream and downstream of the gene, in regions that have been linked to the regulation of PAX6 mRNA expression (17), suggesting that both TEs and an SE regulate this gene (Figure 1C).	human	Epithelial tissues	Low+High throughput	Characterization of enhancers and the role of the transcription factor KLF7 in regulating corneal epithelial differentiation	是	rs6758183	--	Corneal epithelial cell	E_02_0784	Luciferase Reporter Assay,ChIP-seq	"Because of their importance in controlling cell type–specific gene expression, we also defined SEs, using the strength of the H3K27ac mark as described previously (5, 6). We identified 1154 SEs and 12,424 TEs in corneal epithelial cells as well as 76,205 distal regulatory regions, marked by H3K4me1 alone (Fig. 1A).
As expected, the majority of enhancers was found at distal sites in the genome rather than in proximal promoters (Fig. 1B). Although TEs showed a trend toward being localized near genes, SEs were even more strongly enriched near genes; most SEs were found within 50 kb of a transcriptional start site.Together, these data indicate that most epithelial distal regulatory regions are common to multiple epithelial cell types, differing only in the type of enhancer and/or the level of enhancer activity, as indicated by the activation mark H3K27Ac (Fig. 2C)."	Enhancer	--	ChIA-PET	As insulin signaling is important for growth and development of both the corneal epithelium and the stroma, IRS1 is a candidate target for the enhancer containing rs6758183. Consistent with this possibility, in previously published siRNA data for EHF in corneal epithelial cells, we found that knockdown of EHF caused a small but significant increase in IRS1 gene expression (Figure 7G) (18). Together, these data suggest EHF regulates IRS1 through binding to the rs6758183 enhancer and that disruption of the EHF motif causes reduced affinity of EHF for this site, resulting in aberrant IRS1 expression during corneal development. 	HIRS-1	--	--	--	EHF	ESE3, ESE3B, ESEJ	ChIP,siRNA	"We hypothesized that these SNP variants could disrupt transcription factor binding, altering enhancer activity for each allele. At rs6758183, the disease associated A allele increased the strength of a SMAD motif, and decreased the strength of an ETS motif (Figure 7D).
Using ChIP, we found that EHF bound to the WT allele of rs6758183, suggesting disruption of EHF binding by the SNP could result in the observed differences in enhancer activity (Figure 7F). Intriguingly, the WT version of the SNP showed less enhancer activity than the mutant, suggesting EHF binding acts to repress the enhancer region. When this binding is lost, the enhancer becomes overactive, a change that could result in growth imbalances that cause alterations in the curvature and refractive power of the cornea. 
Consistent with this possibility, in previously published siRNA data for EHF in corneal epithelial cells, we found that knockdown of EHF caused a small but significant increase in IRS1 gene expression (Figure 7G) (18). Together, these data suggest EHF regulates IRS1 through binding to the rs6758183 enhancer and that disruption of the EHF motif causes reduced affinity of EHF for this site, resulting in aberrant IRS1 expression during corneal development. "	226136270	Luciferase Reporter Assay	IRS1
28916725	chr2	226998914	227004586	WNT7A	Highly ranked SEs were linked to genes with crucial roles in corneal epithelial identity, including PAX6, WNT7A, and MIR205HG (Figure 1E)	human	Epithelial tissues	Low+High throughput	Characterization of enhancers and the role of the transcription factor KLF7 in regulating corneal epithelial differentiation	是	rs6758183	--	Corneal epithelial cell	E_02_0784	Luciferase Reporter Assay,ChIP-seq	"Because of their importance in controlling cell type–specific gene expression, we also defined SEs, using the strength of the H3K27ac mark as described previously (5, 6). We identified 1154 SEs and 12,424 TEs in corneal epithelial cells as well as 76,205 distal regulatory regions, marked by H3K4me1 alone (Fig. 1A).
As expected, the majority of enhancers was found at distal sites in the genome rather than in proximal promoters (Fig. 1B). Although TEs showed a trend toward being localized near genes, SEs were even more strongly enriched near genes; most SEs were found within 50 kb of a transcriptional start site.Together, these data indicate that most epithelial distal regulatory regions are common to multiple epithelial cell types, differing only in the type of enhancer and/or the level of enhancer activity, as indicated by the activation mark H3K27Ac (Fig. 2C)."	Enhancer	--	ChIA-PET	As insulin signaling is important for growth and development of both the corneal epithelium and the stroma, IRS1 is a candidate target for the enhancer containing rs6758183. Consistent with this possibility, in previously published siRNA data for EHF in corneal epithelial cells, we found that knockdown of EHF caused a small but significant increase in IRS1 gene expression (Figure 7G) (18). Together, these data suggest EHF regulates IRS1 through binding to the rs6758183 enhancer and that disruption of the EHF motif causes reduced affinity of EHF for this site, resulting in aberrant IRS1 expression during corneal development. 	HIRS-1	--	--	--	EHF	ESE3, ESE3B, ESEJ	ChIP,siRNA	"We hypothesized that these SNP variants could disrupt transcription factor binding, altering enhancer activity for each allele. At rs6758183, the disease associated A allele increased the strength of a SMAD motif, and decreased the strength of an ETS motif (Figure 7D).
Using ChIP, we found that EHF bound to the WT allele of rs6758183, suggesting disruption of EHF binding by the SNP could result in the observed differences in enhancer activity (Figure 7F). Intriguingly, the WT version of the SNP showed less enhancer activity than the mutant, suggesting EHF binding acts to repress the enhancer region. When this binding is lost, the enhancer becomes overactive, a change that could result in growth imbalances that cause alterations in the curvature and refractive power of the cornea. 
Consistent with this possibility, in previously published siRNA data for EHF in corneal epithelial cells, we found that knockdown of EHF caused a small but significant increase in IRS1 gene expression (Figure 7G) (18). Together, these data suggest EHF regulates IRS1 through binding to the rs6758183 enhancer and that disruption of the EHF motif causes reduced affinity of EHF for this site, resulting in aberrant IRS1 expression during corneal development. "	226136270	Luciferase Reporter Assay	IRS1
28916223	chr12	56330413	56330909	COL1A1	Pharmacological inhibition of DGKA reduced fibroblast activation markers like expression of col_x0002_lagen 1A1 (COL1A1) and the myofibroblast marker alpha smooth muscle actin (ACTA2), further supporting its involvement in profi_x0002_brotic processes.	human	connective tissue	Low+High throughput	BET-bromodomain inhibitors modulate epigenetic patterns at the diacylglycerol kinase alpha enhancer associated with radiation-induced fibrosis	否	--	Fibrotic Disease	A9 cell	E_02_0785	ChIP-seq,PCR,ChIP	Analysis of publicly available data from the ENCODE project [18] (Fig. 1A), as well as our own ChIP experiments [8] revealed that the DGKA DMR carries H3K27ac. ChIP showed that JQ1 reduced the deposition of H3K27ac levels specifically at the DGKA enhancer site(DMR), but did not affect the upstream DGKA promoter sites 1 and 2 (Fig. 2C). 	Enhancer	--	ChIP,PCR	"From various NHDFs,we selected three fibroblast lines (data not shown) with significant
differences in DGKA DNA methylation at the DGKA enhancer site(Fig. 1A) and inducible DGKA mRNA expression (Fig. 1B). Increased DNA methylation at the DGKA enhancer was associated with a lack of DGKA induction after exposure to bleomycin (Fig. 1B, Fibroblast3), confirming our previous findings in numerous patient-derived NHDF.EGR1 was significantly induced in two NHDF showing high DGKA induction (Fig. 1C)."	DAGK,DAGK1,DGK-alpha	--	--	--	EGR1	AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225	qPCR	Relative DGKA (B) and EGR1 (C) mRNA expression levels in three individual NHDF exposed to bleomycin (40 mM) or vehicle control (DMSO) for 48 h. *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.0001, n.s. not significant.	--	--	DGKA
28916223	chr12	56330413	56330909	ACTA2	Pharmacological inhibition of DGKA reduced fibroblast activation markers like expression of col_x0002_lagen 1A1 (COL1A1) and the myofibroblast marker alpha smooth muscle actin (ACTA2), further supporting its involvement in profi_x0002_brotic processes.	human	connective tissue	Low+High throughput	BET-bromodomain inhibitors modulate epigenetic patterns at the diacylglycerol kinase alpha enhancer associated with radiation-induced fibrosis	否	--	Fibrotic Disease	A9 cell	E_02_0785	ChIP-seq,PCR,ChIP	Analysis of publicly available data from the ENCODE project [18] (Fig. 1A), as well as our own ChIP experiments [8] revealed that the DGKA DMR carries H3K27ac. ChIP showed that JQ1 reduced the deposition of H3K27ac levels specifically at the DGKA enhancer site(DMR), but did not affect the upstream DGKA promoter sites 1 and 2 (Fig. 2C). 	Enhancer	--	ChIP,PCR	"From various NHDFs,we selected three fibroblast lines (data not shown) with significant
differences in DGKA DNA methylation at the DGKA enhancer site(Fig. 1A) and inducible DGKA mRNA expression (Fig. 1B). Increased DNA methylation at the DGKA enhancer was associated with a lack of DGKA induction after exposure to bleomycin (Fig. 1B, Fibroblast3), confirming our previous findings in numerous patient-derived NHDF.EGR1 was significantly induced in two NHDF showing high DGKA induction (Fig. 1C)."	DAGK,DAGK1,DGK-alpha	--	--	--	EGR1	AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225	qPCR	Relative DGKA (B) and EGR1 (C) mRNA expression levels in three individual NHDF exposed to bleomycin (40 mM) or vehicle control (DMSO) for 48 h. *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.0001, n.s. not significant.	--	--	DGKA
28916223	chr12	56330413	56330909	ACTB	Data were normalized to housekeeping gene expression values of beta actin (ACTB), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), hypoxan_x0002_thine phosphoribosyltransferase 1 (HPRT1) and succinate dehy_x0002_drogenase complex subunit A (SDHA) and the average of the normalized expression values was taken for individual samples. Murine mRNA expression was normalized to Actb, Hprt1 and TATA box binding protein (Tbp) signals.	human	connective tissue	Low+High throughput	BET-bromodomain inhibitors modulate epigenetic patterns at the diacylglycerol kinase alpha enhancer associated with radiation-induced fibrosis	否	--	Fibrotic Disease	A9 cell	E_02_0785	ChIP-seq,PCR,ChIP	Analysis of publicly available data from the ENCODE project [18] (Fig. 1A), as well as our own ChIP experiments [8] revealed that the DGKA DMR carries H3K27ac. ChIP showed that JQ1 reduced the deposition of H3K27ac levels specifically at the DGKA enhancer site(DMR), but did not affect the upstream DGKA promoter sites 1 and 2 (Fig. 2C). 	Enhancer	--	ChIP,PCR	"From various NHDFs,we selected three fibroblast lines (data not shown) with significant
differences in DGKA DNA methylation at the DGKA enhancer site(Fig. 1A) and inducible DGKA mRNA expression (Fig. 1B). Increased DNA methylation at the DGKA enhancer was associated with a lack of DGKA induction after exposure to bleomycin (Fig. 1B, Fibroblast3), confirming our previous findings in numerous patient-derived NHDF.EGR1 was significantly induced in two NHDF showing high DGKA induction (Fig. 1C)."	DAGK,DAGK1,DGK-alpha	--	--	--	EGR1	AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225	qPCR	Relative DGKA (B) and EGR1 (C) mRNA expression levels in three individual NHDF exposed to bleomycin (40 mM) or vehicle control (DMSO) for 48 h. *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.0001, n.s. not significant.	--	--	DGKA
28916223	chr12	56330413	56330909	SDHA	Data were normalized to housekeeping gene expression values of beta actin (ACTB), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), hypoxan_x0002_thine phosphoribosyltransferase 1 (HPRT1) and succinate dehy_x0002_drogenase complex subunit A (SDHA) and the average of the normalized expression values was taken for individual samples. Murine mRNA expression was normalized to Actb, Hprt1 and TATA box binding protein (Tbp) signals.	human	connective tissue	Low+High throughput	BET-bromodomain inhibitors modulate epigenetic patterns at the diacylglycerol kinase alpha enhancer associated with radiation-induced fibrosis	否	--	Fibrotic Disease	A9 cell	E_02_0785	ChIP-seq,PCR,ChIP	Analysis of publicly available data from the ENCODE project [18] (Fig. 1A), as well as our own ChIP experiments [8] revealed that the DGKA DMR carries H3K27ac. ChIP showed that JQ1 reduced the deposition of H3K27ac levels specifically at the DGKA enhancer site(DMR), but did not affect the upstream DGKA promoter sites 1 and 2 (Fig. 2C). 	Enhancer	--	ChIP,PCR	"From various NHDFs,we selected three fibroblast lines (data not shown) with significant
differences in DGKA DNA methylation at the DGKA enhancer site(Fig. 1A) and inducible DGKA mRNA expression (Fig. 1B). Increased DNA methylation at the DGKA enhancer was associated with a lack of DGKA induction after exposure to bleomycin (Fig. 1B, Fibroblast3), confirming our previous findings in numerous patient-derived NHDF.EGR1 was significantly induced in two NHDF showing high DGKA induction (Fig. 1C)."	DAGK,DAGK1,DGK-alpha	--	--	--	EGR1	AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225	qPCR	Relative DGKA (B) and EGR1 (C) mRNA expression levels in three individual NHDF exposed to bleomycin (40 mM) or vehicle control (DMSO) for 48 h. *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.0001, n.s. not significant.	--	--	DGKA
28916223	chr12	56330413	56330909	HPRT1	Data were normalized to housekeeping gene expression values of beta actin (ACTB), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), hypoxan_x0002_thine phosphoribosyltransferase 1 (HPRT1) and succinate dehy_x0002_drogenase complex subunit A (SDHA) and the average of the normalized expression values was taken for individual samples. Murine mRNA expression was normalized to Actb, Hprt1 and TATA box binding protein (Tbp) signals.	human	connective tissue	Low+High throughput	BET-bromodomain inhibitors modulate epigenetic patterns at the diacylglycerol kinase alpha enhancer associated with radiation-induced fibrosis	否	--	Fibrotic Disease	A9 cell	E_02_0785	ChIP-seq,PCR,ChIP	Analysis of publicly available data from the ENCODE project [18] (Fig. 1A), as well as our own ChIP experiments [8] revealed that the DGKA DMR carries H3K27ac. ChIP showed that JQ1 reduced the deposition of H3K27ac levels specifically at the DGKA enhancer site(DMR), but did not affect the upstream DGKA promoter sites 1 and 2 (Fig. 2C). 	Enhancer	--	ChIP,PCR	"From various NHDFs,we selected three fibroblast lines (data not shown) with significant
differences in DGKA DNA methylation at the DGKA enhancer site(Fig. 1A) and inducible DGKA mRNA expression (Fig. 1B). Increased DNA methylation at the DGKA enhancer was associated with a lack of DGKA induction after exposure to bleomycin (Fig. 1B, Fibroblast3), confirming our previous findings in numerous patient-derived NHDF.EGR1 was significantly induced in two NHDF showing high DGKA induction (Fig. 1C)."	DAGK,DAGK1,DGK-alpha	--	--	--	EGR1	AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225	qPCR	Relative DGKA (B) and EGR1 (C) mRNA expression levels in three individual NHDF exposed to bleomycin (40 mM) or vehicle control (DMSO) for 48 h. *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.0001, n.s. not significant.	--	--	DGKA
28916223	chr12	56330413	56330909	GAPDH	Data were normalized to housekeeping gene expression values of beta actin (ACTB), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), hypoxan_x0002_thine phosphoribosyltransferase 1 (HPRT1) and succinate dehy_x0002_drogenase complex subunit A (SDHA) and the average of the normalized expression values was taken for individual samples. Murine mRNA expression was normalized to Actb, Hprt1 and TATA box binding protein (Tbp) signals.	human	connective tissue	Low+High throughput	BET-bromodomain inhibitors modulate epigenetic patterns at the diacylglycerol kinase alpha enhancer associated with radiation-induced fibrosis	否	--	Fibrotic Disease	A9 cell	E_02_0785	ChIP-seq,PCR,ChIP	Analysis of publicly available data from the ENCODE project [18] (Fig. 1A), as well as our own ChIP experiments [8] revealed that the DGKA DMR carries H3K27ac. ChIP showed that JQ1 reduced the deposition of H3K27ac levels specifically at the DGKA enhancer site(DMR), but did not affect the upstream DGKA promoter sites 1 and 2 (Fig. 2C). 	Enhancer	--	ChIP,PCR	"From various NHDFs,we selected three fibroblast lines (data not shown) with significant
differences in DGKA DNA methylation at the DGKA enhancer site(Fig. 1A) and inducible DGKA mRNA expression (Fig. 1B). Increased DNA methylation at the DGKA enhancer was associated with a lack of DGKA induction after exposure to bleomycin (Fig. 1B, Fibroblast3), confirming our previous findings in numerous patient-derived NHDF.EGR1 was significantly induced in two NHDF showing high DGKA induction (Fig. 1C)."	DAGK,DAGK1,DGK-alpha	--	--	--	EGR1	AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225	qPCR	Relative DGKA (B) and EGR1 (C) mRNA expression levels in three individual NHDF exposed to bleomycin (40 mM) or vehicle control (DMSO) for 48 h. *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.0001, n.s. not significant.	--	--	DGKA
28916223	chr12	56330413	56330909	TBP	Data were normalized to housekeeping gene expression values of beta actin (ACTB), glyceraldehyde-3-phosphate dehydrogenase (GAPDH), hypoxan_x0002_thine phosphoribosyltransferase 1 (HPRT1) and succinate dehy_x0002_drogenase complex subunit A (SDHA) and the average of the normalized expression values was taken for individual samples. Murine mRNA expression was normalized to Actb, Hprt1 and TATA box binding protein (Tbp) signals.	human	connective tissue	Low+High throughput	BET-bromodomain inhibitors modulate epigenetic patterns at the diacylglycerol kinase alpha enhancer associated with radiation-induced fibrosis	否	--	Fibrotic Disease	A9 cell	E_02_0785	ChIP-seq,PCR,ChIP	Analysis of publicly available data from the ENCODE project [18] (Fig. 1A), as well as our own ChIP experiments [8] revealed that the DGKA DMR carries H3K27ac. ChIP showed that JQ1 reduced the deposition of H3K27ac levels specifically at the DGKA enhancer site(DMR), but did not affect the upstream DGKA promoter sites 1 and 2 (Fig. 2C). 	Enhancer	--	ChIP,PCR	"From various NHDFs,we selected three fibroblast lines (data not shown) with significant
differences in DGKA DNA methylation at the DGKA enhancer site(Fig. 1A) and inducible DGKA mRNA expression (Fig. 1B). Increased DNA methylation at the DGKA enhancer was associated with a lack of DGKA induction after exposure to bleomycin (Fig. 1B, Fibroblast3), confirming our previous findings in numerous patient-derived NHDF.EGR1 was significantly induced in two NHDF showing high DGKA induction (Fig. 1C)."	DAGK,DAGK1,DGK-alpha	--	--	--	EGR1	AT225,G0S30,KROX-24,NGFI-A,TIS8,ZIF-268,ZNF225	qPCR	Relative DGKA (B) and EGR1 (C) mRNA expression levels in three individual NHDF exposed to bleomycin (40 mM) or vehicle control (DMSO) for 48 h. *p < 0.05, **p < 0.01, ***p < 0.005, ****p < 0.0001, n.s. not significant.	--	--	DGKA
28905448	chr11	109985003	109985222	Sox2	We also found that YAP1 can regulate the expression of Sox2 by binding to two distinct DNA binding sites upstream and downstream of the Sox2 gene.	human	bone	Low throughput	Myeloid Zinc Finger 1 and GA Binding Protein Co-Operate with Sox2 in Regulating the Expression of Yes-Associated Protein 1 in Cancer Cells		--	Osteosarcoma	Stem cell	E_02_0786	ChIP-PCR,Luciferase Reporter Assay	"Interestingly, mutation of the Sox2 binding site at mt 11, whose sequence is not con‐
served, had no effect. Mutations at positions m8, m14,and m15 strongly affected the luciferase activity of thereporter plasmid in both cell types. Overexpression of Sox2 did not significantly stimulate the m8, m14, and m15 mutant plasmid activity in 293 cells, indicating that these motifs are critical for enhancer activity."	Enhancer	--	ChIP-PCR	"To further confirm the binding of MZF1 to the YAP1 enhancer region ChIP–PCR was
performed.The results showed binding of MZF1 to specific DNA sequences within the YAP1 enhancer region (Fig. 2C)."	COB1,YAP,YAP2,YAP65,YKI	Osteogenic Differentiation	CRISPR/Cas9,Alkaline Phosphatase Staining	MZF1 binding to the YAP enhancer is essential for the endogenous expression of YAP;Osteogenic differentiation was detected using alkaline phosphatase staining	MZF1,SOX2	MZF-1B,ZFP98,ZNF42,ZSCAN6,MZF1,Sox-2,lcc,ysb	EMSA,Luciferase Reporter Assay	EMSA analysis of the binding of GABP, and MZF1 transcription factor to the YAP enhancer region;A reporter plasmid expressing luciferase under the control of the FGF4 minimal promoter and the YAP enhancer was transfected into 293 cells in combination with different plasmids expressing MZF1, Sox2 and GABP cDNA.	--	--	YAP1
28887413	chr4	94419116	94437803	MED1	To examine the selective loss of function of ERαLQ at ER-binding sites genome-wide, we performed ChIP-seq (chromatin immunoprecipitation [ChIP] com_x0002_bined with high-throughput sequencing) for ERα, Med1, SRCs (using a “pan” SRC antibody), and p300 in both 231/ERαWt and 231/ERαLQ cells after 45 min of E2 treat_x0002_ment (note that Med1, SRCs, and p300 are expressed to similar levels in both cell types) (Supplemental Fig. S1).	human	breast	Low+High throughput	Dynamic assembly and activation of estrogen receptor α enhancers through coregulator switching	否	--	Breast Cancer	231/ERαWt cell,231/ERαLQ cell	E_02_0787	3C-qPCR,ChIP-seq,ChIP-qPCR	3C-qPCR assays showing chromatin looping from a distal ERα-binding site to the OTUB2 promoter in 231/ERαWt and 231/ERαLQ cells with 45 min of E2 treatment. 	Enhancer	3C-qPCR	ChIP-seq,ChIP-qPCR	3C-qPCR assays showing chromatin looping from a distal ERα-binding site to the OTUB2 promoter in 231/ERαWt and 231/ERαLQ cells with 45 min of E2 treatment. 	C14orf137,OTB2,OTU2	--	--	--	--	--	--	--	--	--	OTUB2
28836200	chr6	4438697	4440197	Col1a2	In our previous work, we characterized an enhancer region 17 kb upstream of the Col1a2 gene transcription start site.	mouse		Low+High throughput	Characterization of Mesenchymal-Fibroblast Cells Using the Col1a2 Promoter/Enhancer.	否	--	Fibrotic Disease	Fibroblast	E_02_0788	Luciferase Reporter Assay,DNase I Hypersensitivity Assay,ChIP-seq	Look for regions that have high conservation and good his_x0002_tone peaks and DNase1 peaks; you can use other tracks as exclusion criteria’s, but, generally, these marks are good indica_x0002_tors for enhancers without needing to conduct ChIP-seq or DNaseI hypersensitivity experiments (Fig. 5).	Enhancer	--	Luciferase Reporter Assay,DNase I Hypersensitivity Assay,ChIP-seq	In vivo imaging of transgenic mice that harbor a luciferase gene can be used as a noninvasive longitudinal monitoring of the gene expression. Make sure to determine plateau of constant luciferase activity rather than peak of activity (see Notes 13). You may need to shade high-expressing areas to see other low levels (see Notes 14 and 15).	AA960264,AI325291,Col1a-2,Cola-2,Cola2,oim	--	--	--	--	--	--	--	--	--	Col1a2
28753427	chr6	12490000	12590000	PHACTR1	Genome-wide association studies (GWASs) impli_x0002_cate the PHACTR1 locus (6p24) in risk for five vascular diseases, including coronary artery disease, migraine headache, cervical artery dissection, fibro_x0002_muscular dysplasia, and hypertension.	human	connective tissue	Low throughput	A Genetic Variant Associated with Five Vascular Diseases Is a Distal Regulator of Endothelin-1 Gene Expression	是	rs9349379	Coronary Artery Disease,Migraine Headache,Cervical Artery Dissection,Fibromuscular Dysplasia,Hypertension	HUVEC 	E_02_0789	4C-seq,Luciferase Reporter Assay	"The newly released ENCODE phase 3 data, however, includes four aortic artery samples. In these aortic samples, a strong enhancer signal overlies rs9349379 (Figure 2B), spanning 1 kb.
4C-seq from the rs9349379 site demonstrated a smaller contact region that extended from chr6:12,690,000–13,350,000. There was a possible area of over-lap intergenic to EDN1 and PHACTR1 (Figure 5A). Notably, this region featured high levels of H3K27Ac signal in ECs, consistent with a super enhancer (Figure 5B).
The common contact region contains four distinct peaks of H3K27Ac signal. Reporter assays with each of these four sites cloned into an SV40-driven luciferase plasmid demonstrated that each cis element possessed strong enhancer activity in 293T cells (2- to 12-fold luciferase induction) comparedwith SV40-promoter sequence alone (Figure 5C)."	Super-Enhancer	4C-seq	Luciferase Reporter Assay	"The newly released ENCODE phase 3 data, however, includes four aortic artery samples. In these aortic samples, a strong enhancer signal overlies rs9349379 (Figure 2B), spanning 1 kb.
4C-seq from the rs9349379 site demonstrated a smaller contact region that extended from chr6:12,690,000–13,350,000. There was a possible area of over-lap intergenic to EDN1 and PHACTR1 (Figure 5A). Notably, this region featured high levels of H3K27Ac signal in ECs, consistent with a super enhancer (Figure 5B).
The common contact region contains four distinct peaks of H3K27Ac signal. Reporter assays with each of these four sites cloned into an SV40-driven luciferase plasmid demonstrated that each cis element possessed strong enhancer activity in 293T cells (2- to 12-fold luciferase induction) comparedwith SV40-promoter sequence alone (Figure 5C)."	ARCND3,ET1,HDLCQ7,PPET1,QME	--	--	--	--	--	--	--	12803957	RNA-seq	EDN1
28753427	chr6	12490000	12590000	EDN1	CRISPR-edited stem cell-derived endothelial cells demonstrate rs9349379 regulates expression of endothelin 1 (EDN1), a gene located 600 kb upstream of PHACTR1.	human	connective tissue	Low throughput	A Genetic Variant Associated with Five Vascular Diseases Is a Distal Regulator of Endothelin-1 Gene Expression	是	rs9349379	Coronary Artery Disease,Migraine Headache,Cervical Artery Dissection,Fibromuscular Dysplasia,Hypertension	HUVEC 	E_02_0789	4C-seq,Luciferase Reporter Assay	"The newly released ENCODE phase 3 data, however, includes four aortic artery samples. In these aortic samples, a strong enhancer signal overlies rs9349379 (Figure 2B), spanning 1 kb.
4C-seq from the rs9349379 site demonstrated a smaller contact region that extended from chr6:12,690,000–13,350,000. There was a possible area of over-lap intergenic to EDN1 and PHACTR1 (Figure 5A). Notably, this region featured high levels of H3K27Ac signal in ECs, consistent with a super enhancer (Figure 5B).
The common contact region contains four distinct peaks of H3K27Ac signal. Reporter assays with each of these four sites cloned into an SV40-driven luciferase plasmid demonstrated that each cis element possessed strong enhancer activity in 293T cells (2- to 12-fold luciferase induction) comparedwith SV40-promoter sequence alone (Figure 5C)."	Super-Enhancer	4C-seq	Luciferase Reporter Assay	"The newly released ENCODE phase 3 data, however, includes four aortic artery samples. In these aortic samples, a strong enhancer signal overlies rs9349379 (Figure 2B), spanning 1 kb.
4C-seq from the rs9349379 site demonstrated a smaller contact region that extended from chr6:12,690,000–13,350,000. There was a possible area of over-lap intergenic to EDN1 and PHACTR1 (Figure 5A). Notably, this region featured high levels of H3K27Ac signal in ECs, consistent with a super enhancer (Figure 5B).
The common contact region contains four distinct peaks of H3K27Ac signal. Reporter assays with each of these four sites cloned into an SV40-driven luciferase plasmid demonstrated that each cis element possessed strong enhancer activity in 293T cells (2- to 12-fold luciferase induction) comparedwith SV40-promoter sequence alone (Figure 5C)."	ARCND3,ET1,HDLCQ7,PPET1,QME	--	--	--	--	--	--	--	12803957	RNA-seq	EDN1
28751304	chr7	129854050	129895632	MIR335	This impairs H3K27 methylation and instead favors H3K27 acetylation on MIR335 enhancers	human	Fat	Low+High throughput	A lipodystrophy-causing lamin A mutant alters conformation and epigenetic regulation of the anti-adipogenic MIR335 locu	否	--	--	Adipose progenitor cell	E_02_0790	ChIP-seq,FISH	"We also searched for putative MIR335 short- and long-range Enhancers:to this end, we combined chromatin state modeling data from ENC ODE ChIP-seq experiments showing enrichment in H3K4me1 and/or H3K27ac, histone modifications found on inactive and active Enhancers, respectively (Fig. S5 A), with ENCODE genome-wide chromosome conformation capture of Hi-C data (Rao et al., 2014). The Hi-C data reveal multiple pairwise interactions of these predicted enhancers with the MIR335 
promoter (Fig. S5, B–D), providing six MIR335-predicted distal enhancer sites (regions r6–r11; Fig. S5 D).
Acetylation of H3K27 on MIR335 enhancers detected in ASCLMNA(R482W) after adipogenic induction suggests interac-tions with the MIR335 promoter by chromatin looping (Zhang et al., 2013). We tested this hypothesis by two-color FISH using distinctly labeled promoter and enhancer probes. Probes were generated to cover the MIR335 gene and promoter as well as the distal enhancer element r11 located ?200 kb upstream of MIR335. In both undifferentiated and differentiated ASCs that 
were either native or expressing WT LMNA, these promoter and enhancer elements displayed a relatively low incidence of colocalization on the majority of alleles (?80%; Fig.?6, C and D). After induction of differentiation, however, this proportion markedly increased to 56% of alleles in the LMNA(R482W) mutants, reflecting interaction of a high proportion of MIR335 promoter and enhancer sites (Fig. 6, C and D)."	Enhancer	--	ChIP-seq,FISH	"We also searched for putative MIR335 short- and long-range Enhancers:to this end, we combined chromatin state modeling data from ENC ODE ChIP-seq experiments showing enrichment in H3K4me1 and/or H3K27ac, histone modifications found on inactive and active Enhancers, respectively (Fig. S5 A), with ENCODE genome-wide chromosome conformation capture of Hi-C data (Rao et al., 2014). The Hi-C data reveal multiple pairwise interactions of these predicted enhancers with the MIR335 
promoter (Fig. S5, B–D), providing six MIR335-predicted distal enhancer sites (regions r6–r11; Fig. S5 D).
Acetylation of H3K27 on MIR335 enhancers detected in ASCLMNA(R482W) after adipogenic induction suggests interac-tions with the MIR335 promoter by chromatin looping (Zhang et al., 2013). We tested this hypothesis by two-color FISH using distinctly labeled promoter and enhancer probes. Probes were generated to cover the MIR335 gene and promoter as well as the distal enhancer element r11 located ?200 kb upstream of MIR335. In both undifferentiated and differentiated ASCs that 
were either native or expressing WT LMNA, these promoter and enhancer elements displayed a relatively low incidence of colocalization on the majority of alleles (?80%; Fig.?6, C and D). After induction of differentiation, however, this proportion markedly increased to 56% of alleles in the LMNA(R482W) mutants, reflecting interaction of a high proportion of MIR335 promoter and enhancer sites (Fig. 6, C and D)."	MIRN335,hsa-mir-335,miRNA335,mir-335	--	--	--	--	--	--	--	--	--	MIR335
28751304	chr7	129854050	129895632	LMNA	These findings are supported by recent work showing that although the majority of chromatin domains (so-called lamin-associated domains; LADs) interacting with LMNA are conserved be_x0002_tween fibroblasts of healthy and FPLD2 patients, some are variable (Paulsen et al., 2017).	human	Fat	Low+High throughput	A lipodystrophy-causing lamin A mutant alters conformation and epigenetic regulation of the anti-adipogenic MIR335 locu	否	--	--	Adipose progenitor cell	E_02_0790	ChIP-seq,FISH	"We also searched for putative MIR335 short- and long-range Enhancers:to this end, we combined chromatin state modeling data from ENC ODE ChIP-seq experiments showing enrichment in H3K4me1 and/or H3K27ac, histone modifications found on inactive and active Enhancers, respectively (Fig. S5 A), with ENCODE genome-wide chromosome conformation capture of Hi-C data (Rao et al., 2014). The Hi-C data reveal multiple pairwise interactions of these predicted enhancers with the MIR335 
promoter (Fig. S5, B–D), providing six MIR335-predicted distal enhancer sites (regions r6–r11; Fig. S5 D).
Acetylation of H3K27 on MIR335 enhancers detected in ASCLMNA(R482W) after adipogenic induction suggests interac-tions with the MIR335 promoter by chromatin looping (Zhang et al., 2013). We tested this hypothesis by two-color FISH using distinctly labeled promoter and enhancer probes. Probes were generated to cover the MIR335 gene and promoter as well as the distal enhancer element r11 located ?200 kb upstream of MIR335. In both undifferentiated and differentiated ASCs that 
were either native or expressing WT LMNA, these promoter and enhancer elements displayed a relatively low incidence of colocalization on the majority of alleles (?80%; Fig.?6, C and D). After induction of differentiation, however, this proportion markedly increased to 56% of alleles in the LMNA(R482W) mutants, reflecting interaction of a high proportion of MIR335 promoter and enhancer sites (Fig. 6, C and D)."	Enhancer	--	ChIP-seq,FISH	"We also searched for putative MIR335 short- and long-range Enhancers:to this end, we combined chromatin state modeling data from ENC ODE ChIP-seq experiments showing enrichment in H3K4me1 and/or H3K27ac, histone modifications found on inactive and active Enhancers, respectively (Fig. S5 A), with ENCODE genome-wide chromosome conformation capture of Hi-C data (Rao et al., 2014). The Hi-C data reveal multiple pairwise interactions of these predicted enhancers with the MIR335 
promoter (Fig. S5, B–D), providing six MIR335-predicted distal enhancer sites (regions r6–r11; Fig. S5 D).
Acetylation of H3K27 on MIR335 enhancers detected in ASCLMNA(R482W) after adipogenic induction suggests interac-tions with the MIR335 promoter by chromatin looping (Zhang et al., 2013). We tested this hypothesis by two-color FISH using distinctly labeled promoter and enhancer probes. Probes were generated to cover the MIR335 gene and promoter as well as the distal enhancer element r11 located ?200 kb upstream of MIR335. In both undifferentiated and differentiated ASCs that 
were either native or expressing WT LMNA, these promoter and enhancer elements displayed a relatively low incidence of colocalization on the majority of alleles (?80%; Fig.?6, C and D). After induction of differentiation, however, this proportion markedly increased to 56% of alleles in the LMNA(R482W) mutants, reflecting interaction of a high proportion of MIR335 promoter and enhancer sites (Fig. 6, C and D)."	MIRN335,hsa-mir-335,miRNA335,mir-335	--	--	--	--	--	--	--	--	--	MIR335
28749941	chr10	67853705	67855705	EGR2	The hindbrain is an attractive model to investigate the genetic control of morphogenesis in vertebrates, as it is subject to a transient segmentation process leading to the formation of 7 8 segments called rhombomeres (r) [14,15]. The formation and specification of segments r3 and r5 are governed by the transcription factor KROX20/EGR2 [15 17]. So far three evolutionarily conserved sequences exhibiting enhancer activity in the hindbrain have been identified within the Krox20 locus and are termed A, B and C [13].	mouse		Low+High throughput	Krox20 hindbrain regulation incorporates multiple modes of cooperation between cis-acting elements.	否	--	--	embryonic cell 	E_02_0791	ChIP-seq,4C-seq	To investigate the correlation between the activity of the Krox20 cis-regulatory elements and their chromatin modifications and conformation, we first performed ChIP-seq experiments to analyse two histone modifications: H3K4me1 (broad peaks covering active enhancers) and H3K27ac (punctuated peaks covering active enhancers and promoters).In E8.5 wild type embryo heads, a number of H3K4me1 peaks were observed, including those that expectedly correspond to the A, B and C elements and to a previously known neural crest element (NCE; Fig 4A). 	Enhancer	4C-seq	--	To better characterize the Krox20 regulatory neighborhood, we used circular chromosome conformation capture (4C-seq) on multiple viewpoints in the locus. In samples prepared from total embryos at embryonic day (E) 9.5, when Krox20 is no more transcribed, the Krox20 gene and its distant regulatory element A (separated by over 200 kb) show highly similar distributions of 4C-seq signal (Fig 3A and S2B and S2C Fig) preferentially located in the Krox20 TAD. 	Egr-2,Krox-20,Krox20,NGF1-B,Zfp-25,Zfp-6	Enhancer element C possesses a dual activity: besides its classical Enhancer function, it is also permanently required in cis to potentiate the autoregulatory activity of element A, by increasing its chromatin accessibility.	ChIP-seq	Here, using both enhancer knock-outs and investigations of chromatin organisation, we show that element C possesses a dual activity: besides its classical enhancer function, it is also permanently required in cis to potentiate the autoregulatory activity of element A, by increasing its chromatin accessibility. 	--	--	--	--	--	--	Egr2
28737489	chr3	181432912	181433312	SOX2	In human lung cancers, high NFATc2 expression predicted poor tumor differentiation, adverse recurrence-free and cancer-specific overall survivals. Mechanistic investigations identified NFATc2 response elements in the 3' enhancer region of SOX2, and NFATc2/SOX2 coupling upregulates ALDH1A1 by binding to its 5' enhancer.	human	lung	low throughput	NFATc2 enhances tumor-initiating phenotypes through the NFATc2/SOX2/ALDH axis in lung adenocarcinoma	否	--	Lung Cancer	 Lung adenocarcinoma cell	E_02_0792	Luciferase Reporter Assay,ChIP-qPCR	To further delineate the molecular mechanism of SOX2 regulation by NFATc2, we screened, in silico, the genomic sequences spanning 5 kb up- and downstream of the SOX2 transcription start site (TSS), which identified 4 regions encompassing multiple conserved NFAT binding sequences (Figure 6-figure supplement 1A). Luciferase assays confirmed these regions are active transcriptional regulatory regions (Figure 6-figure supplement 1B). Further evaluation with respective SOX2 luciferase reporter revealed transcriptional activities were mediated by sites 1, 2, 4, and 5 (Figure 6B). Using H441 lung cancer cell line with NFATc2 transient overexpression, we observed only sites 1, 4 and 5 showed statistically significant increased reporter activities while those of sites 4 and 5 were reciprocally abolished by CSA treatment (Figure 6C).	Enhancer	--	Luciferase Reporter Assay,ChIP-qPCR	"To further delineate the molecular mechanism of SOX2 regulation by NFATc2, we screened, in silico, the genomic sequences spanning 5 kb up- and downstream of the SOX2 transcription start site (TSS), which identified 4 regions encompassing multiple conserved NFAT binding sequences (Figure 6-figure supplement 1A). Luciferase assays confirmed these regions are active transcriptional regulatory regions (Figure 6-figure supplement 1B). Further evaluation with respective SOX2 luciferase reporter revealed transcriptional activities were mediated by sites 1, 2, 4, and 5 (Figure 6B). Using H441 lung cancer cell line with NFATc2 transient overexpression, we observed only sites 1, 4 and 5 showed statistically significant increased reporter activities while those of sites 4 and 5 were reciprocally abolished by CSA treatment (Figure 6C). 
"	ANOP3,MCOPS3	--	--	--	NFATC2	NFAT1,NFATP	Luciferase Reporter Assay,ChIP-qPCR	"Finally, site directed mutagenesis of NFAT motifs (GGAAA to GACTA) prevented reporter activities of sites 4 and 5 only (Figure 6D), and the findings were supported by data from A549 and H1299 cells ectopically expressing NFATc2, respectively (Figure 6-figure supplement 1C,D). Thus, the data suggested NFATc2 was highly likely to regulate SOX2 expression through binding to 3’ enhancers at sites 4 and 5. For validation, NFATc2 ChIP-qPCR assays were performed using A549 with NFATc2 upregulation, which showed statistically significant enrichment of sites 4 and 5 sequences compared to vector control (Figure 6F). In HCC827 cells, sites 4 and 5 sequences were significantly enriched by anti-NFATc2 antibody compared to IgG control. Conversely, these sequences were significantly reduced upon NFATc2 knockout in HCC827, compared to their endogenous levels in control cells, indicating de novo physical binding of NFATc2 to SOX2 at sites 4 and 5 (Figure 6G). Together, the data showed NFATc2 upregulates SOX2 by binding to its 3’ enhancer region at around 3.2 kb (site 4) and 3.6 kb (site 5) from the TSS, respectively
"	--	--	SOX2 
28717659	chr14	60973427	60975430	SIX6	To address this question, the SIX6 gene and an already characterized and highly conserved SIX6 enhancer (Ch14:60974427-60974430) were sequenced in two south Indian cohorts, respectively, composed of 65/65 and 200/200 POAG cases/ age-matched controls.	human	eye	low throughput	Identification and characterization of variants and a novel 4 bp deletion in the regulatory region of SIX6, a risk factor for primary open-angle glaucoma	是	rs33912345	Primary Open-Angle Glaucoma		E_02_0793	Transgenic zebrafish,Luciferase Reporter Assay	A evolutionarily conserved enhancer has been shown to control Six6 expression in the vertebrate retina (Conte et al. 2010).We ?rst inserted the entire control human enhancer sequence in the ZED transgenic vector (Bessa et al. 2009) and investigated if the plasmid could drive GFP reporter expression in the retina of zebra?sh embryos, similarly to what has been previously observed for the medaka orthologous region (Conte et al. 2010). We generated 38 F0 transgenic embryos, as determined by RFP expression in the somites (Fig. 4C) that acts as a positive control (Bessa et al.2009). About half of them (18) showed a clear GFP expression driven by the human enhancer element in the eye and occasionally in other CNS regions.	Enhancer	--	Transgenic zebrafish	A evolutionarily conserved enhancer has been shown to control Six6 expression in the vertebrate retina (Conte et al. 2010).We ?rst inserted the entire control human enhancer sequence in the ZED transgenic vector (Bessa et al. 2009) and investigated if the plasmid could drive GFP reporter expression in the retina of zebra?sh embryos, similarly to what has been previously observed for the medaka orthologous region (Conte et al. 2010). We generated 38 F0 transgenic embryos, as determined by RFP expression in the somites (Fig. 4C) that acts as a positive control (Bessa et al.2009). About half of them (18) showed a clear GFP expression driven by the human enhancer element in the eye and occasionally in other CNS regions.	MCOPCT2,ODRMD,OPTX2,Six9	--	--	--	--	--	--	--	60976537	Luciferase Reporter Assay	SIX6 
28671686	chr8	36785613	36985613	CTCF	TADcPcdh in mutant neurons showed abnormal accumulations of CTCF transcriptional regulator and 3D genome organizer at cryptic binding sites, converted into permissive state with DNA cytosine hypomethylation and histone hyperacetylation.	mouse		Low+High throughput	The methyltransferase SETDB1 regulates a large neuron-specific topological chromatin domain.	否	--	Schizophrenia	brain cell 	E_02_0794	ChIP-seq,Hi-C	We then assessed longer-range chromosomal contacts, spanning >200kb of linear genome. We identified genome-wide 110 long-range loop contacts affected in mutant neurons (DESeq2 P<0.05). Unexpectedly, the large majority, 84/110 or 76%, represented clustered, locus-specific ‘loop aggregates’ showing massive weakening, or complete loss, after neuronal Setdb1 ablation (Figure 1d, Supplementary Figure 2c). hese deficits were specific, because ChiP-seq profiling for open chromatin-associated acetyl-H3-lysine 27 (H3K27ac) showed that 96.4% of 1,112 differentially tagged sequences were hyperacetylated in Setdb1-deficient neurons (Figure 2a, Supplementary Tables 1,2).	Enhancer	--	ChIP-seq	Therefore, we predicted that higher order chromatin organization at these positions will be highly conserved in human brain cells, and specifically in neurons, with long-range loopings radiating from ~200kb R1 towards cPCDH promoter and Enhancers primarily anchored in chromatin at and around the Setdb1 peak. To explore, we surveyed with 40kb resolution the cPCDH -bound chromosomal contacts in our in situ Hi-C datasets generated from human neurons and their isogenic neural precursors cells (NPC) and NPC-differentiated astrocytes.	AU022152,ESET,KMT1E,mKIAA0067	--	--	--	Ctcf	AW108038	ChIP-seq	ChIP-seq data from stem cells and CD19+ B lymphocytes significant CTCF motif enrichment.CTCF motif (red) enrichment in sequences H3K9me3 hypomethylated in KO. (e) (Left) FACS plots showing separation of crosslinked NeuN+ from NeuN? nuclei (adult cortex) for cell-type specific CTCF ChIP-seq.	--	--	Setdb1
28667437	chr9	88325101	88326201	Elf2	We describe the existence of an enhancer sequence upstream of the mouse Nt5e minimal promoter and establish that the mouse Nt5e minimal promoter transcriptional activity is negatively regulated by an Elf2-like Ets-related transcription factor in activated mouse liver myofibroblasts. 	mouse		Low throughput	An Elf2-like transcription factor acts as repressor of the mouse ecto-5'-nucleotidase gene expression in hepatic myofibroblasts.	否	--	Hepatic Fibrosis	Myofibroblast	E_02_0795	Luciferase Reporter Assay	The measured luciferase activity noticeably decreased between F1- and F2-Luc constructs, suggesting that F1-Luc construct contains a potential enhancer sequence, which spans approximately 1000 bp (?2069 to ?996 bp) and is absent in the shorter F2-Luc construct.	Enhancer	--	Luciferase Reporter Assay,PCR	Luciferase activity as_x0002_says showed that the ENH1074-F5-Luc construct containing the full putative Enhancer (-2069 to -996 bp) sequence has the ability to enhance the luciferase activity of the identified putative mouse Nt5e promoter.	2210401F01Rik,5'-NT,AI447961,CD73,NT,Nt5,eNT	--	--	--	Elf2	2610036A20Rik,A230104O07Rik,AW111824,BB183398,EU32,NERF,NERF-1A,NERF-1B,NERF-2	Luciferase Reporter Assay	We found that mutation of Elf2 responsive element alone was sufficient to significantly increase the F5-Luc construct luciferase activity (F5-Luc, 11.79 ± 1.41 vs. mut Elf2-F5-Luc,20.48 ± 2.96, **p < 0.01).These data indicate that repression of mouse Nt5e promoter activity is likely mediated by transcription factor(s) acting at the identified Elf2 site in NIH3T3 fibroblasts.	--	--	Nt5e
28637769	Chr11	45846943	45846959	CRY2	Although CRY2 is a core component of the mammalian circadian clock (van der Horst et al., 1999), the mechanism of the circadian transcription of this gene has yet to be analyzed in detail. In the present study, we found that cell-autonomous circadian transcription of the Cry2 gene requires a functionally interdependent tandem E-box motif.	human	Epithelial tissues	Low throughput	Potential contribution of tandem circadian enhancers to nonlinear oscillations in clock gene expression	否	--	--	U-2 OS cell	E_02_0796	Luciferase Reporter Assay	"To identify components necessary for cell-autonomous circadian transcription of the hCry2 gene, a 3-kbp 5'-flanking region upstream from the hCry2 transcription start site was isolated and subcloned into the upstream of the luciferase gene, and the hCry2-driven luciferase activity was monitored in real time using a cell-based system (Figure 1A).To exclude systemic factors such as blood-borne factors and body temperature, it was necessary to examine cell-autonomous transcriptional regulatory mechanisms under an in vitro culture condition. The data clearly showed a robust circadian oscillation of the bioluminescence in U2OS human steosarcoma cells (Figure 1B), indicating that the cloned genomic region contained elements essential for circadian transcription.The 60-bp region is functionally divided into two; a 43-bp region (from -158 to -116) contains elements which enhance oscillation amplitude, while the 17-bp region (from -175 to -159) is indispensable for the generation of transcriptional oscillation. 
After narrowing down the transcriptional regulatory region required for the cell-autonomous circadian transcription of hCry2,and further narrowing down the 
genomic region essential for cell-autonomous circadian transcription,the results strongly suggested that the essential regulatory elements are contained in the region from -175 to -116 (60-bp length) (Figure 1D).
To identify consensus sequences for transcription factor binding within the latter region, we performed an in silico search by sequence alignment, and found 
interspecies-conserved E-boxes within the 17-bp region (E1 and E2, Figure 1C). To investigate whether each of the E-boxes is functional for circadian 
transcription of the hCry2 gene, we produced constructs carrying hCry2 lacking either one of the E-boxes (Figure 2A). To confirm whether the BMAL1 and CLOCK complex actually activates hCry2 transcription via each E-box, we performed dual luciferase assays with these constructs (Figures 2B). The data showed that overexpression of BMAL1 and CLOCK activated hCry2 transcription via the region spanning from -249 to +41, and that deletion of one of the E-boxes produced severe attenuation of transcription, while deletion of both produced an almost complete loss of activation. "	Enhancer	--	Luciferase Reporter Assay	"To identify components necessary for cell-autonomous circadian transcription of the hCry2 gene, a 3-kbp 5'-flanking region upstream from the hCry2 transcription start site was isolated and subcloned into the upstream of the luciferase gene, and the hCry2-driven luciferase activity was monitored in real time using a cell-based system (Figure 1A).To exclude systemic factors such as blood-borne factors and body temperature, it was necessary to examine cell-autonomous transcriptional regulatory mechanisms under an in vitro culture condition. The data clearly showed a robust circadian oscillation of the bioluminescence in U2OS human steosarcoma cells (Figure 1B), indicating that the cloned genomic region contained elements essential for circadian transcription.The 60-bp region is functionally divided into two; a 43-bp region (from -158 to -116) contains elements which enhance oscillation amplitude, while the 17-bp region (from -175 to -159) is indispensable for the generation of transcriptional oscillation. 
After narrowing down the transcriptional regulatory region required for the cell-autonomous circadian transcription of hCry2,and further narrowing down the 
genomic region essential for cell-autonomous circadian transcription,the results strongly suggested that the essential regulatory elements are contained in the region from -175 to -116 (60-bp length) (Figure 1D).
To identify consensus sequences for transcription factor binding within the latter region, we performed an in silico search by sequence alignment, and found 
interspecies-conserved E-boxes within the 17-bp region (E1 and E2, Figure 1C). To investigate whether each of the E-boxes is functional for circadian 
transcription of the hCry2 gene, we produced constructs carrying hCry2 lacking either one of the E-boxes (Figure 2A). To confirm whether the BMAL1 and CLOCK complex actually activates hCry2 transcription via each E-box, we performed dual luciferase assays with these constructs (Figures 2B). The data showed that overexpression of BMAL1 and CLOCK activated hCry2 transcription via the region spanning from -249 to +41, and that deletion of one of the E-boxes produced severe attenuation of transcription, while deletion of both produced an almost complete loss of activation. "	HCRY2,PHLL2	the interdependent behavior of enhancer elements including not only E-boxboxes but also ROR response elements (ROREs) might contribute to limit cycle oscillations by increasing transcriptional nonlinearity.	EMSA	Immunoprecipitation was performed with antibody-conjugated beads, and the immunoprecipitates were eluted with an excess amount of tag-peptide.A mutation of E1 resulted in a severe attenuation of the affinity of the BMAL1 and CLOCK complex to the probe, and the position of the shifted band was slightly changed, probably because of the reduction of the mole ratio between the binding proteins and probe. A mutation of E2 led to almost complete loss of the physical interaction between them. Taken together, the present EMSA data indicate that each of the hCry2 tandem E-boxes physically interacts directly with the BMAL1 and CLOCK complex in an interdependent and not independent manner. 	ARNTL,CLOCK	BMAL1,BMAL1c,JAP3,MOP3,PASD3,TIC,bHLHe5,KAT13D, bHLHe8	EMSA,Pull-down assay	"We therefore performed electrophoretic mobility shift assays (EMSAs) to investigate the physical interaction of purified BMAL1 and CLOCK proteins to double-stranded DNA fragments (Figure 3A).We confirmed that the electrophoretic mobility of the probe was shifted by the physical interaction with BMAL1–CLOCK. 
A mutation of E1 resulted in a severe attenuation of the affinity of the BMAL1 and CLOCK complex to the probe, and the position of the shifted band was slightly changed, probably because of the reduction of the mole ratio between the binding proteins and probe. A mutation of E2 led to almost complete loss of the physical interaction between them. Taken together, the present EMSA data indicate that each of the hCry2 tandem E-boxes physically interacts directly with the BMAL1 and CLOCK complex in an interdependent and not independent manner. 
Next, we performed hCry2-oligodeoxynucleotide (ODN) pull-down assays and confirmed that endogenous BMAL1 and CLOCK expressed in the liver bound to a fragment containing the hCry2 tandem E-boxes (Figure 3B). "	--	--	CRY2
28614915	chr17	62627957	62633457	Ascl1	Further comparative genomic analysis indicated that two evolutionary conserved regions, ECR1 and ECR2, were present within this 5.5 kb region.                                                                                                                                                              Finally, both electrophoretic mobility shift assay and luciferase-based transactivation assay revealed that the transcription factor Ascl1 bound the bHLH consensus binding site in the mesencephalon-specific ephrin-A5 enhancer in vitro.	mouse		Low throughput	Identification of an Enhancer Critical for the ephirn-A5 Gene Expression in the Posterior Region of the Mesencephalon.	否	--	--	Mesencephalon	E_02_0797	Luciferase Reporter Assay	Luciferase activity assay showing that Ascl1- E47 fusion protein induces transcriptional activation through the ephrin-A5 E-box DNA.Taken together, our findings suggest that the mesencephalon-specific enhancer of ephrin-A5 resided in a genomic region that is +11.6 kb to +57.7 kb from the TSS and is within the first intron (Fig. 1A).	Enhancer	--	Luciferase Reporter Assay,PCR	To further restrict the possible locations of the mesencephalon-specific enhancer within the first intron, the 375B7 BAC was modified using a different targeting vector. Importantly, transgenic embryos carrying this recombinant BAC did not show significant LacZ expression in the mesencephalon (Fig. 2C, first panel from the left). This suggested that the deleted 30.4 kb region included the mesencephalon-specific enhancer of ephrin-A5.This suggests that the potential enhancer for ephrin-A5 expression in the mesencephalon was in a 5.5 kb genomic region from +25 kb to +30.5 kb of the TSS.	AL-1,AV158822,EFL-5,Ephrin-A5,Epl7,LERK-7,RAGS	--	--	--	Ascl1	AI225900,ASH1,Mash1,bHLHa46	EMSA,Luciferase Reporter Assay	Finally, both electrophoretic mobility shift assay and luciferase-based transactivation assay revealed that the transcription factor Ascl1 bound the bHLH consensus binding site in the mesencephalon-specific ephrin-A5 enhancer in vitro. 	--	--	Efna5
28578223	chr18	61533339	61545796	SERPINB2	The SERPINB2 gene is strongly upregulated in inflammatory states. In monocytes, it can constitute up to 1% of total cellular protein. It functions in protection from proteotoxic stress and plays a role in angioedema.	human	blood	Low+High throughput	SERPINB2 is regulated by dynamic interactions with pause-release proteins and enhancer RNAs	否	--	--	MonoMac6,K-562 cell	E_02_0798	ChIP-seq,Luciferase Reporter Assay,qRT-PCR	"A cluster of RNAs, not previously annotated, was found approximately 21 kb upstream of the SERPINB2 gene in SLE monocytes (Shi et al.,2014). The RNAs (772, 774, 775) formed a cluster near an enhancer, de?ned by H3K27ac in UCSC Genome Browser. 774 is centered on the H3K27ac peak, 775 is at the proximal edge of the H3K27ac peak and 772 is at the distal shores of the H3K27ac peak. We will refer to this region as Enhancer 1.
We tested the DNA corresponding to the 775 ncRNA in an enhancer assay by sub-cloning it downstream of a minimal thymidine kinase (TK) promoter. The DNA corresponding to the 775 ncRNA location was capable of augmenting luciferase production in this transient transfection assay in two di?erent cell types (K562 and
HEK293), thereby assigning it as a probable enhancer (Fig. 2A and B). For this reason, we will refer to the ncRNAs subsequently as eRNAs. Enhancer RNAs are predicted to have chromatin localization. To validate the remaining eRNAs, we used qRT-PCR from three di?erent cell types to demonstrate tissue speci?city and analyzed eRNA sub-cellular localization by fractionating cells. The eRNAs were found predominantly in monocytes and in the chromatin and nucleoplasm
fractions predominantly (Fig. 2C and D). This demonstration of enhancer activity of the DNA and chromatin localization support the assignment of the ncRNAs as eRNAs."	Enhancer	--	ChIP-seq,Luciferase Reporter Assay,qRT-PCR	"A cluster of RNAs, not previously annotated, was found approximately 21 kb upstream of the SERPINB2 gene in SLE monocytes (Shi et al.,2014). The RNAs (772, 774, 775) formed a cluster near an enhancer, de?ned by H3K27ac in UCSC Genome Browser. 774 is centered on the H3K27ac peak, 775 is at the proximal edge of the H3K27ac peak and 772 is at the distal shores of the H3K27ac peak. We will refer to this region as Enhancer 1.
We tested the DNA corresponding to the 775 ncRNA in an enhancer assay by sub-cloning it downstream of a minimal thymidine kinase (TK) promoter. The DNA corresponding to the 775 ncRNA location was capable of augmenting luciferase production in this transient transfection assay in two di?erent cell types (K562 and
HEK293), thereby assigning it as a probable enhancer (Fig. 2A and B). For this reason, we will refer to the ncRNAs subsequently as eRNAs. Enhancer RNAs are predicted to have chromatin localization. To validate the remaining eRNAs, we used qRT-PCR from three di?erent cell types to demonstrate tissue speci?city and analyzed eRNA sub-cellular localization by fractionating cells. The eRNAs were found predominantly in monocytes and in the chromatin and nucleoplasm
fractions predominantly (Fig. 2C and D). This demonstration of enhancer activity of the DNA and chromatin localization support the assignment of the ncRNAs as eRNAs."	HsT1201,PAI,PAI-2,PAI2,PLANH2	Knock-down of the enhancer RNAs compromised stimulus induction of promoter and enhancer chromatin changes. Conversely,over-expression was associated with enhanced recruitment of c-JUN and increased expression of SERPINB2 mRNA expression.	qRT-PCR	"We knocked down 774 and 775 as SERPINB2-speci?c eRNAs. Knock-down was validated by qRT-PCR of the target eRNAs. Knock-down of 774 and 775 led to inhibition of SERPINB2 mRNAs but not SERPINB10, which is not co-regulated with SERPINB2 (Fig. 3B). We then over-expressed 774 and 775 to determine whether they could regulate SERPIN gene expression when provided in trans. Each over-expression construct was validated as expressing the correct RNA species (Fig. 3C). Over-expression of both 774 and 775 led to higher SERPINB2 RNA but not the distinctly regulated SERPINB10.Ano?-target, control RNA, 477, had no e?ect.
Enhancer RNAs have been hypothesized to regulate gene expression via diverse potential mechanisms. We tested whether they regulated histone modi?cations. To de?ne e?ects related to eRNAs, we used anti-sense oligonucleotides to knock-down 774 and 775.We examined chromatin marks of gene activation in MonoMac6 cells at baseline and after treatment with LPS (Fig. 4C–F). We compared the e?ects of 774 and 775 knock-down with GFP knock-down. Non-transfected cells were included as assay controls for each experiment but are not shown to streamline the ?gures.The GAPDH promoter was una?ected by LPS stimulation and serves as a control. The anti-sense oligonucleotides to 774 and 775 were associated with diminished acquisition of the chromatin marks seen with LPS stimulation at Enhancer 1. The e?ect was limited to LPS-stimulated cells and was not observed in resting cells. Knock-down of 774 and 775 primarily a?ected H3K4me3 and H3K27ac at the promoter. These data demonstrate that eRNAs regulate histone modi?cations not just at the enhancer but also at their target gene promoter. 
"	NSMF,CDK9	HH9,NELF,C-2k,CDC2L4,CTK1,PITALRE,TAK	ChIP	"To examine whether NELF and its major kinase are localized to the promoter and Enhancer of SERPINB2, we performed ChIP studies for NELF and CDK9.
"	--	--	SERPINB2
28536097	chr1	221049243	221051243	DLL4	By assessing the signals responsible for induction of the Notch ligand, Delta-Like 4 (DLL4) in endothelial cells we find that activation of the MAPK/ERK pathway mirrors the rapid and dynamic induction of DLL4 transcription and that this pathway is required for DLL4 expression.	human	connective tissue	Low+High throughput	Dynamic regulation of VEGF-inducible genes by an ERK-ERG-p300 transcriptional network	否	--	--	HUVEC 	E_02_0799	ChIP-seq,Luciferase Reporter Assay,ChIP	"We also performed H3K27ac ChIP-seq and found that 94% of conserved ERG peaks overlapped H3K27ac-enriched regions, supporting their association with active enhancers. We also identified an ERG-bound enhancer, conserved in cows and humans, ~3.0 kb upstream of the gene H2.0-Like Homeobox (HLX) (Fig. 8B; Fig. S8). 
We cloned this conserved H3K27ac- and ERG-enriched -3 kb 5’ putative regulatory region (HLX-3a, 1565 bp fragment) upstream of a minimal promoter (SV40) driving a luciferase reporter, and found that it was VEGF-responsive, and that the basal and VEGF-induced activity of this enhancer required ETS DNA binding sequences (Fig. 9D)."	Enhancer	--	ChIP-seq,Luciferase Reporter Assay	"We also performed H3K27ac ChIP--seq and found that 94% of conserved ERG peaks overlapped H3K27ac--enriched regions, supporting their association with active enhancers. We also identified an ERG--bound enhancer, conserved in cows and humans, ~3.0 kb upstream of the gene H2.0--Like Homeobox (HLX) (Fig. 8B; Fig. S8). 
We cloned this conserved H3K27ac-- and ERG--enriched --3 kb 5’ putative regulatory region (HLX--3a, 1565 bp fragment) upstream of a minimal promoter (SV40) driving a luciferase reporter, and found that it was VEGF--responsive, and that the basal and VEGF--induced activity of this enhancer required ETS DNA binding sequences (Fig. 9D)."	HB241, HLX	A highly-conserved ERG-bound regulatory element was required in the VEGF responsiveness of the angiogenic gene, HLX.	CRISPR/Cas9,PCR	To further test the functional importance of this enhancer, we utilized CRISPR genome editing to delete a portion (1201 bp; see Fig. 8B for schematic) of the H3K27Ac-enriched, ERG-bound region upstream of HLX in TeloHAECs, an immortalized aortic EC line. Several clonal lines (ΔHLX15, ΔHLX17 and ΔHLX21) heterozygous for deletion of this region were generated and confirmed by PCR and DNA sequencing (data not shown). Comparison was made to a clonal line generated following transfection of scrambled control gRNAs (Scr3). While the basal expression of HLX appeared to be unaffected in the deletion lines, the VEGF-dependent induction of HLX was attenuated (Fig. 9G). In contrast, DLL4 induction was unaffected. Furthermore, knock-down of ERG appeared to attenuate the induction of HLX to a greater extent in the control line compared to the deletion lines, implying that ERG acts through the deleted enhancer region. Collectively, these findings demonstrate the requirement of a highly-conserved ERG-bound regulatory element in the VEGF responsiveness of the angiogenic gene, HLX. 	VEGF,ERG	MVCD1,VEGF,VPF,erg-3,p55	Luciferase Reporter Assay	We cloned this conserved H3K27ac- and ERG-enriched -3 kb 5’ putative regulatory region (HLX-3a, 1565 bp fragment) upstream of a minimal promoter (SV40) driving a luciferase reporter, and found that it was VEGF-responsive, and that the basal and VEGF-induced activity of this enhancer required ETS DNA binding sequences (Fig. 9D). 	--	--	HLX
28536097	chr1	221049243	221051243	HLX	Finally, genome_x0002_editing and transgenic approaches demonstrate that a highly conserved ERG-bound enhancer located upstream of HLX (a transcription factor implicated in sprouting angiogenesis) is required for its VEGF-mediated induction.	human	connective tissue	Low+High throughput	Dynamic regulation of VEGF-inducible genes by an ERK-ERG-p300 transcriptional network	否	--	--	HUVEC 	E_02_0799	ChIP-seq,Luciferase Reporter Assay,ChIP	"We also performed H3K27ac ChIP-seq and found that 94% of conserved ERG peaks overlapped H3K27ac-enriched regions, supporting their association with active enhancers. We also identified an ERG-bound enhancer, conserved in cows and humans, ~3.0 kb upstream of the gene H2.0-Like Homeobox (HLX) (Fig. 8B; Fig. S8). 
We cloned this conserved H3K27ac- and ERG-enriched -3 kb 5’ putative regulatory region (HLX-3a, 1565 bp fragment) upstream of a minimal promoter (SV40) driving a luciferase reporter, and found that it was VEGF-responsive, and that the basal and VEGF-induced activity of this enhancer required ETS DNA binding sequences (Fig. 9D)."	Enhancer	--	ChIP-seq,Luciferase Reporter Assay	"We also performed H3K27ac ChIP--seq and found that 94% of conserved ERG peaks overlapped H3K27ac--enriched regions, supporting their association with active enhancers. We also identified an ERG--bound enhancer, conserved in cows and humans, ~3.0 kb upstream of the gene H2.0--Like Homeobox (HLX) (Fig. 8B; Fig. S8). 
We cloned this conserved H3K27ac-- and ERG--enriched --3 kb 5’ putative regulatory region (HLX--3a, 1565 bp fragment) upstream of a minimal promoter (SV40) driving a luciferase reporter, and found that it was VEGF--responsive, and that the basal and VEGF--induced activity of this enhancer required ETS DNA binding sequences (Fig. 9D)."	HB241, HLX	A highly-conserved ERG-bound regulatory element was required in the VEGF responsiveness of the angiogenic gene, HLX.	CRISPR/Cas9,PCR	To further test the functional importance of this enhancer, we utilized CRISPR genome editing to delete a portion (1201 bp; see Fig. 8B for schematic) of the H3K27Ac-enriched, ERG-bound region upstream of HLX in TeloHAECs, an immortalized aortic EC line. Several clonal lines (ΔHLX15, ΔHLX17 and ΔHLX21) heterozygous for deletion of this region were generated and confirmed by PCR and DNA sequencing (data not shown). Comparison was made to a clonal line generated following transfection of scrambled control gRNAs (Scr3). While the basal expression of HLX appeared to be unaffected in the deletion lines, the VEGF-dependent induction of HLX was attenuated (Fig. 9G). In contrast, DLL4 induction was unaffected. Furthermore, knock-down of ERG appeared to attenuate the induction of HLX to a greater extent in the control line compared to the deletion lines, implying that ERG acts through the deleted enhancer region. Collectively, these findings demonstrate the requirement of a highly-conserved ERG-bound regulatory element in the VEGF responsiveness of the angiogenic gene, HLX. 	VEGF,ERG	MVCD1,VEGF,VPF,erg-3,p55	Luciferase Reporter Assay	We cloned this conserved H3K27ac- and ERG-enriched -3 kb 5’ putative regulatory region (HLX-3a, 1565 bp fragment) upstream of a minimal promoter (SV40) driving a luciferase reporter, and found that it was VEGF-responsive, and that the basal and VEGF-induced activity of this enhancer required ETS DNA binding sequences (Fig. 9D). 	--	--	HLX
28511927	chr11	355447	358949	STAT1	The enhancer drove the coordinate expression of IFITM1, 2 and 3 through constitutive long-range interactions and IFNβ-induced STAT1 binding.	human	kidney	Low throughput	Coordinated regulation of IFITM1, 2 and 3 genes by an IFN-responsive enhancer through long-range chromatin interactions	否	--	--	A549,HEK-293 cell	E_02_0800	Luciferase Reporter Assay,CRISPR/Cas9,ChIP,EMSA,3C	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer. Finally, we showed that in vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection. 	Enhancer	CRISPR/Cas9,3C	Luciferase Reporter Assay,EMSA	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.	927,CD225,DSPA2a,IFI17,LEU13,1-8D,DSPA2c,1-8U,DSPA2b,IP15	In vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection.	RT-PCR,Western blot	As IFITM1, 2 and 3 are very important for host to resist infection of IAV [4], [8], we infected wild-type and E2-3-truncated HEK293 cells with IAV Puerto Rico/8/1934 (PR8) at a MOI of 0.1 for 24 h. Although IFITM1, 2 and 3 were induced by PR8 virus in both wild-type and E2-3-truncated HEK293 cells, the inductions were greatly impaired upon truncation of E2-3 (Fig. 5A and B), further confirming the regulation of IFITM1, 2 and 3 expression by the enhancer E2-3. Surprisingly, we did not observe a significant effect on the replication of IAV when enhancer E2-3 was truncated, as revealed by the mRNA and protein levels of virus NP and progeny virus titers determined by TCID50 assay (Fig. S9). Nonetheless, when we treated wild-type and E2-3-truncated HEK293 cells with IFNβ respectively for 24 h before infection of PR8, NP mRNA and protein levels were found to be much higher in mutant HEK293 cells (Fig. 5C and D). Moreover, consistent with virus NP expression, the viral titers were also increased in E2-3-truncated cells (Fig. 5E), indicating that enhancer E2-3 was responsible for IFNβ-induced resistance to IAV infection.	STAT1	CANDF7,IMD31A,IMD31B,IMD31C,ISGF-3,STAT91	ChIP,EMSA,3C	"Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.
"	--	--	IFITM1
28511927	chr11	355447	358949	STAT1	The enhancer drove the coordinate expression of IFITM1, 2 and 3 through constitutive long-range interactions and IFNβ-induced STAT1 binding.	human	kidney	Low throughput	Coordinated regulation of IFITM1, 2 and 3 genes by an IFN-responsive enhancer through long-range chromatin interactions	否	--	--	A549,HEK-293 cell	E_02_0800	Luciferase Reporter Assay,CRISPR/Cas9,ChIP,EMSA,3C	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer. Finally, we showed that in vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection. 	Enhancer	CRISPR/Cas9,3C	Luciferase Reporter Assay,EMSA	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.	927,CD225,DSPA2a,IFI17,LEU13,1-8D,DSPA2c,1-8U,DSPA2b,IP15	In vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection.	RT-PCR,Western blot	As IFITM1, 2 and 3 are very important for host to resist infection of IAV [4], [8], we infected wild-type and E2-3-truncated HEK293 cells with IAV Puerto Rico/8/1934 (PR8) at a MOI of 0.1 for 24 h. Although IFITM1, 2 and 3 were induced by PR8 virus in both wild-type and E2-3-truncated HEK293 cells, the inductions were greatly impaired upon truncation of E2-3 (Fig. 5A and B), further confirming the regulation of IFITM1, 2 and 3 expression by the enhancer E2-3. Surprisingly, we did not observe a significant effect on the replication of IAV when enhancer E2-3 was truncated, as revealed by the mRNA and protein levels of virus NP and progeny virus titers determined by TCID50 assay (Fig. S9). Nonetheless, when we treated wild-type and E2-3-truncated HEK293 cells with IFNβ respectively for 24 h before infection of PR8, NP mRNA and protein levels were found to be much higher in mutant HEK293 cells (Fig. 5C and D). Moreover, consistent with virus NP expression, the viral titers were also increased in E2-3-truncated cells (Fig. 5E), indicating that enhancer E2-3 was responsible for IFNβ-induced resistance to IAV infection.	STAT1	CANDF7,IMD31A,IMD31B,IMD31C,ISGF-3,STAT91	ChIP,EMSA,3C	"Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.
"	--	--	IFITM2
28511927	chr11	355447	358949	STAT1	The enhancer drove the coordinate expression of IFITM1, 2 and 3 through constitutive long-range interactions and IFNβ-induced STAT1 binding.	human	kidney	Low throughput	Coordinated regulation of IFITM1, 2 and 3 genes by an IFN-responsive enhancer through long-range chromatin interactions	否	--	--	A549,HEK-293 cell	E_02_0800	Luciferase Reporter Assay,CRISPR/Cas9,ChIP,EMSA,3C	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer. Finally, we showed that in vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection. 	Enhancer	CRISPR/Cas9,3C	Luciferase Reporter Assay,EMSA	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.	927,CD225,DSPA2a,IFI17,LEU13,1-8D,DSPA2c,1-8U,DSPA2b,IP15	In vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection.	RT-PCR,Western blot	As IFITM1, 2 and 3 are very important for host to resist infection of IAV [4], [8], we infected wild-type and E2-3-truncated HEK293 cells with IAV Puerto Rico/8/1934 (PR8) at a MOI of 0.1 for 24 h. Although IFITM1, 2 and 3 were induced by PR8 virus in both wild-type and E2-3-truncated HEK293 cells, the inductions were greatly impaired upon truncation of E2-3 (Fig. 5A and B), further confirming the regulation of IFITM1, 2 and 3 expression by the enhancer E2-3. Surprisingly, we did not observe a significant effect on the replication of IAV when enhancer E2-3 was truncated, as revealed by the mRNA and protein levels of virus NP and progeny virus titers determined by TCID50 assay (Fig. S9). Nonetheless, when we treated wild-type and E2-3-truncated HEK293 cells with IFNβ respectively for 24 h before infection of PR8, NP mRNA and protein levels were found to be much higher in mutant HEK293 cells (Fig. 5C and D). Moreover, consistent with virus NP expression, the viral titers were also increased in E2-3-truncated cells (Fig. 5E), indicating that enhancer E2-3 was responsible for IFNβ-induced resistance to IAV infection.	STAT1	CANDF7,IMD31A,IMD31B,IMD31C,ISGF-3,STAT91	ChIP,EMSA,3C	"Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.
"	--	--	IFITM3
28511927	chr11	355447	358949	IFITM1	The enhancer drove the coordinate expression of IFITM1, 2 and 3 through constitutive long-range interactions and IFNβ-induced STAT1 binding.	human	kidney	Low throughput	Coordinated regulation of IFITM1, 2 and 3 genes by an IFN-responsive enhancer through long-range chromatin interactions	否	--	--	A549,HEK-293 cell	E_02_0800	Luciferase Reporter Assay,CRISPR/Cas9,ChIP,EMSA,3C	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer. Finally, we showed that in vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection. 	Enhancer	CRISPR/Cas9,3C	Luciferase Reporter Assay,EMSA	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.	927,CD225,DSPA2a,IFI17,LEU13,1-8D,DSPA2c,1-8U,DSPA2b,IP15	In vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection.	RT-PCR,Western blot	As IFITM1, 2 and 3 are very important for host to resist infection of IAV [4], [8], we infected wild-type and E2-3-truncated HEK293 cells with IAV Puerto Rico/8/1934 (PR8) at a MOI of 0.1 for 24 h. Although IFITM1, 2 and 3 were induced by PR8 virus in both wild-type and E2-3-truncated HEK293 cells, the inductions were greatly impaired upon truncation of E2-3 (Fig. 5A and B), further confirming the regulation of IFITM1, 2 and 3 expression by the enhancer E2-3. Surprisingly, we did not observe a significant effect on the replication of IAV when enhancer E2-3 was truncated, as revealed by the mRNA and protein levels of virus NP and progeny virus titers determined by TCID50 assay (Fig. S9). Nonetheless, when we treated wild-type and E2-3-truncated HEK293 cells with IFNβ respectively for 24 h before infection of PR8, NP mRNA and protein levels were found to be much higher in mutant HEK293 cells (Fig. 5C and D). Moreover, consistent with virus NP expression, the viral titers were also increased in E2-3-truncated cells (Fig. 5E), indicating that enhancer E2-3 was responsible for IFNβ-induced resistance to IAV infection.	STAT1	CANDF7,IMD31A,IMD31B,IMD31C,ISGF-3,STAT91	ChIP,EMSA,3C	"Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.
"	--	--	IFITM1
28511927	chr11	355447	358949	IFITM1	The enhancer drove the coordinate expression of IFITM1, 2 and 3 through constitutive long-range interactions and IFNβ-induced STAT1 binding.	human	kidney	Low throughput	Coordinated regulation of IFITM1, 2 and 3 genes by an IFN-responsive enhancer through long-range chromatin interactions	否	--	--	A549,HEK-293 cell	E_02_0800	Luciferase Reporter Assay,CRISPR/Cas9,ChIP,EMSA,3C	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer. Finally, we showed that in vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection. 	Enhancer	CRISPR/Cas9,3C	Luciferase Reporter Assay,EMSA	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.	927,CD225,DSPA2a,IFI17,LEU13,1-8D,DSPA2c,1-8U,DSPA2b,IP15	In vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection.	RT-PCR,Western blot	As IFITM1, 2 and 3 are very important for host to resist infection of IAV [4], [8], we infected wild-type and E2-3-truncated HEK293 cells with IAV Puerto Rico/8/1934 (PR8) at a MOI of 0.1 for 24 h. Although IFITM1, 2 and 3 were induced by PR8 virus in both wild-type and E2-3-truncated HEK293 cells, the inductions were greatly impaired upon truncation of E2-3 (Fig. 5A and B), further confirming the regulation of IFITM1, 2 and 3 expression by the enhancer E2-3. Surprisingly, we did not observe a significant effect on the replication of IAV when enhancer E2-3 was truncated, as revealed by the mRNA and protein levels of virus NP and progeny virus titers determined by TCID50 assay (Fig. S9). Nonetheless, when we treated wild-type and E2-3-truncated HEK293 cells with IFNβ respectively for 24 h before infection of PR8, NP mRNA and protein levels were found to be much higher in mutant HEK293 cells (Fig. 5C and D). Moreover, consistent with virus NP expression, the viral titers were also increased in E2-3-truncated cells (Fig. 5E), indicating that enhancer E2-3 was responsible for IFNβ-induced resistance to IAV infection.	STAT1	CANDF7,IMD31A,IMD31B,IMD31C,ISGF-3,STAT91	ChIP,EMSA,3C	"Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.
"	--	--	IFITM2
28511927	chr11	355447	358949	IFITM1	The enhancer drove the coordinate expression of IFITM1, 2 and 3 through constitutive long-range interactions and IFNβ-induced STAT1 binding.	human	kidney	Low throughput	Coordinated regulation of IFITM1, 2 and 3 genes by an IFN-responsive enhancer through long-range chromatin interactions	否	--	--	A549,HEK-293 cell	E_02_0800	Luciferase Reporter Assay,CRISPR/Cas9,ChIP,EMSA,3C	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer. Finally, we showed that in vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection. 	Enhancer	CRISPR/Cas9,3C	Luciferase Reporter Assay,EMSA	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.	927,CD225,DSPA2a,IFI17,LEU13,1-8D,DSPA2c,1-8U,DSPA2b,IP15	In vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection.	RT-PCR,Western blot	As IFITM1, 2 and 3 are very important for host to resist infection of IAV [4], [8], we infected wild-type and E2-3-truncated HEK293 cells with IAV Puerto Rico/8/1934 (PR8) at a MOI of 0.1 for 24 h. Although IFITM1, 2 and 3 were induced by PR8 virus in both wild-type and E2-3-truncated HEK293 cells, the inductions were greatly impaired upon truncation of E2-3 (Fig. 5A and B), further confirming the regulation of IFITM1, 2 and 3 expression by the enhancer E2-3. Surprisingly, we did not observe a significant effect on the replication of IAV when enhancer E2-3 was truncated, as revealed by the mRNA and protein levels of virus NP and progeny virus titers determined by TCID50 assay (Fig. S9). Nonetheless, when we treated wild-type and E2-3-truncated HEK293 cells with IFNβ respectively for 24 h before infection of PR8, NP mRNA and protein levels were found to be much higher in mutant HEK293 cells (Fig. 5C and D). Moreover, consistent with virus NP expression, the viral titers were also increased in E2-3-truncated cells (Fig. 5E), indicating that enhancer E2-3 was responsible for IFNβ-induced resistance to IAV infection.	STAT1	CANDF7,IMD31A,IMD31B,IMD31C,ISGF-3,STAT91	ChIP,EMSA,3C	"Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.
"	--	--	IFITM3
28511927	chr11	355447	358949	IFITM3	In this study, we surveyed the genomic context around IFITM locus and identified an IFN-responsive enhancer located 35kb upstream of IFITM3 gene promoter.	human	kidney	Low throughput	Coordinated regulation of IFITM1, 2 and 3 genes by an IFN-responsive enhancer through long-range chromatin interactions	否	--	--	A549,HEK-293 cell	E_02_0800	Luciferase Reporter Assay,CRISPR/Cas9,ChIP,EMSA,3C	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer. Finally, we showed that in vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection. 	Enhancer	CRISPR/Cas9,3C	Luciferase Reporter Assay,EMSA	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.	927,CD225,DSPA2a,IFI17,LEU13,1-8D,DSPA2c,1-8U,DSPA2b,IP15	In vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection.	RT-PCR,Western blot	As IFITM1, 2 and 3 are very important for host to resist infection of IAV [4], [8], we infected wild-type and E2-3-truncated HEK293 cells with IAV Puerto Rico/8/1934 (PR8) at a MOI of 0.1 for 24 h. Although IFITM1, 2 and 3 were induced by PR8 virus in both wild-type and E2-3-truncated HEK293 cells, the inductions were greatly impaired upon truncation of E2-3 (Fig. 5A and B), further confirming the regulation of IFITM1, 2 and 3 expression by the enhancer E2-3. Surprisingly, we did not observe a significant effect on the replication of IAV when enhancer E2-3 was truncated, as revealed by the mRNA and protein levels of virus NP and progeny virus titers determined by TCID50 assay (Fig. S9). Nonetheless, when we treated wild-type and E2-3-truncated HEK293 cells with IFNβ respectively for 24 h before infection of PR8, NP mRNA and protein levels were found to be much higher in mutant HEK293 cells (Fig. 5C and D). Moreover, consistent with virus NP expression, the viral titers were also increased in E2-3-truncated cells (Fig. 5E), indicating that enhancer E2-3 was responsible for IFNβ-induced resistance to IAV infection.	STAT1	CANDF7,IMD31A,IMD31B,IMD31C,ISGF-3,STAT91	ChIP,EMSA,3C	"Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.
"	--	--	IFITM1
28511927	chr11	355447	358949	IFITM3	In this study, we surveyed the genomic context around IFITM locus and identified an IFN-responsive enhancer located 35kb upstream of IFITM3 gene promoter.	human	kidney	Low throughput	Coordinated regulation of IFITM1, 2 and 3 genes by an IFN-responsive enhancer through long-range chromatin interactions	否	--	--	A549,HEK-293 cell	E_02_0800	Luciferase Reporter Assay,CRISPR/Cas9,ChIP,EMSA,3C	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer. Finally, we showed that in vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection. 	Enhancer	CRISPR/Cas9,3C	Luciferase Reporter Assay,EMSA	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.	927,CD225,DSPA2a,IFI17,LEU13,1-8D,DSPA2c,1-8U,DSPA2b,IP15	In vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection.	RT-PCR,Western blot	As IFITM1, 2 and 3 are very important for host to resist infection of IAV [4], [8], we infected wild-type and E2-3-truncated HEK293 cells with IAV Puerto Rico/8/1934 (PR8) at a MOI of 0.1 for 24 h. Although IFITM1, 2 and 3 were induced by PR8 virus in both wild-type and E2-3-truncated HEK293 cells, the inductions were greatly impaired upon truncation of E2-3 (Fig. 5A and B), further confirming the regulation of IFITM1, 2 and 3 expression by the enhancer E2-3. Surprisingly, we did not observe a significant effect on the replication of IAV when enhancer E2-3 was truncated, as revealed by the mRNA and protein levels of virus NP and progeny virus titers determined by TCID50 assay (Fig. S9). Nonetheless, when we treated wild-type and E2-3-truncated HEK293 cells with IFNβ respectively for 24 h before infection of PR8, NP mRNA and protein levels were found to be much higher in mutant HEK293 cells (Fig. 5C and D). Moreover, consistent with virus NP expression, the viral titers were also increased in E2-3-truncated cells (Fig. 5E), indicating that enhancer E2-3 was responsible for IFNβ-induced resistance to IAV infection.	STAT1	CANDF7,IMD31A,IMD31B,IMD31C,ISGF-3,STAT91	ChIP,EMSA,3C	"Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.
"	--	--	IFITM2
28511927	chr11	355447	358949	IFITM3	In this study, we surveyed the genomic context around IFITM locus and identified an IFN-responsive enhancer located 35kb upstream of IFITM3 gene promoter.	human	kidney	Low throughput	Coordinated regulation of IFITM1, 2 and 3 genes by an IFN-responsive enhancer through long-range chromatin interactions	否	--	--	A549,HEK-293 cell	E_02_0800	Luciferase Reporter Assay,CRISPR/Cas9,ChIP,EMSA,3C	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer. Finally, we showed that in vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection. 	Enhancer	CRISPR/Cas9,3C	Luciferase Reporter Assay,EMSA	Here, through public data mining, episomal luciferase reporter assay and in vivo CRISPR-Cas9 genome editing, we identified an IFN-responsive enhancer located 35 kb upstream of IFITM3 gene promoter upregulating the IFN-induced expression of IFITM1, 2 and 3 genes. Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.	927,CD225,DSPA2a,IFI17,LEU13,1-8D,DSPA2c,1-8U,DSPA2b,IP15	In vivo truncation of the enhancer impaired IFN-induced resistance to influenza A virus (IAV) infection.	RT-PCR,Western blot	As IFITM1, 2 and 3 are very important for host to resist infection of IAV [4], [8], we infected wild-type and E2-3-truncated HEK293 cells with IAV Puerto Rico/8/1934 (PR8) at a MOI of 0.1 for 24 h. Although IFITM1, 2 and 3 were induced by PR8 virus in both wild-type and E2-3-truncated HEK293 cells, the inductions were greatly impaired upon truncation of E2-3 (Fig. 5A and B), further confirming the regulation of IFITM1, 2 and 3 expression by the enhancer E2-3. Surprisingly, we did not observe a significant effect on the replication of IAV when enhancer E2-3 was truncated, as revealed by the mRNA and protein levels of virus NP and progeny virus titers determined by TCID50 assay (Fig. S9). Nonetheless, when we treated wild-type and E2-3-truncated HEK293 cells with IFNβ respectively for 24 h before infection of PR8, NP mRNA and protein levels were found to be much higher in mutant HEK293 cells (Fig. 5C and D). Moreover, consistent with virus NP expression, the viral titers were also increased in E2-3-truncated cells (Fig. 5E), indicating that enhancer E2-3 was responsible for IFNβ-induced resistance to IAV infection.	STAT1	CANDF7,IMD31A,IMD31B,IMD31C,ISGF-3,STAT91	ChIP,EMSA,3C	"Chromatin immunoprecipitation (ChIP), electrophoretic mobility shift assay (EMSA) and luciferase reporter assay demonstrated that signal transducers and activators of transcription (STAT) 1 bound to the enhancer with the treatment of IFN and was indispensable for the enhancer activity. Furthermore, using chromosome conformation capture technique, we revealed that the IFITM1, 2 and 3 genes physically clustered together and constitutively looped to the distal enhancer through long-range interactions in both HEK293 and A549 cells, providing structural basis for coordinated regulation of IFITM1, 2 and 3 by the enhancer.
"	--	--	IFITM3
28446439	chr11	17666830	17677080	MYOG	P3F uses SEs to setup auto-regulatory loops in collaboration with master transcription factors MYOG, MYOD and MYCN.	human	lung	Low+High throughput	PAX3-FOXO1 establishes myogenic super enhancers and confers BET bromodomain vulnerability	否	--	Alveolar Rhabdomyosarcoma	Human Fibroblast Cell Lines	E_02_0801	ChIP-seq,4C,Luciferase Reporter Assay	We found PAX3-FOXO1 most frequently occupied the strong Enhancer chromatin state , exemplified by known PAX3-FOXO1 target FGFR4 and oncogenes MYC, ALK and MET	Super-Enhancer	4C	ChIP-seq,Luciferase Reporter Assay	We found PAX3-FOXO1 most frequently occupied the strong Enhancer chromatin state , exemplified by known PAX3-FOXO1 target FGFR4 and oncogenes MYC, ALK and MET	MYF3,MYOD,PUM,bHLHc1	--	--	--	PAX3,FOXO1	CDHS,HUP2,WS1,WS3,FKH1,FKHR,FOXO1A	ChIP-qPCR,ChIP-seq	"To gain insight into the epigenetic consequences of PAX3-FOXO1, we mapped the landscape of active and repressive histone marks by sequencing DNA enriched by chromatin immunoprecipitation (ChIP-seq) from a patient derived fusion positive FP-RMS cell line RH4.
"	--	--	MYOD1
28446439	chr11	17666830	17677080	BRD4	Here, we report for the first time that BRD4 inhibition disrupts a hitherto undiscovered PAX3-FOXO1 interaction with BRD4, causes a rapid degradation of the fusion gene, and ablates its transcriptional output, thus revealing a subtype-selective therapeutic vulnerability to BRD4 inhibition.	human	lung	Low+High throughput	PAX3-FOXO1 establishes myogenic super enhancers and confers BET bromodomain vulnerability	否	--	Alveolar Rhabdomyosarcoma	Human Fibroblast Cell Lines	E_02_0801	ChIP-seq,4C,Luciferase Reporter Assay	We found PAX3-FOXO1 most frequently occupied the strong Enhancer chromatin state , exemplified by known PAX3-FOXO1 target FGFR4 and oncogenes MYC, ALK and MET	Super-Enhancer	4C	ChIP-seq,Luciferase Reporter Assay	We found PAX3-FOXO1 most frequently occupied the strong Enhancer chromatin state , exemplified by known PAX3-FOXO1 target FGFR4 and oncogenes MYC, ALK and MET	MYF3,MYOD,PUM,bHLHc1	--	--	--	PAX3,FOXO1	CDHS,HUP2,WS1,WS3,FKH1,FKHR,FOXO1A	ChIP-qPCR,ChIP-seq	"To gain insight into the epigenetic consequences of PAX3-FOXO1, we mapped the landscape of active and repressive histone marks by sequencing DNA enriched by chromatin immunoprecipitation (ChIP-seq) from a patient derived fusion positive FP-RMS cell line RH4.
"	--	--	MYOD1
28378740	chr3	107702615	107714185	CD47	CD47 is a cell surface molecule that inhibits phagocytosis of cells that express it by binding to its receptor, SIRPa, on macrophages and other immune cells.	human	breast	Low+High throughput	A CD47-associated super-enhancer links pro-inflammatory signalling to CD47 upregulation in breast cancer	否	--	Breast Cancer	MCF-7 cell	E_02_0802	ChIP-seq,Luciferase Reporter Assay	"By rank-ordering of enhancer regions based on H3K27ac enrichment, we discovered that T-cell acute lymphoblastic leukemia (T-ALL (RPMI18402, Jurkat and MOLT3)) diffuse large B-cell lymphoma (DLBCL (LY4)) and breast cancer (MCF7 and HCC1954) cell lines have SEs within B200 kb of CD47 (Fig. 1a). 
To validate their function experimentally, we cloned each candidate CD47 enhancer (E1–9) into an EGFP reporter lentiviral construct containing the minimal (basal) promoter for the thymidine kinase (TK) gene7. We found that two of the CD47 enhancers (E5 and E3.2) had MCF7- and Jurkat-speci?c regulatory activity (Fig. 2a–c).First, E5, in the downstream CD47 SE seen in breast cancers (Fig. 1a,b), showed increased reporter activity speci?cally in the MCF7 breast cancer cell line (Fig. 2a). Further analysis of publicly available Paired-End Tag (ChIA-PET) data22,23 con?rmed that E5 and the downstream CD47 SE in MCF7 are connected by a DNA loop containing RNA Polymerase II.Second, we found that E3.2, located within the upstream CD47 SE (Fig. 1a), had increased reporter expression speci?cally
in the Jurkat cell line (Fig. 2b). We also found that a third functional enhancer, E7, located within the upstream CD47 SE (Fig. 1a), drove reporter expression in all of the cancer cell lines tested (Fig. 2d)."	Enhancer	--	ChIP-seq,Luciferase Reporter Assay	"To validate their function experimentally, we cloned each candidate CD47 enhancer (E1–9) into an EGFP reporter lentiviral construct containing the minimal (basal) promoter for the thymidine kinase (TK) gene7. We found that two of the CD47 enhancers (E5 and E3.2) had MCF7- and Jurkat-speci?c regulatory activity (Fig. 2a–c).First, E5, in the downstream CD47 SE seen in breast cancers (Fig. 1a,b), showed increased reporter activity speci?cally in the MCF7 breast cancer cell line (Fig. 2a). Further analysis of publicly available Paired-End Tag (ChIA-PET) data22,23 con?rmed that E5 and the downstream CD47 SE in MCF7 are connected by a DNA loop containing RNA Polymerase II.Second, we found that E3.2, located within the upstream CD47 SE (Fig. 1a), had increased reporter expression speci?cally
in the Jurkat cell line (Fig. 2b). We also found that a third functional enhancer, E7, located within the upstream CD47 SE (Fig. 1a), drove reporter expression in all of the cancer cell lines tested (Fig. 2d)."	IAP,MER6,OA3	--	--	--	NFKB1	CVID12,EBP-1,KBF1,NF-kB,NF-kB1,NF-kappa-B1,NF-kappaB,NFKB-p105,NFKB-p50,NFkappaB,p105,p50	shRNA	We?observed?that?72?h?after?shRNA?transduction,?expression?of?CD47?transcript?and?protein?(measured?by?flow?cytometry)?was?significantly?reduced?by?NFKB1?(Fig.?3b,c)?and?PPARα?(Fig.?3b,?Supplementary?Fig.?3d,e)?shRNAs,?when?compared?to?control?shRNA.?On?the?other?hand,?shRNAs?against?STATs?3,?5?and?6?did?not?reduce?CD47?expression?significantly?(Fig.?3b).?This?information?demonstrates?that?NFKB?and?PPAR?are?involved?in?the?regulation?of?CD47?in?MCF7?cells?and?since?knocking?down?NFKB1?had?the?strongest?effect?on?CD47?gene?expression,?we?focus?this?study?on?the?regulatory?role?of?this?transcription?factor.	--	--	CD47
28335007	chr5	9034150	9036900	CLOCK	It is now known that the central molecular clock is formed by two main feedback loops consisting of core clock genes (1 4). In the first loop, BMAL1 and CLOCK form heterodimers to initiate the expression of Period (Per1/2/3) and Cryptochrome (Cry1/2) genes that in return repress BMAL1/CLOCK activities.	mouse		Low+High throughput	A class of circadian long non-coding RNAs mark enhancers modulating long-range circadian gene regulation.	否	--	--	hepatocyte	E_02_0803	ChIP-seq	On the other hand, the enhancer regions associated with lncRNAs tended to have much higher intensities of H3K27ac marks than the enhancers not associated with lncRNAs (KS test, P-value < 2.2 × 10?16) (Figure ?(Figure2E).2E). The enhancers associated with circadian lncRNAs have even higher levels of H3K27ac marks than those associated with lncRNAs (KS test, P-value = 0.0017). Taken together, there is a strong association between circadian lncRNAs and super-enhancers.	Super-Enhancer	4C	qPCR,RNA-seq,ChIP-seq	The enhancers defined from mouse liver GRO-seq and 5? CAGE technology were consistent with H3K27ac marks of enhancer at this lnc-Crot region (Supplementary Figure S3C). Using RACE assay, we obtained the full-length sequence of lnc-Crot (Figure ?(Figure4B).4B). Both BMAL1 and REV-ERBα binding sites were found on the promoter and gene body of lnc-Crot (Figure ?(Figure4B)4B) but not on the promoters of nearby circadian genes including Crot, Tmem243 and Dmtf1 (Supplementary Figure S3D).By qPCR, we showed that Crot and lnc-Crot were co-expressed (r = 0.8) across adult mouse tissues with elevated expression in liver and kidney (Supplementary Figure S3F).4C signals from three biological replicates at each circadian time were highly reproducible judging from their cross-sample correlations between 0.89 and 0.95. About 44% of 4C signals fell within chromosome 5 where lnc-Crot is situated and the signal profile around lnc-Crot region was displayed in Supplementary Figure S5A. 	lnc-Crot	Enhancer-associated circadian lncRNAs mark the genomic loci modulating long-range circadian gene regulation and shed new lights on the evolutionary origin of lncRNAs.	qPCR,CRISPR/Cas9	Our result points to a model that the lnc-Crot locus and nearby genes first form a scaffold upon which histone modifications and TF bindings then take place to confer tissue- and time-dependent expression (Figure ?(Figure5G).5G). The circadian lncRNAs that we examined may be a result of circadian transcription at the enhancer regions while the lncRNAs themselves do not influence the circadian gene regulation.	Arntl,Nr1d2	Arnt3,BMAL1b,Bmal1,MOP3,bHLHe5,bmal1b',RVR,Rev-erb	ChIP-seq,RNA-seq,Knockout mice	We defined BMAL1 and REV-ERB binding sites from two sets of BMAL1 ChIP-seq studies and two sets of REV-ERB ChIP-seq data in mouse liver respectively, resulting in 8001 BMAL1and 17545REV-ERB binding sites.Atotal of 259 (43%) circadian lncRNA clusters contain either BMAL1 or REV-ERB binding sites.For each lncRNA cluster, we quantified its expression in the BMAL1 knockout and WT mouse livers at CT0 and CT12 using our RNA-seq data.This suggested that circadian lncRNAs were regulated by these two master circadian TFs in the similar way as circadian protein coding genes.Circadian expression of lnc-Crot was disrupted when BMAL1 or REV-ERBα was knocked out, resulting in its downregulation at CT0 in BMAL1 knockout mice and upregulation at CT12 in REV-ERBα knockout mice (Figure ?(Figure4B,4B, Supplementary Figure S3E). This demonstrated that lnc-Crot was directly regulated by BMAL1 and REV-ERBα.	--	--	Gm40264
28335007	chr5	9034150	9036900	Cry1	It is now known that the central molecular clock is formed by two main feedback loops consisting of core clock genes (1 4). In the first loop, BMAL1 and CLOCK form heterodimers to initiate the expression of Period (Per1/2/3) and Cryptochrome (Cry1/2) genes that in return repress BMAL1/CLOCK activities.	mouse		Low+High throughput	A class of circadian long non-coding RNAs mark enhancers modulating long-range circadian gene regulation.	否	--	--	hepatocyte	E_02_0803	ChIP-seq	On the other hand, the enhancer regions associated with lncRNAs tended to have much higher intensities of H3K27ac marks than the enhancers not associated with lncRNAs (KS test, P-value < 2.2 × 10?16) (Figure ?(Figure2E).2E). The enhancers associated with circadian lncRNAs have even higher levels of H3K27ac marks than those associated with lncRNAs (KS test, P-value = 0.0017). Taken together, there is a strong association between circadian lncRNAs and super-enhancers.	Super-Enhancer	4C	qPCR,RNA-seq,ChIP-seq	The enhancers defined from mouse liver GRO-seq and 5? CAGE technology were consistent with H3K27ac marks of enhancer at this lnc-Crot region (Supplementary Figure S3C). Using RACE assay, we obtained the full-length sequence of lnc-Crot (Figure ?(Figure4B).4B). Both BMAL1 and REV-ERBα binding sites were found on the promoter and gene body of lnc-Crot (Figure ?(Figure4B)4B) but not on the promoters of nearby circadian genes including Crot, Tmem243 and Dmtf1 (Supplementary Figure S3D).By qPCR, we showed that Crot and lnc-Crot were co-expressed (r = 0.8) across adult mouse tissues with elevated expression in liver and kidney (Supplementary Figure S3F).4C signals from three biological replicates at each circadian time were highly reproducible judging from their cross-sample correlations between 0.89 and 0.95. About 44% of 4C signals fell within chromosome 5 where lnc-Crot is situated and the signal profile around lnc-Crot region was displayed in Supplementary Figure S5A. 	lnc-Crot	Enhancer-associated circadian lncRNAs mark the genomic loci modulating long-range circadian gene regulation and shed new lights on the evolutionary origin of lncRNAs.	qPCR,CRISPR/Cas9	Our result points to a model that the lnc-Crot locus and nearby genes first form a scaffold upon which histone modifications and TF bindings then take place to confer tissue- and time-dependent expression (Figure ?(Figure5G).5G). The circadian lncRNAs that we examined may be a result of circadian transcription at the enhancer regions while the lncRNAs themselves do not influence the circadian gene regulation.	Arntl,Nr1d2	Arnt3,BMAL1b,Bmal1,MOP3,bHLHe5,bmal1b',RVR,Rev-erb	ChIP-seq,RNA-seq,Knockout mice	We defined BMAL1 and REV-ERB binding sites from two sets of BMAL1 ChIP-seq studies and two sets of REV-ERB ChIP-seq data in mouse liver respectively, resulting in 8001 BMAL1and 17545REV-ERB binding sites.Atotal of 259 (43%) circadian lncRNA clusters contain either BMAL1 or REV-ERB binding sites.For each lncRNA cluster, we quantified its expression in the BMAL1 knockout and WT mouse livers at CT0 and CT12 using our RNA-seq data.This suggested that circadian lncRNAs were regulated by these two master circadian TFs in the similar way as circadian protein coding genes.Circadian expression of lnc-Crot was disrupted when BMAL1 or REV-ERBα was knocked out, resulting in its downregulation at CT0 in BMAL1 knockout mice and upregulation at CT12 in REV-ERBα knockout mice (Figure ?(Figure4B,4B, Supplementary Figure S3E). This demonstrated that lnc-Crot was directly regulated by BMAL1 and REV-ERBα.	--	--	Gm40264
28262837	chr9	97396388	97401553	AKT1	For example, AKT1 stimulates glycolysis by increasing the expression and membrane translocation of glucose trans_x0002_porters, and by phosphorylating key glycolytic enzymes such as hexokinase and phosphofructokinase-22,3.	human	liver	Low+High throughput	Inhibiting histone deacetylases suppresses glucose metabolism and hepatocellular carcinoma growth by restoring FBP1 expression	否	--	Hepatocellular carcinoma	Hepatocellular carcinoma	E_02_0804	ChIP-seq,ChIP,RT-PCR	We noticed that there is a putative H3K4me1-positive enhancer region in the first intron of the FBP1 gene (Fig.?4E).Importantly, we found that at the same region there is a peak of histone H3 lysine-27 acetylation (H3K27Ac) (Fig.?4E), the level of which often correlates with transcriptional activity of the gene. We first examined whether treatment of the HDAC inhibitor NaBu affects H3K27Ac levels in this region. To this end, we erformed chromatin immunoprecipitation (ChIP) assays using H3K27Ac-specific antibody. As demonstrated in Fig.?4F, the H3K27Ac level was readily detectable in the enhancer region of FBP1 gene in both HepG2 and SK-Hep1 cell lines.However, consistent with the finding that NaBu treatment markedly increased expression of FBP1 mRNA (Fig.?2A), it also significantly increased H3K27Ac level in the FBP1 enhancer (Fig.?4F). Similar to the finding that HDAC1 and HDAC2 knockdown induced FBP1 expression, depletion of these proteins alone or together also largely increased H3K27Ac level at this locus (Fig.?4G). This data indicate that the FBP1 gene locus indeed harbors a regulatory region where H3K27Ac level can be modulated by HDAC proteins. Thus, HDAC inhibitor-induced upregulation of H3K27 acetylation in the enhancer of the FBP1 gene correlates with increased expression of FBP1 induced by HDAC inhibitors.	Enhancer	--	ChIP-seq,ChIP,RT-PCR	We noticed that there is a putative H3K4me1-positive enhancer region in the first intron of the FBP1 gene (Fig.?4E).Importantly, we found that at the same region there is a peak of histone H3 lysine-27 acetylation (H3K27Ac) (Fig.?4E), the level of which often correlates with transcriptional activity of the gene. We first examined whether treatment of the HDAC inhibitor NaBu affects H3K27Ac levels in this region. To this end, we erformed chromatin immunoprecipitation (ChIP) assays using H3K27Ac-specific antibody. As demonstrated in Fig.?4F, the H3K27Ac level was readily detectable in the enhancer region of FBP1 gene in both HepG2 and SK-Hep1 cell lines.However, consistent with the finding that NaBu treatment markedly increased expression of FBP1 mRNA (Fig.?2A), it also significantly increased H3K27Ac level in the FBP1 enhancer (Fig.?4F). Similar to the finding that HDAC1 and HDAC2 knockdown induced FBP1 expression, depletion of these proteins alone or together also largely increased H3K27Ac level at this locus (Fig.?4G). This data indicate that the FBP1 gene locus indeed harbors a regulatory region where H3K27Ac level can be modulated by HDAC proteins. Thus, HDAC inhibitor-induced upregulation of H3K27 acetylation in the enhancer of the FBP1 gene correlates with increased expression of FBP1 induced by HDAC inhibitors.	FBP	HDAC-mediated suppression of FBP1 expression correlated with decreased histone H3K27Ac in the FBP1 enhancer.	ChIP,RT-PCR	Real-time PCR analysis of DNA mmunoprecipitated by control IgG or H3K27Ac antibody from HepG2 and SK-Hep1 cells transfected with control or HDAC1- and/or HDAC2-specific siRNAs. Cells harvested for ChIP assay at 48 hours after transfectio.	--	--	--	--	--	--	FBP1
28262837	chr9	97396388	97401553	TIGAR	The p53 protein inhibits the glycolytic pathway by up-regulating the expression of TP53-induced glycolysis and apop_x0002_tosis regulator (TIGAR)	human	liver	Low+High throughput	Inhibiting histone deacetylases suppresses glucose metabolism and hepatocellular carcinoma growth by restoring FBP2 expression	否	--	Hepatocellular carcinoma	Hepatocellular carcinoma	E_02_0804	ChIP-seq,ChIP,RT-PCR	We noticed that there is a putative H3K4me1-positive enhancer region in the first intron of the FBP1 gene (Fig.?4E).Importantly, we found that at the same region there is a peak of histone H3 lysine-27 acetylation (H3K27Ac) (Fig.?4E), the level of which often correlates with transcriptional activity of the gene. We first examined whether treatment of the HDAC inhibitor NaBu affects H3K27Ac levels in this region. To this end, we erformed chromatin immunoprecipitation (ChIP) assays using H3K27Ac-specific antibody. As demonstrated in Fig.?4F, the H3K27Ac level was readily detectable in the enhancer region of FBP1 gene in both HepG2 and SK-Hep1 cell lines.However, consistent with the finding that NaBu treatment markedly increased expression of FBP1 mRNA (Fig.?2A), it also significantly increased H3K27Ac level in the FBP1 enhancer (Fig.?4F). Similar to the finding that HDAC1 and HDAC2 knockdown induced FBP1 expression, depletion of these proteins alone or together also largely increased H3K27Ac level at this locus (Fig.?4G). This data indicate that the FBP1 gene locus indeed harbors a regulatory region where H3K27Ac level can be modulated by HDAC proteins. Thus, HDAC inhibitor-induced upregulation of H3K27 acetylation in the enhancer of the FBP1 gene correlates with increased expression of FBP1 induced by HDAC inhibitors.	Enhancer	--	ChIP-seq,ChIP,RT-PCR	We noticed that there is a putative H3K4me1-positive enhancer region in the first intron of the FBP1 gene (Fig.?4E).Importantly, we found that at the same region there is a peak of histone H3 lysine-27 acetylation (H3K27Ac) (Fig.?4E), the level of which often correlates with transcriptional activity of the gene. We first examined whether treatment of the HDAC inhibitor NaBu affects H3K27Ac levels in this region. To this end, we erformed chromatin immunoprecipitation (ChIP) assays using H3K27Ac-specific antibody. As demonstrated in Fig.?4F, the H3K27Ac level was readily detectable in the enhancer region of FBP1 gene in both HepG2 and SK-Hep1 cell lines.However, consistent with the finding that NaBu treatment markedly increased expression of FBP1 mRNA (Fig.?2A), it also significantly increased H3K27Ac level in the FBP1 enhancer (Fig.?4F). Similar to the finding that HDAC1 and HDAC2 knockdown induced FBP1 expression, depletion of these proteins alone or together also largely increased H3K27Ac level at this locus (Fig.?4G). This data indicate that the FBP1 gene locus indeed harbors a regulatory region where H3K27Ac level can be modulated by HDAC proteins. Thus, HDAC inhibitor-induced upregulation of H3K27 acetylation in the enhancer of the FBP1 gene correlates with increased expression of FBP1 induced by HDAC inhibitors.	FBP	HDAC-mediated suppression of FBP1 expression correlated with decreased histone H3K27Ac in the FBP1 enhancer.	ChIP,RT-PCR	Real-time PCR analysis of DNA mmunoprecipitated by control IgG or H3K27Ac antibody from HepG2 and SK-Hep1 cells transfected with control or HDAC1- and/or HDAC2-specific siRNAs. Cells harvested for ChIP assay at 48 hours after transfectio.	--	--	--	--	--	--	FBP1
28262837	chr9	97396388	97401553	FBP1	FBP1 is a rate-limiting enzyme in gluconeogenesis, and its loss seems to be a critical oncogenic event in epithelial-mesenchymal transition-promoted basal-like breast cancer cell progression5 .	human	liver	Low+High throughput	Inhibiting histone deacetylases suppresses glucose metabolism and hepatocellular carcinoma growth by restoring FBP3 expression	否	--	Hepatocellular carcinoma	Hepatocellular carcinoma	E_02_0804	ChIP-seq,ChIP,RT-PCR	We noticed that there is a putative H3K4me1-positive enhancer region in the first intron of the FBP1 gene (Fig.?4E).Importantly, we found that at the same region there is a peak of histone H3 lysine-27 acetylation (H3K27Ac) (Fig.?4E), the level of which often correlates with transcriptional activity of the gene. We first examined whether treatment of the HDAC inhibitor NaBu affects H3K27Ac levels in this region. To this end, we erformed chromatin immunoprecipitation (ChIP) assays using H3K27Ac-specific antibody. As demonstrated in Fig.?4F, the H3K27Ac level was readily detectable in the enhancer region of FBP1 gene in both HepG2 and SK-Hep1 cell lines.However, consistent with the finding that NaBu treatment markedly increased expression of FBP1 mRNA (Fig.?2A), it also significantly increased H3K27Ac level in the FBP1 enhancer (Fig.?4F). Similar to the finding that HDAC1 and HDAC2 knockdown induced FBP1 expression, depletion of these proteins alone or together also largely increased H3K27Ac level at this locus (Fig.?4G). This data indicate that the FBP1 gene locus indeed harbors a regulatory region where H3K27Ac level can be modulated by HDAC proteins. Thus, HDAC inhibitor-induced upregulation of H3K27 acetylation in the enhancer of the FBP1 gene correlates with increased expression of FBP1 induced by HDAC inhibitors.	Enhancer	--	ChIP-seq,ChIP,RT-PCR	We noticed that there is a putative H3K4me1-positive enhancer region in the first intron of the FBP1 gene (Fig.?4E).Importantly, we found that at the same region there is a peak of histone H3 lysine-27 acetylation (H3K27Ac) (Fig.?4E), the level of which often correlates with transcriptional activity of the gene. We first examined whether treatment of the HDAC inhibitor NaBu affects H3K27Ac levels in this region. To this end, we erformed chromatin immunoprecipitation (ChIP) assays using H3K27Ac-specific antibody. As demonstrated in Fig.?4F, the H3K27Ac level was readily detectable in the enhancer region of FBP1 gene in both HepG2 and SK-Hep1 cell lines.However, consistent with the finding that NaBu treatment markedly increased expression of FBP1 mRNA (Fig.?2A), it also significantly increased H3K27Ac level in the FBP1 enhancer (Fig.?4F). Similar to the finding that HDAC1 and HDAC2 knockdown induced FBP1 expression, depletion of these proteins alone or together also largely increased H3K27Ac level at this locus (Fig.?4G). This data indicate that the FBP1 gene locus indeed harbors a regulatory region where H3K27Ac level can be modulated by HDAC proteins. Thus, HDAC inhibitor-induced upregulation of H3K27 acetylation in the enhancer of the FBP1 gene correlates with increased expression of FBP1 induced by HDAC inhibitors.	FBP	HDAC-mediated suppression of FBP1 expression correlated with decreased histone H3K27Ac in the FBP1 enhancer.	ChIP,RT-PCR	Real-time PCR analysis of DNA mmunoprecipitated by control IgG or H3K27Ac antibody from HepG2 and SK-Hep1 cells transfected with control or HDAC1- and/or HDAC2-specific siRNAs. Cells harvested for ChIP assay at 48 hours after transfectio.	--	--	--	--	--	--	FBP1
28262751	chr4	97123309	97712957	SMARCB1	Of these subunits, several core members are present in most or all SWI/SNF complexes, including SMARCB1 (also known as SNF5, BAF47 and INI1), SMARCC1/SMARCC2 (also known as BAF155 and BAF170), and one of the two mutually exclusive ATPase subunits, SMARCA4 (also known as BRG1) and SMARCA2 (also known as BRM), which utilize energy derived from ATP hydrolysis to mobilize nucleosomes2,3.	mouse		Low+High throughput	The SWI/SNF chromatin remodelling complex is required for maintenance of lineage specific enhancers.	否	--	Malignancies	mouse embryonic fibroblast cell	E_02_0805	ChIP-seq	Following inactivation of either Smarcb1 or Smarca4, we observed little change in H3K27ac levels at promoters, but a marked reduction at many enhancers (Fig. 1b,c). This reduction at enhancers was robust and consistent across replicate experiments performed on MEFs derived from independent mice (Methods, Supplementary Figs 3-7).	Enhancer	--	ChIP-seq,Western blot	To investigate whether SWI/SNF is acting directly at active enhancers, we performed ChIP-Seq for the core SWI/SNF subunits SMARCC1 and SMARCA4 in wild-type and Smarcb1-deficient cells. Because the genome-wide binding profiles of these two subunits were very similar (Supplementary Fig. 3), we considered the average of the two experiments to be representative of SWI/SNF binding for each condition. Interestingly, we found that SWI/SNF was bound at the vast majority of enhancers in wild-type cells-over 95% of enhancers showed enrichment (IP>input; Fig. 2a and Supplementary Fig. 9a). Deletion of the Smarcb1 subunit led to a widespread reduction in SWI/SNF binding (Fig. 2b and Supplementary Fig. 9b).Taken together, the targeting of SWI/SNF to enhancers and the association between loss of SWI/SNF binding and the loss of H3K27ac suggests a direct role for the SWI/SNF complex in regulating the enhancer chromatin landscape in MEFs.	1110047K16Rik,9430022M17Rik,CTF,NF1-A,NF1A	--	--	--	Ep300	A430090G16,A730011L11,KAT3B,p300,p300 HAT	ChIP-seq	To further evaluate how the interaction between SWI/SNF and p300 regulates H3K27ac levels, we immunoprecipitated SWI/SNF complexes using an antibody against the core subunit SMARCC1 and measured histone acetylation activity using recombinant histones as a substrate. With immunoprecipitated SWI/SNF complexes from a RT cell line that lacked SMARCB1, the sample lacked acetyltransferase activity. However, re-expression of SMARCB1 increased H3K27-specific acetyltransferase activity, despite acetylation of H3K9ac being not significantly changed, suggesting the presence of H3K27-specific acetylation activity (Fig. 3d). 	--	--	Nfia
28262751	chr4	97123309	97712957	SMARCC2	Of these subunits, several core members are present in most or all SWI/SNF complexes, including SMARCB1 (also known as SNF5, BAF47 and INI1), SMARCC1/SMARCC2 (also known as BAF155 and BAF170), and one of the two mutually exclusive ATPase subunits, SMARCA4 (also known as BRG1) and SMARCA2 (also known as BRM), which utilize energy derived from ATP hydrolysis to mobilize nucleosomes2,3.	mouse		Low+High throughput	The SWI/SNF chromatin remodelling complex is required for maintenance of lineage specific enhancers.	否	--	Malignancies	mouse embryonic fibroblast cell	E_02_0805	ChIP-seq	Following inactivation of either Smarcb1 or Smarca4, we observed little change in H3K27ac levels at promoters, but a marked reduction at many enhancers (Fig. 1b,c). This reduction at enhancers was robust and consistent across replicate experiments performed on MEFs derived from independent mice (Methods, Supplementary Figs 3-7).	Enhancer	--	ChIP-seq,Western blot	To investigate whether SWI/SNF is acting directly at active enhancers, we performed ChIP-Seq for the core SWI/SNF subunits SMARCC1 and SMARCA4 in wild-type and Smarcb1-deficient cells. Because the genome-wide binding profiles of these two subunits were very similar (Supplementary Fig. 3), we considered the average of the two experiments to be representative of SWI/SNF binding for each condition. Interestingly, we found that SWI/SNF was bound at the vast majority of enhancers in wild-type cells-over 95% of enhancers showed enrichment (IP>input; Fig. 2a and Supplementary Fig. 9a). Deletion of the Smarcb1 subunit led to a widespread reduction in SWI/SNF binding (Fig. 2b and Supplementary Fig. 9b).Taken together, the targeting of SWI/SNF to enhancers and the association between loss of SWI/SNF binding and the loss of H3K27ac suggests a direct role for the SWI/SNF complex in regulating the enhancer chromatin landscape in MEFs.	1110047K16Rik,9430022M17Rik,CTF,NF1-A,NF1A	--	--	--	Ep300	A430090G16,A730011L11,KAT3B,p300,p300 HAT	ChIP-seq	To further evaluate how the interaction between SWI/SNF and p300 regulates H3K27ac levels, we immunoprecipitated SWI/SNF complexes using an antibody against the core subunit SMARCC1 and measured histone acetylation activity using recombinant histones as a substrate. With immunoprecipitated SWI/SNF complexes from a RT cell line that lacked SMARCB1, the sample lacked acetyltransferase activity. However, re-expression of SMARCB1 increased H3K27-specific acetyltransferase activity, despite acetylation of H3K9ac being not significantly changed, suggesting the presence of H3K27-specific acetylation activity (Fig. 3d). 	--	--	Nfia
28262751	chr4	97123309	97712957	SMARCC1	Of these subunits, several core members are present in most or all SWI/SNF complexes, including SMARCB1 (also known as SNF5, BAF47 and INI1), SMARCC1/SMARCC2 (also known as BAF155 and BAF170), and one of the two mutually exclusive ATPase subunits, SMARCA4 (also known as BRG1) and SMARCA2 (also known as BRM), which utilize energy derived from ATP hydrolysis to mobilize nucleosomes2,3.	mouse		Low+High throughput	The SWI/SNF chromatin remodelling complex is required for maintenance of lineage specific enhancers.	否	--	Malignancies	mouse embryonic fibroblast cell	E_02_0805	ChIP-seq	Following inactivation of either Smarcb1 or Smarca4, we observed little change in H3K27ac levels at promoters, but a marked reduction at many enhancers (Fig. 1b,c). This reduction at enhancers was robust and consistent across replicate experiments performed on MEFs derived from independent mice (Methods, Supplementary Figs 3-7).	Enhancer	--	ChIP-seq,Western blot	To investigate whether SWI/SNF is acting directly at active enhancers, we performed ChIP-Seq for the core SWI/SNF subunits SMARCC1 and SMARCA4 in wild-type and Smarcb1-deficient cells. Because the genome-wide binding profiles of these two subunits were very similar (Supplementary Fig. 3), we considered the average of the two experiments to be representative of SWI/SNF binding for each condition. Interestingly, we found that SWI/SNF was bound at the vast majority of enhancers in wild-type cells-over 95% of enhancers showed enrichment (IP>input; Fig. 2a and Supplementary Fig. 9a). Deletion of the Smarcb1 subunit led to a widespread reduction in SWI/SNF binding (Fig. 2b and Supplementary Fig. 9b).Taken together, the targeting of SWI/SNF to enhancers and the association between loss of SWI/SNF binding and the loss of H3K27ac suggests a direct role for the SWI/SNF complex in regulating the enhancer chromatin landscape in MEFs.	1110047K16Rik,9430022M17Rik,CTF,NF1-A,NF1A	--	--	--	Ep300	A430090G16,A730011L11,KAT3B,p300,p300 HAT	ChIP-seq	To further evaluate how the interaction between SWI/SNF and p300 regulates H3K27ac levels, we immunoprecipitated SWI/SNF complexes using an antibody against the core subunit SMARCC1 and measured histone acetylation activity using recombinant histones as a substrate. With immunoprecipitated SWI/SNF complexes from a RT cell line that lacked SMARCB1, the sample lacked acetyltransferase activity. However, re-expression of SMARCB1 increased H3K27-specific acetyltransferase activity, despite acetylation of H3K9ac being not significantly changed, suggesting the presence of H3K27-specific acetylation activity (Fig. 3d). 	--	--	Nfia
28262751	chr4	97123309	97712957	SMARCA2	Of these subunits, several core members are present in most or all SWI/SNF complexes, including SMARCB1 (also known as SNF5, BAF47 and INI1), SMARCC1/SMARCC2 (also known as BAF155 and BAF170), and one of the two mutually exclusive ATPase subunits, SMARCA4 (also known as BRG1) and SMARCA2 (also known as BRM), which utilize energy derived from ATP hydrolysis to mobilize nucleosomes2,3.	mouse		Low+High throughput	The SWI/SNF chromatin remodelling complex is required for maintenance of lineage specific enhancers.	否	--	Malignancies	mouse embryonic fibroblast cell	E_02_0805	ChIP-seq	Following inactivation of either Smarcb1 or Smarca4, we observed little change in H3K27ac levels at promoters, but a marked reduction at many enhancers (Fig. 1b,c). This reduction at enhancers was robust and consistent across replicate experiments performed on MEFs derived from independent mice (Methods, Supplementary Figs 3-7).	Enhancer	--	ChIP-seq,Western blot	To investigate whether SWI/SNF is acting directly at active enhancers, we performed ChIP-Seq for the core SWI/SNF subunits SMARCC1 and SMARCA4 in wild-type and Smarcb1-deficient cells. Because the genome-wide binding profiles of these two subunits were very similar (Supplementary Fig. 3), we considered the average of the two experiments to be representative of SWI/SNF binding for each condition. Interestingly, we found that SWI/SNF was bound at the vast majority of enhancers in wild-type cells-over 95% of enhancers showed enrichment (IP>input; Fig. 2a and Supplementary Fig. 9a). Deletion of the Smarcb1 subunit led to a widespread reduction in SWI/SNF binding (Fig. 2b and Supplementary Fig. 9b).Taken together, the targeting of SWI/SNF to enhancers and the association between loss of SWI/SNF binding and the loss of H3K27ac suggests a direct role for the SWI/SNF complex in regulating the enhancer chromatin landscape in MEFs.	1110047K16Rik,9430022M17Rik,CTF,NF1-A,NF1A	--	--	--	Ep300	A430090G16,A730011L11,KAT3B,p300,p300 HAT	ChIP-seq	To further evaluate how the interaction between SWI/SNF and p300 regulates H3K27ac levels, we immunoprecipitated SWI/SNF complexes using an antibody against the core subunit SMARCC1 and measured histone acetylation activity using recombinant histones as a substrate. With immunoprecipitated SWI/SNF complexes from a RT cell line that lacked SMARCB1, the sample lacked acetyltransferase activity. However, re-expression of SMARCB1 increased H3K27-specific acetyltransferase activity, despite acetylation of H3K9ac being not significantly changed, suggesting the presence of H3K27-specific acetylation activity (Fig. 3d). 	--	--	Nfia
28260788	chr11	8240851	8242851	LMO1	APOBEC signature mutation generates an oncogenic enhancer that drives LMO1 expression in T-ALL.	human	lymph	Low+High throughput	APOBEC signature mutation generates an oncogenic enhancer that drives LMO1 expression in T-ALL	否	--	--	RPMI-8402 cell	E_02_0806	ChIP-seq,Luciferase Reporter Assay,ChIA-PET	"To identify mutations in the T-ALL genome that might signi?cantly alter oncogene expression, we focused our search on aberrant,sample-speci?c enhancers in 10 different human T-ALL cell lines as identi?ed by H3K27ac ChIP-seq. The aberrant active enhancer we identi?ed was present upstream of the LMO1 gene in RPMI-8402 and Jurkat T-ALL cell lines.
To ascertain whether this single base-pair substitution can activate LMO1 gene expression, we cloned a 585-bp genomic DNA fragment from either the C allele or T allele upstream of luciferase and tested the enhancer activity of this fragment in a reporter assay.When introduced into Jurkat cells, the construct containing the T allele exhibited robust reporter activity, which was four-fold greater than that of the fragment containing the C allele (Figure 3f).Taken together, we have shown that the somatically acquired C-to-T mutation that creates a MYB binding motif ~ 4 kb upstream of the proximal transcription start site of LMO1 in T-ALL can generate an active transcriptional enhancer that drives monoallelic overexpression of the LMO1 oncogene.
We also used chromatin interaction analysis with paired-end tag sequencing (ChIA-PET) 24 in Jurkat cells to demonstrate that the stream of the proximal LMO1 transcription start site used by Jurkat cells (Figure 5d and Supplementary Figure S1), indicating that the active enhancer mediated by the acquired MYB binding motif loops to the LMO1 gene promoter region to regulate the transcription of LMO1 (Figure 5e).
"	Enhancer	--	Luciferase Reporter Assay	To ascertain whether this single base-pair substitution can activate LMO1 gene expression, we cloned a 585-bp genomic DNA fragment from either the C allele or T allele upstream of luciferase and tested the enhancer activity of this fragment in a reporter assay.When introduced into Jurkat cells, the construct containing the T allele exhibited robust reporter activity, which was four-fold greater than that of the fragment containing the C allele (Figure 3f).Taken together, we have shown that the somatically acquired C-to-T mutation that creates a MYB binding motif ~ 4 kb upstream of the proximal transcription start site of LMO1 in T-ALL can generate an active transcriptional enhancer that drives monoallelic overexpression of the LMO1 oncogene.	RBTN1,RHOM1,TTG1	--	--	--	MYB	Cmyb, c-myb, c-myb_CDS, efg	ChIP-seq	Analysis of the genomic sequences of both C and T alleles, using UniPROBE and HOCOMOCO databases, identi?ed a de novo-binding motif for the MYB transcription factor (Figure 3a and Supplementary Table S3), while analysis of the MYB and H3K27ac ChIP-seq DNA sequence reads aligned with this site demon-strated that MYB and H3K27ac were bound almost exclusively by the T allele (Figure 3b).Knockdown of MYB expression using lentivirus-transduced shRNA decreased the expression of LMO1 signi?cantly in Jurkat cells (Figure 3d), indicating that MYB binding to the somatically acquired heterozygous MYB binding motif leads to enhanced expression of LMO1 in T-ALL from the same allele.	--	--	LMO1
28244015	chr3	181572712	181574712	SOX2	These findings suggest that physiological levels of BPA increase estrogen receptor-positive breast cancer tumor maintenance through enhanced cancer stem-like cell activity via direct regulation of SOX2 transcription.	human	breast	Low throughput	Bisphenol A Induces Sox2 in ER + Breast Cancer Stem-Like Cells	否	--	--	MCF-7 cell	E_02_0807	ChIP,qPCR	To determine whether BPA-activated pCREB directly regulates SOX2 , ChIP was performed after a 5-minute treatment with either E2 or BPA. pCREB was enriched at an Enhancer region located 143 kilobases downstream of the SOX2 coding region only after BPA treatment (Figure 6), which correlates with gene expression	Enhancer	--	ChIP,qPCR	To determine whether BPA-activated pCREB directly regulates SOX2 , ChIP was performed after a 5-minute treatment with either E2 or BPA. pCREB was enriched at an Enhancer region located 143 kilobases downstream of the SOX2 coding region only after BPA treatment (Figure 6), which correlates with gene expression	ANOP3, MCOPS3	--	--	--	DST	BP240,BPA,BPAG1,CATX-15,CATX15,D6S1101,DMH,DT,EBSB2,HSAN6,MACF2	ChIP	To determine whether BPA-activated pCREB directly regulates SOX2, ChIP was performed after a 5-minute treatment with either E2 or BPA. pCREB was enriched at an Enhancer region located 143 kilobases downstream of the SOX2 coding region only after BPA treatment (Figure 6), which correlates with gene expression.	--	--	SOX2
28213503	chr11	44386118	44393090	STAT3	The receptor for IL-10 activates STAT3 through a JAK1 dependent pathway (12).                                                                                                                                                                                                                                                                                                            In most systems STAT3 is a transcriptional activator and there is little evidence that STAT3 has direct inhibitory function or binds to regulatory regions of IL-10-inhibited genes (13).                        	mouse		Low+High throughput	Inhibition of Inflammatory Gene Transcription by IL-10 Is Associated with Rapid Suppression of Lipopolysaccharide-Induced Enhancer Activation.	否	--	Inflammatory Disease	macrophage	E_02_0808	ChIP-seq	However, following treatment with acute IL-10, H3K27ac was significantly lower at peaks associated with genes from Cluster 2 than at peaks associated with genes from Cluster 1 (p-value <0.01 by Mann-Whitney test, Fig. 6A). Examples of Cluster 1 and Cluster 2 enhancers are shown in Fig. 6B and Fig. 6C, respectively. Interestingly this analysis identified a peak inhibited by acute IL-10 that encompasses a DNAse hypersensitivity site 10 kb upstream of Il12b that has previously been demonstrated in a reporter assay to exhibit enhancer activity (Fig. 6C).	Enhancer	--	ChIP-seq,RT-PCR	To evaluate this issue, we compared induction of Cxcl2 transcription in IL-10-deficient macrophages stimulated with LPS alone, both LPS and IL-10, or stimulated with IL-10 for 1 hour prior to stimulation with LPS. As predicted, LPS rapidly induced Cxcl2 pre-mRNA within 1h hour of stimulation. Surprisingly, addition of IL-10 at the time of LPS stimulation or addition 1 hour prior to LPS stimulation had little influence on Cxcl2 pre-mRNA at 1h post LPS stimulation, although significant suppression was observed at 2h post LPS stimulation (Fig. 8A). 	CINC-2a,GROb,Gro2,MIP-2,MIP-2a,Mgsa-b,Mip2,Scyb,Scyb2	--	--	--	Stat3	1110034C02Rik, AW109958, Aprf	ChIP-seq	To address this possibility, we performed ChIP-seq with an anti-STAT3 antibody to identify STAT3 binding sites.Interestingly, virtually all identified STAT3 binding sites were located within H3K4me1 peaks, suggesting that STAT3 binds to enhancers. As anticipated, we found strong STAT3 binding near Cluster 3 genes induced by IL-10, such as Socs3 (Fig. 7, bottom left), and IL-10 induced an increase in average mean acetylation at STAT3 binding sites associated with genes in Cluster 3, consistent with enhancer activation (Fig. 7, bottom right).	--	--	Cxcl2
28213503	chr11	44386118	44393090	JAK1	The receptor for IL-10 activates STAT3 through a JAK1 dependent pathway (12).                                                                                                                                                                                                                                                                                                            In most systems STAT3 is a transcriptional activator and there is little evidence that STAT3 has direct inhibitory function or binds to regulatory regions of IL-10-inhibited genes (13).                        	mouse		Low+High throughput	Inhibition of Inflammatory Gene Transcription by IL-10 Is Associated with Rapid Suppression of Lipopolysaccharide-Induced Enhancer Activation.	否	--	Inflammatory Disease	macrophage	E_02_0808	ChIP-seq	However, following treatment with acute IL-10, H3K27ac was significantly lower at peaks associated with genes from Cluster 2 than at peaks associated with genes from Cluster 1 (p-value <0.01 by Mann-Whitney test, Fig. 6A). Examples of Cluster 1 and Cluster 2 enhancers are shown in Fig. 6B and Fig. 6C, respectively. Interestingly this analysis identified a peak inhibited by acute IL-10 that encompasses a DNAse hypersensitivity site 10 kb upstream of Il12b that has previously been demonstrated in a reporter assay to exhibit enhancer activity (Fig. 6C).	Enhancer	--	ChIP-seq,RT-PCR	To evaluate this issue, we compared induction of Cxcl2 transcription in IL-10-deficient macrophages stimulated with LPS alone, both LPS and IL-10, or stimulated with IL-10 for 1 hour prior to stimulation with LPS. As predicted, LPS rapidly induced Cxcl2 pre-mRNA within 1h hour of stimulation. Surprisingly, addition of IL-10 at the time of LPS stimulation or addition 1 hour prior to LPS stimulation had little influence on Cxcl2 pre-mRNA at 1h post LPS stimulation, although significant suppression was observed at 2h post LPS stimulation (Fig. 8A). 	CINC-2a,GROb,Gro2,MIP-2,MIP-2a,Mgsa-b,Mip2,Scyb,Scyb2	--	--	--	Stat3	1110034C02Rik, AW109958, Aprf	ChIP-seq	To address this possibility, we performed ChIP-seq with an anti-STAT3 antibody to identify STAT3 binding sites.Interestingly, virtually all identified STAT3 binding sites were located within H3K4me1 peaks, suggesting that STAT3 binds to enhancers. As anticipated, we found strong STAT3 binding near Cluster 3 genes induced by IL-10, such as Socs3 (Fig. 7, bottom left), and IL-10 induced an increase in average mean acetylation at STAT3 binding sites associated with genes in Cluster 3, consistent with enhancer activation (Fig. 7, bottom right).	--	--	Cxcl2
28123038	chrX	55054584	55054678	ALAS2	However, compared with the int-8-GATA site, the int-1-GATA site is more essential for regulating ALAS2 expression through CRISPR/Cas9-mediated site-specific deletion. 	human	bone marrow	Low throughput	Intron 1 GATA site enhances ALAS2 expression indispensably during erythroid differentiation	否	--	--	K-562 CELL	E_02_0809	3C,Luciferase Reporter Assay,RT-qPCR,CRISPR/Cas9	"A luciferase reporter assay conirmed the enhancer activity of this GATA site in vitro (Figure 1E).
Furthermore, the physical proximity between the int-1-GATA and int-8-GATA sites and between the promoter and the int-8-GATA site were veriied by 3C assays (Figure 4H and I), suggesting that the promoter, the int-1-GATA site and the int-8-GATA site could form a potential chromatin enhancer loop.
To further interrogate the speciic role of proximal int-1-GATA and distal int-8-GATA enhancer elements in ALAS2 regulation, we employed CRISPR/Cas9 technol-ogy to separately delete the GATA1 binding sites from the intron 1 or 8 enhancer regions in K562 cells.As expected,GATA site deletion in int1 6 and int8 4 cells entirely disrupted GATA1 occupancy at the intron 1 and 8 enhancer regions, respectively, whereas each deletion did not affect GATA1 occupancy at the other intronic GATA site and the promoter region (Figure 7C). We detected signiicant reductions in ALAS2 expression in both int1 6 and int8 4 cells during cytosine arabinoside (AraC)-inducedK562 erythroid differentiation (Fig-Nucleic Acids Research, 2017, Vol. 45, No. 2 667 ure 7D and E)."	Enhancer	3C,CRISPR/Cas9	Luciferase Reporter Assay,RT-qPCR	"A luciferase reporter assay conirmed the enhancer activity of this GATA site in vitro (Figure 1E).
Furthermore, the physical proximity between the int-1-GATA and int-8-GATA sites and between the promoter and the int-8-GATA site were veriied by 3C assays (Figure 4H and I), suggesting that the promoter, the int-1-GATA site and the int-8-GATA site could form a potential chromatin enhancer loop.
To further interrogate the speciic role of proximal int-1-GATA and distal int-8-GATA enhancer elements in ALAS2 regulation, we employed CRISPR/Cas9 technol-ogy to separately delete the GATA1 binding sites from the intron 1 or 8 enhancer regions in K562 cells.As expected,GATA site deletion in int1 6 and int8 4 cells entirely disrupted GATA1 occupancy at the intron 1 and 8 enhancer regions, respectively, whereas each deletion did not affect GATA1 occupancy at the other intronic GATA site and the promoter region (Figure 7C). We detected signiicant reductions in ALAS2 expression in both int1 6 and int8 4 cells during cytosine arabinoside (AraC)-inducedK562 erythroid differentiation (Fig-Nucleic Acids Research, 2017, Vol. 45, No. 2 667 ure 7D and E)."	ALAS-E,ALASE,ANH1,ASB,SIDBA1,XLDPP,XLEPP,XLSA	--	--	--	GATA1 	ERYF1,GATA-1,GF-1,GF1,NF-E1,NFE1,XLANP,XLTDA,XLTT	ChIP-qPCR	The ChIP-qPCR assay showed the binding of GATA1 to the promoter and the intron 1 and 8 enhancer regions in int1_x0002_6, int8_x0002_4 and WT K562 cells. The DNA sequence at the exon 4-intron 4 junction (exon 4/intron 4) acts as a negative control region. Normal rabbit IgG was employed as the control in all ChIP assays.	--	--	ALAS2
28121289	chr6	88202011	88204330	SUN1	Although this mouse line was reported to be normal, SUN1 overexpression potentially could affect cell phenotype and gene regulation (Chen et al., 2012).	mouse		Low+High throughput	Mapping cell type-specific transcriptional enhancers using high affinity, lineage-specific Ep300 bioChIP-seq.	否	--	--	Endothelial stalk cell	E_02_0810	Luciferase Reporter Assay,ChIP-seq,Western blot	Viewing Ep300fb bioChiP-seq signal at genes selectively expressed in heart or brain confirmed robust tissue-specific differences that overlapped enhancers with known tissue-specific activity.To further functionally validate the transcriptional activity of these heterodimer motifs, we measured their enhancer activity using luciferase reporter assays.	Enhancer	--	Luciferase Reporter Assay,ChIP-seq	At the skeletal muscle specific gene Myod, Myf5Cre drove strong Ep300fb bioChiP-seq signal at a known distal Enhancer (Goldhamer et al., 1992), as well as a second Ep300 bound region about 12 kb upstream from the transcriptional start site.	Gata-2	--	--	--	Ep300	A430090G16,A730011L11,KAT3B,p300,p300 HAT	ChIP-seq	However, antibodies for Ep300 are marginal for robust ChIP-seq, particularly from tissues, leading to low reproducibility, variation between antibody lots, and inefficient Enhancer identification.	--	--	Gata2
28104492	chr15	97898854	97902854	CYP24A1	Transient transfection of Caco-2 cells with a constitutively active mutant K-RAS (G12V) significantly reduced 1,25(OH)2D-induced activity of both a human 25-hydroxyvitamin D, 24 hydroxyase (CYP24A1) promoter-luciferase and an artificial 3X vitamin D response element (VDRE) promoter-luciferase reporter gene.                                                                                                                                                                                                                                                                  However, chromatin accessibility to the VDR gene at the proximal promoter ( 300 bp), an enhancer region at 6 kb, and an enhancer region located in exon 3 was significantly reduced in RAS transformed YAMC cells (YAMC-RAS).	mouse		Low throughput	Constitutively active RAS signaling reduces 1,25 dihydroxyvitamin D-mediated gene transcription in intestinal epithelial cells by reducing vitamin D receptor expression.	否	--	Colon Cancer	YAMC Cell	E_02_0811	Luciferase Reporter Assay,Western blot,DNaseI-seq	Zella et al. [22] found that transcription of the mouse VDR gene is regulated at seven promoter and enhancer regions (Fig. 5A) in the mouse osteoblast cell line MC3T3-E1. In addition, the ENCODE project has identified DNAse I hypersensitive sites in the mouse large intestine that overlap with these regions.	Enhancer	--	Luciferase Reporter Assay,Western blot	However, chromatin accessibility to the VDR gene at the proximal promoter (_x0001_300 bp), an Enhancer region at _x0001_6 kb, and an Enhancer region located in exon 7 was significantly reduced in RAS transformed YAMC cells (YAMC-RAS).	Nr1i1	--	--	--	--	--	--	--	--	--	Vdr
28104492	chr15	97898854	97902854	VDR	Transient transfection of Caco-2 cells with a constitutively active mutant K-RAS (G12V) significantly reduced 1,25(OH)2D-induced activity of both a human 25-hydroxyvitamin D, 24 hydroxyase (CYP24A1) promoter-luciferase and an artificial 3X vitamin D response element (VDRE) promoter-luciferase reporter gene.                                                                                                                                                                                                                                                                  However, chromatin accessibility to the VDR gene at the proximal promoter ( 300 bp), an enhancer region at 6 kb, and an enhancer region located in exon 3 was significantly reduced in RAS transformed YAMC cells (YAMC-RAS).	mouse		Low throughput	Constitutively active RAS signaling reduces 1,25 dihydroxyvitamin D-mediated gene transcription in intestinal epithelial cells by reducing vitamin D receptor expression.	否	--	Colon Cancer	YAMC Cell	E_02_0811	Luciferase Reporter Assay,Western blot,DNaseI-seq	Zella et al. [22] found that transcription of the mouse VDR gene is regulated at seven promoter and enhancer regions (Fig. 5A) in the mouse osteoblast cell line MC3T3-E1. In addition, the ENCODE project has identified DNAse I hypersensitive sites in the mouse large intestine that overlap with these regions.	Enhancer	--	Luciferase Reporter Assay,Western blot	However, chromatin accessibility to the VDR gene at the proximal promoter (_x0001_300 bp), an Enhancer region at _x0001_6 kb, and an Enhancer region located in exon 7 was significantly reduced in RAS transformed YAMC cells (YAMC-RAS).	Nr1i1	--	--	--	--	--	--	--	--	--	Vdr
28087634	chr2	105072843	105076843	SOX9	SRY and SOX9 control the differentiation of Sertoli cells by triggering a dramatic transcriptional reprogramming of bipotential progenitor cells within just 24 h, leading to the upregulation of over 200 genes important for Sertoli cell development and downregulation of 100 pregranulosa cell-expressed genes that were expressed at the bipotential stage (Munger et al., 2013).	mouse		Low+High throughput	Genome-wide identification of regulatory elements in Sertoli cells.	否	--	Genitourinary Defects	Sustentacular cell	E_02_0812	ChIP-seq,DNaseI-seq	H3K27ac ChIP-seq on E13.5 Sertoli cells identified >28,000 H3K27ac peaks, ?70% of which overlapped a DHS in our E13.5 Sertoli cell dataset (Fig. 3A, Fig. S4).H3K27ac-positive DHSs, which are indicative of active enhancers, were significantly enriched specifically in neighboring Sertoli cell-expressed genes (Fig. 3D), as expected.	Enhancer	--	ChIP-seq,DNaseI-seq	To demonstrate this, we performed a transient transgenic assay with a putative active enhancer of the Wt1 gene (Fig. 5A,B).We identified a DHS peak located 50?kb upstream of Wt1 that was unique to E13.5 and E15.5 Sertoli cells compared with the other cell types we examined, and marked by H3K27ac, suggesting that it functions as an active enhancer.	D630046I19Rik,Wt-1	--	--	--	--	--	--	--	--	--	Wt1 
28087634	chr2	105072843	105076843	SRY	SRY and SOX9 control the differentiation of Sertoli cells by triggering a dramatic transcriptional reprogramming of bipotential progenitor cells within just 24 h, leading to the upregulation of over 200 genes important for Sertoli cell development and downregulation of 100 pregranulosa cell-expressed genes that were expressed at the bipotential stage (Munger et al., 2013).	mouse		Low+High throughput	Genome-wide identification of regulatory elements in Sertoli cells.	否	--	Genitourinary Defects	Sustentacular cell	E_02_0812	ChIP-seq,DNaseI-seq	H3K27ac ChIP-seq on E13.5 Sertoli cells identified >28,000 H3K27ac peaks, ?70% of which overlapped a DHS in our E13.5 Sertoli cell dataset (Fig. 3A, Fig. S4).H3K27ac-positive DHSs, which are indicative of active enhancers, were significantly enriched specifically in neighboring Sertoli cell-expressed genes (Fig. 3D), as expected.	Enhancer	--	ChIP-seq,DNaseI-seq	To demonstrate this, we performed a transient transgenic assay with a putative active enhancer of the Wt1 gene (Fig. 5A,B).We identified a DHS peak located 50?kb upstream of Wt1 that was unique to E13.5 and E15.5 Sertoli cells compared with the other cell types we examined, and marked by H3K27ac, suggesting that it functions as an active enhancer.	D630046I19Rik,Wt-1	--	--	--	--	--	--	--	--	--	Wt1 
28082341	chr3	46988575	46990242	GATA1	 In conclusion, we herein show a long-distance regulatory region with GATA1 binding sites as being a strong enhancer for NBEAL2 expression.	human	bone marrow	Low throughput	The transcription factor GATA1 regulates NBEAL2 expression through a long-distance enhancer	否	--	--	K-562 CELL	E_02_0813	Luciferase Reporter Assay,ChIP,RT-PCR	Chromatin immunoprecipitation sequencing revealed 5 GATA binding sites in a regulatory region 31 kb upstream of NBEAL2 covered by a H3K4Me1 mark indicative of an Enhancer locus.Luciferase reporter constructs containing this region confirmed its Enhancer activity in K562 cells, and mutagenesis of the GATA1 binding sites resulted in significantly reduced Enhancer activity. 	Enhancer	--	Luciferase Reporter Assay,ChIP,RT-PCR	Chromatin immunoprecipitation sequencing revealed 5 GATA binding sites in a regulatory region 31 kb upstream of NBEAL2 covered by a H3K4Me1 mark indicative of an Enhancer locus.Luciferase reporter constructs containing this region confirmed its Enhancer activity in K562 cells, and mutagenesis of the GATA1 binding sites resulted in significantly reduced Enhancer activity. 	BDPLT4,GPS	--	--	--	GATA1	ERYF1,GATA-1,GF-1,GF1,NF-E1,NFE1,XLANP,XLTDA,XLTT	Immunoblot	Immunoblot analysis for NBEAL2 with a rabbit polyclonal antibody and integrin β3 were performed (left) using total protein MK lysates at days 8 and 11 for the control and day 11 for GATA1 D218Y (right) using total protein MK lysates at day 13 for the control and GATA1 D218G.	--	--	NBEAL2
28045957	chr11	112769210	112772210	Sox9	Here, we present functional analysis of TES/TESCO, using CRISPR/Cas9 genome editing in mice. Deletion of TESCO or TES reduced Sox9 expression levels in XY fetal gonads to 60 or 45% respectively relative to wild type gonads, and reduced expression of the SOX9 target Amh. Although human patients heterozygous for null mutations in SOX9, which are assumed to have 50% of normal expression, often show XY female sex reversal, mice deleted for one copy of Sox9 do not. Consistent with this, we did not observe sex reversal in either TESCO-/- or TES-/- XY embryos or adult mice. However, embryos carrying both a conditional Sox9 null allele and the TES deletion developed ovotestes. Quantitative analysis of these revealed levels of 23% expression of Sox9 compared to wild type, and a significant increase in the expression of the granulosa cell marker Foxl2. This indicates that the threshold in mice where sex reversal begins to be seen is about half that of the ~50% levels predicted in humans. Our results demonstrate that TES/TESCO is a crucial enhancer regulating Sox9 expression in the gonad, but point to the existence of additional enhancers that act redundantly.	mouse	connective tissue	Low throughput	Normal Levels of Sox9 Expression in the Developing Mouse Testis Depend on the TES/TESCO Enhancer, but This Does Not Act Alone	否	--	--	Testis somatic cell	E_02_0814	Transgenic mice,CRISPR/Cas9,qRT-PCR	During mouse sex determination, transient expression of the Y-linked gene Sry up-regulates its direct target gene Sox9, via a 3.2 kb testis specific enhancer of Sox9 (TES), which includes a core 1.4 kb element, TESCO. SOX9 activity leads to differentiation of Sertoli cells, rather than granulosa cells from the bipotential supporting cell precursor lineage. Here, we present functional analysis of TES/TESCO, using CRISPR/Cas9 genome editing in mice. Deletion of TESCO or TES reduced Sox9 expression levels in XY fetal gonads to 60 or 45% respectively relative to wild type gonads, and reduced expression of the SOX9 target Amh. 	Enhancer	--	qRT-PCR	These results of qRT-PCR clearly indicate that the TESCO Enhancer is an important regulator of Sox9 expression throughout testis development, accounting for around 40% of its expression levels.	2010306G03Rik,AV220920,mKIAA4243	reduced expression of the SOX9 target Amh.	CRISPR/Cas9	Here, we present functional analysis of TES/TESCO, using CRISPR/Cas9 genome editing in mice. Deletion of TESCO or TES reduced Sox9 expression levels in XY fetal gonads to 60 or 45% respectively relative to wild type gonads, and reduced expression of the SOX9 target Amh.	--	--	--	--	--	--	Sox9 
28045957	chr11	112769210	112772210	TES	Here, we present functional analysis of TES/TESCO, using CRISPR/Cas9 genome editing in mice. Deletion of TESCO or TES reduced Sox9 expression levels in XY fetal gonads to 60 or 45% respectively relative to wild type gonads, and reduced expression of the SOX9 target Amh. Although human patients heterozygous for null mutations in SOX9, which are assumed to have 50% of normal expression, often show XY female sex reversal, mice deleted for one copy of Sox9 do not. Consistent with this, we did not observe sex reversal in either TESCO-/- or TES-/- XY embryos or adult mice. However, embryos carrying both a conditional Sox9 null allele and the TES deletion developed ovotestes. Quantitative analysis of these revealed levels of 23% expression of Sox9 compared to wild type, and a significant increase in the expression of the granulosa cell marker Foxl2. This indicates that the threshold in mice where sex reversal begins to be seen is about half that of the ~50% levels predicted in humans. Our results demonstrate that TES/TESCO is a crucial enhancer regulating Sox9 expression in the gonad, but point to the existence of additional enhancers that act redundantly.	mouse	connective tissue	Low throughput	Normal Levels of Sox9 Expression in the Developing Mouse Testis Depend on the TES/TESCO Enhancer, but This Does Not Act Alone	否	--	--	Testis somatic cell	E_02_0814	Transgenic mice,CRISPR/Cas9,qRT-PCR	During mouse sex determination, transient expression of the Y-linked gene Sry up-regulates its direct target gene Sox9, via a 3.2 kb testis specific enhancer of Sox9 (TES), which includes a core 1.4 kb element, TESCO. SOX9 activity leads to differentiation of Sertoli cells, rather than granulosa cells from the bipotential supporting cell precursor lineage. Here, we present functional analysis of TES/TESCO, using CRISPR/Cas9 genome editing in mice. Deletion of TESCO or TES reduced Sox9 expression levels in XY fetal gonads to 60 or 45% respectively relative to wild type gonads, and reduced expression of the SOX9 target Amh. 	Enhancer	--	qRT-PCR	These results of qRT-PCR clearly indicate that the TESCO Enhancer is an important regulator of Sox9 expression throughout testis development, accounting for around 40% of its expression levels.	2010306G03Rik,AV220920,mKIAA4243	reduced expression of the SOX9 target Amh.	CRISPR/Cas9	Here, we present functional analysis of TES/TESCO, using CRISPR/Cas9 genome editing in mice. Deletion of TESCO or TES reduced Sox9 expression levels in XY fetal gonads to 60 or 45% respectively relative to wild type gonads, and reduced expression of the SOX9 target Amh.	--	--	--	--	--	--	Sox9 
27989796	chr17	69541883	69542989	SOX9	SR4 activity and the observed SOX9 expression pattern suggest that SR4 may function as a Sox9 genital tubercle enhancer. 	human	testis	Low throughput	Altered SOX9 genital tubercle enhancer region in hypospadias	否	--	Disorders Of Sexual Development	TM4 cell	E_02_0815	Luciferase Reporter Assay,PCR,Transgenic mice,Immunofluorescence	"Our previous work involving the genomic analysis of isolated DSD patients revealed a 78 kb minimal sex determining region (RevSex) far upstream of SOX9 that was duplicated in 46,XX and deleted in 46,XY DSDs. It was postulated that RevSex contains a gonadal enhancer. However, the most highly conserved sub-region within RevSex, called SR4, was neither responsive to sex determining factors in vitro nor active in the gonads of transgenic mice, suggesting that SR4 may not be functioning as a testicular enhancer. Interestingly, SR4 transgenic mice showed reporter activity in the genital tubercle, the primordium of the penis and clitoris, a previously unreported domain of Sox9 expression. SOX9 protein was detected in the genital tubercle, notably in the urethral plate epithelium, 
preputial glands, ventral surface ectoderm and corpus cavernosa. SR4 may therefore function as a Sox9 genital tubercle enhancer, mutations of which could possibly lead to hypospadias, a birth defect seen in the DSD patients in the RevSex study. SR4 activity and the observed SOX9 expression pattern suggest that SR4 may function as a Sox9 genital tubercle enhancer. However, conditional ablation of Sox9 in the genital tubercle using Shh-Cre/+;Sox9flox/flox mice revealed no genital tubercle abnormalities, possibly due to compensation by similar Sox factors. To conclude, we have identified a novel regulatory enhancer driving Sox9 expression during external genitalia development. "	Enhancer	--	Transgenic mice,Immunofluorescence	The transcriptional activity of the SR4 enhancer in the genital tubercle led us to investigate whether SOX9 protein was also expressed there. Immunofluorescence using a SOX9 antibody on genital tubercle sections from E15.5 mouse embryos was performed (Fig. 5). SOX9 was detected in the genital tubercle of both sexes, specifically in the preputial glands, the urethral plate epithelium, ventral surface ectoderm and the corpus cavernosa. 	CMD1,CMPD1,SRA1,SRXX2,SRXY10	--	--	--	SOX9	CMD1,CMPD1,SRA1,SRXX2,SRXY10	Luciferase Reporter Assay	SR4 and TESC luciferase constructs containing an E1b minimal promoter, as well as the empty E1b-Luc vector, were transiently co-transfected into TM4 cells with expression plasmids bearing SF-1 and SRY, or SF-1 and SOX9. While activation of the TESCO enhancer was observed in luciferase assays, SR4 was not activated by the transcription factors tested. Data are represented in the form of relative luciferase activity.	--	--	SOX9
27986456	chr18	69656860	69683465	TCF4	We report that TCF4 comprises two transcriptional isoforms, both of which are required for optimal pDC development in vitro. The long Tcf4 isoform is expressed specifically in pDCs, and its deletion in mice impaired pDCs development and led to the expansion of non-canonical CD8 cDCs. The expression of Tcf4 commenced in progenitors and was further upregulated in pDCs, correlating with stage-specific activity of multiple enhancer elements. A conserved enhancer downstream of Tcf4 was required for its upregulation during pDC differentiation, revealing a positive feedback loop. The expression of Tcf4 and the resulting pDC differentiation were selectively sensitive to the inhibition of enhancer-binding BET protein activity. Thus, lineage-specifying function of E proteins is facilitated by lineage-specific isoform expression and by BET-dependent feedback regulation through distal regulatory elements. 	mouse	connective tissue	Low+High throughput	Isoform-Specific Expression and Feedback Regulation of E Protein TCF4 Control Dendritic Cell Lineage Specification	否	--	--	HoxB8-FL cell	E_02_0816	ATAC-seq	ATAC-Seq analysis of Tcf4 locus in primary DCs. Shown are ATAC-Seq peaks across ~1.5 Mb of the Tcf4 locus; indicated are proximal promoters of Tcf4L (green) and Tcf4S (purple), the 3′ enhancer (orange) and the cluster of 5′ regulatory elements (yellow). In this and subsequent panels, the scale was adjusted between different samples based on signals from housekeeping genes.We analyzed the 3′ region by ChIP during the differentiation of HoxB8-FL cells. Histone modifications associated with active enhancers, including histone 3 lysine 4 monomethylation (H3K4me1) and lysine 27 acetylation (H3K27ac), were induced in this region on day 4, i.e. at the onset of pDC differentiation (Fig. 5D).	Super-Enhancer	CRISPR/Cas9	ChIP-seq,ATAC-seq	ChIP analysis of histone modifications (H3K4me1 and H3K27ac) and of TCF4 binding to the 3′ Enhancer in differentiating HoxB8-FL cells.	5730422P05Rik,ASPI2,E2-2,E2.2,ITF-2,ITF-2b,ITF2,ME2,MITF-2A,MITF-2B,SEF-2,SEF2,SEF2-1,TFE,Tcf-4,bHLHb19	A conserved Enhancer downstream of Tcf4 was required for its upregulation during pDC differentiation, revealing a positive feedback loop	qRT-PCR,CRISPR/Cas9	By qRT-PCR, Tcf4S was prominently expressed in pDCs but also present in other cell types including B cells and cDCs	Tcf4	5730422P05Rik,ASPI2,E2-2,E2.2,ITF-2,ITF-2b,ITF2,ME2,MITF-2A,MITF-2B,SEF-2,SEF2,SEF2-1,TFE,Tcf-4,bHLHb19	qRT-PCR	"By qRT-PCR, Tcf4S was prominently expressed in pDCs but also present in other cell types including B cells and cDCs. 
"	--	--	Tcf4
27980063	chr1	24601612	24626812	GRHL3	Together, our findings support a function for BRD4 in promoting basal mammary cell epithelial differentiation, at least in part, by regulating FOXO factor function on enhancers to activate TP63 and GRHL3 expression.	human		Low+High throughput	BRD4 promotes p63 and GRHL3 expression downstream of FOXO in mammary epithelial cells	否	--	Breast Cancer	B cell	E_02_0817	ChIP-seq,Western blot	"ChIP analyses of BRD4 and RNAPII occupancy revealed that decreased BRD4 occupanc on enhancers in response to JQ1 or OTX015 treatment leads to a signiicant concomitant reduction in RNAPII occupancy on these regions (Figure 4H, I and K, L). While BRD4 occupancy was not significantly affected around the Np63 TSS, the potential enhancers displayed a substantial reduction in the occupancy of both BRD4 and RNAPII (Figure 4HandI).
Most importantly, BRD4 inhibition resulted in the down regulation of the putative TP63-- and GRHL3--associated eRNAs (Figure 4J and N)."	Enhancer	--	ChIP	"ChIP analyses of BRD4 and RNAPII occupancy revealed that decreased BRD4 occupanc on enhancers in response to JQ1 or OTX015 treatment leads to a significant concomitant reduction in RNAPII occupancy on these regions (Figure 4H, I and K, L).Altogether, these studies demonstrate an enhancer--associated function of BRD4 in modulating the expression of TP63 and GRHL3.
"	SOM,TFCP2L4,VWS2	This Enhancer is located in a region where a long-range chromatin interaction among the promoters and promoter-Enhancer of several genes has been described, possibly affecting their expression simultaneously.	Luciferase Reporter Assay	In the present work, by integrating several strategies, we have uncovered the variant most strongly associated with MS in the region. This variant also affects the activity of an Enhancer in an allele-dependent and orientation-dependent manner and correlates with the expression of five genes of the locus.	FOXO,GRHL3	FOXO,SOM,TFCP2L4,VWS2	Western blot	Western blot analyses of MCF10A protein ysates showing total p63 and GRHL3 expression with 100 nM and 1 _x0002_M of FOXO1 inhibitor AS1842856 (FOXO1i) for 24 h after removal of EGF and Insulin (-EGF/-Ins) for 48 h.	--	--	GRHL3
27941798	chr15	63833002	63863200	ARID1A	These tumors lack deregulation of APC/β-catenin signaling components, which are crucial gatekeepers in common forms of intestinal cancer. We find that ARID1A normally targets SWI/SNF complexes to enhancers, where they function in coordination with transcription factors to facilitate gene activation. ARID1B preserves SWI/SNF function in ARID1A-deficient cells, but defects in SWI/SNF targeting and control of enhancer activity cause extensive dysregulation of gene expression. These findings represent an advance in colon cancer modeling and implicate enhancer-mediated gene regulation as a principal tumor-suppressor function of ARID1A.	mouse	connective tissue	Low+High throughput	ARID1A loss impairs enhancer-mediated gene regulation and drives colon cancer in mice	否	--	Colon Cancer	HCT116 cell	E_02_0818	ChIP-seq	To determine if control of enhancer activity by SWI/SNF complexes is coordinated with TFs, we analyzed sequence motifs at enhancers sensitive to ARID1A loss. The CTCF motif was relatively depleted in regions of H3K27ac loss, implying CTCF-bound insulator regions may resist modulation, while the AP1 (JUND/FOSL1) motif was most enriched (Fig. 5a, Supplementary Table 5).Among factors assessed in HCT116 cells, binding of these TFs correlated most strongly with SWI/SNF occupancy (Supplementary Fig. 6b) and was higher at enhancers that lost activity than at enhancers that were unaffected by ARID1A deficiency (Fig. 5c). 	Super-Enhancer	--	ChIP-seq,ChIP-qPCR	To determine if ARID1A loss impairs enhancer activity?in vivo, we examined H3K27ac and gene expression in the colonic epithelium of wildtype and Villin-CreER-T2?Arid1afl/fl?mice. Again, whereas promoter activation states were changed little (Fig. 5d), the effects on H3K27ac at enhancers were significant and were correlated with changes in mRNA levels of the nearest genes (Fig. 5e).?	1110030E03Rik, BAF250a, Osa1, Smarcf1	--	--	--	Jun,Cebpb	AP-1c,c-jun,Jun,C/EBPbeta,CRP2,IL-6DBP,LAP,LIP,NF-IL6,NF-M,Nfil6	ChIP-seq	ChIP-Seq profiles for HCT116 cells, including those generated by ENCODE21 (Encyclopedia of DNA Elements, Supplementary Table 6), revealed further that H3K27ac loss was most strongly associated with sites bound in WT cells by SWI/SNF complexes and/or TFs including AP1, CEBPB, and TEAD4 (Fig. 5b). Among factors assessed in HCT116 cells, binding of these TFs correlated most strongly with SWI/SNF occupancy (Supplementary Fig. 6b) and was higher at enhancers that lost activity than at enhancers that were unaffected by ARID1A deficiency (Fig. 5c)	--	--	Arid1a
27920250	chr5	137465620	137479420	Epo	We prepared various Epo gene-reporter constructs utilizing a bacterial artificial chromosome and generated a number of transgenic-mouse lines. We observed that deletion of the CURE region (δCURE) abrogated Epo gene expression in REP cells. Although transgenic expression of the δCURE construct rescued Epo-deficient mice from embryonic lethality, the rescued mice had severe EPO-dependent anemia. These mouse lines serve as an elaborate model for the search for erythroid stimulatory activity and are referred to as AnRED (anemic model with renal EPO deficiency) mice. We also dissected the CURE region by exploiting a minigene harboring four phylogenetically conserved elements in reporter transgenic-mouse analyses. Our analyses revealed that Epo gene regulation in REP cells is a complex process that utilizes multiple regulatory influences.	mouse	epithelial tissue	Low throughput	Renal Anemia Model Mouse Established by Transgenic Rescue with an Erythropoietin Gene Lacking Kidney-Specific Regulatory Elements	否	--	Renal Anemia	Nephrocyte	E_02_0819	Luciferase Reporter Assay,Transgenic mice	17k-GFP contains the 17-kb upstream and 15-kb downstream regions, whereas 17kXM-GFP contains only the 17-kb upstream region as a regulatory element. As in 22k-GFP mice, GFP expression was observed in the kidney and liver in 17k-GFP mice under anemic conditions (Fig. 1C).	Enhancer	--	Luciferase Reporter Assay,qRT-PCR	we generated a series of transgenic GFP reporter constructs using 60k-GFP and 22k-GFP as the starting materia GFP expression was observed in the kidney but not in the liver in 17kXM-GFP mice.By means of long genomic PCR assays utilizing a primer set recognizing sequences located 18.6 kb upstream (forward primer) and 3.7 kb downstream (reverse primer) from the Epo gene transcription start site, we confirmed that the bulk of the Epo-BAC DNA containing a 17-kb upstream region and a downstream hepatic enhancer region was integrated into the genome of the transgenic mice in the right order (Fig. 4C).	Epo	--	--	--	--	--	--	--	--	--	Epo
27895109	chr9	78368337	78376479	SHH	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	SHH	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	HBB	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	HBB	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	Tet1	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	Tet1	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	Sall1	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	Sall1	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	Sox2	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	Sox2	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	Etl4	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	Etl4	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	Mcl1	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	Mcl1	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	Ooep	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	Ooep	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	Dppa5a	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	Dppa5a	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	Esrrb	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	Esrrb	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	Cbfa2t2	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	Cbfa2t2	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	Ranbp17	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	Ranbp17	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	Med13l	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	Med13l	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	AU018091	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	AU018091	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27895109	chr9	78368337	78376479	Prkcg	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Dppa5a
27895109	chr9	78368337	78376479	Prkcg	In addition, select super-enhancers and enhancers were identified that regulated clusters of paralogous genes. We conclude that, whereas robust transcriptional output can be achieved by an isolated enhancer, clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	mouse	epithelial tissue	Low+High throughput	Enhancers and super-enhancers have an equivalent regulatory role in embryonic stem cells through regulation of single or multiple genes	否	--	--	embryonic stem cell	E_02_0820	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B). Deletion of the entire EC(DppUp) significantly affects the expression of both Dppa5a and Ooep, although the effect on Ooep is much greater (92% reduction compared to a 36% reduction).Enhancer activity was identified in a reporter assay for the ?1 enhancer and the ?5.8 enhancer within the EC(DppUpA) and EC(DppUpB) regions, respectively.	Enhancer	--	Luciferase Reporter Assay,RT-qPCR,ChIP-seq	We found that the enhancer cluster EC(DppUp), which lies between the Dppa5a and Ooep genes, regulated both Dppa5a and Ooep in cis. We considered two alternatives for the mechanism underlying this observation: Either this region contained two distinct regulatory modules, one for Dppa5a and one for Ooep, or each of the enhancers within the cluster contributed to the expression of both genes. To differentiate between these two alternatives, we split the EC into two segments and deleted each individually (Fig. 2). The region closest to Ooep, EC(DppUpB), contains one MTL bound by four transcription factors, whereas the region closest to Dppa5a, EC(DppUpA), contains three separate MTLs. Reporter assays revealed that each of these regions contained an active enhancer (Fig. 2B).	AA536857,Dppa5,Esg1,ecat2,2410146L05Rik,Floped,Moep19,Sddr	Robust transcriptional output can be achieved by an isolated enhancer,clusters of enhancers acting on a common target gene act in a partially redundant manner to fine tune transcriptional output of their target genes.	ChIP-seq	This occurs despite the fact that deletion of EC(DppDn) alone has only a modest effect on both Dppa5a (16% reduction) and Ooep (15% reduction) ex_x0002_pression (Table 1). This finding indicates partially redundant control of Dppa5a and Ooep by Enhancers in the upstream and downstream EC.	--	--	--	--	--	--	Ooep
27881681	chr7	129554284	129564284	SOX9	Here, we aimed to determine the role of the novel SOX9-binding site in intron 6. We prepared reporter constructs that contain a Col2a1 promoter, intron 1 with or without intron 6, and the luciferase gene. Although the reporter constructs were not activated by SOX9 alone, the construct that contained both introns 1 and 6 was activated 5-10-fold by the SOX9/SOX5 or the SOX9/SOX6 combination in transient-transfection assays in 293T cells. This enhancement was also observed in rat chondrosarcoma cells that stably expressed the construct. CRISPR/Cas9-induced deletion of intron 6 in RCS cells revealed that a 10-bp region of intron 6 is necessary both for Col2a1 expression and SOX9 binding. Furthermore, SOX9, but not SOX5, binds to this region as demonstrated in an electrophoretic mobility shift assay, although both SOX9 and SOX5 bind to a larger 325-bp fragment of intron 6 containing this small sequence. These findings suggest a novel mechanism of action of SOX5/6; namely, the SOX9/5/6 combination enhances Col2a1 transcription through a novel enhancer in intron 6 together with the enhancer in intron 1.	mouse	epithelial tissue	Low+High throughput	A Novel Regulatory Mechanism of Type II Collagen Expression via a SOX9-dependent Enhancer in Intron 6	否	--	Skeletal Diseases	Chondrosarcoma Cell	E_02_0821	Luciferase Reporter Assay,ChIP-seq	However, ChIP sequencing revealed that SOX9 does not strongly bind to intron 1, but rather it binds to intron 6 and a site 30 kb upstream of the transcription start site. Here, we aimed to determine the role of the novel SOX9-binding site in intron 6. We prepared reporter constructs that contain a Col2a1 promoter, intron 1 with or without intron 6, and the luciferase gene. 	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,ChIP-seq	the ChIP-Seq data of SOX9 in the Col2a1 gene using rat chondrosarcoma cells (RCS cells)show that there is a strong SOX9-binding site in intron 6 and a weaker binding site in intron 1.Although the reporter constructs were not activated by SOX9 alone, the construct that contained both introns 1 and 6 was activated 5–10-fold by the SOX9/SOX5 or the SOX9/SOX6 combination in transient-transfection assays in 293T cells. This enhancement was also observed in rat chondrosarcoma cells that stably expressed the construct. CRISPR/Cas9-induced deletion of intron 6 in RCS cells revealed that a 10-bp region of intron 6 is necessary both for Col2a1 expression and SOX9 binding. 	Col2,Col2a,Col2a-1,Del1,Dmm,Lpk,M100413,Rgsc413,Rgsc856	--	--	--	Sox9	2010306G03Rik,AV220920,mKIAA4243	ChIP-seq,ChIP-qPCR,EMSA	SOX9 bind to intron 6 and the binding of SOX5/SOX6 to intron 6 may facilitate the binding of SOX9 to the intron 1.To explore this possibility, we tested whether SOX9 and SOX5 bound to the SB2 fragment(600bp)shownabove or an even shorter fragment by means of an EMSA.	--	--	Col2a1
27881681	chr7	129554284	129564284	Col2a1	Here, we aimed to determine the role of the novel SOX9-binding site in intron 6. We prepared reporter constructs that contain a Col2a1 promoter, intron 1 with or without intron 6, and the luciferase gene. Although the reporter constructs were not activated by SOX9 alone, the construct that contained both introns 1 and 6 was activated 5-10-fold by the SOX9/SOX5 or the SOX9/SOX6 combination in transient-transfection assays in 293T cells. This enhancement was also observed in rat chondrosarcoma cells that stably expressed the construct. CRISPR/Cas9-induced deletion of intron 6 in RCS cells revealed that a 10-bp region of intron 6 is necessary both for Col2a1 expression and SOX9 binding. Furthermore, SOX9, but not SOX5, binds to this region as demonstrated in an electrophoretic mobility shift assay, although both SOX9 and SOX5 bind to a larger 325-bp fragment of intron 6 containing this small sequence. These findings suggest a novel mechanism of action of SOX5/6; namely, the SOX9/5/6 combination enhances Col2a1 transcription through a novel enhancer in intron 6 together with the enhancer in intron 1.	mouse	epithelial tissue	Low+High throughput	A Novel Regulatory Mechanism of Type II Collagen Expression via a SOX9-dependent Enhancer in Intron 6	否	--	Skeletal Diseases	Chondrosarcoma Cell	E_02_0821	Luciferase Reporter Assay,ChIP-seq	However, ChIP sequencing revealed that SOX9 does not strongly bind to intron 1, but rather it binds to intron 6 and a site 30 kb upstream of the transcription start site. Here, we aimed to determine the role of the novel SOX9-binding site in intron 6. We prepared reporter constructs that contain a Col2a1 promoter, intron 1 with or without intron 6, and the luciferase gene. 	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,ChIP-seq	the ChIP-Seq data of SOX9 in the Col2a1 gene using rat chondrosarcoma cells (RCS cells)show that there is a strong SOX9-binding site in intron 6 and a weaker binding site in intron 1.Although the reporter constructs were not activated by SOX9 alone, the construct that contained both introns 1 and 6 was activated 5–10-fold by the SOX9/SOX5 or the SOX9/SOX6 combination in transient-transfection assays in 293T cells. This enhancement was also observed in rat chondrosarcoma cells that stably expressed the construct. CRISPR/Cas9-induced deletion of intron 6 in RCS cells revealed that a 10-bp region of intron 6 is necessary both for Col2a1 expression and SOX9 binding. 	Col2,Col2a,Col2a-1,Del1,Dmm,Lpk,M100413,Rgsc413,Rgsc856	--	--	--	Sox9	2010306G03Rik,AV220920,mKIAA4243	ChIP-seq,ChIP-qPCR,EMSA	SOX9 bind to intron 6 and the binding of SOX5/SOX6 to intron 6 may facilitate the binding of SOX9 to the intron 1.To explore this possibility, we tested whether SOX9 and SOX5 bound to the SB2 fragment(600bp)shownabove or an even shorter fragment by means of an EMSA.	--	--	Col2a1
27881681	chr7	129554284	129564284	SOX5	Here, we aimed to determine the role of the novel SOX9-binding site in intron 6. We prepared reporter constructs that contain a Col2a1 promoter, intron 1 with or without intron 6, and the luciferase gene. Although the reporter constructs were not activated by SOX9 alone, the construct that contained both introns 1 and 6 was activated 5-10-fold by the SOX9/SOX5 or the SOX9/SOX6 combination in transient-transfection assays in 293T cells. This enhancement was also observed in rat chondrosarcoma cells that stably expressed the construct. CRISPR/Cas9-induced deletion of intron 6 in RCS cells revealed that a 10-bp region of intron 6 is necessary both for Col2a1 expression and SOX9 binding. Furthermore, SOX9, but not SOX5, binds to this region as demonstrated in an electrophoretic mobility shift assay, although both SOX9 and SOX5 bind to a larger 325-bp fragment of intron 6 containing this small sequence. These findings suggest a novel mechanism of action of SOX5/6; namely, the SOX9/5/6 combination enhances Col2a1 transcription through a novel enhancer in intron 6 together with the enhancer in intron 1.	mouse	epithelial tissue	Low+High throughput	A Novel Regulatory Mechanism of Type II Collagen Expression via a SOX9-dependent Enhancer in Intron 6	否	--	Skeletal Diseases	Chondrosarcoma Cell	E_02_0821	Luciferase Reporter Assay,ChIP-seq	However, ChIP sequencing revealed that SOX9 does not strongly bind to intron 1, but rather it binds to intron 6 and a site 30 kb upstream of the transcription start site. Here, we aimed to determine the role of the novel SOX9-binding site in intron 6. We prepared reporter constructs that contain a Col2a1 promoter, intron 1 with or without intron 6, and the luciferase gene. 	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,ChIP-seq	the ChIP-Seq data of SOX9 in the Col2a1 gene using rat chondrosarcoma cells (RCS cells)show that there is a strong SOX9-binding site in intron 6 and a weaker binding site in intron 1.Although the reporter constructs were not activated by SOX9 alone, the construct that contained both introns 1 and 6 was activated 5–10-fold by the SOX9/SOX5 or the SOX9/SOX6 combination in transient-transfection assays in 293T cells. This enhancement was also observed in rat chondrosarcoma cells that stably expressed the construct. CRISPR/Cas9-induced deletion of intron 6 in RCS cells revealed that a 10-bp region of intron 6 is necessary both for Col2a1 expression and SOX9 binding. 	Col2,Col2a,Col2a-1,Del1,Dmm,Lpk,M100413,Rgsc413,Rgsc856	--	--	--	Sox9	2010306G03Rik,AV220920,mKIAA4243	ChIP-seq,ChIP-qPCR,EMSA	SOX9 bind to intron 6 and the binding of SOX5/SOX6 to intron 6 may facilitate the binding of SOX9 to the intron 1.To explore this possibility, we tested whether SOX9 and SOX5 bound to the SB2 fragment(600bp)shownabove or an even shorter fragment by means of an EMSA.	--	--	Col2a1
27881681	chr7	129554284	129564284	SOX6	Here, we aimed to determine the role of the novel SOX9-binding site in intron 6. We prepared reporter constructs that contain a Col2a1 promoter, intron 1 with or without intron 6, and the luciferase gene. Although the reporter constructs were not activated by SOX9 alone, the construct that contained both introns 1 and 6 was activated 5-10-fold by the SOX9/SOX5 or the SOX9/SOX6 combination in transient-transfection assays in 293T cells. This enhancement was also observed in rat chondrosarcoma cells that stably expressed the construct. CRISPR/Cas9-induced deletion of intron 6 in RCS cells revealed that a 10-bp region of intron 6 is necessary both for Col2a1 expression and SOX9 binding. Furthermore, SOX9, but not SOX5, binds to this region as demonstrated in an electrophoretic mobility shift assay, although both SOX9 and SOX5 bind to a larger 325-bp fragment of intron 6 containing this small sequence. These findings suggest a novel mechanism of action of SOX5/6; namely, the SOX9/5/6 combination enhances Col2a1 transcription through a novel enhancer in intron 6 together with the enhancer in intron 1.	mouse	epithelial tissue	Low+High throughput	A Novel Regulatory Mechanism of Type II Collagen Expression via a SOX9-dependent Enhancer in Intron 6	否	--	Skeletal Diseases	Chondrosarcoma Cell	E_02_0821	Luciferase Reporter Assay,ChIP-seq	However, ChIP sequencing revealed that SOX9 does not strongly bind to intron 1, but rather it binds to intron 6 and a site 30 kb upstream of the transcription start site. Here, we aimed to determine the role of the novel SOX9-binding site in intron 6. We prepared reporter constructs that contain a Col2a1 promoter, intron 1 with or without intron 6, and the luciferase gene. 	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay,ChIP-seq	the ChIP-Seq data of SOX9 in the Col2a1 gene using rat chondrosarcoma cells (RCS cells)show that there is a strong SOX9-binding site in intron 6 and a weaker binding site in intron 1.Although the reporter constructs were not activated by SOX9 alone, the construct that contained both introns 1 and 6 was activated 5–10-fold by the SOX9/SOX5 or the SOX9/SOX6 combination in transient-transfection assays in 293T cells. This enhancement was also observed in rat chondrosarcoma cells that stably expressed the construct. CRISPR/Cas9-induced deletion of intron 6 in RCS cells revealed that a 10-bp region of intron 6 is necessary both for Col2a1 expression and SOX9 binding. 	Col2,Col2a,Col2a-1,Del1,Dmm,Lpk,M100413,Rgsc413,Rgsc856	--	--	--	Sox9	2010306G03Rik,AV220920,mKIAA4243	ChIP-seq,ChIP-qPCR,EMSA	SOX9 bind to intron 6 and the binding of SOX5/SOX6 to intron 6 may facilitate the binding of SOX9 to the intron 1.To explore this possibility, we tested whether SOX9 and SOX5 bound to the SB2 fragment(600bp)shownabove or an even shorter fragment by means of an EMSA.	--	--	Col2a1
27869826	chr11	2219531	2239062	IRS4	We demonstrate that IRS4 overexpression in lung cancer is associated with recurrent deletions in cis, and we present evidence supporting a tumor-promoting role.	human	lung	Low+High throughput	Pan-cancer analysis of somatic copy-number alterations implicates IRS4 and IGF2 in enhancer hijacking	否	--	Lung Cancer	HCC-15 cell	E_02_0822	ChIP-seq,Luciferase Reporter Assay	"We next performed ChIP-Seq at the IGF2 locus, detecting an accumulation of the active chromatin mark H3K27ac at a previously identified IGF2 enhancer66 herein referred to as IGF2 cognate enhancer (Fig. 5a, Supplementary Fig. 11). An even more pronounced H3K27ac peak, however, intersected with an element previously inferred to represent a lineage-specific super-enhancer in CRC cell lines (VACO-400 and VACO-9M)46.To verify enhancer function, we performed luciferase assays revealing enhancer activity of cloned fragments of this previously inferred super-enhancer46 in the HCT116 colon cancer but not in a control (HeLa) cancer cell line (Supplementary Fig. 12 and Supplementary Table 6).
"	Super-Enhancer	--	Luciferase Reporter Assay	To verify enhancer function, we performed luciferase assays revealing enhancer activity of cloned fragments of this previously inferred super-enhancer46 in the HCT116 colon cancer but not in a control (HeLa) cancer cell line (Supplementary Fig. 12 and Supplementary Table 6).	C11orf43,GRDF,IGF-II,PP9974	this IGF2 region indeed interacts with and hence represents a candidate IGF2 Enhancer.	4C-seq	we additionally performed 4C-Seq (chromosome conformation capture sequencing63) experiments employing the putative CRE downstream of IRS4 as a viewpoint	--	--	--	--	--	--	IGF2
27333824	chr1	183149939	183150336	CDX2	Regulation of Laminin γ2 Expression by CDX2 in Colonic Epithelial Cells Is Impaired During Active Inflammation.	human	Intestinal epithelium	Low throughput	Regulation of Laminin γ2 Expression by CDX2 in Colonic Epithelial Cells Is Impaired During Active Inflammation	否	--	--	enterocyte	E_02_0823	Luciferase Reporter Assay	"To determine whether CDX2 regulates the basal LAMC2 gene activity, a luciferase reporter gene driven by the LAMC2 promoter with and without the upstream LAMC2 enhancer identi?ed previously [Boyd et al., 2014] was transfected into Caco-2 cells without or with concomitant CDX2 expression plasmid. Over-expression of CDX2 increased the luciferase activity driven by the enhancer-less construct of LAMC2 by 2.5-fold (P?0.028) relative to cells transfected with the LAMC2 reporter vector alone, whereas the LAMC2 promoter with enhancer construct gave a fourfold increase (P?0.006) in reporter signal when co-transfected with CDX2 expression plasmid relative to cells transfected with the LAMC2 promoter/enhancer reporter vector alone (Fig. 1A).
The LAMC2 luciferase reporter constructs were: pGL3-LAMC2 containing the 1.2 kb human LAMC2 promoter region upstream of transcription start site [Olsen et al., 2000], and pGL3-LAMC2+ Enhancer containing the 1.2 kb LAMC2 promoter and the enhancer region at chr1:183,149,939–183,150,336 (hg19) [Boyd et al., 2014]."	Enhancer	--	Luciferase Reporter Assay	To determine whether CDX2 regulates the basal LAMC2 gene activity, a luciferase reporter gene driven by the LAMC2 promoter with and without the upstream LAMC2 enhancer identi?ed previously [Boyd et al., 2014] was transfected into Caco-2 cells without or with concomitant CDX2 expression plasmid. Over-expression of CDX2 increased the luciferase activity driven by the enhancer-less construct of LAMC2 by 2.5-fold (P?0.028) relative to cells transfected with the LAMC2 reporter vector alone, whereas the LAMC2 promoter with enhancer construct gave a fourfold increase (P?0.006) in reporter signal when co-transfected with CDX2 expression plasmid relative to cells transfected with the LAMC2 promoter/enhancer reporter vector alone (Fig. 1A).	B2T,BM600,CSF,EBR2,EBR2A,LAMB2T,LAMNB2	--	--	--	CDX2	CDX-3/AS, CDX3, CDX2	ChIP-seq	Thus, to further analyze,whether LAMC2 is a direct target of CDX2 also in the native chromatin environment, we performed ChIP experiments with Caco-2 and with cells purified from human colonic tissue samples.	--	--	LAMC2
27207652	chr11	95817801	95818824	DNMT3B	This condensed chromatin structure is associated with binding of DNMT3B and decreased occupancy of OCT1 transcription factor at MAML2 enhancer, suggesting a role of DNMT3B in increasing methylation of MAML2 after stilbenoid treatment. Our results deliver a novel insight into epigenetic regulation of oncogenic signals in cancer and provide support for epigenetic-targeting strategies as an effective anticancer approac	human	connective tissue	Low+High throughput	Stilbenoids remodel the DNA methylation patterns in breast cancer cells and inhibit oncogenic NOTCH signaling through epigenetic regulation of MAML2 transcriptional activity	否	--	Breast Cancer	MCF10CA1h,MCF10CA1a cell	E_02_0824	ChIP,qPCR,Transfection,Western blot	"The difference in DNA meth_x0002_ylation within MAML2 in RSV treated versus control cells was 
determined as 0.37 in MCF10CA1h and 0.1 in MCF10CA1a cells based on the array data. These elevated levels of methylation were identified in a fragment corresponding to the predic_x0002_tive enhancer within MAML2 gene body. It has been demonstrated that active enhancers are enriched with H3K27ac.We confirmed by ChIP assay that this histone mark is present at MAML2 in 
cancer cells and its occupancy is significantly reduced by RSV.These data strongly support the role of this region as a gene enhancer and the role of RSV in decreasing the activ_x0002_ity of this enhancer."	Enhancer 	--	ChIP,Transfection,Western blot	"MAML2, a coactivator of NOTCH targets, is methylated at the enhancer region and transcriptionally silenced in response to stilbenoids, possibly explaining the downregulation 
of NOTCH target genes.It has been demonstrated that active enhancers are enriched with H3K27ac.We confirmed by ChIP assay that this histone mark is present at MAML2 in 
cancer cells and its occupancy is significantly reduced by RSV."	MAM-3,MAM2,MAM3,MLL-MAML2	--	--	--	POU2F1	OCT1,OTF1,oct-1B	ChIP,qPCR	Using ChIP, we confirmed OCT1 binding to MAML2 enhancer (Figure?6C, control cells). The binding dramati_x0002_cally decreases upon treatment of MCF10CA1a with 15?μM RSV.The lack of OCT1 binding may be directly linked to MAML2 transcriptional silencing. To test this hypothesis, we depleted OCT1 in MCF10CA1a cells using SmartPool siRNA mixture and four siRNA sequences separately, as confirmed by QPCR and western blot and tested the effect of OCT1 absence on MAML2 expression.	--	--	MAML2
27166834	chr8	120876144	120876856	CTCF	We describe enhancer-blocking or boundary elements on either side of the locus that are bound in vivo by the transcription factor CTCF, but we found that they do not coincide with transitions in nuclease sensitivity flanking the locus or with patterns of histone modifications within it. 	mouse		Low+High throughput	A Complex Chromatin Landscape Revealed by Patterns of Nuclease Sensitivity and Histone Modification within the Mouse 尾-Globin Locus	否	--	--	embryonic cell 	E_02_0825	3C,ChIP-seq	To identify the presence of physical interaction between the 11 enhancer candidates and the Foxf1 promoter, 3C assays were performed. Among 11 selected regions, three enhancer candidates demonstrated interactions with the Foxf1 promoter.	Enhancer 	3C	RT-qPCR,DNaseI-seq,Transgenic mice	"To investigate the in vivo activity of the discovered enhanc_x0002_ers and compare the location of activity with Foxf1-express_x0002_ing regions, we generated enhancer-driven lacZ-reporter 
mice 5′e207mFoxf1-lacZ and 5′e201mFoxf1-lacZ.Foxf1 mRNA was expressed in the maxilla, mandible, limbs, sclerotome and gut of wild-type mouse embryos at E12 (Fig. 2a), whereas 
lacZ-positive cells were observed in part of the forebrain and neural tube in 5′e207mFoxf1-lacZ transgenic mice at E11 and E12 as well as 5′e201mFoxf1-lacZ transgenic mouse embryos at E11 after x-gal staining.Foxf1 was also expressed in the mesenchyme surrounding 
epithelial buds in lungs at E12."	AI450827,FREAC1a,Freac-1,HFH-8,Hfh8,Foxf1	--	--	--	Gli1,Gli2,Gli3 	AV235269,Zfp-5,Zfp5;Gli2,AI854843,AU023367,Bph,GLI3-190,GLI3FL,Pdn,Xt,add	RT-qPCR,Luciferase Reporter Assay	Schematic drawing of luciferase reporter constructs containing 112 bp 5′e207mFoxf1 and 173 bp 5′e201mFoxf1 fragments with Gli binding sites is shown. Luciferase reporter constructs were assayed for luciferase activity without or with Gli1 over-expression vector at 50 or 100 ng. 	--	--	Foxf1
27149122	chr5	110175800	110176600	TSLP	Knockdown of the transcription factor predicted to bind the enhancer region (NHLH1) in a human cell line (HEK293) expressing NHLH1 resulted in lower TSLP expression.	human	heart	low throughput	Discovery of Genetic Variation on Chromosome 5q22 Associated with Mortality in Heart Failure	是	rs9885413	Heart Failure	293T cell	E_02_0826	Luciferase Reporter Assay	To experimentally test the effect of rs9885413 on enhancer activity, the 100 bp region flanking the SNP (50 bp on either side) was cloned into a reporter vector and transfected into HEK293 cells expressing NHLH1 (S1 Text). Luciferase activity measured after 24 hours was 4-fold higher with a construct corresponding to the risk allele as compared to the wild-type allele (S4 Fig, P < 0.001), indicating that the risk allele of rs9885413 substantially increases enhancer activity.	enhancer	--	Luciferase Reporter Assay	To experimentally test the effect of rs9885413 on enhancer activity, the 100 bp region flanking the SNP (50 bp on either side) was cloned into a reporter vector and transfected into HEK293 cells expressing NHLH1 (S1 Text). Luciferase activity measured after 24 hours was 4-fold higher with a construct corresponding to the risk allele as compared to the wild-type allele (S4 Fig, P < 0.001), indicating that the risk allele of rs9885413 substantially increases enhancer activity.	TSLP	--	--	--	--	--	--	--	110176128	Transfection,Luciferase Reporter Assay	TSLP
26937964	chr7	35156353	35161233	Runx1	CRISPR/Cas9-mediated replacement of the wild-type enhancer with a variant mutant in its seven Ets sites leads to 20-fold reduction of Cebpa mRNA in the 32Dcl3 myeloid cell line. To determine the effect of deleting the enhancer in vivo, we now characterize C57BL/6 mice in which loxP sites flank a 688 bp DNA segment containing the enhancer. CMV-Cre mediated germline deletion resulted in diminution of the expected number of viable Enh(f/f);CMV-Cre offspring, with 28-fold reduction in marrow Cebpa mRNA but normal levels in liver, lung, adipose, intestine, muscle, and kidney. Cre-transduction of lineage-negative marrow cells in vitro reduced Cebpa mRNA 12-fold, with impairment of granulocytic maturation, morphologic blast accumulation, and IL-3 dependent myeloid colony replating for >12 generations. Exposure of Enh(f/f);Mx1-Cre mice to pIpC led to 14-fold reduction of Cebpa mRNA in GMP or CMP, 30-fold reduction in LSK, and <2-fold reduction in the LSK/SLAM subset. FACS analysis of marrow from these mice revealed 10-fold reduced neutrophils, 3-fold decreased GMP, and 3-fold increased LSK cells. Progenitor cell cycle progression was mildly impaired. Granulocyte and B lymphoid colony forming units were reduced while monocytic and erythroid colonies were increased, with reduced Pu.1 and Gfi1 and increased Egr1 and Klf4 in GMP. Finally, competitive transplantation indicated preservation of functional long-term hematopoietic stem cells upon enhancer deletion and confirmed marrow-intrinsic impairment of granulopoiesis and B cell generation with LSK and monocyte lineage expansion. These findings demonstrate a critical role for the +37 kb Cebpa enhancer for hematopoietic-specific Cebpa expression, with enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	mouse	connective tissue	Low+High throughput	In Vivo Deletion of the Cebpa +37 kb Enhancer Markedly Reduces Cebpa mRNA in Myeloid Progenitors but Not in Non-Hematopoietic Tissues to Impair Granulopoiesis	否	--	--	bone marrow cell	E_02_0827	ChIP-seq,CRISPR/Cas9,Transgenic mice	To determine the effect of deleting the enhancer in vivo, we now characterize C57BL/6 mice in which loxP sites flank a 688 bp DNA segment containing the enhancer. 	Enhancer	CRISPR/Cas9	ChIP-seq	These findings demonstrate a critical role for the +37 kb Cebpa Enhancer for hematopoietic-specific Cebpa expression,with Enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	C/ebpalpha,CBF-A,Cebp	These findings demonstrate a critical role for the +37 kb Cebpa enhancer for hematopoietic-specific Cebpa expression, with enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	CRISPR/Cas9,PCR,Western blot	Together, these data indicate that reduced Cebpa expression consequent to +37 kb Enhancer deletion impairs hematopoietic cell autonomous granulopoiesis in vitro, leading to preservation of immature myeloid progenitors capable of long-term, IL-3-dependent proliferation without complete terminal maturation,a preleukemic phenotype.	Runx1	AML1,CBF-alpha-2,Cbfa2,Pebp2a2,Pebpa2b	ChIP-seq	Runx1,C/EBPα,Spi1,Erg,Fli-1,GATA2,Scl,Meis1,and Gfi-1b bind chromatin in the region of this Enhancer in hematopoietic cells as determined by ChIP-Seq.	--	--	Cebpa
26937964	chr7	35156353	35161233	GATA2	CRISPR/Cas9-mediated replacement of the wild-type enhancer with a variant mutant in its seven Ets sites leads to 20-fold reduction of Cebpa mRNA in the 32Dcl3 myeloid cell line. To determine the effect of deleting the enhancer in vivo, we now characterize C57BL/6 mice in which loxP sites flank a 688 bp DNA segment containing the enhancer. CMV-Cre mediated germline deletion resulted in diminution of the expected number of viable Enh(f/f);CMV-Cre offspring, with 28-fold reduction in marrow Cebpa mRNA but normal levels in liver, lung, adipose, intestine, muscle, and kidney. Cre-transduction of lineage-negative marrow cells in vitro reduced Cebpa mRNA 12-fold, with impairment of granulocytic maturation, morphologic blast accumulation, and IL-3 dependent myeloid colony replating for >12 generations. Exposure of Enh(f/f);Mx1-Cre mice to pIpC led to 14-fold reduction of Cebpa mRNA in GMP or CMP, 30-fold reduction in LSK, and <2-fold reduction in the LSK/SLAM subset. FACS analysis of marrow from these mice revealed 10-fold reduced neutrophils, 3-fold decreased GMP, and 3-fold increased LSK cells. Progenitor cell cycle progression was mildly impaired. Granulocyte and B lymphoid colony forming units were reduced while monocytic and erythroid colonies were increased, with reduced Pu.1 and Gfi1 and increased Egr1 and Klf4 in GMP. Finally, competitive transplantation indicated preservation of functional long-term hematopoietic stem cells upon enhancer deletion and confirmed marrow-intrinsic impairment of granulopoiesis and B cell generation with LSK and monocyte lineage expansion. These findings demonstrate a critical role for the +37 kb Cebpa enhancer for hematopoietic-specific Cebpa expression, with enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	mouse	connective tissue	Low+High throughput	In Vivo Deletion of the Cebpa +37 kb Enhancer Markedly Reduces Cebpa mRNA in Myeloid Progenitors but Not in Non-Hematopoietic Tissues to Impair Granulopoiesis	否	--	--	bone marrow cell	E_02_0827	ChIP-seq,CRISPR/Cas9,Transgenic mice	To determine the effect of deleting the enhancer in vivo, we now characterize C57BL/6 mice in which loxP sites flank a 688 bp DNA segment containing the enhancer. 	Enhancer	CRISPR/Cas9	ChIP-seq	These findings demonstrate a critical role for the +37 kb Cebpa Enhancer for hematopoietic-specific Cebpa expression,with Enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	C/ebpalpha,CBF-A,Cebp	These findings demonstrate a critical role for the +37 kb Cebpa enhancer for hematopoietic-specific Cebpa expression, with enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	CRISPR/Cas9,PCR,Western blot	Together, these data indicate that reduced Cebpa expression consequent to +37 kb Enhancer deletion impairs hematopoietic cell autonomous granulopoiesis in vitro, leading to preservation of immature myeloid progenitors capable of long-term, IL-3-dependent proliferation without complete terminal maturation,a preleukemic phenotype.	Runx1	AML1,CBF-alpha-2,Cbfa2,Pebp2a2,Pebpa2b	ChIP-seq	Runx1,C/EBPα,Spi1,Erg,Fli-1,GATA2,Scl,Meis1,and Gfi-1b bind chromatin in the region of this Enhancer in hematopoietic cells as determined by ChIP-Seq.	--	--	Cebpa
26937964	chr7	35156353	35161233	Egr1	CRISPR/Cas9-mediated replacement of the wild-type enhancer with a variant mutant in its seven Ets sites leads to 20-fold reduction of Cebpa mRNA in the 32Dcl3 myeloid cell line. To determine the effect of deleting the enhancer in vivo, we now characterize C57BL/6 mice in which loxP sites flank a 688 bp DNA segment containing the enhancer. CMV-Cre mediated germline deletion resulted in diminution of the expected number of viable Enh(f/f);CMV-Cre offspring, with 28-fold reduction in marrow Cebpa mRNA but normal levels in liver, lung, adipose, intestine, muscle, and kidney. Cre-transduction of lineage-negative marrow cells in vitro reduced Cebpa mRNA 12-fold, with impairment of granulocytic maturation, morphologic blast accumulation, and IL-3 dependent myeloid colony replating for >12 generations. Exposure of Enh(f/f);Mx1-Cre mice to pIpC led to 14-fold reduction of Cebpa mRNA in GMP or CMP, 30-fold reduction in LSK, and <2-fold reduction in the LSK/SLAM subset. FACS analysis of marrow from these mice revealed 10-fold reduced neutrophils, 3-fold decreased GMP, and 3-fold increased LSK cells. Progenitor cell cycle progression was mildly impaired. Granulocyte and B lymphoid colony forming units were reduced while monocytic and erythroid colonies were increased, with reduced Pu.1 and Gfi1 and increased Egr1 and Klf4 in GMP. Finally, competitive transplantation indicated preservation of functional long-term hematopoietic stem cells upon enhancer deletion and confirmed marrow-intrinsic impairment of granulopoiesis and B cell generation with LSK and monocyte lineage expansion. These findings demonstrate a critical role for the +37 kb Cebpa enhancer for hematopoietic-specific Cebpa expression, with enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	mouse	connective tissue	Low+High throughput	In Vivo Deletion of the Cebpa +37 kb Enhancer Markedly Reduces Cebpa mRNA in Myeloid Progenitors but Not in Non-Hematopoietic Tissues to Impair Granulopoiesis	否	--	--	bone marrow cell	E_02_0827	ChIP-seq,CRISPR/Cas9,Transgenic mice	To determine the effect of deleting the enhancer in vivo, we now characterize C57BL/6 mice in which loxP sites flank a 688 bp DNA segment containing the enhancer. 	Enhancer	CRISPR/Cas9	ChIP-seq	These findings demonstrate a critical role for the +37 kb Cebpa Enhancer for hematopoietic-specific Cebpa expression,with Enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	C/ebpalpha,CBF-A,Cebp	These findings demonstrate a critical role for the +37 kb Cebpa enhancer for hematopoietic-specific Cebpa expression, with enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	CRISPR/Cas9,PCR,Western blot	Together, these data indicate that reduced Cebpa expression consequent to +37 kb Enhancer deletion impairs hematopoietic cell autonomous granulopoiesis in vitro, leading to preservation of immature myeloid progenitors capable of long-term, IL-3-dependent proliferation without complete terminal maturation,a preleukemic phenotype.	Runx1	AML1,CBF-alpha-2,Cbfa2,Pebp2a2,Pebpa2b	ChIP-seq	Runx1,C/EBPα,Spi1,Erg,Fli-1,GATA2,Scl,Meis1,and Gfi-1b bind chromatin in the region of this Enhancer in hematopoietic cells as determined by ChIP-Seq.	--	--	Cebpa
26937964	chr7	35156353	35161233	Klf4	CRISPR/Cas9-mediated replacement of the wild-type enhancer with a variant mutant in its seven Ets sites leads to 20-fold reduction of Cebpa mRNA in the 32Dcl3 myeloid cell line. To determine the effect of deleting the enhancer in vivo, we now characterize C57BL/6 mice in which loxP sites flank a 688 bp DNA segment containing the enhancer. CMV-Cre mediated germline deletion resulted in diminution of the expected number of viable Enh(f/f);CMV-Cre offspring, with 28-fold reduction in marrow Cebpa mRNA but normal levels in liver, lung, adipose, intestine, muscle, and kidney. Cre-transduction of lineage-negative marrow cells in vitro reduced Cebpa mRNA 12-fold, with impairment of granulocytic maturation, morphologic blast accumulation, and IL-3 dependent myeloid colony replating for >12 generations. Exposure of Enh(f/f);Mx1-Cre mice to pIpC led to 14-fold reduction of Cebpa mRNA in GMP or CMP, 30-fold reduction in LSK, and <2-fold reduction in the LSK/SLAM subset. FACS analysis of marrow from these mice revealed 10-fold reduced neutrophils, 3-fold decreased GMP, and 3-fold increased LSK cells. Progenitor cell cycle progression was mildly impaired. Granulocyte and B lymphoid colony forming units were reduced while monocytic and erythroid colonies were increased, with reduced Pu.1 and Gfi1 and increased Egr1 and Klf4 in GMP. Finally, competitive transplantation indicated preservation of functional long-term hematopoietic stem cells upon enhancer deletion and confirmed marrow-intrinsic impairment of granulopoiesis and B cell generation with LSK and monocyte lineage expansion. These findings demonstrate a critical role for the +37 kb Cebpa enhancer for hematopoietic-specific Cebpa expression, with enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	mouse	connective tissue	Low+High throughput	In Vivo Deletion of the Cebpa +37 kb Enhancer Markedly Reduces Cebpa mRNA in Myeloid Progenitors but Not in Non-Hematopoietic Tissues to Impair Granulopoiesis	否	--	--	bone marrow cell	E_02_0827	ChIP-seq,CRISPR/Cas9,Transgenic mice	To determine the effect of deleting the enhancer in vivo, we now characterize C57BL/6 mice in which loxP sites flank a 688 bp DNA segment containing the enhancer. 	Enhancer	CRISPR/Cas9	ChIP-seq	These findings demonstrate a critical role for the +37 kb Cebpa Enhancer for hematopoietic-specific Cebpa expression,with Enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	C/ebpalpha,CBF-A,Cebp	These findings demonstrate a critical role for the +37 kb Cebpa enhancer for hematopoietic-specific Cebpa expression, with enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	CRISPR/Cas9,PCR,Western blot	Together, these data indicate that reduced Cebpa expression consequent to +37 kb Enhancer deletion impairs hematopoietic cell autonomous granulopoiesis in vitro, leading to preservation of immature myeloid progenitors capable of long-term, IL-3-dependent proliferation without complete terminal maturation,a preleukemic phenotype.	Runx1	AML1,CBF-alpha-2,Cbfa2,Pebp2a2,Pebpa2b	ChIP-seq	Runx1,C/EBPα,Spi1,Erg,Fli-1,GATA2,Scl,Meis1,and Gfi-1b bind chromatin in the region of this Enhancer in hematopoietic cells as determined by ChIP-Seq.	--	--	Cebpa
26937964	chr7	35156353	35161233	Gfi1	CRISPR/Cas9-mediated replacement of the wild-type enhancer with a variant mutant in its seven Ets sites leads to 20-fold reduction of Cebpa mRNA in the 32Dcl3 myeloid cell line. To determine the effect of deleting the enhancer in vivo, we now characterize C57BL/6 mice in which loxP sites flank a 688 bp DNA segment containing the enhancer. CMV-Cre mediated germline deletion resulted in diminution of the expected number of viable Enh(f/f);CMV-Cre offspring, with 28-fold reduction in marrow Cebpa mRNA but normal levels in liver, lung, adipose, intestine, muscle, and kidney. Cre-transduction of lineage-negative marrow cells in vitro reduced Cebpa mRNA 12-fold, with impairment of granulocytic maturation, morphologic blast accumulation, and IL-3 dependent myeloid colony replating for >12 generations. Exposure of Enh(f/f);Mx1-Cre mice to pIpC led to 14-fold reduction of Cebpa mRNA in GMP or CMP, 30-fold reduction in LSK, and <2-fold reduction in the LSK/SLAM subset. FACS analysis of marrow from these mice revealed 10-fold reduced neutrophils, 3-fold decreased GMP, and 3-fold increased LSK cells. Progenitor cell cycle progression was mildly impaired. Granulocyte and B lymphoid colony forming units were reduced while monocytic and erythroid colonies were increased, with reduced Pu.1 and Gfi1 and increased Egr1 and Klf4 in GMP. Finally, competitive transplantation indicated preservation of functional long-term hematopoietic stem cells upon enhancer deletion and confirmed marrow-intrinsic impairment of granulopoiesis and B cell generation with LSK and monocyte lineage expansion. These findings demonstrate a critical role for the +37 kb Cebpa enhancer for hematopoietic-specific Cebpa expression, with enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	mouse	connective tissue	Low+High throughput	In Vivo Deletion of the Cebpa +37 kb Enhancer Markedly Reduces Cebpa mRNA in Myeloid Progenitors but Not in Non-Hematopoietic Tissues to Impair Granulopoiesis	否	--	--	bone marrow cell	E_02_0827	ChIP-seq,CRISPR/Cas9,Transgenic mice	To determine the effect of deleting the enhancer in vivo, we now characterize C57BL/6 mice in which loxP sites flank a 688 bp DNA segment containing the enhancer. 	Enhancer	CRISPR/Cas9	ChIP-seq	These findings demonstrate a critical role for the +37 kb Cebpa Enhancer for hematopoietic-specific Cebpa expression,with Enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	C/ebpalpha,CBF-A,Cebp	These findings demonstrate a critical role for the +37 kb Cebpa enhancer for hematopoietic-specific Cebpa expression, with enhancer deletion leading to impaired myelopoiesis and potentially preleukemic progenitor expansion.	CRISPR/Cas9,PCR,Western blot	Together, these data indicate that reduced Cebpa expression consequent to +37 kb Enhancer deletion impairs hematopoietic cell autonomous granulopoiesis in vitro, leading to preservation of immature myeloid progenitors capable of long-term, IL-3-dependent proliferation without complete terminal maturation,a preleukemic phenotype.	Runx1	AML1,CBF-alpha-2,Cbfa2,Pebp2a2,Pebpa2b	ChIP-seq	Runx1,C/EBPα,Spi1,Erg,Fli-1,GATA2,Scl,Meis1,and Gfi-1b bind chromatin in the region of this Enhancer in hematopoietic cells as determined by ChIP-Seq.	--	--	Cebpa
26916345	chr1	67739940	67741075	IL12RB2	The proportion of IFN-γ+ CD4+ T-cells was increased in 'A/A' homozygotes (p=0.004), but neither IL23R nor IL12RB2 mRNA was affected.	human	bone	low throughput	An ankylosing spondylitis-associated genetic variant in the IL23R-IL12RB2 intergenic region modulates enhancer activity and is associated with increased Th1-cell differentiation	是	rs11209026	Ankylosing Spondylitis	Lymphoblastoid cell lines	E_02_0828	DNase I Hypersensitivity Assay	We identified a PRE (Chr1:67739940–67741075) located 14.2 kb downstream of IL23R and 33.1 kb upstream of IL12RB2.This region is DNase I hypersensitive (in Th1-cells, but not Th17-cells) and exhibits TF binding (lymphoblastoid cell line; GM12878) and enhancer-associated H3K4me1 methylation (CD4+ CD25? IL-17A? T-cells; PMA and ionomycin-stimulated).	enhancer	--	DNase I Hypersensitivity Assay	We identified a PRE (Chr1:67739940–67741075) located 14.2 kb downstream of IL23R and 33.1 kb upstream of IL12RB2.This region is DNase I hypersensitive (in Th1-cells, but not Th17-cells) and exhibits TF binding (lymphoblastoid cell line; GM12878) and enhancer-associated H3K4me1 methylation (CD4+ CD25? IL-17A? T-cells; PMA and ionomycin-stimulated).	IL23R	--	--	--	--	--	--	--	67705958	DNase I Hypersensitivity Assay,Luciferase Reporter Assay	IL23R
26886256	chr6	43891400	43898360	VEGFA	Further analyses of a hypomethylated ESSE downstream to the VEGFA gene revealed a novel regulatory circuit affecting VEGFA transcript levels across cancers and patients.	human	lymph	Low+High throughput	Embryonic Stem Cell (ES)-Specific Enhancers Specify the Expression Potential of ES Genes in Cancer		--	--	K-562 CELL	E_02_0829	ChIP-seq	We termed these promoter-distal elements, which carry the H3K4me1 mark in ES but not in hematopoietic cells,the ES-specific enhancers (ESSEs) of the hematopoietic cell lineage.	enhancer	4C-seq,CRISPR/Cas9	Luciferase Reporter Assay	To determine whether this ESSE is able to enhance transcription, a 1,500 bp fragment surrounding the ESSE methylation site was cloned upstream to a minimal SV40 promoter in a luciferase reporter plasmid and transfected to K562 cells.Indeed, the ESSE segment significantly enhanced expression when placed upstream or downstream to the minimal promoter. Thus,the DNA element surrounding the ESSE site is a transcriptional enhancer in leukemia cells.The Circularized Chromosome Conformation Capture (4C-seqencing) assay allowed mapping the interactions between the VEGFA promoter and DNA sequences across the K562 cell genome.To determine whether VEGFA expression depends upon the ESSE, we mutated the ESSE site in K562 cells by utilization of the CRISPR/Cas9 genome-editing system.	MVCD1, VEGF, VPF	--	--	--	STAT1/2	CANDF7,IMD31A,IMD31B,IMD31C,ISGF-3,STAT91,IMD44,ISGF-3,P113,STAT113	ChIP-seq	Focused (<600 bp) cluster of transcription factor binding sites (Chip-seq data) within the predicted enhancer. The factors bound in K562 cells are listed. This is the only cluster within 20 kb around the ESSE.	--	--	VEGFA 
26884396	chr14	61121917	61123917	Six2	We compared the regulatory actions of Six2 in mouse and human nephron progenitors by chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq).	human		Low+High throughput	Differential regulation of mouse and human nephron progenitors by the Six family of transcriptional regulators	否	--	--	nephron progenitor cell	E_02_0830	ChIP-seq	ChIP-seq was performed on 17 week fetal kidneys and E16.5 mouse kidneys to assess chromatin marks associated with active genes and enhancers (H3K27ac) and transcriptionally silenced chromatin (H3K27me3). Similarly, the human SIX1 locus was bound by SIX2 at multiple conserved elements and displayed prominent H3K27ac throughout the gene body and the SIX2-bound regions (Fig. 3A).	Enhancer	--	RNA-seq	"Using RNA-seq data from nephron progenitors, we compared expression of genes between human
and mouse and identified genes that were >5-fold enriched in either species and were also a species-specific target (Fig. 2E, right panel,highlighted genes). SIX1 is expressed in the human ITGA8+progenitors, but not in mouse nephron progenitors, identifying SIX1 as a human specific target on the basis of both cis-interactions around the SIX1 gene and active SIX1 expression (right panelFig. 2E; Table S3)."	BOS3,DFNA23,TIP39	--	--	--	SIX2	SIX2	ChIP	The differing number of peaks was due to lower levels of SIX2 ChIP enrichment in the second replicate (Fig. S1C). Examination of SIX2 binding near MEOX1 and WT1 highlighted the similar binding profiles for SIX2 replicates(Fig. 1B).	--	--	SIX1
26884396	chr14	61121917	61123917	Six3	We compared the regulatory actions of Six3 in mouse and human nephron progenitors by chromatin immunoprecipitation followed by DNA sequencing (ChIP-seq).	human		Low+High throughput	Differential regulation of mouse and human nephron progenitors by the Six family of transcriptional regulators	否	--	--	nephron progenitor cell	E_02_0830	ChIP-seq	ChIP-seq was performed on 17 week fetal kidneys and E16.5 mouse kidneys to assess chromatin marks associated with active genes and enhancers (H3K27ac) and transcriptionally silenced chromatin (H3K27me3). Similarly, the human SIX1 locus was bound by SIX2 at multiple conserved elements and displayed prominent H3K27ac throughout the gene body and the SIX2-bound regions (Fig. 3A).	Enhancer	--	RNA-seq	"Using RNA-seq data from nephron progenitors, we compared expression of genes between human
and mouse and identified genes that were >5-fold enriched in either species and were also a species-specific target (Fig. 2E, right panel,highlighted genes). SIX1 is expressed in the human ITGA8+progenitors, but not in mouse nephron progenitors, identifying SIX1 as a human specific target on the basis of both cis-interactions around the SIX1 gene and active SIX1 expression (right panelFig. 2E; Table S3)."	BOS3,DFNA23,TIP39	--	--	--	SIX2	SIX2	ChIP	The differing number of peaks was due to lower levels of SIX2 ChIP enrichment in the second replicate (Fig. S1C). Examination of SIX2 binding near MEOX1 and WT1 highlighted the similar binding profiles for SIX2 replicates(Fig. 1B).	--	--	SIX1
26864944	chr14	24435744	24437744	DHRS4	The human DHRS4 gene cluster consists of DHRS4 and two immediately downstream homologous genes, DHRS4L2 and DHRS4L1, generated by evolutionarily gene-duplication events.	human	Cancer tissues	Low throughput	Enhancer RNA-driven looping enhances the transcription of the long noncoding RNA DHRS4-AS1, a controller of the DHRS4 gene cluster	否	--	--	Hep G2,HL-7702 cell	E_02_0831	Luciferase Reporter Assay,ChIP	we searched for and identified a putative enhancer region located 13.8 kb downstream from the TSS of DHRS4-AS117,18. We performed chromatin immunoprecipitation (ChIP) to confirm the enrichment of histone modifications in hepatocellular carcinoma cells (HepG2) and normal hepatocytes (HL7702) (Fig.?1D). We then examined the potential enhancement of luciferase reporter activity by using luciferase reporter assays in HepG2 and HL7702 cells (Fig.?1E). 	Enhancer	3C	Luciferase Reporter Assay,ChIP,qPCR	In a search of the DHRS4-AS1 region for nearby enhancers, we identified an enhancer located 13.8 kb downstream of the DHRS4-AS1 transcriptional start site. We further showed, by using a chromosome conformation capture (3C) assay, that this enhancer is capable of physically interacting with the DHRS4-AS1 promoter through chromosomal looping. 	AS1DHRS4,C14orf167,C14orf67,DHRS4AS1,PRO1488	--	--	--	EP300	KAT3B,MKHK2,RSTS2,p300	ChIP	"RNA pol II and the transcriptional coactivator p300/CBP occupy enhancer regions and target gene promoters to maintain chromatin loops29. We next characterized the effect of AS1eRNA knockdown on the binding levels of RNA pol II and p300 at the AS1 enhancer and the 
DHRS4-AS1 promoter (Fig.?4A,B)."	--	--	DHRS4-AS1
26829750	chr9	14538685	14540685	TP63	MYB also binds enhancers that drive different regulatory programs in alternate cell lineages in ACC, cooperating with TP63 in myoepithelial cells and a Notch program in luminal epithelial cells.	human	lymph	Low+High throughput	An oncogenic MYB feedback loop drives alternate cell fates in adenoid cystic carcinoma		--	Adenoid Cystic Carcinoma	MCF-7 cell	E_02_0832	Luciferase Reporter Assay,RT-PCR,ChIP,ChIP-seq	Here we identify super-enhancer translocations that drive overexpression of the oncogenic transcription factor MYB as a recurrent theme in adenoid cystic carcinoma (ACC). Whole-genome sequencing data and chromatin maps highlight distinct chromosomal rearrangements that juxtapose super-enhancers to the MYB locus. Chromosome conformation capture confirms that the translocated enhancers interact with the MYB promoter.	Enhancer	3C	ChIP,ChIP-seq	To test whether specific enhancers within the translocated super_x0002_enhancers might activate the MYB promoter, we examined their physical proximity to the promoter using chromosome conforma_x0002_tion capture (3C). First, we examined an ACC with a translocation involving MYB and the NFIB locus. 	CTF,HMGIC/NFIB,MACID,NF-I/B,NF1-B,NFI-B,NFI-RED2,NFIB3,NFIB	Here we identify the juxtaposition of super-enhancer regions to the MYB locus as the unifying feature of ACC translocations.Detailed genomic and epigenomic analyses of ACCs identify alternate rearrangements that translocate super-enhancers in the NFIB and	3C	To test whether specific enhancers within the translocated super_x0002_enhancers might activate the MYB promoter, we examined their physical proximity to the promoter using chromosome conforma_x0002_tion capture (3C).These data suggest that the translocations reposition super-enhancers that subsequently loop to the MYB promoter and sustain high-level MYB expression.	TP63 	AIS, B(p51A), B(p51B), EEC3, KET, LMS, NBP, OFC8, RHS, SHFM4, TP53CP, TP53L, TP73L, p40, p51, p53CP, p63, p73H, p73L	ChIP-seq	To directly test whether TP63 co-binds with MYB, we mapped binding of this transcription factor by ChIP-seq.Remarkably, we found that 81% of TP63-binding sites in ACC were co-bound by MYB.These data suggest that MYB,TP63 and Notch signaling may coordinately orchestrate the diverse expression programs in ACC.	--	--	NFIB
26813977	chr6	30904342	30904788	POU5F2	Unexpectedly, we also discovered a new class of enhancers that contribute to POU5F1 transcription in an unusual way: Disruption of such sequences led to a temporary loss of POU5F2 transcription that is fully restored after a few rounds of cell division.	human	Early embryos	Low throughput	A new class of temporarily phenotypic enhancers identified by CRISPR/Cas11-mediated genetic screening	否	--	--	embryonic stem cell	E_02_0833	CRISPR/Cas9,Luciferase Reporter Assay,4C-seq	"We designed 1964 sgRNA sequences (Supplemental Table S2) targeting these putative cis-regulatory elements with an average of 11 sgRNA per element (Supplemental Fig. S1A). To eliminate these false positives,we required that a positive cis-regulatory element should have at least two distinct sgRNAs enriched by twofold or more in the eGFP? population in at least three out of the four independent experiments (Supplemental Table S3; Supplemental Fig. S2A). By use of this criterion, no negative control sgRNA passed the filter, while six cis-regulatory elements were identified as positives (Fig. 2A).
Next, we tested whether the identified elements could function as enhancers in the classical reporter assays (DHS_37,CTCF_38, DHS_65, DHS_108, and DHS_115).We cloned genomic fragments corresponding to each element into a reporter plasmid containing the 360-bp POU5F1 core promoter region and a luciferase reporter gene. All elements, with the exception of DHS_65, exhibited significant enhancer activities in the H1 cells compared with the control plasmid containing only the POU5F1 core promoter sequence (Fig. 2C).
We found that all Temp Enhancers, namely, DHS_37, DHS_65, and DHS_108, are located near regions that show high levels of chromatin interactions with the POU5F1 promoter. To confirm this observation, we also performed 4C-seq experiments in H1 POU5F1-eGFP cells. Again, we found these elements near regions displaying high and consistent interaction frequencies with the POU5F1 promoter (Fig. 4D)."	Enhancer	4C-seq	Luciferase Reporter Assay	"Next, we tested whether the identified elements could function as enhancers in the classical reporter assays (DHS_37,CTCF_38, DHS_65, DHS_108, and DHS_115).We cloned genomic fragments corresponding to each element into a reporter plasmid containing the 360-bp POU5F1 core promoter region and a luciferase reporter gene. All elements, with the exception of DHS_65, exhibited significant enhancer activities in the H1 cells compared with the control plasmid containing only the POU5F1 core promoter sequence (Fig. 2C).
We found that all Temp Enhancers, namely, DHS_37, DHS_65, and DHS_108, are located near regions that show high levels of chromatin interactions with the POU5F1 promoter. To confirm this observation, we also performed 4C-seq experiments in H1 POU5F1-eGFP cells. Again, we found these elements near regions displaying high and consistent interaction frequencies with the POU5F1 promoter (Fig. 4D)."	OCT3, OCT4, OTF-3, OTF3, OTF4, Oct-3, Oct-4	DHS_65 and DHS_108 act in cis to regulate POU5F1 expression	CRISPR/Cas9	Those results support our model that DHS_65 and DHS_108 act in cis to regulate POU5F1 transcription.	--	--	--	--	--	--	POU5F1
26813977	chr6	30904342	30904788	POU5F1	We identified two classical regulatory elements - including a promoter and a proximal enhancer - that are essential for POU5F1 transcription in the hESCs.	human	Embryonic tissues	Low throughput	A New Class of Temporarily Phenotypic Enhancers Identified by CRISPR/Cas9 Mediated Genetic Screening	相关	--	--	embryonic stem cell	E_02_0833	CRISPR/Cas9,Luciferase Reporter Assay,4C-seq	"We designed 1964 sgRNA sequences (Supplemental Table S2) targeting these putative cis-regulatory elements with an average of 11 sgRNA per element (Supplemental Fig. S1A). To eliminate these false positives,we required that a positive cis-regulatory element should have at least two distinct sgRNAs enriched by twofold or more in the eGFP? population in at least three out of the four independent experiments (Supplemental Table S3; Supplemental Fig. S2A). By use of this criterion, no negative control sgRNA passed the filter, while six cis-regulatory elements were identified as positives (Fig. 2A).
Next, we tested whether the identified elements could function as enhancers in the classical reporter assays (DHS_37,CTCF_38, DHS_65, DHS_108, and DHS_115).We cloned genomic fragments corresponding to each element into a reporter plasmid containing the 360-bp POU5F1 core promoter region and a luciferase reporter gene. All elements, with the exception of DHS_65, exhibited significant enhancer activities in the H1 cells compared with the control plasmid containing only the POU5F1 core promoter sequence (Fig. 2C).
We found that all Temp Enhancers, namely, DHS_37, DHS_65, and DHS_108, are located near regions that show high levels of chromatin interactions with the POU5F1 promoter. To confirm this observation, we also performed 4C-seq experiments in H1 POU5F1-eGFP cells. Again, we found these elements near regions displaying high and consistent interaction frequencies with the POU5F1 promoter (Fig. 4D)."	Enhancer	4C-seq	Luciferase Reporter Assay	"Next, we tested whether the identified elements could function as enhancers in the classical reporter assays (DHS_37,CTCF_38, DHS_65, DHS_108, and DHS_115).We cloned genomic fragments corresponding to each element into a reporter plasmid containing the 360-bp POU5F1 core promoter region and a luciferase reporter gene. All elements, with the exception of DHS_65, exhibited significant enhancer activities in the H1 cells compared with the control plasmid containing only the POU5F1 core promoter sequence (Fig. 2C).
We found that all Temp Enhancers, namely, DHS_37, DHS_65, and DHS_108, are located near regions that show high levels of chromatin interactions with the POU5F1 promoter. To confirm this observation, we also performed 4C-seq experiments in H1 POU5F1-eGFP cells. Again, we found these elements near regions displaying high and consistent interaction frequencies with the POU5F1 promoter (Fig. 4D)."	OCT3, OCT4, OTF-3, OTF3, OTF4, Oct-3, Oct-4	DHS_65 and DHS_108 act in cis to regulate POU5F1 expression	CRISPR/Cas9	Those results support our model that DHS_65 and DHS_108 act in cis to regulate POU5F1 transcription.	--	--	--	--	--	--	POU5F1
26808502	chr2	10136078	10138078	Gata3	Here, we determined that the canonical Gata3 promoter is insufficient for Gata3 transcriptional activation in T cells in vivo, precluding the possibility that promoter binding by a host of previously implicated transcription factors alone is responsible for Gata3 expression in T cells. Instead, we demonstrated that multiple lineage-affiliated transcription factors bind to Tce1 and that this enhancer confers T lymphocyte-specific Gata3 activation in vivo, as targeted deletion of Tce1 in a mouse model abrogated critical functions of this T cell-regulatory element. Together, our data show that Tce1 is both necessary and sufficient for critical aspects of Gata3 T cell-specific transcriptional activity.	mouse	connective tissue	Low throughput	Lineage-affiliated transcription factors bind the Gata3 Tce1 enhancer to mediate lineage-specific programs	否	--	--	T cell	E_02_0834	CRISPR/Cas9,ChIP,RT-PCR	We next asked whether this 1.2-kb Gata3 Tce1 fragment was also necessary for the transcription of a reporter gene in T cells. To answer this question, we prepared another EGFP reporter plasmid in which the 1.2-kb sequence was deleted from full-length Tce1 (Figure 5A) and generated additional F0 Tg mice (TgΔ1.2 mice). None of the F0 TgΔ1.2 mice expressed EGFP in peripheral CD4 T cells (Table 1 and Supplemental Figure 5C) or in thymocytes (Figure 5, B and C), except possibly at the DN4 stage (Table 2). We also analyzed TgΔ1.7, TgΔ1.5, and TgΔ2.7 mice and found that all of them expressed EGFP in peripheral CD4 T cells (Tables 1 and ?and2).2). Therefore, the EGFP expression in those mice confirmed that these sequences were not required for Tce1 enhancer activity in peripheral CD4 T cells. These data show that the 1.2-kb T cell enhancer fragment within Tce1 is also necessary for reporter gene transcription in T cells and, taken together with the data shown in Figure 1, that this fragment functions as an enhancer core element in vivo for Gata3 T cell–specific transcription. 	Enhancer	CRISPR/Cas9	ChIP,PCR	As anticipated, homozygous loss of Tce1 (Tce1–/–) led to a reduction in the number of ETPs (62% of that of heterozygous controls), and Gata3 mRNA in the remaining ETPs was only 52% of that of controls (Figure 1B). In contrast, the number of Tce1–/– DN2 and DN3 stage cells was unaltered compared with that of controls, although Gata3 mRNA levels in DN2 thymocytes were reduced (83% of that of heterozygous controls; Figure 1B). 	Gata-3,jal	Together, our data show that Tce1 is both necessary and sufficient for critical aspects of Gata3 T cell–specific transcriptional activity.	CRISPR/Cas9,ChIP,RT-PCR	Instead, we demonstrated that multiple lineage-affiliated transcription factors bind to Tce1 and that this enhancer confers T lymphocyte–specific Gata3 activation in vivo, as targeted deletion of Tce1 in a mouse model abrogated critical functions of this T cell–regulatory element.	Tcf7,Tcf12,Rbpj	AI465550,TCF-1,Tcf1,A130037E08Rik,ALF1,HEB,HEBAlt,HTF-4,HTF4,ME1,REB,bHLHb20,AI843960,CBF1,Igkjrb,Igkrsbp,RBP-J,RBP-Jkappa,RBP-Jkappa,RBPjk,Rbpsuh	ChIP	We therefore examined the association of CSL/RBP-J with predicted binding sites within Tce1. CSL/RBP-J binding to the Cd25 locus, a robust direct Notch target gene, was used as a positive control with an anti–RBP-J antibody in ChIP assays.Taken together, these data show that at least 3 critical T cell–affiliated transcription factors, TCF-1, HEB, and CSL/RBP-J, occupy binding sites within Tce1 at different developmental stages.Since all 3 have been shown to vitally affect T cell development, it seems likely that these factors and their associated signaling pathways directly modulate Gata3 expression through their binding to multiple consensus sites within Tce1.	--	--	Gata3
26795348	chr2	202120390	202125986	CASP8	we implicate three regulatory variants at 2q33 that target CASP8 (rs3769823,rs3769821 in CASP8, and rs10197246 in ALS2CR12) as func- tionally relevant. We conclude that nested discordant haplo- type sequencing is a promising approach to aid mapping of low-risk association loci. 	human	connective tissue	Low+High throughput	Discordant Haplotype Sequencing Identifies Functional Variants at the 2q33 Breast Cancer Risk Locus.	否	--	Breast Cancer	Chronic lymphocytic leukemia cell	E_02_0835	PCR,Luciferase Reporter Assay,ChIP-seq	Variants rs3769823, rs3769821, and rs10197246 were chosen to investigate for ability to affect enhancer activity. To create the enhancer constructs, we performed PCR using genomic DNA from T-47D, which is homozygous for risk alleles at all three SNPs, and MCF10A, which is homozygous for neutral alleles, using the following primer pairs.	Enhancer	--	DNase I Hypersensitivity Assay	To prioritize further, we used expression-quantitative trait locus analysis of RNA sequencing from breast tissues, gene regulation annota_x0002_tions from the ENCODE consortium, and functional assays for differential enhancer activities. Notably, we implicate three regulatory variants at 2q33 that target CASP8 (rs3769823, rs3769821 in CASP8, and rs10197246 in ALS2CR12) as func_x0002_tionally relevant.	CASP-8, FLICE, MACH, Mch5	--	--	--	STAT3,MYC,CTCF	1110034C02Rik, AW109958, Aprf,MRTLC,bHLHe39,c-Myc,MYC,MRD21	DNase I Hypersensitivity Assay,ChIP-seq	The first two reside 435 bp apart in a promoter proximal region that exhibits DNAse I hypersensitivity in mammary epithelial and breast cancer cell lines, and binds multiple transcription factors(STAT3, MYC, Pol2, and CTCF) based on ENCODE data (22).Also notable are results from an eQTL study in blood (23),indicating highly significant decreased CASP8 expression associ_x0002_ated with these cFSVs and suggesting the expression signature is also readily observed in blood.	--	--	CASP8
26766440	chr8	23448386	23454886	GATA2	Here we compare the enhancer landscape, transcriptional factor occupancy, and transcriptomic changes in human fetal and adult hematopoietic stem/progenitor cells and committed erythroid progenitors. We find that enhancers are modulated pervasively and direct lineage- and stage-specific transcription. GATA2-to-GATA1 switch is prevalent at dynamic enhancers and drives erythroid enhancer commissioning. Examination of lineage-specific enhancers identifies transcription factors and their combinatorial patterns in enhancer turnover. Importantly, by CRISPR/Cas9-mediated genomic editing, we uncover functional hierarchy of constituent enhancers within the SLC25A37 super-enhancer. Despite indistinguishable chromatin features, we reveal through genomic editing the functional diversity of several GATA switch enhancers in which enhancers with opposing functions cooperate to coordinate transcription. Thus, genome-wide enhancer profiling coupled with in situ enhancer editing provide critical insights into the functional complexity of enhancers during development.	human	epithelial tissue	Low+High throughput	Dynamic Control of Enhancer Repertoires Drives Lineage and Stage-Specific Transcription during Hematopoiesis	否	--	--	Erythroid lineage cell	E_02_0836	CRISPR/Cas9,ChIP-seq	"The enhancer cluster upstream of the SLC25A37 gene, consisting of three distinct constituent enhancers as measured by H3K4me1 and H3K27ac ChIP-seq, is defined 
as an erythroid-specific super-enhancer in both human (A5 ProE) and mouse (G1ER) erythroid cells (Figure 3A; Table S4).
To define the regulatory components of the SLC25A37 super-enhancer, we asked whether the function of each constituent enhancer depends on the activity of neighboring enhancers in situ. We employed site-directed loss-of-function analysis of the SLC25A37 super-enhancer constituents using CRISPR/Cas9-mediated genomic engineering.We focused on the orthologous mouse super-enhancer in the murine G1E/G1ER erythroid cell model (Welch et al., 2004).
We designed sequence-specific guide RNAs (or sgRNAs) flanking each constituent enhancer (E1, E2 and E3) or the promoter (P) (Figure 3B). Upon transfection into undifferentiated G1E cells together with an SpCas9 expressing construct, we screened and obtained multiple independent single cell-derived clones containing bi-allelic deletion of each enhancer (Figure S2B,C). Surprisingly, knockout of individual enhancers confer markedly varying effects on Slc25a37 expression. Specifically, while deletion of E1 or E2 individually only modestly or slightly impairs Slc25a37 activation during differentiation, respectively, E3 deletion abolishes its activation resulting in a 15-fold decrease in expression (48h after β-estradiol treatment; Figure 3C). "	Enhancer	CRISPR/Cas9	ChIP-seq	"The enhancer cluster upstream of the SLC25A37 gene, consisting of three distinct constituent enhancers as measured by H3K4me1 and H3K27ac ChIP-seq, is defined 
as an erythroid-specific super-enhancer in both human (A5 ProE) and mouse (G1ER) erythroid cells (Figure 3A; Table S4).
To define the regulatory components of the SLC25A37 super-enhancer, we asked whether the function of each constituent enhancer depends on the activity of neighboring enhancers in situ. We employed site-directed loss-of-function analysis of the SLC25A37 super-enhancer constituents using CRISPR/Cas9-mediated genomic engineering.We focused on the orthologous mouse super-enhancer in the murine G1E/G1ER erythroid cell model (Welch et al., 2004).
Surprisingly, knockout of individual enhancers confer markedly varying effects on Slc25a37 expression. Specifically, while deletion of E1 or E2 individually only modestly or slightly impairs Slc25a37 activation during differentiation, respectively, E3 deletion abolishes its activation resulting in a 15-fold decrease in expression (48h after β-estradiol treatment; Figure 3C). "	HT015,MFRN,MFRN1,MSC,MSCP,PRO1278,PRO1584,PRO2217	GATA2-to-GATA1 switch is prevalent at dynamic enhancers and drives erythroid enhancer commissioning.	CRISPR/Cas9	While the E2 and E3 Enhancers are indispensable for maximal Gata2 activation in stem/progenitor cells, the E1 Enhancer is required to maintain Gata2 repression in committed erythroid cells. 	GATA1,TAL1	ERYF1,GATA-1,GF-1,GF1,NF-E1,NFE1,XLANP,XLTDA,XLTT,SCL,TCL5,bHLHa17,tal-1	ChIP-seq	Strikingly, while only 3% (22,570 of 707,718) of the GATA1 motif-matched loci are covered by GATA1 ChIP-seq at a genome scale in ProEs, 34% of identified GATA1 motifs are covered by GATA1 within the Enhancer context.Similar pattern is observed for another principal erythroid regulator TAL1.	--	--	SLC25A37 
26766440	chr8	23448386	23454886	GATA1	Here we compare the enhancer landscape, transcriptional factor occupancy, and transcriptomic changes in human fetal and adult hematopoietic stem/progenitor cells and committed erythroid progenitors. We find that enhancers are modulated pervasively and direct lineage- and stage-specific transcription. GATA2-to-GATA1 switch is prevalent at dynamic enhancers and drives erythroid enhancer commissioning. Examination of lineage-specific enhancers identifies transcription factors and their combinatorial patterns in enhancer turnover. Importantly, by CRISPR/Cas9-mediated genomic editing, we uncover functional hierarchy of constituent enhancers within the SLC25A37 super-enhancer. Despite indistinguishable chromatin features, we reveal through genomic editing the functional diversity of several GATA switch enhancers in which enhancers with opposing functions cooperate to coordinate transcription. Thus, genome-wide enhancer profiling coupled with in situ enhancer editing provide critical insights into the functional complexity of enhancers during development.	human	epithelial tissue	Low+High throughput	Dynamic Control of Enhancer Repertoires Drives Lineage and Stage-Specific Transcription during Hematopoiesis	否	--	--	Erythroid lineage cell	E_02_0836	CRISPR/Cas9,ChIP-seq	"The enhancer cluster upstream of the SLC25A37 gene, consisting of three distinct constituent enhancers as measured by H3K4me1 and H3K27ac ChIP-seq, is defined 
as an erythroid-specific super-enhancer in both human (A5 ProE) and mouse (G1ER) erythroid cells (Figure 3A; Table S4).
To define the regulatory components of the SLC25A37 super-enhancer, we asked whether the function of each constituent enhancer depends on the activity of neighboring enhancers in situ. We employed site-directed loss-of-function analysis of the SLC25A37 super-enhancer constituents using CRISPR/Cas9-mediated genomic engineering.We focused on the orthologous mouse super-enhancer in the murine G1E/G1ER erythroid cell model (Welch et al., 2004).
We designed sequence-specific guide RNAs (or sgRNAs) flanking each constituent enhancer (E1, E2 and E3) or the promoter (P) (Figure 3B). Upon transfection into undifferentiated G1E cells together with an SpCas9 expressing construct, we screened and obtained multiple independent single cell-derived clones containing bi-allelic deletion of each enhancer (Figure S2B,C). Surprisingly, knockout of individual enhancers confer markedly varying effects on Slc25a37 expression. Specifically, while deletion of E1 or E2 individually only modestly or slightly impairs Slc25a37 activation during differentiation, respectively, E3 deletion abolishes its activation resulting in a 15-fold decrease in expression (48h after β-estradiol treatment; Figure 3C). "	Enhancer	CRISPR/Cas9	ChIP-seq	"The enhancer cluster upstream of the SLC25A37 gene, consisting of three distinct constituent enhancers as measured by H3K4me1 and H3K27ac ChIP-seq, is defined 
as an erythroid-specific super-enhancer in both human (A5 ProE) and mouse (G1ER) erythroid cells (Figure 3A; Table S4).
To define the regulatory components of the SLC25A37 super-enhancer, we asked whether the function of each constituent enhancer depends on the activity of neighboring enhancers in situ. We employed site-directed loss-of-function analysis of the SLC25A37 super-enhancer constituents using CRISPR/Cas9-mediated genomic engineering.We focused on the orthologous mouse super-enhancer in the murine G1E/G1ER erythroid cell model (Welch et al., 2004).
Surprisingly, knockout of individual enhancers confer markedly varying effects on Slc25a37 expression. Specifically, while deletion of E1 or E2 individually only modestly or slightly impairs Slc25a37 activation during differentiation, respectively, E3 deletion abolishes its activation resulting in a 15-fold decrease in expression (48h after β-estradiol treatment; Figure 3C). "	HT015,MFRN,MFRN1,MSC,MSCP,PRO1278,PRO1584,PRO2217	GATA2-to-GATA1 switch is prevalent at dynamic enhancers and drives erythroid enhancer commissioning.	CRISPR/Cas9	While the E2 and E3 Enhancers are indispensable for maximal Gata2 activation in stem/progenitor cells, the E1 Enhancer is required to maintain Gata2 repression in committed erythroid cells. 	GATA1,TAL1	ERYF1,GATA-1,GF-1,GF1,NF-E1,NFE1,XLANP,XLTDA,XLTT,SCL,TCL5,bHLHa17,tal-1	ChIP-seq	Strikingly, while only 3% (22,570 of 707,718) of the GATA1 motif-matched loci are covered by GATA1 ChIP-seq at a genome scale in ProEs, 34% of identified GATA1 motifs are covered by GATA1 within the Enhancer context.Similar pattern is observed for another principal erythroid regulator TAL1.	--	--	SLC25A37 
26766440	chr8	23448386	23454886	SLC25A37	Here we compare the enhancer landscape, transcriptional factor occupancy, and transcriptomic changes in human fetal and adult hematopoietic stem/progenitor cells and committed erythroid progenitors. We find that enhancers are modulated pervasively and direct lineage- and stage-specific transcription. GATA2-to-GATA1 switch is prevalent at dynamic enhancers and drives erythroid enhancer commissioning. Examination of lineage-specific enhancers identifies transcription factors and their combinatorial patterns in enhancer turnover. Importantly, by CRISPR/Cas9-mediated genomic editing, we uncover functional hierarchy of constituent enhancers within the SLC25A37 super-enhancer. Despite indistinguishable chromatin features, we reveal through genomic editing the functional diversity of several GATA switch enhancers in which enhancers with opposing functions cooperate to coordinate transcription. Thus, genome-wide enhancer profiling coupled with in situ enhancer editing provide critical insights into the functional complexity of enhancers during development.	human	epithelial tissue	Low+High throughput	Dynamic Control of Enhancer Repertoires Drives Lineage and Stage-Specific Transcription during Hematopoiesis	否	--	--	Erythroid lineage cell	E_02_0836	CRISPR/Cas9,ChIP-seq	"The enhancer cluster upstream of the SLC25A37 gene, consisting of three distinct constituent enhancers as measured by H3K4me1 and H3K27ac ChIP-seq, is defined 
as an erythroid-specific super-enhancer in both human (A5 ProE) and mouse (G1ER) erythroid cells (Figure 3A; Table S4).
To define the regulatory components of the SLC25A37 super-enhancer, we asked whether the function of each constituent enhancer depends on the activity of neighboring enhancers in situ. We employed site-directed loss-of-function analysis of the SLC25A37 super-enhancer constituents using CRISPR/Cas9-mediated genomic engineering.We focused on the orthologous mouse super-enhancer in the murine G1E/G1ER erythroid cell model (Welch et al., 2004).
We designed sequence-specific guide RNAs (or sgRNAs) flanking each constituent enhancer (E1, E2 and E3) or the promoter (P) (Figure 3B). Upon transfection into undifferentiated G1E cells together with an SpCas9 expressing construct, we screened and obtained multiple independent single cell-derived clones containing bi-allelic deletion of each enhancer (Figure S2B,C). Surprisingly, knockout of individual enhancers confer markedly varying effects on Slc25a37 expression. Specifically, while deletion of E1 or E2 individually only modestly or slightly impairs Slc25a37 activation during differentiation, respectively, E3 deletion abolishes its activation resulting in a 15-fold decrease in expression (48h after β-estradiol treatment; Figure 3C). "	Enhancer	CRISPR/Cas9	ChIP-seq	"The enhancer cluster upstream of the SLC25A37 gene, consisting of three distinct constituent enhancers as measured by H3K4me1 and H3K27ac ChIP-seq, is defined 
as an erythroid-specific super-enhancer in both human (A5 ProE) and mouse (G1ER) erythroid cells (Figure 3A; Table S4).
To define the regulatory components of the SLC25A37 super-enhancer, we asked whether the function of each constituent enhancer depends on the activity of neighboring enhancers in situ. We employed site-directed loss-of-function analysis of the SLC25A37 super-enhancer constituents using CRISPR/Cas9-mediated genomic engineering.We focused on the orthologous mouse super-enhancer in the murine G1E/G1ER erythroid cell model (Welch et al., 2004).
Surprisingly, knockout of individual enhancers confer markedly varying effects on Slc25a37 expression. Specifically, while deletion of E1 or E2 individually only modestly or slightly impairs Slc25a37 activation during differentiation, respectively, E3 deletion abolishes its activation resulting in a 15-fold decrease in expression (48h after β-estradiol treatment; Figure 3C). "	HT015,MFRN,MFRN1,MSC,MSCP,PRO1278,PRO1584,PRO2217	GATA2-to-GATA1 switch is prevalent at dynamic enhancers and drives erythroid enhancer commissioning.	CRISPR/Cas9	While the E2 and E3 Enhancers are indispensable for maximal Gata2 activation in stem/progenitor cells, the E1 Enhancer is required to maintain Gata2 repression in committed erythroid cells. 	GATA1,TAL1	ERYF1,GATA-1,GF-1,GF1,NF-E1,NFE1,XLANP,XLTDA,XLTT,SCL,TCL5,bHLHa17,tal-1	ChIP-seq	Strikingly, while only 3% (22,570 of 707,718) of the GATA1 motif-matched loci are covered by GATA1 ChIP-seq at a genome scale in ProEs, 34% of identified GATA1 motifs are covered by GATA1 within the Enhancer context.Similar pattern is observed for another principal erythroid regulator TAL1.	--	--	SLC25A37 
26766440	chr8	23448386	23454886	Entpd4	Here we compare the enhancer landscape, transcriptional factor occupancy, and transcriptomic changes in human fetal and adult hematopoietic stem/progenitor cells and committed erythroid progenitors. We find that enhancers are modulated pervasively and direct lineage- and stage-specific transcription. GATA2-to-GATA1 switch is prevalent at dynamic enhancers and drives erythroid enhancer commissioning. Examination of lineage-specific enhancers identifies transcription factors and their combinatorial patterns in enhancer turnover. Importantly, by CRISPR/Cas9-mediated genomic editing, we uncover functional hierarchy of constituent enhancers within the SLC25A37 super-enhancer. Despite indistinguishable chromatin features, we reveal through genomic editing the functional diversity of several GATA switch enhancers in which enhancers with opposing functions cooperate to coordinate transcription. Thus, genome-wide enhancer profiling coupled with in situ enhancer editing provide critical insights into the functional complexity of enhancers during development.	human	epithelial tissue	Low+High throughput	Dynamic Control of Enhancer Repertoires Drives Lineage and Stage-Specific Transcription during Hematopoiesis	否	--	--	Erythroid lineage cell	E_02_0836	CRISPR/Cas9,ChIP-seq	"The enhancer cluster upstream of the SLC25A37 gene, consisting of three distinct constituent enhancers as measured by H3K4me1 and H3K27ac ChIP-seq, is defined 
as an erythroid-specific super-enhancer in both human (A5 ProE) and mouse (G1ER) erythroid cells (Figure 3A; Table S4).
To define the regulatory components of the SLC25A37 super-enhancer, we asked whether the function of each constituent enhancer depends on the activity of neighboring enhancers in situ. We employed site-directed loss-of-function analysis of the SLC25A37 super-enhancer constituents using CRISPR/Cas9-mediated genomic engineering.We focused on the orthologous mouse super-enhancer in the murine G1E/G1ER erythroid cell model (Welch et al., 2004).
We designed sequence-specific guide RNAs (or sgRNAs) flanking each constituent enhancer (E1, E2 and E3) or the promoter (P) (Figure 3B). Upon transfection into undifferentiated G1E cells together with an SpCas9 expressing construct, we screened and obtained multiple independent single cell-derived clones containing bi-allelic deletion of each enhancer (Figure S2B,C). Surprisingly, knockout of individual enhancers confer markedly varying effects on Slc25a37 expression. Specifically, while deletion of E1 or E2 individually only modestly or slightly impairs Slc25a37 activation during differentiation, respectively, E3 deletion abolishes its activation resulting in a 15-fold decrease in expression (48h after β-estradiol treatment; Figure 3C). "	Enhancer	CRISPR/Cas9	ChIP-seq	"The enhancer cluster upstream of the SLC25A37 gene, consisting of three distinct constituent enhancers as measured by H3K4me1 and H3K27ac ChIP-seq, is defined 
as an erythroid-specific super-enhancer in both human (A5 ProE) and mouse (G1ER) erythroid cells (Figure 3A; Table S4).
To define the regulatory components of the SLC25A37 super-enhancer, we asked whether the function of each constituent enhancer depends on the activity of neighboring enhancers in situ. We employed site-directed loss-of-function analysis of the SLC25A37 super-enhancer constituents using CRISPR/Cas9-mediated genomic engineering.We focused on the orthologous mouse super-enhancer in the murine G1E/G1ER erythroid cell model (Welch et al., 2004).
Surprisingly, knockout of individual enhancers confer markedly varying effects on Slc25a37 expression. Specifically, while deletion of E1 or E2 individually only modestly or slightly impairs Slc25a37 activation during differentiation, respectively, E3 deletion abolishes its activation resulting in a 15-fold decrease in expression (48h after β-estradiol treatment; Figure 3C). "	HT015,MFRN,MFRN1,MSC,MSCP,PRO1278,PRO1584,PRO2217	GATA2-to-GATA1 switch is prevalent at dynamic enhancers and drives erythroid enhancer commissioning.	CRISPR/Cas9	While the E2 and E3 Enhancers are indispensable for maximal Gata2 activation in stem/progenitor cells, the E1 Enhancer is required to maintain Gata2 repression in committed erythroid cells. 	GATA1,TAL1	ERYF1,GATA-1,GF-1,GF1,NF-E1,NFE1,XLANP,XLTDA,XLTT,SCL,TCL5,bHLHa17,tal-1	ChIP-seq	Strikingly, while only 3% (22,570 of 707,718) of the GATA1 motif-matched loci are covered by GATA1 ChIP-seq at a genome scale in ProEs, 34% of identified GATA1 motifs are covered by GATA1 within the Enhancer context.Similar pattern is observed for another principal erythroid regulator TAL1.	--	--	SLC25A37 
26748758	chr2	172513228	172520500	Foxd3	Using mouse embryonic stem cells as an in vitro model to study the transcriptional regulatory principles orchestrating peri-implantation development, here we show that the transcription factor Foxd3 is necessary for exit from naive pluripotency and progression to a primed pluripotent state. During this transition, Foxd3 acts as a repressor that dismantles a significant fraction of the naive pluripotency expression program through decommissioning of active enhancers associated with key naive pluripotency and early germline genes. Subsequently, Foxd3 needs to be silenced in primed pluripotent cells to allow re-activation of relevant genes required for proper PGC specification. Our findings therefore uncover a cycle of activation and deactivation of Foxd3 required for exit from naive pluripotency and subsequent PGC specification.	mouse	epithelial tissue	Low+High throughput	Foxd3 Promotes Exit from Naive Pluripotency through Enhancer Decommissioning and Inhibits Germline Specification	否	--	--	embryonic stem cell	E_02_0837	ChIP-seq,RT-qPCR	To test if Foxd3 was indeed able to silence na?ve pluripotency enhancers, we evaluated the impact of Foxd3 overexpression on some of these regulatory elements. tetOn Foxd3 mESC were treated with Dox and the levels of various histone modifications (i.e. H3K27ac, H3K27me2, H3K4me1, H3K4me2) at selected enhancers were evaluated by ChIP-qPCR. Compared to control cells, tetOn Foxd3 cells displayed lower levels of H3K27ac and H3K4me2 (active enhancers) , increased H3K27me2 (inactive enhancers) and minor changes in H3K4me1 levels (active and inactive enhancers)at most of the analysed na?ve enhancers (Figure 4B-C, Figure S5A-B).	Enhancer	--	ChIP-seq,RT-qPCR	ChIP-Seq profiles generated in Foxd3-FH mES cells with anti-HA and anti-Flag antibodies around a representative locus (i.e.,Tfap2c).	AA409384,AP2gamma,Ap-2.2,Stra2,Tcfap2c	--	--	--	Foxd3	CWH3,Genesis,Hfh2	ChIP-qPCR	To test if Foxd3 was indeed able to silence naive pluripotency enhancers, we evaluated the impact of Foxd3 overexpression on some of these regulatory elements. tetOn Foxd3 mESCs were treated with Dox, and the levels of various histone modifications (i.e., H3K27ac, H3K27me2, H3K4me1, and H3K4me2) at selected enhancers were evaluated by ChIP-qPCR. Compared to control cells, tetOn Foxd3 cells displayed lower levels of H3K27ac and H3K4me2 (active enhancers) , increased H3K27me2 (inactive enhancers) and minor changes in H3K4me1 levels (active and inactive enhancers)at most of the analysed na?ve enhancers (Figure 4B-C, Figure S5A-B).Using RT-qPCR, we found that Foxd3 overexpression significantly reduced eRNA levels at most of the analysed enhancers (Figure S5C). The role of Foxd3 was similarly evaluated using Foxd3?/? mESC, which displayed increased levels of H3K27ac and H3K4me2 (Figure 4D-E) and minor changes in H3K27me2 (Figure S5D) at most of the analysed enhancers.	--	--	Tfap2C
26748758	chr2	172513228	172520500	Otx2	Using mouse embryonic stem cells as an in vitro model to study the transcriptional regulatory principles orchestrating peri-implantation development, here we show that the transcription factor Foxd3 is necessary for exit from naive pluripotency and progression to a primed pluripotent state. During this transition, Foxd3 acts as a repressor that dismantles a significant fraction of the naive pluripotency expression program through decommissioning of active enhancers associated with key naive pluripotency and early germline genes. Subsequently, Foxd3 needs to be silenced in primed pluripotent cells to allow re-activation of relevant genes required for proper PGC specification. Our findings therefore uncover a cycle of activation and deactivation of Foxd3 required for exit from naive pluripotency and subsequent PGC specification.	mouse	epithelial tissue	Low+High throughput	Foxd3 Promotes Exit from Naive Pluripotency through Enhancer Decommissioning and Inhibits Germline Specification	否	--	--	embryonic stem cell	E_02_0837	ChIP-seq,RT-qPCR	To test if Foxd3 was indeed able to silence na?ve pluripotency enhancers, we evaluated the impact of Foxd3 overexpression on some of these regulatory elements. tetOn Foxd3 mESC were treated with Dox and the levels of various histone modifications (i.e. H3K27ac, H3K27me2, H3K4me1, H3K4me2) at selected enhancers were evaluated by ChIP-qPCR. Compared to control cells, tetOn Foxd3 cells displayed lower levels of H3K27ac and H3K4me2 (active enhancers) , increased H3K27me2 (inactive enhancers) and minor changes in H3K4me1 levels (active and inactive enhancers)at most of the analysed na?ve enhancers (Figure 4B-C, Figure S5A-B).	Enhancer	--	ChIP-seq,RT-qPCR	ChIP-Seq profiles generated in Foxd3-FH mES cells with anti-HA and anti-Flag antibodies around a representative locus (i.e.,Tfap2c).	AA409384,AP2gamma,Ap-2.2,Stra2,Tcfap2c	--	--	--	Foxd3	CWH3,Genesis,Hfh2	ChIP-qPCR	To test if Foxd3 was indeed able to silence naive pluripotency enhancers, we evaluated the impact of Foxd3 overexpression on some of these regulatory elements. tetOn Foxd3 mESCs were treated with Dox, and the levels of various histone modifications (i.e., H3K27ac, H3K27me2, H3K4me1, and H3K4me2) at selected enhancers were evaluated by ChIP-qPCR. Compared to control cells, tetOn Foxd3 cells displayed lower levels of H3K27ac and H3K4me2 (active enhancers) , increased H3K27me2 (inactive enhancers) and minor changes in H3K4me1 levels (active and inactive enhancers)at most of the analysed na?ve enhancers (Figure 4B-C, Figure S5A-B).Using RT-qPCR, we found that Foxd3 overexpression significantly reduced eRNA levels at most of the analysed enhancers (Figure S5C). The role of Foxd3 was similarly evaluated using Foxd3?/? mESC, which displayed increased levels of H3K27ac and H3K4me2 (Figure 4D-E) and minor changes in H3K27me2 (Figure S5D) at most of the analysed enhancers.	--	--	Tfap2C
26745862	chr6	36640937	36642937	CDK9	ChIP and functional analyses reason for a prominent role of CDK9 itself and elongation factor complexes PAF1c and SEC involved in pause and elongation control.	human	lymph	Low throughput	The Establishment of a Hyperactive Structure Allows the Tumour Suppressor Protein p53 to Function through P-TEFb during Limited CDK9 Kinase Inhibition		--	Tumour	T cell	E_02_0838	ChIP,qPCR	"Our ChIP experiments showed that prior to activation p53 was exclusively found at the upstream enhancer that harbors a high-affinity, near-consen_x0002_sus binding site for p53 (Fig 5A). Occupancy of this site increased incrementally after 1.5 and 4 hours of CDK9 inhibition (Fig 5B). In contrast to this pre-loaded ""primary"" enhancer, treat_x0002_ment with 067 was followed by de novo recruitment of p53 to additional, secondary binding sites, most notably to an intronic region that maps to position +4 kb downstream of the p21 TSS and contains another near-consensus p53 motif (Fig 5A). After four hours of treatment,p53 occupancy of this site reached similar levels as found at the upstream enhancer (Fig 5B)."	Enhancer	--	ChIP-qPCR	"Our ChIP experiments showed that prior to activation p53 was exclusively found at the upstream enhancer that harbors a high-affinity, near-consen_x0002_sus binding site for p53 (Fig 5A). Occupancy of this site increased incrementally after 1.5 and 4 hours of CDK9 inhibition (Fig 5B). In contrast to this pre-loaded ""primary"" enhancer, treat_x0002_ment with 067 was followed by de novo recruitment of p53 to additional, secondary binding sites, most notably to an intronic region that maps to position +4 kb downstream of the p21 TSS and contains another near-consensus p53 motif (Fig 5A). After four hours of treatment,p53 occupancy of this site reached similar levels as found at the upstream enhancer (Fig 5B)."	CAP20, CDKN1, CIP1, MDA-6,?P21, SDI1, WAF1, p21CIP1	--	--	--	TP53	BCC7, BMFS5, LFS1,?P53, TRP53	qPCR	MCF7 cells, which harbour functional wild-type p53, were treated for 20 minutes to 4 hours with 10 μM 067 and both nascent unspliced precursor (pre) and mature spliced mRNA was analyzed by quantitative PCR (qPCR). Inhibitor treatment led to significant(2.5-fold) repression of nascent RNA synthesis of the p53 target gene p21 within 20 minutes (Fig1A).	--	--	CDKN1A
26745862	chr6	36640937	36642937	CDK10	ChIP and functional analyses reason for a prominent role of CDK9 itself and elongation factor complexes PAF2c and SEC involved in pause and elongation control.	human	lymph	Low throughput	The Establishment of a Hyperactive Structure Allows the Tumour Suppressor Protein p53 to Function through P-TEFb during Limited CDK10 Kinase Inhibition		--	Tumour	T cell	E_02_0838	ChIP,qPCR	"Our ChIP experiments showed that prior to activation p53 was exclusively found at the upstream enhancer that harbors a high-affinity, near-consen_x0002_sus binding site for p53 (Fig 5A). Occupancy of this site increased incrementally after 1.5 and 4 hours of CDK9 inhibition (Fig 5B). In contrast to this pre-loaded ""primary"" enhancer, treat_x0002_ment with 067 was followed by de novo recruitment of p53 to additional, secondary binding sites, most notably to an intronic region that maps to position +4 kb downstream of the p21 TSS and contains another near-consensus p53 motif (Fig 5A). After four hours of treatment,p53 occupancy of this site reached similar levels as found at the upstream enhancer (Fig 5B)."	Enhancer	--	ChIP-qPCR	"Our ChIP experiments showed that prior to activation p53 was exclusively found at the upstream enhancer that harbors a high-affinity, near-consen_x0002_sus binding site for p53 (Fig 5A). Occupancy of this site increased incrementally after 1.5 and 4 hours of CDK9 inhibition (Fig 5B). In contrast to this pre-loaded ""primary"" enhancer, treat_x0002_ment with 067 was followed by de novo recruitment of p53 to additional, secondary binding sites, most notably to an intronic region that maps to position +4 kb downstream of the p21 TSS and contains another near-consensus p53 motif (Fig 5A). After four hours of treatment,p53 occupancy of this site reached similar levels as found at the upstream enhancer (Fig 5B)."	CAP20, CDKN1, CIP1, MDA-6,?P21, SDI1, WAF1, p21CIP1	--	--	--	TP53	BCC7, BMFS5, LFS1,?P53, TRP53	qPCR	MCF7 cells, which harbour functional wild-type p53, were treated for 20 minutes to 4 hours with 10 μM 067 and both nascent unspliced precursor (pre) and mature spliced mRNA was analyzed by quantitative PCR (qPCR). Inhibitor treatment led to significant(2.5-fold) repression of nascent RNA synthesis of the p53 target gene p21 within 20 minutes (Fig1A).	--	--	CDKN1A
26728555	chr12	109528035	109532509	AFF3	Here, we report that AFF3 can specifically bind both gametic DMRs (gDMRs) and enhancers within imprinted loci in an allele-specific manner. 	mouse		Low+High throughput	Regulation of the imprinted Dlk1-Dio3 locus by allele-specific enhancer activity	否	--	--	embryonic stem cell	E_02_0839	ChIP-seq,ChIP	"By performing ChIP-seq in different mESC lines and using two different antibodies, we were able to identify 973 high-confidence AFF3-binding sites.AFF3 is also de_x0002_tected in the intergenic regions within the Dlk1-Dio3 locus, which harbors a paternally methylated gDMR/
ICR (Fig. 1A). Two discrete AFF3-binding sites are located 12 kb (distal AFF3 peak) and 10 kb (proximal AFF3 peak)upstream of the promoter region of the maternally ex_x0002_pressed gene Meg3 (Fig. 1B).This AFF3 peak resides within the intergenic DMR (IG-DMR) of the Dlk1-Dio3 cluster and corresponds to the Meg3-proximal enhancer peak located just 2.4 kb from the Meg3-distal gDMR peak (Figs. 1B, 3A). While bisulfite sequencing of ChIP DNA demonstrated that AFF3 is on the inactive allele at the Meg3-distal gDMR,AFF3 is restricted to the unmethylated allele at the Meg3-proximal enhancer (Fig. 3B,C; Supplemental Fig. S4)."	Enhancer	--	ChIP-seq,ChIP	This AFF3 peak resides within the intergenic DMR (IG-DMR) of the Dlk1-Dio3 cluster and corresponds to the Meg3-proximal enhancer peak located just 2.4 kb from the Meg3-distal gDMR peak (Figs. 1B, 3A). While bisulfite sequencing of ChIP DNA demonstrated that AFF3 is on the inactive allele at the Meg3-distal gDMR,AFF3 is restricted to the unmethylated allele at the Meg3-proximal enhancer (Fig. 3B,C; Supplemental Fig. S4).	2900016C05Rik,3110050O07Rik,6330408G06Rik,AI425946,AW108224,D12Bwg1266e,Gtl2,R74756,R75394	--	--	--	Aff3	LAF4,MLLT2-like	ChIP,ChIP-seq	"This AFF3 peak resides within the intergenic DMR (IG-DMR) of the Dlk1-Dio3 cluster and corresponds to the Meg3-proximal enhancer peak located just 2.4 kb from the Meg3-distal gDMR peak (Figs. 1B, 3A). While bisulfite sequencing of ChIP DNA demonstrated that AFF3 is on the inactive allele at the Meg3-distal gDMR,AFF3 is restricted to the unmethylated allele at the Meg3-proximal enhancer (Fig. 3B,C; Supplemental Fig. S4).Knockdown of AFF3 leads to reduced H3K27ac at the Meg3-proximal enhancer, indicating that AFF3 is required to maintain its active chromatin state (Fig. 3D; Supple_x0002_mental Table 2). Furthermore, the expression levels of
Meg3 and the downstream maternally expressed noncod_x0002_ing genes within the Dlk1-Dio3 locus are also reduced in AFF3 knockdown ESCs (Fig. 3E; Supplemental Fig. S5A),suggesting that an activating function of AFF3 might beexerted from the nearby Meg3-proximal enhancer."	--	--	Meg3
26673704	chr7	117038917	117040917	CFTR	" We showed previously that intronic and ex_x0002_tragenic enhancers, when occupied by specific tran_x0002_scription factors, are recruited to the CFTR promoter
by a looping mechanism to drive gene expression."	human	lung	Low throughput	Differential contribution of cis-regulatory elements to higher order chromatin structure and expression of the CFTR locus		--	--	Caco-2,Calu3 cell	E_02_0840	RT-qPCR,4C,ChIP,CRISPR/Cas9	"Two pairs of gRNAs ?anking the ?20.9 kb CTCF site
and the intron 11 enhancer core were identifed using the
CRISPR Design Program"	Enhancer	CRISPR/Cas9	--	Here we use a combination of CRISPR/Cas9 editing of cis-regulatory elements and siRNA-mediated depletion of architectural proteins to determine the relative contribution of structural elements and enhancers to the higher order structure and expression of the CFTR locus.	ABC35,ABCC7,CF,CFTR/MRP,MRP7,TNR-CFTR,dJ760C5.1	--	--	--	FOXA1,FOXA2,HNF1A,CDX2	HNF3A,TCF3A,HNF3B,TCF3B,HNF-1A,HNF1,HNF4A,IDDM20,LFB1,MODY3,TCF-1,TCF1,CDX-3/AS, CDX3, CDX2	4C,ChIP,CRISPR/Cas9	Approximately 1.2 encompass_x0002_ing the binding sites for critical transcription factors driving the intron 11 Enhancer (FOXA1/2,HNF1 and CDX2).	--	--	CFTR
26673693	chr14	54227135	54228033	Ets1	We found that while Ets1 binding at distal sites was associated with active genes at both DN and DP stages, its enhancer activity was attained at the DP stage, as reflected by levels of the core transcriptional hallmarks H3K4me1/3, RNA Polymerase II and eRNA. This dual, stage-specific ability reflected a switch from non-T hematopoietic toward T-cell specific gene expression programs during the DN-to-DP transition, as indicated by transcriptome analyses of Ets1(-/-) thymic cells. Coincidentally, Ets1 associates more specifically with Runx1 in DN and with TCF1 in DP cells. We also provide evidence that Ets1 predominantly binds distal nucleosome-occupied regions in DN and nucleosome-depleted regions in DP. Finally and importantly, we demonstrate that Ets1 induces chromatin remodeling by displacing H3K4me1-marked nucleosomes. Our results thus provide an original model whereby the ability of a transcription factor to bind nucleosomal DNA changes during differentiation with consequences on its cognate enhancer activity.	mouse	epithelial tissue	Low+High throughput	Dynamic recruitment of Ets1 to both nucleosome-occupied and -depleted enhancer regions mediates a transcriptional program switch during early T-cell differentiation	否	--	--	P5424,CD4+ CD8+ DP cell	E_02_0841	ChIP-seq,ChIP	We found that eRNAs essentially reca_x0002_pitulated Pol II patterns during DN to DP transition as wellas those of Ets1 in DP only, suggesting highest enhancer ac_x0002_tivity in class 4 at the DN stage and classes 4–5 at the DP stage (Figure 3C). Thus, distal Ets1 enhancers broadly re_x0002_cruit Pol II that is able to generate paused transcripts.Significance of gene expression differences by increasing Ets1-fold change. Expression fold changes for all classes, shown as a boxplot. Significance levels for each comparison are indicated above, with 1 star denoting P < 0.05, 2 stars denoting P < 0.01 and 3 stars denoting P < 0.005.	Enhancer	--	ChIP-seq,Western blot,ChIP-qPCR	We further validated the dy_x0002_namic recruitment of TCF1 and Runx1 by ChIP-qPCR at the Tcra Enhancer, which is bound by similar levels of Ets1 in both DN and DP thymocytes.UCSC genome browser screenshot of the Tcra (left) and Cd2 loci (right)showing increased H3K4me1 signal at the Ets1 binding site following knockdown in the P5424 cell line.	AI323713	--	--	--	Ets1,Tcf1,Runx1	AI196000,AI448617,D230050P06,Ets-1,Tpl1,p54,vs,AI465550,TCF-1,Tcf1,AML1,CBF-alpha-2,Cbfa2,Pebp2a2,Pebpa2b	ChIP-qPCR,Western blot	We further validated the dynamic recruitment of TCF1 and Runx1 by ChIP-qPCR at the Tcra Enhancer, which is bound by similar levels of Ets1 in both DN and DP thymocytes.	--	--	Dad1
26673693	chr14	54227135	54228033	Runx1	We found that while Ets1 binding at distal sites was associated with active genes at both DN and DP stages, its enhancer activity was attained at the DP stage, as reflected by levels of the core transcriptional hallmarks H3K4me1/3, RNA Polymerase II and eRNA. This dual, stage-specific ability reflected a switch from non-T hematopoietic toward T-cell specific gene expression programs during the DN-to-DP transition, as indicated by transcriptome analyses of Ets1(-/-) thymic cells. Coincidentally, Ets1 associates more specifically with Runx1 in DN and with TCF1 in DP cells. We also provide evidence that Ets1 predominantly binds distal nucleosome-occupied regions in DN and nucleosome-depleted regions in DP. Finally and importantly, we demonstrate that Ets1 induces chromatin remodeling by displacing H3K4me1-marked nucleosomes. Our results thus provide an original model whereby the ability of a transcription factor to bind nucleosomal DNA changes during differentiation with consequences on its cognate enhancer activity.	mouse	epithelial tissue	Low+High throughput	Dynamic recruitment of Ets1 to both nucleosome-occupied and -depleted enhancer regions mediates a transcriptional program switch during early T-cell differentiation	否	--	--	P5424,CD4+ CD8+ DP cell	E_02_0841	ChIP-seq,ChIP	We found that eRNAs essentially reca_x0002_pitulated Pol II patterns during DN to DP transition as wellas those of Ets1 in DP only, suggesting highest enhancer ac_x0002_tivity in class 4 at the DN stage and classes 4–5 at the DP stage (Figure 3C). Thus, distal Ets1 enhancers broadly re_x0002_cruit Pol II that is able to generate paused transcripts.Significance of gene expression differences by increasing Ets1-fold change. Expression fold changes for all classes, shown as a boxplot. Significance levels for each comparison are indicated above, with 1 star denoting P < 0.05, 2 stars denoting P < 0.01 and 3 stars denoting P < 0.005.	Enhancer	--	ChIP-seq,Western blot,ChIP-qPCR	We further validated the dy_x0002_namic recruitment of TCF1 and Runx1 by ChIP-qPCR at the Tcra Enhancer, which is bound by similar levels of Ets1 in both DN and DP thymocytes.UCSC genome browser screenshot of the Tcra (left) and Cd2 loci (right)showing increased H3K4me1 signal at the Ets1 binding site following knockdown in the P5424 cell line.	AI323713	--	--	--	Ets1,Tcf1,Runx1	AI196000,AI448617,D230050P06,Ets-1,Tpl1,p54,vs,AI465550,TCF-1,Tcf1,AML1,CBF-alpha-2,Cbfa2,Pebp2a2,Pebpa2b	ChIP-qPCR,Western blot	We further validated the dynamic recruitment of TCF1 and Runx1 by ChIP-qPCR at the Tcra Enhancer, which is bound by similar levels of Ets1 in both DN and DP thymocytes.	--	--	Dad1
26673693	chr14	54227135	54228033	Il2ra	We found that while Ets1 binding at distal sites was associated with active genes at both DN and DP stages, its enhancer activity was attained at the DP stage, as reflected by levels of the core transcriptional hallmarks H3K4me1/3, RNA Polymerase II and eRNA. This dual, stage-specific ability reflected a switch from non-T hematopoietic toward T-cell specific gene expression programs during the DN-to-DP transition, as indicated by transcriptome analyses of Ets1(-/-) thymic cells. Coincidentally, Ets1 associates more specifically with Runx1 in DN and with TCF1 in DP cells. We also provide evidence that Ets1 predominantly binds distal nucleosome-occupied regions in DN and nucleosome-depleted regions in DP. Finally and importantly, we demonstrate that Ets1 induces chromatin remodeling by displacing H3K4me1-marked nucleosomes. Our results thus provide an original model whereby the ability of a transcription factor to bind nucleosomal DNA changes during differentiation with consequences on its cognate enhancer activity.	mouse	epithelial tissue	Low+High throughput	Dynamic recruitment of Ets1 to both nucleosome-occupied and -depleted enhancer regions mediates a transcriptional program switch during early T-cell differentiation	否	--	--	P5424,CD4+ CD8+ DP cell	E_02_0841	ChIP-seq,ChIP	We found that eRNAs essentially reca_x0002_pitulated Pol II patterns during DN to DP transition as wellas those of Ets1 in DP only, suggesting highest enhancer ac_x0002_tivity in class 4 at the DN stage and classes 4–5 at the DP stage (Figure 3C). Thus, distal Ets1 enhancers broadly re_x0002_cruit Pol II that is able to generate paused transcripts.Significance of gene expression differences by increasing Ets1-fold change. Expression fold changes for all classes, shown as a boxplot. Significance levels for each comparison are indicated above, with 1 star denoting P < 0.05, 2 stars denoting P < 0.01 and 3 stars denoting P < 0.005.	Enhancer	--	ChIP-seq,Western blot,ChIP-qPCR	We further validated the dy_x0002_namic recruitment of TCF1 and Runx1 by ChIP-qPCR at the Tcra Enhancer, which is bound by similar levels of Ets1 in both DN and DP thymocytes.UCSC genome browser screenshot of the Tcra (left) and Cd2 loci (right)showing increased H3K4me1 signal at the Ets1 binding site following knockdown in the P5424 cell line.	AI323713	--	--	--	Ets1,Tcf1,Runx1	AI196000,AI448617,D230050P06,Ets-1,Tpl1,p54,vs,AI465550,TCF-1,Tcf1,AML1,CBF-alpha-2,Cbfa2,Pebp2a2,Pebpa2b	ChIP-qPCR,Western blot	We further validated the dynamic recruitment of TCF1 and Runx1 by ChIP-qPCR at the Tcra Enhancer, which is bound by similar levels of Ets1 in both DN and DP thymocytes.	--	--	Dad1
26673693	chr14	54227135	54228033	Cd44	We found that while Ets1 binding at distal sites was associated with active genes at both DN and DP stages, its enhancer activity was attained at the DP stage, as reflected by levels of the core transcriptional hallmarks H3K4me1/3, RNA Polymerase II and eRNA. This dual, stage-specific ability reflected a switch from non-T hematopoietic toward T-cell specific gene expression programs during the DN-to-DP transition, as indicated by transcriptome analyses of Ets1(-/-) thymic cells. Coincidentally, Ets1 associates more specifically with Runx1 in DN and with TCF1 in DP cells. We also provide evidence that Ets1 predominantly binds distal nucleosome-occupied regions in DN and nucleosome-depleted regions in DP. Finally and importantly, we demonstrate that Ets1 induces chromatin remodeling by displacing H3K4me1-marked nucleosomes. Our results thus provide an original model whereby the ability of a transcription factor to bind nucleosomal DNA changes during differentiation with consequences on its cognate enhancer activity.	mouse	epithelial tissue	Low+High throughput	Dynamic recruitment of Ets1 to both nucleosome-occupied and -depleted enhancer regions mediates a transcriptional program switch during early T-cell differentiation	否	--	--	P5424,CD4+ CD8+ DP cell	E_02_0841	ChIP-seq,ChIP	We found that eRNAs essentially reca_x0002_pitulated Pol II patterns during DN to DP transition as wellas those of Ets1 in DP only, suggesting highest enhancer ac_x0002_tivity in class 4 at the DN stage and classes 4–5 at the DP stage (Figure 3C). Thus, distal Ets1 enhancers broadly re_x0002_cruit Pol II that is able to generate paused transcripts.Significance of gene expression differences by increasing Ets1-fold change. Expression fold changes for all classes, shown as a boxplot. Significance levels for each comparison are indicated above, with 1 star denoting P < 0.05, 2 stars denoting P < 0.01 and 3 stars denoting P < 0.005.	Enhancer	--	ChIP-seq,Western blot,ChIP-qPCR	We further validated the dy_x0002_namic recruitment of TCF1 and Runx1 by ChIP-qPCR at the Tcra Enhancer, which is bound by similar levels of Ets1 in both DN and DP thymocytes.UCSC genome browser screenshot of the Tcra (left) and Cd2 loci (right)showing increased H3K4me1 signal at the Ets1 binding site following knockdown in the P5424 cell line.	AI323713	--	--	--	Ets1,Tcf1,Runx1	AI196000,AI448617,D230050P06,Ets-1,Tpl1,p54,vs,AI465550,TCF-1,Tcf1,AML1,CBF-alpha-2,Cbfa2,Pebp2a2,Pebpa2b	ChIP-qPCR,Western blot	We further validated the dynamic recruitment of TCF1 and Runx1 by ChIP-qPCR at the Tcra Enhancer, which is bound by similar levels of Ets1 in both DN and DP thymocytes.	--	--	Dad1
26673693	chr14	54227135	54228033	Il7r	We found that while Ets1 binding at distal sites was associated with active genes at both DN and DP stages, its enhancer activity was attained at the DP stage, as reflected by levels of the core transcriptional hallmarks H3K4me1/3, RNA Polymerase II and eRNA. This dual, stage-specific ability reflected a switch from non-T hematopoietic toward T-cell specific gene expression programs during the DN-to-DP transition, as indicated by transcriptome analyses of Ets1(-/-) thymic cells. Coincidentally, Ets1 associates more specifically with Runx1 in DN and with TCF1 in DP cells. We also provide evidence that Ets1 predominantly binds distal nucleosome-occupied regions in DN and nucleosome-depleted regions in DP. Finally and importantly, we demonstrate that Ets1 induces chromatin remodeling by displacing H3K4me1-marked nucleosomes. Our results thus provide an original model whereby the ability of a transcription factor to bind nucleosomal DNA changes during differentiation with consequences on its cognate enhancer activity.	mouse	epithelial tissue	Low+High throughput	Dynamic recruitment of Ets1 to both nucleosome-occupied and -depleted enhancer regions mediates a transcriptional program switch during early T-cell differentiation	否	--	--	P5424,CD4+ CD8+ DP cell	E_02_0841	ChIP-seq,ChIP	We found that eRNAs essentially reca_x0002_pitulated Pol II patterns during DN to DP transition as wellas those of Ets1 in DP only, suggesting highest enhancer ac_x0002_tivity in class 4 at the DN stage and classes 4–5 at the DP stage (Figure 3C). Thus, distal Ets1 enhancers broadly re_x0002_cruit Pol II that is able to generate paused transcripts.Significance of gene expression differences by increasing Ets1-fold change. Expression fold changes for all classes, shown as a boxplot. Significance levels for each comparison are indicated above, with 1 star denoting P < 0.05, 2 stars denoting P < 0.01 and 3 stars denoting P < 0.005.	Enhancer	--	ChIP-seq,Western blot,ChIP-qPCR	We further validated the dy_x0002_namic recruitment of TCF1 and Runx1 by ChIP-qPCR at the Tcra Enhancer, which is bound by similar levels of Ets1 in both DN and DP thymocytes.UCSC genome browser screenshot of the Tcra (left) and Cd2 loci (right)showing increased H3K4me1 signal at the Ets1 binding site following knockdown in the P5424 cell line.	AI323713	--	--	--	Ets1,Tcf1,Runx1	AI196000,AI448617,D230050P06,Ets-1,Tpl1,p54,vs,AI465550,TCF-1,Tcf1,AML1,CBF-alpha-2,Cbfa2,Pebp2a2,Pebpa2b	ChIP-qPCR,Western blot	We further validated the dynamic recruitment of TCF1 and Runx1 by ChIP-qPCR at the Tcra Enhancer, which is bound by similar levels of Ets1 in both DN and DP thymocytes.	--	--	Dad1
26673693	chr14	54227135	54228033	Ptcra	We found that while Ets1 binding at distal sites was associated with active genes at both DN and DP stages, its enhancer activity was attained at the DP stage, as reflected by levels of the core transcriptional hallmarks H3K4me1/3, RNA Polymerase II and eRNA. This dual, stage-specific ability reflected a switch from non-T hematopoietic toward T-cell specific gene expression programs during the DN-to-DP transition, as indicated by transcriptome analyses of Ets1(-/-) thymic cells. Coincidentally, Ets1 associates more specifically with Runx1 in DN and with TCF1 in DP cells. We also provide evidence that Ets1 predominantly binds distal nucleosome-occupied regions in DN and nucleosome-depleted regions in DP. Finally and importantly, we demonstrate that Ets1 induces chromatin remodeling by displacing H3K4me1-marked nucleosomes. Our results thus provide an original model whereby the ability of a transcription factor to bind nucleosomal DNA changes during differentiation with consequences on its cognate enhancer activity.	mouse	epithelial tissue	Low+High throughput	Dynamic recruitment of Ets1 to both nucleosome-occupied and -depleted enhancer regions mediates a transcriptional program switch during early T-cell differentiation	否	--	--	P5424,CD4+ CD8+ DP cell	E_02_0841	ChIP-seq,ChIP	We found that eRNAs essentially reca_x0002_pitulated Pol II patterns during DN to DP transition as wellas those of Ets1 in DP only, suggesting highest enhancer ac_x0002_tivity in class 4 at the DN stage and classes 4–5 at the DP stage (Figure 3C). Thus, distal Ets1 enhancers broadly re_x0002_cruit Pol II that is able to generate paused transcripts.Significance of gene expression differences by increasing Ets1-fold change. Expression fold changes for all classes, shown as a boxplot. Significance levels for each comparison are indicated above, with 1 star denoting P < 0.05, 2 stars denoting P < 0.01 and 3 stars denoting P < 0.005.	Enhancer	--	ChIP-seq,Western blot,ChIP-qPCR	We further validated the dy_x0002_namic recruitment of TCF1 and Runx1 by ChIP-qPCR at the Tcra Enhancer, which is bound by similar levels of Ets1 in both DN and DP thymocytes.UCSC genome browser screenshot of the Tcra (left) and Cd2 loci (right)showing increased H3K4me1 signal at the Ets1 binding site following knockdown in the P5424 cell line.	AI323713	--	--	--	Ets1,Tcf1,Runx1	AI196000,AI448617,D230050P06,Ets-1,Tpl1,p54,vs,AI465550,TCF-1,Tcf1,AML1,CBF-alpha-2,Cbfa2,Pebp2a2,Pebpa2b	ChIP-qPCR,Western blot	We further validated the dynamic recruitment of TCF1 and Runx1 by ChIP-qPCR at the Tcra Enhancer, which is bound by similar levels of Ets1 in both DN and DP thymocytes.	--	--	Dad1
26663721	chr12	85515101	85543901	GC	We conclude that enhancer divergence underlies the difference in transcriptional activation after GC treatment between mouse and human macrophages. Only the shared inducible loci show evidence of selection, and therefore these loci may be important for the subset of responses to GC that is shared between species.	mouse	connective tissue	Low+High throughput	Enhancer Turnover Is Associated with a Divergent Transcriptional Response to Glucocorticoid in Mouse and Human Macrophages	否	--	--	Peripheral blood mononuclear cell	E_02_0842	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	Enhancer	--	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	D12Rfj1,c-fos,cFos,Jundm2,Jundp2,TIF	--	--	--	--	--	--	--	--	--	Fos-Jdp2?
26663721	chr12	85515101	85543901	CSF1	We conclude that enhancer divergence underlies the difference in transcriptional activation after GC treatment between mouse and human macrophages. Only the shared inducible loci show evidence of selection, and therefore these loci may be important for the subset of responses to GC that is shared between species.	mouse	connective tissue	Low+High throughput	Enhancer Turnover Is Associated with a Divergent Transcriptional Response to Glucocorticoid in Mouse and Human Macrophages	否	--	--	Peripheral blood mononuclear cell	E_02_0842	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	Enhancer	--	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	D12Rfj1,c-fos,cFos,Jundm2,Jundp2,TIF	--	--	--	--	--	--	--	--	--	Fos-Jdp2?
26663721	chr12	85515101	85543901	Fos	We conclude that enhancer divergence underlies the difference in transcriptional activation after GC treatment between mouse and human macrophages. Only the shared inducible loci show evidence of selection, and therefore these loci may be important for the subset of responses to GC that is shared between species.	mouse	connective tissue	Low+High throughput	Enhancer Turnover Is Associated with a Divergent Transcriptional Response to Glucocorticoid in Mouse and Human Macrophages	否	--	--	Peripheral blood mononuclear cell	E_02_0842	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	Enhancer	--	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	D12Rfj1,c-fos,cFos,Jundm2,Jundp2,TIF	--	--	--	--	--	--	--	--	--	Fos-Jdp2?
26663721	chr12	85515101	85543901	Hivep2	We conclude that enhancer divergence underlies the difference in transcriptional activation after GC treatment between mouse and human macrophages. Only the shared inducible loci show evidence of selection, and therefore these loci may be important for the subset of responses to GC that is shared between species.	mouse	connective tissue	Low+High throughput	Enhancer Turnover Is Associated with a Divergent Transcriptional Response to Glucocorticoid in Mouse and Human Macrophages	否	--	--	Peripheral blood mononuclear cell	E_02_0842	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	Enhancer	--	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	D12Rfj1,c-fos,cFos,Jundm2,Jundp2,TIF	--	--	--	--	--	--	--	--	--	Fos-Jdp2?
26663721	chr12	85515101	85543901	Klf4	We conclude that enhancer divergence underlies the difference in transcriptional activation after GC treatment between mouse and human macrophages. Only the shared inducible loci show evidence of selection, and therefore these loci may be important for the subset of responses to GC that is shared between species.	mouse	connective tissue	Low+High throughput	Enhancer Turnover Is Associated with a Divergent Transcriptional Response to Glucocorticoid in Mouse and Human Macrophages	否	--	--	Peripheral blood mononuclear cell	E_02_0842	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	Enhancer	--	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	D12Rfj1,c-fos,cFos,Jundm2,Jundp2,TIF	--	--	--	--	--	--	--	--	--	Fos-Jdp2?
26663721	chr12	85515101	85543901	Ncoa5	We conclude that enhancer divergence underlies the difference in transcriptional activation after GC treatment between mouse and human macrophages. Only the shared inducible loci show evidence of selection, and therefore these loci may be important for the subset of responses to GC that is shared between species.	mouse	connective tissue	Low+High throughput	Enhancer Turnover Is Associated with a Divergent Transcriptional Response to Glucocorticoid in Mouse and Human Macrophages	否	--	--	Peripheral blood mononuclear cell	E_02_0842	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	Enhancer	--	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	D12Rfj1,c-fos,cFos,Jundm2,Jundp2,TIF	--	--	--	--	--	--	--	--	--	Fos-Jdp2?
26663721	chr12	85515101	85543901	Plau	We conclude that enhancer divergence underlies the difference in transcriptional activation after GC treatment between mouse and human macrophages. Only the shared inducible loci show evidence of selection, and therefore these loci may be important for the subset of responses to GC that is shared between species.	mouse	connective tissue	Low+High throughput	Enhancer Turnover Is Associated with a Divergent Transcriptional Response to Glucocorticoid in Mouse and Human Macrophages	否	--	--	Peripheral blood mononuclear cell	E_02_0842	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	Enhancer	--	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	D12Rfj1,c-fos,cFos,Jundm2,Jundp2,TIF	--	--	--	--	--	--	--	--	--	Fos-Jdp2?
26663721	chr12	85515101	85543901	Egr2	We conclude that enhancer divergence underlies the difference in transcriptional activation after GC treatment between mouse and human macrophages. Only the shared inducible loci show evidence of selection, and therefore these loci may be important for the subset of responses to GC that is shared between species.	mouse	connective tissue	Low+High throughput	Enhancer Turnover Is Associated with a Divergent Transcriptional Response to Glucocorticoid in Mouse and Human Macrophages	否	--	--	Peripheral blood mononuclear cell	E_02_0842	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	Enhancer	--	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	D12Rfj1,c-fos,cFos,Jundm2,Jundp2,TIF	--	--	--	--	--	--	--	--	--	Fos-Jdp2?
26663721	chr12	85515101	85543901	Rgs2	We conclude that enhancer divergence underlies the difference in transcriptional activation after GC treatment between mouse and human macrophages. Only the shared inducible loci show evidence of selection, and therefore these loci may be important for the subset of responses to GC that is shared between species.	mouse	connective tissue	Low+High throughput	Enhancer Turnover Is Associated with a Divergent Transcriptional Response to Glucocorticoid in Mouse and Human Macrophages	否	--	--	Peripheral blood mononuclear cell	E_02_0842	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	Enhancer	--	ChIP-seq	To identify the sites involved in the GC response in the two species,Chromatin immunoprecipitation for GR and sequencing (ChIP-seq) was performed 2 h after dexamethasone treatment in both mBMDM and hMDM. Representative UCSC browser tracks for GR binding in mBMDM and hMDM are shown in Fig. 2A and 2C.ChIP-seq data tracks from the UCSC browser for the Fos – Jdp2 region, for GR binding in mBMDM. Data from ChIP with anti-GR antibodies after treatment with 100nM dexamethasone for 2h (Dex GR IP), input material (Dex input) and immunoprecipitated material from a vehicle treated control (Vehicle GR IP) are shown. Enriched motifs found de novo within GR bound sites in mBMDM and hMDM.	D12Rfj1,c-fos,cFos,Jundm2,Jundp2,TIF	--	--	--	--	--	--	--	--	--	Fos-Jdp2?
26659182	chr2	168744572	168752225	Chaf1a	To further elucidate regulatory pathways that safeguard the somatic state, we performed two comprehensive RNA interference (RNAi) screens targeting chromatin factors during transcription-factor-mediated reprogramming of mouse fibroblasts to induced pluripotent stem cells (iPS cells). Subunits of the chromatin assembly factor-1 (CAF-1) complex, including Chaf1a and Chaf1b, emerged as the most prominent hits from both screens, followed by modulators of lysine sumoylation and heterochromatin maintenance. Optimal modulation of both CAF-1 and transcription factor levels increased reprogramming efficiency by several orders of magnitude and facilitated iPS cell formation in as little as 4 days. Mechanistically, CAF-1 suppression led to a more accessible chromatin structure at enhancer elements early during reprogramming. These changes were accompanied by a decrease in somatic heterochromatin domains, increased binding of Sox2 to pluripotency-specific targets and activation of associated genes. Notably, suppression of CAF-1 also enhanced the direct conversion of B cells into macrophages and fibroblasts into neurons. Together, our findings reveal the histone chaperone CAF-1 to be a novel regulator of somatic cell identity during transcription-factor-induced cell-fate transitions and provide a potential strategy to modulate cellular plasticity in a regenerative setting.	mouse	epithelial tissue	Low+High throughput	The histone chaperone CAF-1 safeguards somatic cell identity	否	--	--	MEF,iPS,ES,MEFs,HSP cell	E_02_0843	ChIP-seq,ATAC-seq,CRISPR/Cas9	To validate these observations with an independent, higher resolution method, we performed Assay of Transposase Accessible Chromatin using sequencing (ATAC-seq), which detects integration of the Tn5 transposase in open chromatin regions27 (Extended Data Fig. 7c). Consistent with the SONO-seq data, ATAC-seq analysis of early reprogramming intermediates showed a more accessible chromatin configuration at regulatory regions including ESC-specific enhancers upon suppression of Chaf1a (Fig. 5a; P value <10?15). Moreover, Chaf1a knockdown caused a significant increase in chromatin accessibility across ESC-specific super-enhancers at day 3 of iPSC formation (Supplementary Table 3 and Extended Data Fig. 7d,e; P value <5.3×10?16). Of note, super-enhancers linked to specialized cell types such as macrophages, lymphocytes and muscle cells were also significantly more accessible in Chaf1a depleted reprogramming intermediates compared to controls (Extended Data Fig. 7f). 	Super-Enhancer	--	ChIP-seq,ATAC-seq	Moreover,Chaf1a knockdown caused a significant increase in Chromatin accessibility across ES-cell-specific Super-Enhancers at day 3 of iPS cell formation.	5730441M18Rik,AA407717,AL022809,AW536104,C330011P20Rik,C78083,C78563,Tex20	--	--	--	Sox2	Sox-2,lcc,ysb	ChIP-seq,ATAC-seq	Next,we performed ChIP-seq analysis for Sox2 at day 3 of OKSM expression in order to test our hypothesis that increased Chromatin accessibility at Enhancer lements influences reprogramming factor binding. Of the Sox2-bound super-Enhancers unique to CAF-1 knockdown cells, a subset also showed a more accessible chromatin structure by ATAC-seq analysis. 	--	--	Sall4
26659182	chr2	168744572	168752225	Chaf1b	To further elucidate regulatory pathways that safeguard the somatic state, we performed two comprehensive RNA interference (RNAi) screens targeting chromatin factors during transcription-factor-mediated reprogramming of mouse fibroblasts to induced pluripotent stem cells (iPS cells). Subunits of the chromatin assembly factor-1 (CAF-1) complex, including Chaf1a and Chaf1b, emerged as the most prominent hits from both screens, followed by modulators of lysine sumoylation and heterochromatin maintenance. Optimal modulation of both CAF-1 and transcription factor levels increased reprogramming efficiency by several orders of magnitude and facilitated iPS cell formation in as little as 4 days. Mechanistically, CAF-1 suppression led to a more accessible chromatin structure at enhancer elements early during reprogramming. These changes were accompanied by a decrease in somatic heterochromatin domains, increased binding of Sox2 to pluripotency-specific targets and activation of associated genes. Notably, suppression of CAF-1 also enhanced the direct conversion of B cells into macrophages and fibroblasts into neurons. Together, our findings reveal the histone chaperone CAF-1 to be a novel regulator of somatic cell identity during transcription-factor-induced cell-fate transitions and provide a potential strategy to modulate cellular plasticity in a regenerative setting.	mouse	epithelial tissue	Low+High throughput	The histone chaperone CAF-1 safeguards somatic cell identity	否	--	--	MEF,iPS,ES,MEFs,HSP cell	E_02_0843	ChIP-seq,ATAC-seq,CRISPR/Cas9	To validate these observations with an independent, higher resolution method, we performed Assay of Transposase Accessible Chromatin using sequencing (ATAC-seq), which detects integration of the Tn5 transposase in open chromatin regions27 (Extended Data Fig. 7c). Consistent with the SONO-seq data, ATAC-seq analysis of early reprogramming intermediates showed a more accessible chromatin configuration at regulatory regions including ESC-specific enhancers upon suppression of Chaf1a (Fig. 5a; P value <10?15). Moreover, Chaf1a knockdown caused a significant increase in chromatin accessibility across ESC-specific super-enhancers at day 3 of iPSC formation (Supplementary Table 3 and Extended Data Fig. 7d,e; P value <5.3×10?16). Of note, super-enhancers linked to specialized cell types such as macrophages, lymphocytes and muscle cells were also significantly more accessible in Chaf1a depleted reprogramming intermediates compared to controls (Extended Data Fig. 7f). 	Super-Enhancer	--	ChIP-seq,ATAC-seq	Moreover,Chaf1a knockdown caused a significant increase in Chromatin accessibility across ES-cell-specific Super-Enhancers at day 3 of iPS cell formation.	5730441M18Rik,AA407717,AL022809,AW536104,C330011P20Rik,C78083,C78563,Tex20	--	--	--	Sox2	Sox-2,lcc,ysb	ChIP-seq,ATAC-seq	Next,we performed ChIP-seq analysis for Sox2 at day 3 of OKSM expression in order to test our hypothesis that increased Chromatin accessibility at Enhancer lements influences reprogramming factor binding. Of the Sox2-bound super-Enhancers unique to CAF-1 knockdown cells, a subset also showed a more accessible chromatin structure by ATAC-seq analysis. 	--	--	Sall4
26659182	chr2	168744572	168752225	Sox2	To further elucidate regulatory pathways that safeguard the somatic state, we performed two comprehensive RNA interference (RNAi) screens targeting chromatin factors during transcription-factor-mediated reprogramming of mouse fibroblasts to induced pluripotent stem cells (iPS cells). Subunits of the chromatin assembly factor-1 (CAF-1) complex, including Chaf1a and Chaf1b, emerged as the most prominent hits from both screens, followed by modulators of lysine sumoylation and heterochromatin maintenance. Optimal modulation of both CAF-1 and transcription factor levels increased reprogramming efficiency by several orders of magnitude and facilitated iPS cell formation in as little as 4 days. Mechanistically, CAF-1 suppression led to a more accessible chromatin structure at enhancer elements early during reprogramming. These changes were accompanied by a decrease in somatic heterochromatin domains, increased binding of Sox2 to pluripotency-specific targets and activation of associated genes. Notably, suppression of CAF-1 also enhanced the direct conversion of B cells into macrophages and fibroblasts into neurons. Together, our findings reveal the histone chaperone CAF-1 to be a novel regulator of somatic cell identity during transcription-factor-induced cell-fate transitions and provide a potential strategy to modulate cellular plasticity in a regenerative setting.	mouse	epithelial tissue	Low+High throughput	The histone chaperone CAF-1 safeguards somatic cell identity	否	--	--	MEF,iPS,ES,MEFs,HSP cell	E_02_0843	ChIP-seq,ATAC-seq,CRISPR/Cas9	To validate these observations with an independent, higher resolution method, we performed Assay of Transposase Accessible Chromatin using sequencing (ATAC-seq), which detects integration of the Tn5 transposase in open chromatin regions27 (Extended Data Fig. 7c). Consistent with the SONO-seq data, ATAC-seq analysis of early reprogramming intermediates showed a more accessible chromatin configuration at regulatory regions including ESC-specific enhancers upon suppression of Chaf1a (Fig. 5a; P value <10?15). Moreover, Chaf1a knockdown caused a significant increase in chromatin accessibility across ESC-specific super-enhancers at day 3 of iPSC formation (Supplementary Table 3 and Extended Data Fig. 7d,e; P value <5.3×10?16). Of note, super-enhancers linked to specialized cell types such as macrophages, lymphocytes and muscle cells were also significantly more accessible in Chaf1a depleted reprogramming intermediates compared to controls (Extended Data Fig. 7f). 	Super-Enhancer	--	ChIP-seq,ATAC-seq	Moreover,Chaf1a knockdown caused a significant increase in Chromatin accessibility across ES-cell-specific Super-Enhancers at day 3 of iPS cell formation.	5730441M18Rik,AA407717,AL022809,AW536104,C330011P20Rik,C78083,C78563,Tex20	--	--	--	Sox2	Sox-2,lcc,ysb	ChIP-seq,ATAC-seq	Next,we performed ChIP-seq analysis for Sox2 at day 3 of OKSM expression in order to test our hypothesis that increased Chromatin accessibility at Enhancer lements influences reprogramming factor binding. Of the Sox2-bound super-Enhancers unique to CAF-1 knockdown cells, a subset also showed a more accessible chromatin structure by ATAC-seq analysis. 	--	--	Sall4
26659182	chr2	168744572	168752225	Ube2i	To further elucidate regulatory pathways that safeguard the somatic state, we performed two comprehensive RNA interference (RNAi) screens targeting chromatin factors during transcription-factor-mediated reprogramming of mouse fibroblasts to induced pluripotent stem cells (iPS cells). Subunits of the chromatin assembly factor-1 (CAF-1) complex, including Chaf1a and Chaf1b, emerged as the most prominent hits from both screens, followed by modulators of lysine sumoylation and heterochromatin maintenance. Optimal modulation of both CAF-1 and transcription factor levels increased reprogramming efficiency by several orders of magnitude and facilitated iPS cell formation in as little as 4 days. Mechanistically, CAF-1 suppression led to a more accessible chromatin structure at enhancer elements early during reprogramming. These changes were accompanied by a decrease in somatic heterochromatin domains, increased binding of Sox2 to pluripotency-specific targets and activation of associated genes. Notably, suppression of CAF-1 also enhanced the direct conversion of B cells into macrophages and fibroblasts into neurons. Together, our findings reveal the histone chaperone CAF-1 to be a novel regulator of somatic cell identity during transcription-factor-induced cell-fate transitions and provide a potential strategy to modulate cellular plasticity in a regenerative setting.	mouse	epithelial tissue	Low+High throughput	The histone chaperone CAF-1 safeguards somatic cell identity	否	--	--	MEF,iPS,ES,MEFs,HSP cell	E_02_0843	ChIP-seq,ATAC-seq,CRISPR/Cas9	To validate these observations with an independent, higher resolution method, we performed Assay of Transposase Accessible Chromatin using sequencing (ATAC-seq), which detects integration of the Tn5 transposase in open chromatin regions27 (Extended Data Fig. 7c). Consistent with the SONO-seq data, ATAC-seq analysis of early reprogramming intermediates showed a more accessible chromatin configuration at regulatory regions including ESC-specific enhancers upon suppression of Chaf1a (Fig. 5a; P value <10?15). Moreover, Chaf1a knockdown caused a significant increase in chromatin accessibility across ESC-specific super-enhancers at day 3 of iPSC formation (Supplementary Table 3 and Extended Data Fig. 7d,e; P value <5.3×10?16). Of note, super-enhancers linked to specialized cell types such as macrophages, lymphocytes and muscle cells were also significantly more accessible in Chaf1a depleted reprogramming intermediates compared to controls (Extended Data Fig. 7f). 	Super-Enhancer	--	ChIP-seq,ATAC-seq	Moreover,Chaf1a knockdown caused a significant increase in Chromatin accessibility across ES-cell-specific Super-Enhancers at day 3 of iPS cell formation.	5730441M18Rik,AA407717,AL022809,AW536104,C330011P20Rik,C78083,C78563,Tex20	--	--	--	Sox2	Sox-2,lcc,ysb	ChIP-seq,ATAC-seq	Next,we performed ChIP-seq analysis for Sox2 at day 3 of OKSM expression in order to test our hypothesis that increased Chromatin accessibility at Enhancer lements influences reprogramming factor binding. Of the Sox2-bound super-Enhancers unique to CAF-1 knockdown cells, a subset also showed a more accessible chromatin structure by ATAC-seq analysis. 	--	--	Sall4
26659182	chr2	168744572	168752225	Setdb1	To further elucidate regulatory pathways that safeguard the somatic state, we performed two comprehensive RNA interference (RNAi) screens targeting chromatin factors during transcription-factor-mediated reprogramming of mouse fibroblasts to induced pluripotent stem cells (iPS cells). Subunits of the chromatin assembly factor-1 (CAF-1) complex, including Chaf1a and Chaf1b, emerged as the most prominent hits from both screens, followed by modulators of lysine sumoylation and heterochromatin maintenance. Optimal modulation of both CAF-1 and transcription factor levels increased reprogramming efficiency by several orders of magnitude and facilitated iPS cell formation in as little as 4 days. Mechanistically, CAF-1 suppression led to a more accessible chromatin structure at enhancer elements early during reprogramming. These changes were accompanied by a decrease in somatic heterochromatin domains, increased binding of Sox2 to pluripotency-specific targets and activation of associated genes. Notably, suppression of CAF-1 also enhanced the direct conversion of B cells into macrophages and fibroblasts into neurons. Together, our findings reveal the histone chaperone CAF-1 to be a novel regulator of somatic cell identity during transcription-factor-induced cell-fate transitions and provide a potential strategy to modulate cellular plasticity in a regenerative setting.	mouse	epithelial tissue	Low+High throughput	The histone chaperone CAF-1 safeguards somatic cell identity	否	--	--	MEF,iPS,ES,MEFs,HSP cell	E_02_0843	ChIP-seq,ATAC-seq,CRISPR/Cas9	To validate these observations with an independent, higher resolution method, we performed Assay of Transposase Accessible Chromatin using sequencing (ATAC-seq), which detects integration of the Tn5 transposase in open chromatin regions27 (Extended Data Fig. 7c). Consistent with the SONO-seq data, ATAC-seq analysis of early reprogramming intermediates showed a more accessible chromatin configuration at regulatory regions including ESC-specific enhancers upon suppression of Chaf1a (Fig. 5a; P value <10?15). Moreover, Chaf1a knockdown caused a significant increase in chromatin accessibility across ESC-specific super-enhancers at day 3 of iPSC formation (Supplementary Table 3 and Extended Data Fig. 7d,e; P value <5.3×10?16). Of note, super-enhancers linked to specialized cell types such as macrophages, lymphocytes and muscle cells were also significantly more accessible in Chaf1a depleted reprogramming intermediates compared to controls (Extended Data Fig. 7f). 	Super-Enhancer	--	ChIP-seq,ATAC-seq	Moreover,Chaf1a knockdown caused a significant increase in Chromatin accessibility across ES-cell-specific Super-Enhancers at day 3 of iPS cell formation.	5730441M18Rik,AA407717,AL022809,AW536104,C330011P20Rik,C78083,C78563,Tex20	--	--	--	Sox2	Sox-2,lcc,ysb	ChIP-seq,ATAC-seq	Next,we performed ChIP-seq analysis for Sox2 at day 3 of OKSM expression in order to test our hypothesis that increased Chromatin accessibility at Enhancer lements influences reprogramming factor binding. Of the Sox2-bound super-Enhancers unique to CAF-1 knockdown cells, a subset also showed a more accessible chromatin structure by ATAC-seq analysis. 	--	--	Sall4
26659182	chr2	168744572	168752225	Utf1	To further elucidate regulatory pathways that safeguard the somatic state, we performed two comprehensive RNA interference (RNAi) screens targeting chromatin factors during transcription-factor-mediated reprogramming of mouse fibroblasts to induced pluripotent stem cells (iPS cells). Subunits of the chromatin assembly factor-1 (CAF-1) complex, including Chaf1a and Chaf1b, emerged as the most prominent hits from both screens, followed by modulators of lysine sumoylation and heterochromatin maintenance. Optimal modulation of both CAF-1 and transcription factor levels increased reprogramming efficiency by several orders of magnitude and facilitated iPS cell formation in as little as 4 days. Mechanistically, CAF-1 suppression led to a more accessible chromatin structure at enhancer elements early during reprogramming. These changes were accompanied by a decrease in somatic heterochromatin domains, increased binding of Sox2 to pluripotency-specific targets and activation of associated genes. Notably, suppression of CAF-1 also enhanced the direct conversion of B cells into macrophages and fibroblasts into neurons. Together, our findings reveal the histone chaperone CAF-1 to be a novel regulator of somatic cell identity during transcription-factor-induced cell-fate transitions and provide a potential strategy to modulate cellular plasticity in a regenerative setting.	mouse	epithelial tissue	Low+High throughput	The histone chaperone CAF-1 safeguards somatic cell identity	否	--	--	MEF,iPS,ES,MEFs,HSP cell	E_02_0843	ChIP-seq,ATAC-seq,CRISPR/Cas9	To validate these observations with an independent, higher resolution method, we performed Assay of Transposase Accessible Chromatin using sequencing (ATAC-seq), which detects integration of the Tn5 transposase in open chromatin regions27 (Extended Data Fig. 7c). Consistent with the SONO-seq data, ATAC-seq analysis of early reprogramming intermediates showed a more accessible chromatin configuration at regulatory regions including ESC-specific enhancers upon suppression of Chaf1a (Fig. 5a; P value <10?15). Moreover, Chaf1a knockdown caused a significant increase in chromatin accessibility across ESC-specific super-enhancers at day 3 of iPSC formation (Supplementary Table 3 and Extended Data Fig. 7d,e; P value <5.3×10?16). Of note, super-enhancers linked to specialized cell types such as macrophages, lymphocytes and muscle cells were also significantly more accessible in Chaf1a depleted reprogramming intermediates compared to controls (Extended Data Fig. 7f). 	Super-Enhancer	--	ChIP-seq,ATAC-seq	Moreover,Chaf1a knockdown caused a significant increase in Chromatin accessibility across ES-cell-specific Super-Enhancers at day 3 of iPS cell formation.	5730441M18Rik,AA407717,AL022809,AW536104,C330011P20Rik,C78083,C78563,Tex20	--	--	--	Sox2	Sox-2,lcc,ysb	ChIP-seq,ATAC-seq	Next,we performed ChIP-seq analysis for Sox2 at day 3 of OKSM expression in order to test our hypothesis that increased Chromatin accessibility at Enhancer lements influences reprogramming factor binding. Of the Sox2-bound super-Enhancers unique to CAF-1 knockdown cells, a subset also showed a more accessible chromatin structure by ATAC-seq analysis. 	--	--	Sall4
26659182	chr2	168744572	168752225	Epcam	To further elucidate regulatory pathways that safeguard the somatic state, we performed two comprehensive RNA interference (RNAi) screens targeting chromatin factors during transcription-factor-mediated reprogramming of mouse fibroblasts to induced pluripotent stem cells (iPS cells). Subunits of the chromatin assembly factor-1 (CAF-1) complex, including Chaf1a and Chaf1b, emerged as the most prominent hits from both screens, followed by modulators of lysine sumoylation and heterochromatin maintenance. Optimal modulation of both CAF-1 and transcription factor levels increased reprogramming efficiency by several orders of magnitude and facilitated iPS cell formation in as little as 4 days. Mechanistically, CAF-1 suppression led to a more accessible chromatin structure at enhancer elements early during reprogramming. These changes were accompanied by a decrease in somatic heterochromatin domains, increased binding of Sox2 to pluripotency-specific targets and activation of associated genes. Notably, suppression of CAF-1 also enhanced the direct conversion of B cells into macrophages and fibroblasts into neurons. Together, our findings reveal the histone chaperone CAF-1 to be a novel regulator of somatic cell identity during transcription-factor-induced cell-fate transitions and provide a potential strategy to modulate cellular plasticity in a regenerative setting.	mouse	epithelial tissue	Low+High throughput	The histone chaperone CAF-1 safeguards somatic cell identity	否	--	--	MEF,iPS,ES,MEFs,HSP cell	E_02_0843	ChIP-seq,ATAC-seq,CRISPR/Cas9	To validate these observations with an independent, higher resolution method, we performed Assay of Transposase Accessible Chromatin using sequencing (ATAC-seq), which detects integration of the Tn5 transposase in open chromatin regions27 (Extended Data Fig. 7c). Consistent with the SONO-seq data, ATAC-seq analysis of early reprogramming intermediates showed a more accessible chromatin configuration at regulatory regions including ESC-specific enhancers upon suppression of Chaf1a (Fig. 5a; P value <10?15). Moreover, Chaf1a knockdown caused a significant increase in chromatin accessibility across ESC-specific super-enhancers at day 3 of iPSC formation (Supplementary Table 3 and Extended Data Fig. 7d,e; P value <5.3×10?16). Of note, super-enhancers linked to specialized cell types such as macrophages, lymphocytes and muscle cells were also significantly more accessible in Chaf1a depleted reprogramming intermediates compared to controls (Extended Data Fig. 7f). 	Super-Enhancer	--	ChIP-seq,ATAC-seq	Moreover,Chaf1a knockdown caused a significant increase in Chromatin accessibility across ES-cell-specific Super-Enhancers at day 3 of iPS cell formation.	5730441M18Rik,AA407717,AL022809,AW536104,C330011P20Rik,C78083,C78563,Tex20	--	--	--	Sox2	Sox-2,lcc,ysb	ChIP-seq,ATAC-seq	Next,we performed ChIP-seq analysis for Sox2 at day 3 of OKSM expression in order to test our hypothesis that increased Chromatin accessibility at Enhancer lements influences reprogramming factor binding. Of the Sox2-bound super-Enhancers unique to CAF-1 knockdown cells, a subset also showed a more accessible chromatin structure by ATAC-seq analysis. 	--	--	Sall4
26659182	chr2	168744572	168752225	Nr0b1	To further elucidate regulatory pathways that safeguard the somatic state, we performed two comprehensive RNA interference (RNAi) screens targeting chromatin factors during transcription-factor-mediated reprogramming of mouse fibroblasts to induced pluripotent stem cells (iPS cells). Subunits of the chromatin assembly factor-1 (CAF-1) complex, including Chaf1a and Chaf1b, emerged as the most prominent hits from both screens, followed by modulators of lysine sumoylation and heterochromatin maintenance. Optimal modulation of both CAF-1 and transcription factor levels increased reprogramming efficiency by several orders of magnitude and facilitated iPS cell formation in as little as 4 days. Mechanistically, CAF-1 suppression led to a more accessible chromatin structure at enhancer elements early during reprogramming. These changes were accompanied by a decrease in somatic heterochromatin domains, increased binding of Sox2 to pluripotency-specific targets and activation of associated genes. Notably, suppression of CAF-1 also enhanced the direct conversion of B cells into macrophages and fibroblasts into neurons. Together, our findings reveal the histone chaperone CAF-1 to be a novel regulator of somatic cell identity during transcription-factor-induced cell-fate transitions and provide a potential strategy to modulate cellular plasticity in a regenerative setting.	mouse	epithelial tissue	Low+High throughput	The histone chaperone CAF-1 safeguards somatic cell identity	否	--	--	MEF,iPS,ES,MEFs,HSP cell	E_02_0843	ChIP-seq,ATAC-seq,CRISPR/Cas9	To validate these observations with an independent, higher resolution method, we performed Assay of Transposase Accessible Chromatin using sequencing (ATAC-seq), which detects integration of the Tn5 transposase in open chromatin regions27 (Extended Data Fig. 7c). Consistent with the SONO-seq data, ATAC-seq analysis of early reprogramming intermediates showed a more accessible chromatin configuration at regulatory regions including ESC-specific enhancers upon suppression of Chaf1a (Fig. 5a; P value <10?15). Moreover, Chaf1a knockdown caused a significant increase in chromatin accessibility across ESC-specific super-enhancers at day 3 of iPSC formation (Supplementary Table 3 and Extended Data Fig. 7d,e; P value <5.3×10?16). Of note, super-enhancers linked to specialized cell types such as macrophages, lymphocytes and muscle cells were also significantly more accessible in Chaf1a depleted reprogramming intermediates compared to controls (Extended Data Fig. 7f). 	Super-Enhancer	--	ChIP-seq,ATAC-seq	Moreover,Chaf1a knockdown caused a significant increase in Chromatin accessibility across ES-cell-specific Super-Enhancers at day 3 of iPS cell formation.	5730441M18Rik,AA407717,AL022809,AW536104,C330011P20Rik,C78083,C78563,Tex20	--	--	--	Sox2	Sox-2,lcc,ysb	ChIP-seq,ATAC-seq	Next,we performed ChIP-seq analysis for Sox2 at day 3 of OKSM expression in order to test our hypothesis that increased Chromatin accessibility at Enhancer lements influences reprogramming factor binding. Of the Sox2-bound super-Enhancers unique to CAF-1 knockdown cells, a subset also showed a more accessible chromatin structure by ATAC-seq analysis. 	--	--	Sall4
26659182	chr2	168744572	168752225	Tdgf1	To further elucidate regulatory pathways that safeguard the somatic state, we performed two comprehensive RNA interference (RNAi) screens targeting chromatin factors during transcription-factor-mediated reprogramming of mouse fibroblasts to induced pluripotent stem cells (iPS cells). Subunits of the chromatin assembly factor-1 (CAF-1) complex, including Chaf1a and Chaf1b, emerged as the most prominent hits from both screens, followed by modulators of lysine sumoylation and heterochromatin maintenance. Optimal modulation of both CAF-1 and transcription factor levels increased reprogramming efficiency by several orders of magnitude and facilitated iPS cell formation in as little as 4 days. Mechanistically, CAF-1 suppression led to a more accessible chromatin structure at enhancer elements early during reprogramming. These changes were accompanied by a decrease in somatic heterochromatin domains, increased binding of Sox2 to pluripotency-specific targets and activation of associated genes. Notably, suppression of CAF-1 also enhanced the direct conversion of B cells into macrophages and fibroblasts into neurons. Together, our findings reveal the histone chaperone CAF-1 to be a novel regulator of somatic cell identity during transcription-factor-induced cell-fate transitions and provide a potential strategy to modulate cellular plasticity in a regenerative setting.	mouse	epithelial tissue	Low+High throughput	The histone chaperone CAF-1 safeguards somatic cell identity	否	--	--	MEF,iPS,ES,MEFs,HSP cell	E_02_0843	ChIP-seq,ATAC-seq,CRISPR/Cas9	To validate these observations with an independent, higher resolution method, we performed Assay of Transposase Accessible Chromatin using sequencing (ATAC-seq), which detects integration of the Tn5 transposase in open chromatin regions27 (Extended Data Fig. 7c). Consistent with the SONO-seq data, ATAC-seq analysis of early reprogramming intermediates showed a more accessible chromatin configuration at regulatory regions including ESC-specific enhancers upon suppression of Chaf1a (Fig. 5a; P value <10?15). Moreover, Chaf1a knockdown caused a significant increase in chromatin accessibility across ESC-specific super-enhancers at day 3 of iPSC formation (Supplementary Table 3 and Extended Data Fig. 7d,e; P value <5.3×10?16). Of note, super-enhancers linked to specialized cell types such as macrophages, lymphocytes and muscle cells were also significantly more accessible in Chaf1a depleted reprogramming intermediates compared to controls (Extended Data Fig. 7f). 	Super-Enhancer	--	ChIP-seq,ATAC-seq	Moreover,Chaf1a knockdown caused a significant increase in Chromatin accessibility across ES-cell-specific Super-Enhancers at day 3 of iPS cell formation.	5730441M18Rik,AA407717,AL022809,AW536104,C330011P20Rik,C78083,C78563,Tex20	--	--	--	Sox2	Sox-2,lcc,ysb	ChIP-seq,ATAC-seq	Next,we performed ChIP-seq analysis for Sox2 at day 3 of OKSM expression in order to test our hypothesis that increased Chromatin accessibility at Enhancer lements influences reprogramming factor binding. Of the Sox2-bound super-Enhancers unique to CAF-1 knockdown cells, a subset also showed a more accessible chromatin structure by ATAC-seq analysis. 	--	--	Sall4
26659182	chr2	168744572	168752225	Sall4	To further elucidate regulatory pathways that safeguard the somatic state, we performed two comprehensive RNA interference (RNAi) screens targeting chromatin factors during transcription-factor-mediated reprogramming of mouse fibroblasts to induced pluripotent stem cells (iPS cells). Subunits of the chromatin assembly factor-1 (CAF-1) complex, including Chaf1a and Chaf1b, emerged as the most prominent hits from both screens, followed by modulators of lysine sumoylation and heterochromatin maintenance. Optimal modulation of both CAF-1 and transcription factor levels increased reprogramming efficiency by several orders of magnitude and facilitated iPS cell formation in as little as 4 days. Mechanistically, CAF-1 suppression led to a more accessible chromatin structure at enhancer elements early during reprogramming. These changes were accompanied by a decrease in somatic heterochromatin domains, increased binding of Sox2 to pluripotency-specific targets and activation of associated genes. Notably, suppression of CAF-1 also enhanced the direct conversion of B cells into macrophages and fibroblasts into neurons. Together, our findings reveal the histone chaperone CAF-1 to be a novel regulator of somatic cell identity during transcription-factor-induced cell-fate transitions and provide a potential strategy to modulate cellular plasticity in a regenerative setting.	mouse	epithelial tissue	Low+High throughput	The histone chaperone CAF-1 safeguards somatic cell identity	否	--	--	MEF,iPS,ES,MEFs,HSP cell	E_02_0843	ChIP-seq,ATAC-seq,CRISPR/Cas9	To validate these observations with an independent, higher resolution method, we performed Assay of Transposase Accessible Chromatin using sequencing (ATAC-seq), which detects integration of the Tn5 transposase in open chromatin regions27 (Extended Data Fig. 7c). Consistent with the SONO-seq data, ATAC-seq analysis of early reprogramming intermediates showed a more accessible chromatin configuration at regulatory regions including ESC-specific enhancers upon suppression of Chaf1a (Fig. 5a; P value <10?15). Moreover, Chaf1a knockdown caused a significant increase in chromatin accessibility across ESC-specific super-enhancers at day 3 of iPSC formation (Supplementary Table 3 and Extended Data Fig. 7d,e; P value <5.3×10?16). Of note, super-enhancers linked to specialized cell types such as macrophages, lymphocytes and muscle cells were also significantly more accessible in Chaf1a depleted reprogramming intermediates compared to controls (Extended Data Fig. 7f). 	Super-Enhancer	--	ChIP-seq,ATAC-seq	Moreover,Chaf1a knockdown caused a significant increase in Chromatin accessibility across ES-cell-specific Super-Enhancers at day 3 of iPS cell formation.	5730441M18Rik,AA407717,AL022809,AW536104,C330011P20Rik,C78083,C78563,Tex20	--	--	--	Sox2	Sox-2,lcc,ysb	ChIP-seq,ATAC-seq	Next,we performed ChIP-seq analysis for Sox2 at day 3 of OKSM expression in order to test our hypothesis that increased Chromatin accessibility at Enhancer lements influences reprogramming factor binding. Of the Sox2-bound super-Enhancers unique to CAF-1 knockdown cells, a subset also showed a more accessible chromatin structure by ATAC-seq analysis. 	--	--	Sall4
26659182	chr2	168744572	168752225	IL3	To further elucidate regulatory pathways that safeguard the somatic state, we performed two comprehensive RNA interference (RNAi) screens targeting chromatin factors during transcription-factor-mediated reprogramming of mouse fibroblasts to induced pluripotent stem cells (iPS cells). Subunits of the chromatin assembly factor-1 (CAF-1) complex, including Chaf1a and Chaf1b, emerged as the most prominent hits from both screens, followed by modulators of lysine sumoylation and heterochromatin maintenance. Optimal modulation of both CAF-1 and transcription factor levels increased reprogramming efficiency by several orders of magnitude and facilitated iPS cell formation in as little as 4 days. Mechanistically, CAF-1 suppression led to a more accessible chromatin structure at enhancer elements early during reprogramming. These changes were accompanied by a decrease in somatic heterochromatin domains, increased binding of Sox2 to pluripotency-specific targets and activation of associated genes. Notably, suppression of CAF-1 also enhanced the direct conversion of B cells into macrophages and fibroblasts into neurons. Together, our findings reveal the histone chaperone CAF-1 to be a novel regulator of somatic cell identity during transcription-factor-induced cell-fate transitions and provide a potential strategy to modulate cellular plasticity in a regenerative setting.	mouse	epithelial tissue	Low+High throughput	The histone chaperone CAF-1 safeguards somatic cell identity	否	--	--	MEF,iPS,ES,MEFs,HSP cell	E_02_0843	ChIP-seq,ATAC-seq,CRISPR/Cas9	To validate these observations with an independent, higher resolution method, we performed Assay of Transposase Accessible Chromatin using sequencing (ATAC-seq), which detects integration of the Tn5 transposase in open chromatin regions27 (Extended Data Fig. 7c). Consistent with the SONO-seq data, ATAC-seq analysis of early reprogramming intermediates showed a more accessible chromatin configuration at regulatory regions including ESC-specific enhancers upon suppression of Chaf1a (Fig. 5a; P value <10?15). Moreover, Chaf1a knockdown caused a significant increase in chromatin accessibility across ESC-specific super-enhancers at day 3 of iPSC formation (Supplementary Table 3 and Extended Data Fig. 7d,e; P value <5.3×10?16). Of note, super-enhancers linked to specialized cell types such as macrophages, lymphocytes and muscle cells were also significantly more accessible in Chaf1a depleted reprogramming intermediates compared to controls (Extended Data Fig. 7f). 	Super-Enhancer	--	ChIP-seq,ATAC-seq	Moreover,Chaf1a knockdown caused a significant increase in Chromatin accessibility across ES-cell-specific Super-Enhancers at day 3 of iPS cell formation.	5730441M18Rik,AA407717,AL022809,AW536104,C330011P20Rik,C78083,C78563,Tex20	--	--	--	Sox2	Sox-2,lcc,ysb	ChIP-seq,ATAC-seq	Next,we performed ChIP-seq analysis for Sox2 at day 3 of OKSM expression in order to test our hypothesis that increased Chromatin accessibility at Enhancer lements influences reprogramming factor binding. Of the Sox2-bound super-Enhancers unique to CAF-1 knockdown cells, a subset also showed a more accessible chromatin structure by ATAC-seq analysis. 	--	--	Sall4
26659182	chr2	168744572	168752225	IL6	To further elucidate regulatory pathways that safeguard the somatic state, we performed two comprehensive RNA interference (RNAi) screens targeting chromatin factors during transcription-factor-mediated reprogramming of mouse fibroblasts to induced pluripotent stem cells (iPS cells). Subunits of the chromatin assembly factor-1 (CAF-1) complex, including Chaf1a and Chaf1b, emerged as the most prominent hits from both screens, followed by modulators of lysine sumoylation and heterochromatin maintenance. Optimal modulation of both CAF-1 and transcription factor levels increased reprogramming efficiency by several orders of magnitude and facilitated iPS cell formation in as little as 4 days. Mechanistically, CAF-1 suppression led to a more accessible chromatin structure at enhancer elements early during reprogramming. These changes were accompanied by a decrease in somatic heterochromatin domains, increased binding of Sox2 to pluripotency-specific targets and activation of associated genes. Notably, suppression of CAF-1 also enhanced the direct conversion of B cells into macrophages and fibroblasts into neurons. Together, our findings reveal the histone chaperone CAF-1 to be a novel regulator of somatic cell identity during transcription-factor-induced cell-fate transitions and provide a potential strategy to modulate cellular plasticity in a regenerative setting.	mouse	epithelial tissue	Low+High throughput	The histone chaperone CAF-1 safeguards somatic cell identity	否	--	--	MEF,iPS,ES,MEFs,HSP cell	E_02_0843	ChIP-seq,ATAC-seq,CRISPR/Cas9	To validate these observations with an independent, higher resolution method, we performed Assay of Transposase Accessible Chromatin using sequencing (ATAC-seq), which detects integration of the Tn5 transposase in open chromatin regions27 (Extended Data Fig. 7c). Consistent with the SONO-seq data, ATAC-seq analysis of early reprogramming intermediates showed a more accessible chromatin configuration at regulatory regions including ESC-specific enhancers upon suppression of Chaf1a (Fig. 5a; P value <10?15). Moreover, Chaf1a knockdown caused a significant increase in chromatin accessibility across ESC-specific super-enhancers at day 3 of iPSC formation (Supplementary Table 3 and Extended Data Fig. 7d,e; P value <5.3×10?16). Of note, super-enhancers linked to specialized cell types such as macrophages, lymphocytes and muscle cells were also significantly more accessible in Chaf1a depleted reprogramming intermediates compared to controls (Extended Data Fig. 7f). 	Super-Enhancer	--	ChIP-seq,ATAC-seq	Moreover,Chaf1a knockdown caused a significant increase in Chromatin accessibility across ES-cell-specific Super-Enhancers at day 3 of iPS cell formation.	5730441M18Rik,AA407717,AL022809,AW536104,C330011P20Rik,C78083,C78563,Tex20	--	--	--	Sox2	Sox-2,lcc,ysb	ChIP-seq,ATAC-seq	Next,we performed ChIP-seq analysis for Sox2 at day 3 of OKSM expression in order to test our hypothesis that increased Chromatin accessibility at Enhancer lements influences reprogramming factor binding. Of the Sox2-bound super-Enhancers unique to CAF-1 knockdown cells, a subset also showed a more accessible chromatin structure by ATAC-seq analysis. 	--	--	Sall4
26615198	chr7	117011495	117063767	CFTR	We demonstrate that two of these novel interacting regions cooperatively increase CFTR expression, and suggest that the new enhancer elements located on either side of the gene are brought together through chromatin looping via CTCF.	human	Nose, skin	Low+High throughput	Analysis of long-range interactions in primary human cells identifies cooperative CFTR regulatory elements	否	--	Cystic Fibrosis	adepithelial cell,skin fibroblast	E_02_0844	Hi-C,5C,Luciferase Reporter Assay,PCR	We tested whether any of the newly identiied looping regions displayed enhancer activity in a reporter assay. As shown in Figure 4A, two of our interacting regions significantly enhanced CFTR promoter activity.The fragment encompassing a DHS in the region E displayed a strong Enhancer function with almost 6-fold effect on the CFTR promoter.	Enhancer	--	Luciferase Reporter Assay	As shown in Figure 4A, two of our interacting regions significantly enhanced CFTR promoter activity.The fragment encompassing a DHS in the region E displayed a strong Enhancer function with almost 6-fold effect on the CFTR promoter.	ABC35,ABCC7,CF,CFTR/MRP,MRP7,TNR-CFTR,dJ760C5.1	--	--	--	--	--	--	--	--	--	CFTR
26595656	chr12	85433906	85439068	Fos	Here we demonstrate that multiple enhancers surrounding the c-fos gene are crucial for ensuring robust c-fos response to various stimuli. Membrane depolarization, brain-derived neurotrophic factor (BDNF) and forskolin activate distinct subsets of the enhancers to induce c-fos transcription in neurons, suggesting that stimulus-specific combinatorial activation of multiple enhancers underlies the broad inducibility of the c-fos gene. Accordingly, the functional requirement of key transcription factors varies depending on the type of stimulation. Combinatorial enhancer activation also occurs in the brain. Providing a comprehensive picture of the c-fos induction mechanism beyond the minimal promoter, our study should help in understanding the physiological nature of c-fos induction in relation to neural activity and plasticity.	mouse	nervous tissue	Low+High throughput	Stimulus-specific combinatorial functionality of neuronal c-fos enhancers	否	--	--	neuron,neuroglioform cell	E_02_0845	ChIP-seq,Luciferase Reporter Assay	These enhancers, which we identified in primary cultures of mouse cortical neurons, appear to be active in the intact brain throughout development, as all of them were tightly aligned with the chroma_x0002_tin immunoprecipitation (ChIP)-seq peaks of the active enhancer marker, acetylated H3K27 (H3K27ac)(Supplementary Fig. 1).	Enhancer	3C	--	Characterizing individual c-fos Enhancers by chromosome-conformation capture (3C) analysis and an Enhancer reporter assay, we have corroborated the idea that eRNA is a reliable marker for identifying activated Enhancers.	D12Rfj1,c-fos,cFos	These results demonstrate that the combinatorial activation of the c-fosenhancers enables the c-fos gene to be broadly responsive to various signaling pathways.	CRISPRi,RT-qPCR	We also evaluated the functionality of individual enhancers in their native context by targeted transcription silencing via CRISPR interference (CRISPRi). Using eRNA as a proxy for enhancer activity, we found that distinc_x0002_tive subsets of the c-fos enhancers are activated in the intact brain following chemically induced seizure or light stimulation.	Creb,srf,Mef2a,Mef2d,Mef2c,Npas4	CREB,CREB-1,MCM1,ADCAD1,RSRFC4,RSRFC9,mef2,C5DELq14.3,DEL5q14.3,Le-PAS,NXF,PASD10,bHLHe79	ChIP-seq	ChIP-_x0002_seq analysis has revealed that the c-fos promoter and enhancers were bound by different combinations of several activity-regulated TFs6 (Supplementary Fig. 1).Knockdown of CREB, MEF2A and NPAS4 significantly impaired c-fos induction by Cl-mediated membrane depolarization (Fig. 4a and Supplementary Fig. 4). Although knockdown of MEF2 family members MEF2D and MEF2C showed a slight decrease in c-fos expression, it was not significant and had a weaker impact than MEF2A knockdown. The decrease in c-fos expression was paralleled with little effect on eRNA transcription (Supplementary Fig. 5).	--	--	Fos
26595656	chr12	85433906	85439068	BDNF	Here we demonstrate that multiple enhancers surrounding the c-fos gene are crucial for ensuring robust c-fos response to various stimuli. Membrane depolarization, brain-derived neurotrophic factor (BDNF) and forskolin activate distinct subsets of the enhancers to induce c-fos transcription in neurons, suggesting that stimulus-specific combinatorial activation of multiple enhancers underlies the broad inducibility of the c-fos gene. Accordingly, the functional requirement of key transcription factors varies depending on the type of stimulation. Combinatorial enhancer activation also occurs in the brain. Providing a comprehensive picture of the c-fos induction mechanism beyond the minimal promoter, our study should help in understanding the physiological nature of c-fos induction in relation to neural activity and plasticity.	mouse	nervous tissue	Low+High throughput	Stimulus-specific combinatorial functionality of neuronal c-fos enhancers	否	--	--	neuron,neuroglioform cell	E_02_0845	ChIP-seq,Luciferase Reporter Assay	These enhancers, which we identified in primary cultures of mouse cortical neurons, appear to be active in the intact brain throughout development, as all of them were tightly aligned with the chroma_x0002_tin immunoprecipitation (ChIP)-seq peaks of the active enhancer marker, acetylated H3K27 (H3K27ac)(Supplementary Fig. 1).	Enhancer	3C	--	Characterizing individual c-fos Enhancers by chromosome-conformation capture (3C) analysis and an Enhancer reporter assay, we have corroborated the idea that eRNA is a reliable marker for identifying activated Enhancers.	D12Rfj1,c-fos,cFos	These results demonstrate that the combinatorial activation of the c-fosenhancers enables the c-fos gene to be broadly responsive to various signaling pathways.	CRISPRi,RT-qPCR	We also evaluated the functionality of individual enhancers in their native context by targeted transcription silencing via CRISPR interference (CRISPRi). Using eRNA as a proxy for enhancer activity, we found that distinc_x0002_tive subsets of the c-fos enhancers are activated in the intact brain following chemically induced seizure or light stimulation.	Creb,srf,Mef2a,Mef2d,Mef2c,Npas4	CREB,CREB-1,MCM1,ADCAD1,RSRFC4,RSRFC9,mef2,C5DELq14.3,DEL5q14.3,Le-PAS,NXF,PASD10,bHLHe79	ChIP-seq	ChIP-_x0002_seq analysis has revealed that the c-fos promoter and enhancers were bound by different combinations of several activity-regulated TFs6 (Supplementary Fig. 1).Knockdown of CREB, MEF2A and NPAS4 significantly impaired c-fos induction by Cl-mediated membrane depolarization (Fig. 4a and Supplementary Fig. 4). Although knockdown of MEF2 family members MEF2D and MEF2C showed a slight decrease in c-fos expression, it was not significant and had a weaker impact than MEF2A knockdown. The decrease in c-fos expression was paralleled with little effect on eRNA transcription (Supplementary Fig. 5).	--	--	Fos
26595656	chr12	85433906	85439068	SRF	Here we demonstrate that multiple enhancers surrounding the c-fos gene are crucial for ensuring robust c-fos response to various stimuli. Membrane depolarization, brain-derived neurotrophic factor (BDNF) and forskolin activate distinct subsets of the enhancers to induce c-fos transcription in neurons, suggesting that stimulus-specific combinatorial activation of multiple enhancers underlies the broad inducibility of the c-fos gene. Accordingly, the functional requirement of key transcription factors varies depending on the type of stimulation. Combinatorial enhancer activation also occurs in the brain. Providing a comprehensive picture of the c-fos induction mechanism beyond the minimal promoter, our study should help in understanding the physiological nature of c-fos induction in relation to neural activity and plasticity.	mouse	nervous tissue	Low+High throughput	Stimulus-specific combinatorial functionality of neuronal c-fos enhancers	否	--	--	neuron,neuroglioform cell	E_02_0845	ChIP-seq,Luciferase Reporter Assay	These enhancers, which we identified in primary cultures of mouse cortical neurons, appear to be active in the intact brain throughout development, as all of them were tightly aligned with the chroma_x0002_tin immunoprecipitation (ChIP)-seq peaks of the active enhancer marker, acetylated H3K27 (H3K27ac)(Supplementary Fig. 1).	Enhancer	3C	--	Characterizing individual c-fos Enhancers by chromosome-conformation capture (3C) analysis and an Enhancer reporter assay, we have corroborated the idea that eRNA is a reliable marker for identifying activated Enhancers.	D12Rfj1,c-fos,cFos	These results demonstrate that the combinatorial activation of the c-fosenhancers enables the c-fos gene to be broadly responsive to various signaling pathways.	CRISPRi,RT-qPCR	We also evaluated the functionality of individual enhancers in their native context by targeted transcription silencing via CRISPR interference (CRISPRi). Using eRNA as a proxy for enhancer activity, we found that distinc_x0002_tive subsets of the c-fos enhancers are activated in the intact brain following chemically induced seizure or light stimulation.	Creb,srf,Mef2a,Mef2d,Mef2c,Npas4	CREB,CREB-1,MCM1,ADCAD1,RSRFC4,RSRFC9,mef2,C5DELq14.3,DEL5q14.3,Le-PAS,NXF,PASD10,bHLHe79	ChIP-seq	ChIP-_x0002_seq analysis has revealed that the c-fos promoter and enhancers were bound by different combinations of several activity-regulated TFs6 (Supplementary Fig. 1).Knockdown of CREB, MEF2A and NPAS4 significantly impaired c-fos induction by Cl-mediated membrane depolarization (Fig. 4a and Supplementary Fig. 4). Although knockdown of MEF2 family members MEF2D and MEF2C showed a slight decrease in c-fos expression, it was not significant and had a weaker impact than MEF2A knockdown. The decrease in c-fos expression was paralleled with little effect on eRNA transcription (Supplementary Fig. 5).	--	--	Fos
26595656	chr12	85433906	85439068	NPAS4	Here we demonstrate that multiple enhancers surrounding the c-fos gene are crucial for ensuring robust c-fos response to various stimuli. Membrane depolarization, brain-derived neurotrophic factor (BDNF) and forskolin activate distinct subsets of the enhancers to induce c-fos transcription in neurons, suggesting that stimulus-specific combinatorial activation of multiple enhancers underlies the broad inducibility of the c-fos gene. Accordingly, the functional requirement of key transcription factors varies depending on the type of stimulation. Combinatorial enhancer activation also occurs in the brain. Providing a comprehensive picture of the c-fos induction mechanism beyond the minimal promoter, our study should help in understanding the physiological nature of c-fos induction in relation to neural activity and plasticity.	mouse	nervous tissue	Low+High throughput	Stimulus-specific combinatorial functionality of neuronal c-fos enhancers	否	--	--	neuron,neuroglioform cell	E_02_0845	ChIP-seq,Luciferase Reporter Assay	These enhancers, which we identified in primary cultures of mouse cortical neurons, appear to be active in the intact brain throughout development, as all of them were tightly aligned with the chroma_x0002_tin immunoprecipitation (ChIP)-seq peaks of the active enhancer marker, acetylated H3K27 (H3K27ac)(Supplementary Fig. 1).	Enhancer	3C	--	Characterizing individual c-fos Enhancers by chromosome-conformation capture (3C) analysis and an Enhancer reporter assay, we have corroborated the idea that eRNA is a reliable marker for identifying activated Enhancers.	D12Rfj1,c-fos,cFos	These results demonstrate that the combinatorial activation of the c-fosenhancers enables the c-fos gene to be broadly responsive to various signaling pathways.	CRISPRi,RT-qPCR	We also evaluated the functionality of individual enhancers in their native context by targeted transcription silencing via CRISPR interference (CRISPRi). Using eRNA as a proxy for enhancer activity, we found that distinc_x0002_tive subsets of the c-fos enhancers are activated in the intact brain following chemically induced seizure or light stimulation.	Creb,srf,Mef2a,Mef2d,Mef2c,Npas4	CREB,CREB-1,MCM1,ADCAD1,RSRFC4,RSRFC9,mef2,C5DELq14.3,DEL5q14.3,Le-PAS,NXF,PASD10,bHLHe79	ChIP-seq	ChIP-_x0002_seq analysis has revealed that the c-fos promoter and enhancers were bound by different combinations of several activity-regulated TFs6 (Supplementary Fig. 1).Knockdown of CREB, MEF2A and NPAS4 significantly impaired c-fos induction by Cl-mediated membrane depolarization (Fig. 4a and Supplementary Fig. 4). Although knockdown of MEF2 family members MEF2D and MEF2C showed a slight decrease in c-fos expression, it was not significant and had a weaker impact than MEF2A knockdown. The decrease in c-fos expression was paralleled with little effect on eRNA transcription (Supplementary Fig. 5).	--	--	Fos
26595656	chr12	85433906	85439068	MEF2A	Here we demonstrate that multiple enhancers surrounding the c-fos gene are crucial for ensuring robust c-fos response to various stimuli. Membrane depolarization, brain-derived neurotrophic factor (BDNF) and forskolin activate distinct subsets of the enhancers to induce c-fos transcription in neurons, suggesting that stimulus-specific combinatorial activation of multiple enhancers underlies the broad inducibility of the c-fos gene. Accordingly, the functional requirement of key transcription factors varies depending on the type of stimulation. Combinatorial enhancer activation also occurs in the brain. Providing a comprehensive picture of the c-fos induction mechanism beyond the minimal promoter, our study should help in understanding the physiological nature of c-fos induction in relation to neural activity and plasticity.	mouse	nervous tissue	Low+High throughput	Stimulus-specific combinatorial functionality of neuronal c-fos enhancers	否	--	--	neuron,neuroglioform cell	E_02_0845	ChIP-seq,Luciferase Reporter Assay	These enhancers, which we identified in primary cultures of mouse cortical neurons, appear to be active in the intact brain throughout development, as all of them were tightly aligned with the chroma_x0002_tin immunoprecipitation (ChIP)-seq peaks of the active enhancer marker, acetylated H3K27 (H3K27ac)(Supplementary Fig. 1).	Enhancer	3C	--	Characterizing individual c-fos Enhancers by chromosome-conformation capture (3C) analysis and an Enhancer reporter assay, we have corroborated the idea that eRNA is a reliable marker for identifying activated Enhancers.	D12Rfj1,c-fos,cFos	These results demonstrate that the combinatorial activation of the c-fosenhancers enables the c-fos gene to be broadly responsive to various signaling pathways.	CRISPRi,RT-qPCR	We also evaluated the functionality of individual enhancers in their native context by targeted transcription silencing via CRISPR interference (CRISPRi). Using eRNA as a proxy for enhancer activity, we found that distinc_x0002_tive subsets of the c-fos enhancers are activated in the intact brain following chemically induced seizure or light stimulation.	Creb,srf,Mef2a,Mef2d,Mef2c,Npas4	CREB,CREB-1,MCM1,ADCAD1,RSRFC4,RSRFC9,mef2,C5DELq14.3,DEL5q14.3,Le-PAS,NXF,PASD10,bHLHe79	ChIP-seq	ChIP-_x0002_seq analysis has revealed that the c-fos promoter and enhancers were bound by different combinations of several activity-regulated TFs6 (Supplementary Fig. 1).Knockdown of CREB, MEF2A and NPAS4 significantly impaired c-fos induction by Cl-mediated membrane depolarization (Fig. 4a and Supplementary Fig. 4). Although knockdown of MEF2 family members MEF2D and MEF2C showed a slight decrease in c-fos expression, it was not significant and had a weaker impact than MEF2A knockdown. The decrease in c-fos expression was paralleled with little effect on eRNA transcription (Supplementary Fig. 5).	--	--	Fos
26595656	chr12	85433906	85439068	MEF2C	Here we demonstrate that multiple enhancers surrounding the c-fos gene are crucial for ensuring robust c-fos response to various stimuli. Membrane depolarization, brain-derived neurotrophic factor (BDNF) and forskolin activate distinct subsets of the enhancers to induce c-fos transcription in neurons, suggesting that stimulus-specific combinatorial activation of multiple enhancers underlies the broad inducibility of the c-fos gene. Accordingly, the functional requirement of key transcription factors varies depending on the type of stimulation. Combinatorial enhancer activation also occurs in the brain. Providing a comprehensive picture of the c-fos induction mechanism beyond the minimal promoter, our study should help in understanding the physiological nature of c-fos induction in relation to neural activity and plasticity.	mouse	nervous tissue	Low+High throughput	Stimulus-specific combinatorial functionality of neuronal c-fos enhancers	否	--	--	neuron,neuroglioform cell	E_02_0845	ChIP-seq,Luciferase Reporter Assay	These enhancers, which we identified in primary cultures of mouse cortical neurons, appear to be active in the intact brain throughout development, as all of them were tightly aligned with the chroma_x0002_tin immunoprecipitation (ChIP)-seq peaks of the active enhancer marker, acetylated H3K27 (H3K27ac)(Supplementary Fig. 1).	Enhancer	3C	--	Characterizing individual c-fos Enhancers by chromosome-conformation capture (3C) analysis and an Enhancer reporter assay, we have corroborated the idea that eRNA is a reliable marker for identifying activated Enhancers.	D12Rfj1,c-fos,cFos	These results demonstrate that the combinatorial activation of the c-fosenhancers enables the c-fos gene to be broadly responsive to various signaling pathways.	CRISPRi,RT-qPCR	We also evaluated the functionality of individual enhancers in their native context by targeted transcription silencing via CRISPR interference (CRISPRi). Using eRNA as a proxy for enhancer activity, we found that distinc_x0002_tive subsets of the c-fos enhancers are activated in the intact brain following chemically induced seizure or light stimulation.	Creb,srf,Mef2a,Mef2d,Mef2c,Npas4	CREB,CREB-1,MCM1,ADCAD1,RSRFC4,RSRFC9,mef2,C5DELq14.3,DEL5q14.3,Le-PAS,NXF,PASD10,bHLHe79	ChIP-seq	ChIP-_x0002_seq analysis has revealed that the c-fos promoter and enhancers were bound by different combinations of several activity-regulated TFs6 (Supplementary Fig. 1).Knockdown of CREB, MEF2A and NPAS4 significantly impaired c-fos induction by Cl-mediated membrane depolarization (Fig. 4a and Supplementary Fig. 4). Although knockdown of MEF2 family members MEF2D and MEF2C showed a slight decrease in c-fos expression, it was not significant and had a weaker impact than MEF2A knockdown. The decrease in c-fos expression was paralleled with little effect on eRNA transcription (Supplementary Fig. 5).	--	--	Fos
26595656	chr12	85433906	85439068	MEF2D	Here we demonstrate that multiple enhancers surrounding the c-fos gene are crucial for ensuring robust c-fos response to various stimuli. Membrane depolarization, brain-derived neurotrophic factor (BDNF) and forskolin activate distinct subsets of the enhancers to induce c-fos transcription in neurons, suggesting that stimulus-specific combinatorial activation of multiple enhancers underlies the broad inducibility of the c-fos gene. Accordingly, the functional requirement of key transcription factors varies depending on the type of stimulation. Combinatorial enhancer activation also occurs in the brain. Providing a comprehensive picture of the c-fos induction mechanism beyond the minimal promoter, our study should help in understanding the physiological nature of c-fos induction in relation to neural activity and plasticity.	mouse	nervous tissue	Low+High throughput	Stimulus-specific combinatorial functionality of neuronal c-fos enhancers	否	--	--	neuron,neuroglioform cell	E_02_0845	ChIP-seq,Luciferase Reporter Assay	These enhancers, which we identified in primary cultures of mouse cortical neurons, appear to be active in the intact brain throughout development, as all of them were tightly aligned with the chroma_x0002_tin immunoprecipitation (ChIP)-seq peaks of the active enhancer marker, acetylated H3K27 (H3K27ac)(Supplementary Fig. 1).	Enhancer	3C	--	Characterizing individual c-fos Enhancers by chromosome-conformation capture (3C) analysis and an Enhancer reporter assay, we have corroborated the idea that eRNA is a reliable marker for identifying activated Enhancers.	D12Rfj1,c-fos,cFos	These results demonstrate that the combinatorial activation of the c-fosenhancers enables the c-fos gene to be broadly responsive to various signaling pathways.	CRISPRi,RT-qPCR	We also evaluated the functionality of individual enhancers in their native context by targeted transcription silencing via CRISPR interference (CRISPRi). Using eRNA as a proxy for enhancer activity, we found that distinc_x0002_tive subsets of the c-fos enhancers are activated in the intact brain following chemically induced seizure or light stimulation.	Creb,srf,Mef2a,Mef2d,Mef2c,Npas4	CREB,CREB-1,MCM1,ADCAD1,RSRFC4,RSRFC9,mef2,C5DELq14.3,DEL5q14.3,Le-PAS,NXF,PASD10,bHLHe79	ChIP-seq	ChIP-_x0002_seq analysis has revealed that the c-fos promoter and enhancers were bound by different combinations of several activity-regulated TFs6 (Supplementary Fig. 1).Knockdown of CREB, MEF2A and NPAS4 significantly impaired c-fos induction by Cl-mediated membrane depolarization (Fig. 4a and Supplementary Fig. 4). Although knockdown of MEF2 family members MEF2D and MEF2C showed a slight decrease in c-fos expression, it was not significant and had a weaker impact than MEF2A knockdown. The decrease in c-fos expression was paralleled with little effect on eRNA transcription (Supplementary Fig. 5).	--	--	Fos
26595656	chr12	85433906	85439068	SETDB1	Here we demonstrate that multiple enhancers surrounding the c-fos gene are crucial for ensuring robust c-fos response to various stimuli. Membrane depolarization, brain-derived neurotrophic factor (BDNF) and forskolin activate distinct subsets of the enhancers to induce c-fos transcription in neurons, suggesting that stimulus-specific combinatorial activation of multiple enhancers underlies the broad inducibility of the c-fos gene. Accordingly, the functional requirement of key transcription factors varies depending on the type of stimulation. Combinatorial enhancer activation also occurs in the brain. Providing a comprehensive picture of the c-fos induction mechanism beyond the minimal promoter, our study should help in understanding the physiological nature of c-fos induction in relation to neural activity and plasticity.	mouse	nervous tissue	Low+High throughput	Stimulus-specific combinatorial functionality of neuronal c-fos enhancers	否	--	--	neuron,neuroglioform cell	E_02_0845	ChIP-seq,Luciferase Reporter Assay	These enhancers, which we identified in primary cultures of mouse cortical neurons, appear to be active in the intact brain throughout development, as all of them were tightly aligned with the chroma_x0002_tin immunoprecipitation (ChIP)-seq peaks of the active enhancer marker, acetylated H3K27 (H3K27ac)(Supplementary Fig. 1).	Enhancer	3C	--	Characterizing individual c-fos Enhancers by chromosome-conformation capture (3C) analysis and an Enhancer reporter assay, we have corroborated the idea that eRNA is a reliable marker for identifying activated Enhancers.	D12Rfj1,c-fos,cFos	These results demonstrate that the combinatorial activation of the c-fosenhancers enables the c-fos gene to be broadly responsive to various signaling pathways.	CRISPRi,RT-qPCR	We also evaluated the functionality of individual enhancers in their native context by targeted transcription silencing via CRISPR interference (CRISPRi). Using eRNA as a proxy for enhancer activity, we found that distinc_x0002_tive subsets of the c-fos enhancers are activated in the intact brain following chemically induced seizure or light stimulation.	Creb,srf,Mef2a,Mef2d,Mef2c,Npas4	CREB,CREB-1,MCM1,ADCAD1,RSRFC4,RSRFC9,mef2,C5DELq14.3,DEL5q14.3,Le-PAS,NXF,PASD10,bHLHe79	ChIP-seq	ChIP-_x0002_seq analysis has revealed that the c-fos promoter and enhancers were bound by different combinations of several activity-regulated TFs6 (Supplementary Fig. 1).Knockdown of CREB, MEF2A and NPAS4 significantly impaired c-fos induction by Cl-mediated membrane depolarization (Fig. 4a and Supplementary Fig. 4). Although knockdown of MEF2 family members MEF2D and MEF2C showed a slight decrease in c-fos expression, it was not significant and had a weaker impact than MEF2A knockdown. The decrease in c-fos expression was paralleled with little effect on eRNA transcription (Supplementary Fig. 5).	--	--	Fos
26595656	chr12	85433906	85439068	EGR1	Here we demonstrate that multiple enhancers surrounding the c-fos gene are crucial for ensuring robust c-fos response to various stimuli. Membrane depolarization, brain-derived neurotrophic factor (BDNF) and forskolin activate distinct subsets of the enhancers to induce c-fos transcription in neurons, suggesting that stimulus-specific combinatorial activation of multiple enhancers underlies the broad inducibility of the c-fos gene. Accordingly, the functional requirement of key transcription factors varies depending on the type of stimulation. Combinatorial enhancer activation also occurs in the brain. Providing a comprehensive picture of the c-fos induction mechanism beyond the minimal promoter, our study should help in understanding the physiological nature of c-fos induction in relation to neural activity and plasticity.	mouse	nervous tissue	Low+High throughput	Stimulus-specific combinatorial functionality of neuronal c-fos enhancers	否	--	--	neuron,neuroglioform cell	E_02_0845	ChIP-seq,Luciferase Reporter Assay	These enhancers, which we identified in primary cultures of mouse cortical neurons, appear to be active in the intact brain throughout development, as all of them were tightly aligned with the chroma_x0002_tin immunoprecipitation (ChIP)-seq peaks of the active enhancer marker, acetylated H3K27 (H3K27ac)(Supplementary Fig. 1).	Enhancer	3C	--	Characterizing individual c-fos Enhancers by chromosome-conformation capture (3C) analysis and an Enhancer reporter assay, we have corroborated the idea that eRNA is a reliable marker for identifying activated Enhancers.	D12Rfj1,c-fos,cFos	These results demonstrate that the combinatorial activation of the c-fosenhancers enables the c-fos gene to be broadly responsive to various signaling pathways.	CRISPRi,RT-qPCR	We also evaluated the functionality of individual enhancers in their native context by targeted transcription silencing via CRISPR interference (CRISPRi). Using eRNA as a proxy for enhancer activity, we found that distinc_x0002_tive subsets of the c-fos enhancers are activated in the intact brain following chemically induced seizure or light stimulation.	Creb,srf,Mef2a,Mef2d,Mef2c,Npas4	CREB,CREB-1,MCM1,ADCAD1,RSRFC4,RSRFC9,mef2,C5DELq14.3,DEL5q14.3,Le-PAS,NXF,PASD10,bHLHe79	ChIP-seq	ChIP-_x0002_seq analysis has revealed that the c-fos promoter and enhancers were bound by different combinations of several activity-regulated TFs6 (Supplementary Fig. 1).Knockdown of CREB, MEF2A and NPAS4 significantly impaired c-fos induction by Cl-mediated membrane depolarization (Fig. 4a and Supplementary Fig. 4). Although knockdown of MEF2 family members MEF2D and MEF2C showed a slight decrease in c-fos expression, it was not significant and had a weaker impact than MEF2A knockdown. The decrease in c-fos expression was paralleled with little effect on eRNA transcription (Supplementary Fig. 5).	--	--	Fos
26581162	chr3	108015219	108015290	CD83	CD83 is a marker for T-cell activation,41 and the observed presence of upregulated CD83 points to TNFα's potential T-cell–activating role not observed in sg362F/dCas9-VP64 transfected cells.	human	lymph	Low throughput	Potent and Targeted Activation of Latent HIV-1 Using the CRISPR/dCas9 Activator Complex		--	--	293T cell	E_02_0846	Luciferase Reporter Assay,Transient Transfection Assay,RNA-seq,PCR	In this study, we identify a targeted hotspot for CRISPR acti_x0002_vation within the long terminal repeat (LTR) enhancer region,at the junction between two nuclear factor (NF)-κB transcrip_x0002_tion factor–binding sites.Twenty-three possible NGG Streptococcus pyogenes(Sp) Cas9 photospacer adjacent motif (PAM) sites for targeting of sgRNAs were identified in the U3 region of the LTR, upstream of the HIV transcriptional start site(TSS) (?450 to 0 bp; HIV genome HXB2) within the enhancer and modulatory region of the promoter. 	Enhancer	CRISPR/Cas9	Luciferase Reporter Assay	All sgRNAs were named according to the 3′ adjacent sense strand nucleotide cleavage site catalyzed by nuclease-active Cas9 (Figure? 1a) and were screened together with dCas9-VP64 or dCas9-VP160 for their activation properties by transient transfection with the reporter NL4-3.Luc.R_x005f_x0002_E-，a full-length HIV molec_x0002_ular clone where luciferase is driven by the viral LTR.	B7-H5,B7-H7,B7H7,B7y	--	--	--	NFKB1	CVID12,EBP-1,KBF1,NF-kB,NF-kB1,NF-kappa-B1,NF-kappaB,NFKB-p105,NFKB-p50,NFkappaB,p105,p50	CRISPR/Cas9	Since sg362F fully occupies the sequence across both NF-κB–binding sites, we next determined if CRISPR activation via the sg362F target site was coupled to NF-κB function. these data strongly support a conclusion where sg362F/dCas9-VP64 functions independently of NF-κB as a stand-alone transactivator of LTR activation. 	--	--	HHLA2
26560027	chr11	8271697	8279492	LMO1	These findings indicate that a recently evolved polymorphism within a super-enhancer element in the first intron of LMO1 influences neuroblastoma susceptibility through differential GATA transcription factor binding and direct modulation of LMO1 expression in cis, and this leads to an oncogenic dependency in tumour cells.	human		Low+High throughput	Genetic predisposition to neuroblastoma mediated by a LMO1 super-enhancer polymorphism	相关	--	Neuroblastoma	neuroblastoma cell lines	E_02_0847	ChIP-seq,Luciferase Reporter Assay	"Acetylation of histone H3 at lysine 27 (H3K27ac) is a hallmark of active enhancers, and ChIP-seq analysis of SHSY5Y (G/G; not MYCN amplified), KELLY (G/?; MYCN amplified), BE2 (G/T; MYCN amplified) and NGP (G/T; MYCN amplified) neuroblastoma cells showed extensive H3K27 acetylation in the first intron of LMO1 across 
rs2168101, which was not observed in BE2C (T/? ; MYCN amplified; Fig. 3c). This region is classified as a super-enhancer in G-allele-containing lines SHSY5Y, KELLY and BE2 based on enhancer clustering and especially high H3K27ac signal (NGP was just below the threshold; see Methods), a pattern also observed for other known oncogenes and tumour suppressor genes in this disease12 (Fig. 3d and Extended Data Fig. 6a). 
We next performed luciferase reporter assays to measure the effect of rs2168101 alleles on enhancer activity. HEK293T cells transfected with constructs containing the risk G allele demonstrated 30–300-fold higher normalized luminescence compared to the T allele (t-test P = 0.002, Fig. 3e), whereas luciferase activity of the T allele was not significantly different from empty vector, indicating that the intact GATA motif is required for robust enhancer activity. "	Super-Enhancer	--	ChIP-seq,Luciferase Reporter Assay	"Acetylation of histone H3 at lysine 27 (H3K27ac) is a hallmark of active enhancers, and ChIP-seq analysis of SHSY5Y (G/G; not MYCN amplified), KELLY (G/?; MYCN amplified), BE2 (G/T; MYCN amplified) and NGP (G/T; MYCN amplified) neuroblastoma cells showed extensive H3K27 acetylation in the first intron of LMO1 across 
rs2168101, which was not observed in BE2C (T/? ; MYCN amplified; Fig. 3c). This region is classified as a super-enhancer in G-allele-containing lines SHSY5Y, KELLY and BE2 based on enhancer clustering and especially high H3K27ac signal (NGP was just below the threshold; see Methods), a pattern also observed for other known oncogenes and tumour suppressor genes in this disease12 (Fig. 3d and Extended Data Fig. 6a). 
We next performed luciferase reporter assays to measure the effect of rs2168101 alleles on enhancer activity. HEK293T cells transfected with constructs containing the risk G allele demonstrated 30–300-fold higher normalized luminescence compared to the T allele (t-test P = 0.002, Fig. 3e), whereas luciferase activity of the T allele was not significantly different from empty vector, indicating that the intact GATA motif is required for robust enhancer activity. "	RBTN1,RHOM1,TTG1	--	--	--	GATA3	HDR, HDRS	Luciferase Reporter Assay,RNAi	HEK293T cells transfected with constructs containing the risk G allele demonstrated 30–300-fold higher normalized luminescence compared to the T allele (t-test P = 0.002, Fig. 3e), whereas luciferase activity of the T allele was not significantly different from empty vector, indicating that the intact GATA motif is required for robust enhancer activity. Finally, knockdown of GATA3 in SHSY5Y and KELLY cells resulted in both decreased LMO1 protein levels and suppression of cell growth that was rescued by LMO1 overexpression (Fig. 3f and Extended Data Fig. 7), indicating the central role of GATA3 in regulating LMO1 expression levels in neuroblastoma.Finally, knockdown of GATA3 in SHSY5Y and KELLY cells resulted in both decreased LMO1 protein levels and suppression of cell growth that was rescued by LMO1 overexpression (Fig. 3f and Extended Data Fig. 7), indicating the central role of GATA3 in regulating LMO1 expression levels in neuroblastoma.	--	--	LMO1
26550034	chr4	55565908	55608014	KAT5	The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation. The comparison of genome-wide binding profiles of Tip60 and c-Myc, a somatic cell reprogramming factor that binds predominantly to active genes in mESCs, demonstrate that Tip60 and c-Myc co-bind at 50–60 % of their binding sites. We also show that the Tip60 complex binds to a subset of bivalent developmental genes and defines a set of mESC specific enhancer as well as super-enhancer regions.	mouse	epithelial tissue	Low+High throughput	Tip60 complex binds to active PolII promoters and a subset of enhancers and co-regulates the c-Myc network in mouse embryonic stem cells	否	--	--	E14,CD1 feeder cell,wt cell	E_02_0848	ChIP-seq,ChIP	"The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-
containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation."	Super-Enhancer	--	ChIP-seq	As two of the so-called ‘super Enhancer’ regions of the Nanog gene and the Enhancer of the Klf4 gene are bound by Tip60,but not by Nsl1 and Msl1(Fig.?7a, b).	EZF,Gklf,Zie	--	--	--	Kat5	AI839539,CPLA2,Htatip,Htatip1,PLIP,Tip55,Tip60	ChIP-qPCR,ChIP-seq	"The validation of several randomly selected ChIP-seq positive sites by ChIP-qPCR indicated specific Tip60 enrichments at these sites, when compared to control IgG ChIP signals and to background enrichment at an intergenic region negative for Tip60 binding (Fig.?1b).These results, together with the ChIP-qPCR validation (Fig.? 1b), indicate that the 
obtained anti-Tip60 ChIP-seq signal is specific."	--	--	Klf4
26550034	chr4	55565908	55608014	KAT8	The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation. The comparison of genome-wide binding profiles of Tip60 and c-Myc, a somatic cell reprogramming factor that binds predominantly to active genes in mESCs, demonstrate that Tip60 and c-Myc co-bind at 50–60 % of their binding sites. We also show that the Tip60 complex binds to a subset of bivalent developmental genes and defines a set of mESC specific enhancer as well as super-enhancer regions.	mouse	epithelial tissue	Low+High throughput	Tip60 complex binds to active PolII promoters and a subset of enhancers and co-regulates the c-Myc network in mouse embryonic stem cells	否	--	--	E14,CD1 feeder cell,wt cell	E_02_0848	ChIP-seq,ChIP	"The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-
containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation."	Super-Enhancer	--	ChIP-seq	As two of the so-called ‘super Enhancer’ regions of the Nanog gene and the Enhancer of the Klf4 gene are bound by Tip60,but not by Nsl1 and Msl1(Fig.?7a, b).	EZF,Gklf,Zie	--	--	--	Kat5	AI839539,CPLA2,Htatip,Htatip1,PLIP,Tip55,Tip60	ChIP-qPCR,ChIP-seq	"The validation of several randomly selected ChIP-seq positive sites by ChIP-qPCR indicated specific Tip60 enrichments at these sites, when compared to control IgG ChIP signals and to background enrichment at an intergenic region negative for Tip60 binding (Fig.?1b).These results, together with the ChIP-qPCR validation (Fig.? 1b), indicate that the 
obtained anti-Tip60 ChIP-seq signal is specific."	--	--	Klf4
26550034	chr4	55565908	55608014	Nanog	The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation. The comparison of genome-wide binding profiles of Tip60 and c-Myc, a somatic cell reprogramming factor that binds predominantly to active genes in mESCs, demonstrate that Tip60 and c-Myc co-bind at 50–60 % of their binding sites. We also show that the Tip60 complex binds to a subset of bivalent developmental genes and defines a set of mESC specific enhancer as well as super-enhancer regions.	mouse	epithelial tissue	Low+High throughput	Tip60 complex binds to active PolII promoters and a subset of enhancers and co-regulates the c-Myc network in mouse embryonic stem cells	否	--	--	E14,CD1 feeder cell,wt cell	E_02_0848	ChIP-seq,ChIP	"The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-
containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation."	Super-Enhancer	--	ChIP-seq	As two of the so-called ‘super Enhancer’ regions of the Nanog gene and the Enhancer of the Klf4 gene are bound by Tip60,but not by Nsl1 and Msl1(Fig.?7a, b).	EZF,Gklf,Zie	--	--	--	Kat5	AI839539,CPLA2,Htatip,Htatip1,PLIP,Tip55,Tip60	ChIP-qPCR,ChIP-seq	"The validation of several randomly selected ChIP-seq positive sites by ChIP-qPCR indicated specific Tip60 enrichments at these sites, when compared to control IgG ChIP signals and to background enrichment at an intergenic region negative for Tip60 binding (Fig.?1b).These results, together with the ChIP-qPCR validation (Fig.? 1b), indicate that the 
obtained anti-Tip60 ChIP-seq signal is specific."	--	--	Klf4
26550034	chr4	55565908	55608014	Klf4	The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation. The comparison of genome-wide binding profiles of Tip60 and c-Myc, a somatic cell reprogramming factor that binds predominantly to active genes in mESCs, demonstrate that Tip60 and c-Myc co-bind at 50–60 % of their binding sites. We also show that the Tip60 complex binds to a subset of bivalent developmental genes and defines a set of mESC specific enhancer as well as super-enhancer regions.	mouse	epithelial tissue	Low+High throughput	Tip60 complex binds to active PolII promoters and a subset of enhancers and co-regulates the c-Myc network in mouse embryonic stem cells	否	--	--	E14,CD1 feeder cell,wt cell	E_02_0848	ChIP-seq,ChIP	"The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-
containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation."	Super-Enhancer	--	ChIP-seq	As two of the so-called ‘super Enhancer’ regions of the Nanog gene and the Enhancer of the Klf4 gene are bound by Tip60,but not by Nsl1 and Msl1(Fig.?7a, b).	EZF,Gklf,Zie	--	--	--	Kat5	AI839539,CPLA2,Htatip,Htatip1,PLIP,Tip55,Tip60	ChIP-qPCR,ChIP-seq	"The validation of several randomly selected ChIP-seq positive sites by ChIP-qPCR indicated specific Tip60 enrichments at these sites, when compared to control IgG ChIP signals and to background enrichment at an intergenic region negative for Tip60 binding (Fig.?1b).These results, together with the ChIP-qPCR validation (Fig.? 1b), indicate that the 
obtained anti-Tip60 ChIP-seq signal is specific."	--	--	Klf4
26550034	chr4	55565908	55608014	Sox2	The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation. The comparison of genome-wide binding profiles of Tip60 and c-Myc, a somatic cell reprogramming factor that binds predominantly to active genes in mESCs, demonstrate that Tip60 and c-Myc co-bind at 50–60 % of their binding sites. We also show that the Tip60 complex binds to a subset of bivalent developmental genes and defines a set of mESC specific enhancer as well as super-enhancer regions.	mouse	epithelial tissue	Low+High throughput	Tip60 complex binds to active PolII promoters and a subset of enhancers and co-regulates the c-Myc network in mouse embryonic stem cells	否	--	--	E14,CD1 feeder cell,wt cell	E_02_0848	ChIP-seq,ChIP	"The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-
containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation."	Super-Enhancer	--	ChIP-seq	As two of the so-called ‘super Enhancer’ regions of the Nanog gene and the Enhancer of the Klf4 gene are bound by Tip60,but not by Nsl1 and Msl1(Fig.?7a, b).	EZF,Gklf,Zie	--	--	--	Kat5	AI839539,CPLA2,Htatip,Htatip1,PLIP,Tip55,Tip60	ChIP-qPCR,ChIP-seq	"The validation of several randomly selected ChIP-seq positive sites by ChIP-qPCR indicated specific Tip60 enrichments at these sites, when compared to control IgG ChIP signals and to background enrichment at an intergenic region negative for Tip60 binding (Fig.?1b).These results, together with the ChIP-qPCR validation (Fig.? 1b), indicate that the 
obtained anti-Tip60 ChIP-seq signal is specific."	--	--	Klf4
26550034	chr4	55565908	55608014	E2f1	The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation. The comparison of genome-wide binding profiles of Tip60 and c-Myc, a somatic cell reprogramming factor that binds predominantly to active genes in mESCs, demonstrate that Tip60 and c-Myc co-bind at 50–60 % of their binding sites. We also show that the Tip60 complex binds to a subset of bivalent developmental genes and defines a set of mESC specific enhancer as well as super-enhancer regions.	mouse	epithelial tissue	Low+High throughput	Tip60 complex binds to active PolII promoters and a subset of enhancers and co-regulates the c-Myc network in mouse embryonic stem cells	否	--	--	E14,CD1 feeder cell,wt cell	E_02_0848	ChIP-seq,ChIP	"The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-
containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation."	Super-Enhancer	--	ChIP-seq	As two of the so-called ‘super Enhancer’ regions of the Nanog gene and the Enhancer of the Klf4 gene are bound by Tip60,but not by Nsl1 and Msl1(Fig.?7a, b).	EZF,Gklf,Zie	--	--	--	Kat5	AI839539,CPLA2,Htatip,Htatip1,PLIP,Tip55,Tip60	ChIP-qPCR,ChIP-seq	"The validation of several randomly selected ChIP-seq positive sites by ChIP-qPCR indicated specific Tip60 enrichments at these sites, when compared to control IgG ChIP signals and to background enrichment at an intergenic region negative for Tip60 binding (Fig.?1b).These results, together with the ChIP-qPCR validation (Fig.? 1b), indicate that the 
obtained anti-Tip60 ChIP-seq signal is specific."	--	--	Klf4
26550034	chr4	55565908	55608014	Zfx	The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation. The comparison of genome-wide binding profiles of Tip60 and c-Myc, a somatic cell reprogramming factor that binds predominantly to active genes in mESCs, demonstrate that Tip60 and c-Myc co-bind at 50–60 % of their binding sites. We also show that the Tip60 complex binds to a subset of bivalent developmental genes and defines a set of mESC specific enhancer as well as super-enhancer regions.	mouse	epithelial tissue	Low+High throughput	Tip60 complex binds to active PolII promoters and a subset of enhancers and co-regulates the c-Myc network in mouse embryonic stem cells	否	--	--	E14,CD1 feeder cell,wt cell	E_02_0848	ChIP-seq,ChIP	"The genome-wide mapping of Tip60 binding in mESCs by chromatin immunoprecipitation (ChIP) coupled with high-throughput sequencing (ChIP-seq) shows that the Tip60 complex is present at promoter regions of predominantly active genes that are bound by RNA polymerase II (Pol II) and contain the H3K4me3 histone mark. The coactivator HAT complexes, Tip60- and Mof (KAT8)-
containing (NSL and MSL), show a global overlap at promoters, whereas distinct binding profiles at enhancers suggest different regulatory functions of each essential HAT complex. Interestingly, Tip60 enrichment peaks at about 200 bp downstream of the transcription start sites suggesting a function for the Tip60 complexes in addition to histone acetylation."	Super-Enhancer	--	ChIP-seq	As two of the so-called ‘super Enhancer’ regions of the Nanog gene and the Enhancer of the Klf4 gene are bound by Tip60,but not by Nsl1 and Msl1(Fig.?7a, b).	EZF,Gklf,Zie	--	--	--	Kat5	AI839539,CPLA2,Htatip,Htatip1,PLIP,Tip55,Tip60	ChIP-qPCR,ChIP-seq	"The validation of several randomly selected ChIP-seq positive sites by ChIP-qPCR indicated specific Tip60 enrichments at these sites, when compared to control IgG ChIP signals and to background enrichment at an intergenic region negative for Tip60 binding (Fig.?1b).These results, together with the ChIP-qPCR validation (Fig.? 1b), indicate that the 
obtained anti-Tip60 ChIP-seq signal is specific."	--	--	Klf4
26537192	chr4	29115647	29140947	Lef1	To get insight into the mechanism of how EphA7 gene expression is regulated during the dorsal specification of the dien- and mesencephalon, we investigated the cis-acting regulatory sequence driving EphA7 to the dorsal midline of the dien- and mesencephalon. Transgenic LacZ reporter analysis, using overlapping EphA7 BACs, was used to narrow down the dorsal midline-specific enhancer, revealing the 25.3 kb genomic region as the enhancer candidate. Strikingly, this genomic DNA was located far downstream of the EphA7 transcription start site, +302.6 kb to +327.9 kb. Further enhancer mapping, using comparative genomic analysis and transgenic methods, showed that the 187 bp genomic DNA alone, approximately 305 kb downstream of the EphA7 transcription start site, was sufficient to act as the dorsal midline-specific enhancer of EphA7. Importantly, our results indicate that the 187 bp dorsal midline-specific enhancer is critically regulated by homeobox transcription factors during the development of the dien- and mesencephalon.	mouse	nervous tissue	Low throughput	Identification of the 187 bp EphA7 Genomic DNA as the Dorsal Midline-Specific Enhancer of the Diencephalon and Mesencephalon	否	--	--	neural cell	E_02_0849	PCR,Transgenic mice	"Transgenic LacZ reporter analysis, using overlapping EphA7 BACs, was used to narrow down the 
dorsal midline-specific enhancer, revealing the 25.3 kb genomic region as the enhancer candidate. Strikingly, this genomic DNA was located far downstream of the EphA7 transcription start site, +302.6 kb to +327.9 kb."	Enhancer	--	PCR,Transgenic mice	Further enhancer mapping, using comparative genomic analysis and transgenic methods, showed that the 187 bp genomic DNA alone, approximately 305 kb downstream of the EphA7 transcription start site, was sufficient to act as the dorsal midline-specific enhancer of EphA7.	Cek11,Ebk,Ehk3,Hek11,Mdk1	The 187 bp dorsal midline-specific enhancer is critically regulated by homeobox transcription factors during the development of the dien- and mesencephalon.	PCR	Importantly, we found that transgenic embryos carrying ECR3, but not ECR1 or 2, displayed LacZ expression in the dorsal midline of the dien- and mesencephalon	Sbe3	ECR3	PCR	To investigate whether the conserved transcription factor binding sites are functionally important for the 187 bp ECR3 enhancer activity, three putative transcription factor binding sites were selected for deletion. The deleted ECR3 DNA was examined for its effect on the enhancer activity by creating transgenic mouse embryos (Figs. 4A and 4B).	--	--	Epha7
26537192	chr4	29115647	29140947	Msx1	To get insight into the mechanism of how EphA7 gene expression is regulated during the dorsal specification of the dien- and mesencephalon, we investigated the cis-acting regulatory sequence driving EphA7 to the dorsal midline of the dien- and mesencephalon. Transgenic LacZ reporter analysis, using overlapping EphA7 BACs, was used to narrow down the dorsal midline-specific enhancer, revealing the 25.3 kb genomic region as the enhancer candidate. Strikingly, this genomic DNA was located far downstream of the EphA7 transcription start site, +302.6 kb to +327.9 kb. Further enhancer mapping, using comparative genomic analysis and transgenic methods, showed that the 187 bp genomic DNA alone, approximately 305 kb downstream of the EphA7 transcription start site, was sufficient to act as the dorsal midline-specific enhancer of EphA7. Importantly, our results indicate that the 187 bp dorsal midline-specific enhancer is critically regulated by homeobox transcription factors during the development of the dien- and mesencephalon.	mouse	nervous tissue	Low throughput	Identification of the 187 bp EphA7 Genomic DNA as the Dorsal Midline-Specific Enhancer of the Diencephalon and Mesencephalon	否	--	--	neural cell	E_02_0849	PCR,Transgenic mice	"Transgenic LacZ reporter analysis, using overlapping EphA7 BACs, was used to narrow down the 
dorsal midline-specific enhancer, revealing the 25.3 kb genomic region as the enhancer candidate. Strikingly, this genomic DNA was located far downstream of the EphA7 transcription start site, +302.6 kb to +327.9 kb."	Enhancer	--	PCR,Transgenic mice	Further enhancer mapping, using comparative genomic analysis and transgenic methods, showed that the 187 bp genomic DNA alone, approximately 305 kb downstream of the EphA7 transcription start site, was sufficient to act as the dorsal midline-specific enhancer of EphA7.	Cek11,Ebk,Ehk3,Hek11,Mdk1	The 187 bp dorsal midline-specific enhancer is critically regulated by homeobox transcription factors during the development of the dien- and mesencephalon.	PCR	Importantly, we found that transgenic embryos carrying ECR3, but not ECR1 or 2, displayed LacZ expression in the dorsal midline of the dien- and mesencephalon	Sbe3	ECR3	PCR	To investigate whether the conserved transcription factor binding sites are functionally important for the 187 bp ECR3 enhancer activity, three putative transcription factor binding sites were selected for deletion. The deleted ECR3 DNA was examined for its effect on the enhancer activity by creating transgenic mouse embryos (Figs. 4A and 4B).	--	--	Epha7
26537192	chr4	29115647	29140947	Wnt1	To get insight into the mechanism of how EphA7 gene expression is regulated during the dorsal specification of the dien- and mesencephalon, we investigated the cis-acting regulatory sequence driving EphA7 to the dorsal midline of the dien- and mesencephalon. Transgenic LacZ reporter analysis, using overlapping EphA7 BACs, was used to narrow down the dorsal midline-specific enhancer, revealing the 25.3 kb genomic region as the enhancer candidate. Strikingly, this genomic DNA was located far downstream of the EphA7 transcription start site, +302.6 kb to +327.9 kb. Further enhancer mapping, using comparative genomic analysis and transgenic methods, showed that the 187 bp genomic DNA alone, approximately 305 kb downstream of the EphA7 transcription start site, was sufficient to act as the dorsal midline-specific enhancer of EphA7. Importantly, our results indicate that the 187 bp dorsal midline-specific enhancer is critically regulated by homeobox transcription factors during the development of the dien- and mesencephalon.	mouse	nervous tissue	Low throughput	Identification of the 187 bp EphA7 Genomic DNA as the Dorsal Midline-Specific Enhancer of the Diencephalon and Mesencephalon	否	--	--	neural cell	E_02_0849	PCR,Transgenic mice	"Transgenic LacZ reporter analysis, using overlapping EphA7 BACs, was used to narrow down the 
dorsal midline-specific enhancer, revealing the 25.3 kb genomic region as the enhancer candidate. Strikingly, this genomic DNA was located far downstream of the EphA7 transcription start site, +302.6 kb to +327.9 kb."	Enhancer	--	PCR,Transgenic mice	Further enhancer mapping, using comparative genomic analysis and transgenic methods, showed that the 187 bp genomic DNA alone, approximately 305 kb downstream of the EphA7 transcription start site, was sufficient to act as the dorsal midline-specific enhancer of EphA7.	Cek11,Ebk,Ehk3,Hek11,Mdk1	The 187 bp dorsal midline-specific enhancer is critically regulated by homeobox transcription factors during the development of the dien- and mesencephalon.	PCR	Importantly, we found that transgenic embryos carrying ECR3, but not ECR1 or 2, displayed LacZ expression in the dorsal midline of the dien- and mesencephalon	Sbe3	ECR3	PCR	To investigate whether the conserved transcription factor binding sites are functionally important for the 187 bp ECR3 enhancer activity, three putative transcription factor binding sites were selected for deletion. The deleted ECR3 DNA was examined for its effect on the enhancer activity by creating transgenic mouse embryos (Figs. 4A and 4B).	--	--	Epha7
26505625	chr7	95210132	95260132	MET	The exonic single nucleotide variant rs11762213 located in the MET oncogene has recently been identified as a prognostic marker in clear cell renal cell carcinoma (ccRCC).	human		Low+High throughput	Validation and genomic interrogation of the MET variant rs11762213 as a predictor of adverse outcomes in clear cell renal cell carcinoma	是	--	Clear Cell Renal Cell Carcinoma	ccRCC cell	E_02_0850	ChIP,ChIP-seq	rs11762213 alone is found in a regulatory element of MET likely in an enhancer domain, and this has implications for its interaction both with MET itself and with potentially other cis-acting target genes.To further characterize the functional significance of rs11762213 we used our previously generated genome-wide chromatin annotation maps using cultured human proximal tubular epithelial cells (HKC8) and overlaid them with previously generated gene regulatory annotation maps from a panel of ChIP-seq data using the hidden Markov model-based ChromHMM chromatin segmentation program (Figure 4). Notably, rs11762213 maps to an H3K4me1 histone modification mark, which serves as an enhancer marker and is therefore consistent with the hypothesis that the SNP has a regulatory function.Mapping of rs11762213 to regulatory regions within the genome suggests that it may impact a DNA enhancer region.	Enhancer	--	ChIP,RNA-seq	Next, we assessed the impact of rs11762213 on MET steady-state mRNA and protein tumor expression using available RNA seq data and reverse phase protein array (RPPA) data from the TCGA. We found no difference in tumor MET expression by SNP status (p=0.47 Mann Whitney) including all detected MET isoforms (n=18) (Supplemental figure 2A). Since rs11762213 is located in the coding region of exon 2 we further explored exon level expression differences by genotype and again did not find any difference by genotype for exon 2 MET expression (p=0.29) of any other exon (Supplemental figure 3). Additionally, we did not see differences in tumor MET protein (p=0.88) or MET phospho-protein expression (Y1235) (Supplemental figure 2B and 2C).rs11762213 was associated with higher normal tissue MET expression (p=0.019), however, in an independent normal kidney Affymetrix mRNA array data set this finding did not validate (n=95) (data not shown).	AI838057,HGF,HGFR,Par4,c-Met	--	--	--	--	--	--	--	--	--	MET
26494787	chr10	61403948	61408233	Lhx1	Here we demonstrate Smad4/Eomes-dependent Lhx1 expression in the epiblast marks the entire definitive endoderm lineage, the anterior mesendoderm, and midline progenitors. Conditional inactivation of Lhx1 disrupts anterior definitive endoderm development and impedes node and midline morphogenesis in part due to severe disturbances in visceral endoderm displacement. Transcriptional profiling and ChIP-seq (chromatin immunoprecipitation [ChIP] followed by high-throughput sequencing) experiments identified Lhx1 target genes, including numerous anterior definitive endoderm markers and components of the Wnt signaling pathway. Interestingly, Lhx1-binding sites were enriched at enhancers, including the Nodal-proximal epiblast enhancer element and enhancer regions controlling Otx2 and Foxa2 expression. Moreover, in proteomic experiments, we characterized a complex comprised of Lhx1, Otx2, and Foxa2 as well as the chromatin-looping protein Ldb1. These partnerships cooperatively regulate development of the anterior mesendoderm, node, and midline cell populations responsible for establishment of the left-right body axis and head formation.	mouse	epithelial tissue	Low+High throughput	Lhx1 functions together with Otx2, Foxa2,and Ldb1 to govern anterior mesendoderm,node, and midline development	否	--	--	embryonic stem cell	E_02_0851	ChIP,ChIP-seq	ChIP (red) and input (blue) wiggle plot overlays showing enrichment of Lhx1 ChIP-seq density at Hesx1,Fzd8,Embigin,Nodal,Otx2,and Foxa3. Purple boxes indicate the positions of previously mapped Nodal Enhancer elements.	Enhancer	--	ChIP,ChIP-seq	Conditional inactivation of Lhx1 dis_x0002_rupts anterior definitive endoderm development and impedes node and midline morphogenesis in part due to severe disturbances in visceral endoderm displacement. Transcriptional profiling and ChIP-seq (chromatin immunopre_x0002_cipitation [ChIP] followed by high-throughput sequencing) experiments identified Lhx1 target genes, including numerous anterior definitive endoderm markers and components of the Wnt signaling pathway. Interestingly, Lhx1-binding sites were enriched at enhancers, including the Nodal-proximal epiblast enhancer element and enhancer regions controlling Otx2 and Foxa2 expression. 	Tg.413d	--	--	--	Lhx1,Eomes	Lim1,C77258,TBR-2,Tbr2	ChIP	Several putative Lhx1 target genes were represented in our ChIP data set. For example, Lhx1 binding was detected at two distinct regions at the Hesx1 locus, including a regulatory element in the 5′ untranslated region (containing two Lhx1-binding motifs) and a 3′ distal enhancer. Lhx1 ChIP peaks were also present upstream of Embigin exon 1.	--	--	Nodal
26494787	chr10	61403948	61408233	Otx2	Here we demonstrate Smad4/Eomes-dependent Lhx1 expression in the epiblast marks the entire definitive endoderm lineage, the anterior mesendoderm, and midline progenitors. Conditional inactivation of Lhx1 disrupts anterior definitive endoderm development and impedes node and midline morphogenesis in part due to severe disturbances in visceral endoderm displacement. Transcriptional profiling and ChIP-seq (chromatin immunoprecipitation [ChIP] followed by high-throughput sequencing) experiments identified Lhx1 target genes, including numerous anterior definitive endoderm markers and components of the Wnt signaling pathway. Interestingly, Lhx1-binding sites were enriched at enhancers, including the Nodal-proximal epiblast enhancer element and enhancer regions controlling Otx2 and Foxa2 expression. Moreover, in proteomic experiments, we characterized a complex comprised of Lhx1, Otx2, and Foxa2 as well as the chromatin-looping protein Ldb1. These partnerships cooperatively regulate development of the anterior mesendoderm, node, and midline cell populations responsible for establishment of the left-right body axis and head formation.	mouse	epithelial tissue	Low+High throughput	Lhx1 functions together with Otx2, Foxa2,and Ldb1 to govern anterior mesendoderm,node, and midline development	否	--	--	embryonic stem cell	E_02_0851	ChIP,ChIP-seq	ChIP (red) and input (blue) wiggle plot overlays showing enrichment of Lhx1 ChIP-seq density at Hesx1,Fzd8,Embigin,Nodal,Otx2,and Foxa3. Purple boxes indicate the positions of previously mapped Nodal Enhancer elements.	Enhancer	--	ChIP,ChIP-seq	Conditional inactivation of Lhx1 dis_x0002_rupts anterior definitive endoderm development and impedes node and midline morphogenesis in part due to severe disturbances in visceral endoderm displacement. Transcriptional profiling and ChIP-seq (chromatin immunopre_x0002_cipitation [ChIP] followed by high-throughput sequencing) experiments identified Lhx1 target genes, including numerous anterior definitive endoderm markers and components of the Wnt signaling pathway. Interestingly, Lhx1-binding sites were enriched at enhancers, including the Nodal-proximal epiblast enhancer element and enhancer regions controlling Otx2 and Foxa2 expression. 	Tg.413d	--	--	--	Lhx1,Eomes	Lim1,C77258,TBR-2,Tbr2	ChIP	Several putative Lhx1 target genes were represented in our ChIP data set. For example, Lhx1 binding was detected at two distinct regions at the Hesx1 locus, including a regulatory element in the 5′ untranslated region (containing two Lhx1-binding motifs) and a 3′ distal enhancer. Lhx1 ChIP peaks were also present upstream of Embigin exon 1.	--	--	Nodal
26494787	chr10	61403948	61408233	Foxa2	Here we demonstrate Smad4/Eomes-dependent Lhx1 expression in the epiblast marks the entire definitive endoderm lineage, the anterior mesendoderm, and midline progenitors. Conditional inactivation of Lhx1 disrupts anterior definitive endoderm development and impedes node and midline morphogenesis in part due to severe disturbances in visceral endoderm displacement. Transcriptional profiling and ChIP-seq (chromatin immunoprecipitation [ChIP] followed by high-throughput sequencing) experiments identified Lhx1 target genes, including numerous anterior definitive endoderm markers and components of the Wnt signaling pathway. Interestingly, Lhx1-binding sites were enriched at enhancers, including the Nodal-proximal epiblast enhancer element and enhancer regions controlling Otx2 and Foxa2 expression. Moreover, in proteomic experiments, we characterized a complex comprised of Lhx1, Otx2, and Foxa2 as well as the chromatin-looping protein Ldb1. These partnerships cooperatively regulate development of the anterior mesendoderm, node, and midline cell populations responsible for establishment of the left-right body axis and head formation.	mouse	epithelial tissue	Low+High throughput	Lhx1 functions together with Otx2, Foxa2,and Ldb1 to govern anterior mesendoderm,node, and midline development	否	--	--	embryonic stem cell	E_02_0851	ChIP,ChIP-seq	ChIP (red) and input (blue) wiggle plot overlays showing enrichment of Lhx1 ChIP-seq density at Hesx1,Fzd8,Embigin,Nodal,Otx2,and Foxa3. Purple boxes indicate the positions of previously mapped Nodal Enhancer elements.	Enhancer	--	ChIP,ChIP-seq	Conditional inactivation of Lhx1 dis_x0002_rupts anterior definitive endoderm development and impedes node and midline morphogenesis in part due to severe disturbances in visceral endoderm displacement. Transcriptional profiling and ChIP-seq (chromatin immunopre_x0002_cipitation [ChIP] followed by high-throughput sequencing) experiments identified Lhx1 target genes, including numerous anterior definitive endoderm markers and components of the Wnt signaling pathway. Interestingly, Lhx1-binding sites were enriched at enhancers, including the Nodal-proximal epiblast enhancer element and enhancer regions controlling Otx2 and Foxa2 expression. 	Tg.413d	--	--	--	Lhx1,Eomes	Lim1,C77258,TBR-2,Tbr2	ChIP	Several putative Lhx1 target genes were represented in our ChIP data set. For example, Lhx1 binding was detected at two distinct regions at the Hesx1 locus, including a regulatory element in the 5′ untranslated region (containing two Lhx1-binding motifs) and a 3′ distal enhancer. Lhx1 ChIP peaks were also present upstream of Embigin exon 1.	--	--	Nodal
26494787	chr10	61403948	61408233	Ldb1	Here we demonstrate Smad4/Eomes-dependent Lhx1 expression in the epiblast marks the entire definitive endoderm lineage, the anterior mesendoderm, and midline progenitors. Conditional inactivation of Lhx1 disrupts anterior definitive endoderm development and impedes node and midline morphogenesis in part due to severe disturbances in visceral endoderm displacement. Transcriptional profiling and ChIP-seq (chromatin immunoprecipitation [ChIP] followed by high-throughput sequencing) experiments identified Lhx1 target genes, including numerous anterior definitive endoderm markers and components of the Wnt signaling pathway. Interestingly, Lhx1-binding sites were enriched at enhancers, including the Nodal-proximal epiblast enhancer element and enhancer regions controlling Otx2 and Foxa2 expression. Moreover, in proteomic experiments, we characterized a complex comprised of Lhx1, Otx2, and Foxa2 as well as the chromatin-looping protein Ldb1. These partnerships cooperatively regulate development of the anterior mesendoderm, node, and midline cell populations responsible for establishment of the left-right body axis and head formation.	mouse	epithelial tissue	Low+High throughput	Lhx1 functions together with Otx2, Foxa2,and Ldb1 to govern anterior mesendoderm,node, and midline development	否	--	--	embryonic stem cell	E_02_0851	ChIP,ChIP-seq	ChIP (red) and input (blue) wiggle plot overlays showing enrichment of Lhx1 ChIP-seq density at Hesx1,Fzd8,Embigin,Nodal,Otx2,and Foxa3. Purple boxes indicate the positions of previously mapped Nodal Enhancer elements.	Enhancer	--	ChIP,ChIP-seq	Conditional inactivation of Lhx1 dis_x0002_rupts anterior definitive endoderm development and impedes node and midline morphogenesis in part due to severe disturbances in visceral endoderm displacement. Transcriptional profiling and ChIP-seq (chromatin immunopre_x0002_cipitation [ChIP] followed by high-throughput sequencing) experiments identified Lhx1 target genes, including numerous anterior definitive endoderm markers and components of the Wnt signaling pathway. Interestingly, Lhx1-binding sites were enriched at enhancers, including the Nodal-proximal epiblast enhancer element and enhancer regions controlling Otx2 and Foxa2 expression. 	Tg.413d	--	--	--	Lhx1,Eomes	Lim1,C77258,TBR-2,Tbr2	ChIP	Several putative Lhx1 target genes were represented in our ChIP data set. For example, Lhx1 binding was detected at two distinct regions at the Hesx1 locus, including a regulatory element in the 5′ untranslated region (containing two Lhx1-binding motifs) and a 3′ distal enhancer. Lhx1 ChIP peaks were also present upstream of Embigin exon 1.	--	--	Nodal
26494787	chr10	61403948	61408233	Smad4	Here we demonstrate Smad4/Eomes-dependent Lhx1 expression in the epiblast marks the entire definitive endoderm lineage, the anterior mesendoderm, and midline progenitors. Conditional inactivation of Lhx1 disrupts anterior definitive endoderm development and impedes node and midline morphogenesis in part due to severe disturbances in visceral endoderm displacement. Transcriptional profiling and ChIP-seq (chromatin immunoprecipitation [ChIP] followed by high-throughput sequencing) experiments identified Lhx1 target genes, including numerous anterior definitive endoderm markers and components of the Wnt signaling pathway. Interestingly, Lhx1-binding sites were enriched at enhancers, including the Nodal-proximal epiblast enhancer element and enhancer regions controlling Otx2 and Foxa2 expression. Moreover, in proteomic experiments, we characterized a complex comprised of Lhx1, Otx2, and Foxa2 as well as the chromatin-looping protein Ldb1. These partnerships cooperatively regulate development of the anterior mesendoderm, node, and midline cell populations responsible for establishment of the left-right body axis and head formation.	mouse	epithelial tissue	Low+High throughput	Lhx1 functions together with Otx2, Foxa2,and Ldb1 to govern anterior mesendoderm,node, and midline development	否	--	--	embryonic stem cell	E_02_0851	ChIP,ChIP-seq	ChIP (red) and input (blue) wiggle plot overlays showing enrichment of Lhx1 ChIP-seq density at Hesx1,Fzd8,Embigin,Nodal,Otx2,and Foxa3. Purple boxes indicate the positions of previously mapped Nodal Enhancer elements.	Enhancer	--	ChIP,ChIP-seq	Conditional inactivation of Lhx1 dis_x0002_rupts anterior definitive endoderm development and impedes node and midline morphogenesis in part due to severe disturbances in visceral endoderm displacement. Transcriptional profiling and ChIP-seq (chromatin immunopre_x0002_cipitation [ChIP] followed by high-throughput sequencing) experiments identified Lhx1 target genes, including numerous anterior definitive endoderm markers and components of the Wnt signaling pathway. Interestingly, Lhx1-binding sites were enriched at enhancers, including the Nodal-proximal epiblast enhancer element and enhancer regions controlling Otx2 and Foxa2 expression. 	Tg.413d	--	--	--	Lhx1,Eomes	Lim1,C77258,TBR-2,Tbr2	ChIP	Several putative Lhx1 target genes were represented in our ChIP data set. For example, Lhx1 binding was detected at two distinct regions at the Hesx1 locus, including a regulatory element in the 5′ untranslated region (containing two Lhx1-binding motifs) and a 3′ distal enhancer. Lhx1 ChIP peaks were also present upstream of Embigin exon 1.	--	--	Nodal
26494787	chr10	61403948	61408233	Eomes	Here we demonstrate Smad4/Eomes-dependent Lhx1 expression in the epiblast marks the entire definitive endoderm lineage, the anterior mesendoderm, and midline progenitors. Conditional inactivation of Lhx1 disrupts anterior definitive endoderm development and impedes node and midline morphogenesis in part due to severe disturbances in visceral endoderm displacement. Transcriptional profiling and ChIP-seq (chromatin immunoprecipitation [ChIP] followed by high-throughput sequencing) experiments identified Lhx1 target genes, including numerous anterior definitive endoderm markers and components of the Wnt signaling pathway. Interestingly, Lhx1-binding sites were enriched at enhancers, including the Nodal-proximal epiblast enhancer element and enhancer regions controlling Otx2 and Foxa2 expression. Moreover, in proteomic experiments, we characterized a complex comprised of Lhx1, Otx2, and Foxa2 as well as the chromatin-looping protein Ldb1. These partnerships cooperatively regulate development of the anterior mesendoderm, node, and midline cell populations responsible for establishment of the left-right body axis and head formation.	mouse	epithelial tissue	Low+High throughput	Lhx1 functions together with Otx2, Foxa2,and Ldb1 to govern anterior mesendoderm,node, and midline development	否	--	--	embryonic stem cell	E_02_0851	ChIP,ChIP-seq	ChIP (red) and input (blue) wiggle plot overlays showing enrichment of Lhx1 ChIP-seq density at Hesx1,Fzd8,Embigin,Nodal,Otx2,and Foxa3. Purple boxes indicate the positions of previously mapped Nodal Enhancer elements.	Enhancer	--	ChIP,ChIP-seq	Conditional inactivation of Lhx1 dis_x0002_rupts anterior definitive endoderm development and impedes node and midline morphogenesis in part due to severe disturbances in visceral endoderm displacement. Transcriptional profiling and ChIP-seq (chromatin immunopre_x0002_cipitation [ChIP] followed by high-throughput sequencing) experiments identified Lhx1 target genes, including numerous anterior definitive endoderm markers and components of the Wnt signaling pathway. Interestingly, Lhx1-binding sites were enriched at enhancers, including the Nodal-proximal epiblast enhancer element and enhancer regions controlling Otx2 and Foxa2 expression. 	Tg.413d	--	--	--	Lhx1,Eomes	Lim1,C77258,TBR-2,Tbr2	ChIP	Several putative Lhx1 target genes were represented in our ChIP data set. For example, Lhx1 binding was detected at two distinct regions at the Hesx1 locus, including a regulatory element in the 5′ untranslated region (containing two Lhx1-binding motifs) and a 3′ distal enhancer. Lhx1 ChIP peaks were also present upstream of Embigin exon 1.	--	--	Nodal
26445536	chr22	35686840	35687280	MAF	Interestingly, Bach1, a nuclear protein shown to associate with small MAF proteins and serve as a repressor of HO-1 gene expression	human	blood	Low throughput	Gold nanoparticles induce heme oxygenase-1 expression through Nrf2 activation and Bach1 export in human vascular endothelial cells		--	--	Endothelial cell	E_02_0852	ChIP,RT-PCR,qPCR	To investigate whether the translocated Nrf2 interacted with the HO-1 promoter region, the primer sets for the enhancer region (E2) and promoter region near transcription start site were synthesized for ChIP assays (Figure 5A, upper panel schematic). The ChIP analyses demonstrated that AuNP treatment significantly induced Nrf2 binding to the human HO-1 E2 enhancer region, but not to the promoter region near the transcription start site. The binding to the enhancer region was concentration dependent, as determined by RT-PCR and real-time PCR (Figure 5B and C).	Enhancer	--	ChIP,RT-PCR,qPCR	To investigate whether the translocated Nrf2 interacted with the HO-1 promoter region, the primer sets for the enhancer region (E2) and promoter region near transcription start site were synthesized for ChIP assays (Figure 5A, upper panel schematic). The ChIP analyses demonstrated that AuNP treatment significantly induced Nrf2 binding to the human HO-1 E2 enhancer region, but not to the promoter region near the transcription start site. The binding to the enhancer region was concentration dependent, as determined by RT-PCR and real-time PCR (Figure 5B and C).	HMOX1D,HO-1,HSP32,bK286B10	--	--	--	--	--	--	--	--	--	HMOX1
26443845	chr16	49740654	49742654	GATA1	"Here we examined whether enhancers physically contact the gene segments transcribed by RNAPII.Initial results at the β-globin locus are consistent with elongation-dependent LCR–β-globin gene body contacts.To overcome the inherent resolution limitations of chromosome conformation capture (3C) studies associated with a small gene such as β-globin,we carried out our studies at the Kit locus. His locus has a well-characterized enhancer residing 114 kb upstream of the transcription start site (TSS),and its coding region encompasses∼82 kb,thus lending itself to finely space- and time-resolved 3C analysis (Jing et al. 2008). Using timed elongation block and release experiments,we found that the−114 enhancer forms stable contacts with the promoterproximal region throughout transcription elongation. Notably,additional dynamic contacts of the enhancer with
the coding region were observed at the positions of elongating RNAPII.Similar dynamic enhancer gene body contacts were identified at the CD47 locus.These results are compatible with a dynamic folding pattern during transcription elongation in which the gene body is reeled past a stable enhancer–promoter complex,providing a physical platform upon which enhancers might impact on transcription elongation."	mouse	connective tissue	Low throughput	Dynamic enhancer–gene body contacts during transcription elongation	否	--	--	G1E cell	E_02_0853	RT-qPCR,ChIP	CD47 gene contacts with its distal enhancer at ?80 kb dur_x0002_ing synchronized transcriptional elongation. (A) Map of the CD47 lo_x0002_cus. Blue bars indicate fragments of BglII, and red bars indicate the regions used for ChIP and RT-qPCR.	Enhancer	3C	RT-qPCR,ChIP	This locus has a well-character- ized Enhancer residing 114 kb upstream of the transcrip- tion start site (TSS),and its coding region encompasses ～82 kb,thus lending itself to finely space-and time-re- solved 3C analysis (Jing et al. 2008) No- tably,additional dynamic contacts of the Enhancer with the coding region were observed at the positions of elon- gating RNAPII. Similar dynamic Enhancer gene body con- tacts were identified at the CD47 locus.CD47 gene contacts with its distal enhancer at ?80 kb dur_x0002_ing synchronized transcriptional elongation. (A) Map of the CD47 lo_x0002_cus. Blue bars indicate fragments of BglII, and red bars indicate the regions used for ChIP and RT-qPCR.	9130415E20Rik,AA407862,AI848868,AW108519,B430305P08Rik,IAP,Itgp	--	--	--	--	--	--	--	--	--	Cd47
26443845	chr16	49740654	49742654	Kit	"Here we examined whether enhancers physically contact the gene segments transcribed by RNAPII.Initial results at the β-globin locus are consistent with elongation-dependent LCR–β-globin gene body contacts.To overcome the inherent resolution limitations of chromosome conformation capture (3C) studies associated with a small gene such as β-globin,we carried out our studies at the Kit locus. His locus has a well-characterized enhancer residing 114 kb upstream of the transcription start site (TSS),and its coding region encompasses∼82 kb,thus lending itself to finely space- and time-resolved 3C analysis (Jing et al. 2008). Using timed elongation block and release experiments,we found that the−114 enhancer forms stable contacts with the promoterproximal region throughout transcription elongation. Notably,additional dynamic contacts of the enhancer with
the coding region were observed at the positions of elongating RNAPII.Similar dynamic enhancer gene body contacts were identified at the CD47 locus.These results are compatible with a dynamic folding pattern during transcription elongation in which the gene body is reeled past a stable enhancer–promoter complex,providing a physical platform upon which enhancers might impact on transcription elongation."	mouse	connective tissue	Low throughput	Dynamic enhancer–gene body contacts during transcription elongation	否	--	--	G1E cell	E_02_0853	RT-qPCR,ChIP	CD47 gene contacts with its distal enhancer at ?80 kb dur_x0002_ing synchronized transcriptional elongation. (A) Map of the CD47 lo_x0002_cus. Blue bars indicate fragments of BglII, and red bars indicate the regions used for ChIP and RT-qPCR.	Enhancer	3C	RT-qPCR,ChIP	This locus has a well-character- ized Enhancer residing 114 kb upstream of the transcrip- tion start site (TSS),and its coding region encompasses ～82 kb,thus lending itself to finely space-and time-re- solved 3C analysis (Jing et al. 2008) No- tably,additional dynamic contacts of the Enhancer with the coding region were observed at the positions of elon- gating RNAPII. Similar dynamic Enhancer gene body con- tacts were identified at the CD47 locus.CD47 gene contacts with its distal enhancer at ?80 kb dur_x0002_ing synchronized transcriptional elongation. (A) Map of the CD47 lo_x0002_cus. Blue bars indicate fragments of BglII, and red bars indicate the regions used for ChIP and RT-qPCR.	9130415E20Rik,AA407862,AI848868,AW108519,B430305P08Rik,IAP,Itgp	--	--	--	--	--	--	--	--	--	Cd47
26443845	chr16	49740654	49742654	CD47	"Here we examined whether enhancers physically contact the gene segments transcribed by RNAPII.Initial results at the β-globin locus are consistent with elongation-dependent LCR–β-globin gene body contacts.To overcome the inherent resolution limitations of chromosome conformation capture (3C) studies associated with a small gene such as β-globin,we carried out our studies at the Kit locus. His locus has a well-characterized enhancer residing 114 kb upstream of the transcription start site (TSS),and its coding region encompasses∼82 kb,thus lending itself to finely space- and time-resolved 3C analysis (Jing et al. 2008). Using timed elongation block and release experiments,we found that the−114 enhancer forms stable contacts with the promoterproximal region throughout transcription elongation. Notably,additional dynamic contacts of the enhancer with
the coding region were observed at the positions of elongating RNAPII.Similar dynamic enhancer gene body contacts were identified at the CD47 locus.These results are compatible with a dynamic folding pattern during transcription elongation in which the gene body is reeled past a stable enhancer–promoter complex,providing a physical platform upon which enhancers might impact on transcription elongation."	mouse	connective tissue	Low throughput	Dynamic enhancer–gene body contacts during transcription elongation	否	--	--	G1E cell	E_02_0853	RT-qPCR,ChIP	CD47 gene contacts with its distal enhancer at ?80 kb dur_x0002_ing synchronized transcriptional elongation. (A) Map of the CD47 lo_x0002_cus. Blue bars indicate fragments of BglII, and red bars indicate the regions used for ChIP and RT-qPCR.	Enhancer	3C	RT-qPCR,ChIP	This locus has a well-character- ized Enhancer residing 114 kb upstream of the transcrip- tion start site (TSS),and its coding region encompasses ～82 kb,thus lending itself to finely space-and time-re- solved 3C analysis (Jing et al. 2008) No- tably,additional dynamic contacts of the Enhancer with the coding region were observed at the positions of elon- gating RNAPII. Similar dynamic Enhancer gene body con- tacts were identified at the CD47 locus.CD47 gene contacts with its distal enhancer at ?80 kb dur_x0002_ing synchronized transcriptional elongation. (A) Map of the CD47 lo_x0002_cus. Blue bars indicate fragments of BglII, and red bars indicate the regions used for ChIP and RT-qPCR.	9130415E20Rik,AA407862,AI848868,AW108519,B430305P08Rik,IAP,Itgp	--	--	--	--	--	--	--	--	--	Cd47
26443845	chr16	49740654	49742654	IFT57	"Here we examined whether enhancers physically contact the gene segments transcribed by RNAPII.Initial results at the β-globin locus are consistent with elongation-dependent LCR–β-globin gene body contacts.To overcome the inherent resolution limitations of chromosome conformation capture (3C) studies associated with a small gene such as β-globin,we carried out our studies at the Kit locus. His locus has a well-characterized enhancer residing 114 kb upstream of the transcription start site (TSS),and its coding region encompasses∼82 kb,thus lending itself to finely space- and time-resolved 3C analysis (Jing et al. 2008). Using timed elongation block and release experiments,we found that the−114 enhancer forms stable contacts with the promoterproximal region throughout transcription elongation. Notably,additional dynamic contacts of the enhancer with
the coding region were observed at the positions of elongating RNAPII.Similar dynamic enhancer gene body contacts were identified at the CD47 locus.These results are compatible with a dynamic folding pattern during transcription elongation in which the gene body is reeled past a stable enhancer–promoter complex,providing a physical platform upon which enhancers might impact on transcription elongation."	mouse	connective tissue	Low throughput	Dynamic enhancer–gene body contacts during transcription elongation	否	--	--	G1E cell	E_02_0853	RT-qPCR,ChIP	CD47 gene contacts with its distal enhancer at ?80 kb dur_x0002_ing synchronized transcriptional elongation. (A) Map of the CD47 lo_x0002_cus. Blue bars indicate fragments of BglII, and red bars indicate the regions used for ChIP and RT-qPCR.	Enhancer	3C	RT-qPCR,ChIP	This locus has a well-character- ized Enhancer residing 114 kb upstream of the transcrip- tion start site (TSS),and its coding region encompasses ～82 kb,thus lending itself to finely space-and time-re- solved 3C analysis (Jing et al. 2008) No- tably,additional dynamic contacts of the Enhancer with the coding region were observed at the positions of elon- gating RNAPII. Similar dynamic Enhancer gene body con- tacts were identified at the CD47 locus.CD47 gene contacts with its distal enhancer at ?80 kb dur_x0002_ing synchronized transcriptional elongation. (A) Map of the CD47 lo_x0002_cus. Blue bars indicate fragments of BglII, and red bars indicate the regions used for ChIP and RT-qPCR.	9130415E20Rik,AA407862,AI848868,AW108519,B430305P08Rik,IAP,Itgp	--	--	--	--	--	--	--	--	--	Cd47
26364592	chr10	78046488	78046636	Aire	Here, we characterize a conserved noncoding sequence 1 (CNS1) containing two NF-κB binding sites upstream of the Aire coding region. We show that CNS1-deficient mice lack thymic expression of Aire and share several features of Aire-knockout mice, including downregulation of Aire-dependent genes, impaired terminal differentiation of the mTEC population, and reduced production of thymic Treg cells. In addition, we show that CNS1 is indispensable for RANK-induced Aire expression and that CNS1 is activated by NF-κB pathway complexes containing RelA. Together, our results indicate that CNS1 is a critical link between RANK signaling, NF-κB activation, and thymic expression of Aire.	mouse	epithelial tissue	Low throughput	A highly conserved NF-κB-responsive enhancer is critical for thymic expression of Aire in mice	否	--	--	epithelial cell of thymus	E_02_0854	qPCR	To determine the in vivo function of the Aire enhancer region,we generated knockout mice (CNS1-KO) with a deletion of 45 bp within CNS1 including both NF-κB sites.We first studied thymic expression of Aire in purified thymic epithelial cell subsets-cTEC, mTEClo, and mTEChi-from homozygous CNS1-KO mice by qPCR targeting exons 7–9. Strik_x0002_ingly, Aire was not expressed in mTEChi from CNS1-KO mice,whereas the gene was highly expressed in mTEChi from WT mice(Fig. 2A).	Enhancer	--	qPCR,Immunofluorescence,RT-PCR	"To determine whether the upstream CNS1 region regulates these variants, we analyzed the expression levels of the majority of exons in the Aire coding region by qPCR.Aire-KO mouse results are shown in Supporting Information Fig.2B), indicating that CNS1 is required for the thymic expression of the majority of, if not all, Aire splice variants.Deficiency of Aire
protein expression was confirmed in situ by immunofluorescence staining, which showed no Aire protein in the thymi of CNS1-KO(Fig. 2D). These results established that the CNS1 region is critical for Aire mRNA and protein expression in the mouse thymus."	Aire	CNS1 is indispensable for RANK-induced Aire expression and that CNS1 is activated by NF-κB pathway complexes containing RelA.	3C,Luciferase Reporter Assay,EMSA	To further examine the role of CNS1 in Aire gene regulation, we evaluated the spa_x0002_tial proximity between the CNS1 Enhancer and Aire promoter by chromosome conformation capture (3C) method.This result suggests that these distant regulatory regions are brought close to each other in intact chromatin.	Nfkb1	NF-KB1,NF-kappaB,NF-kappaB1,p105,p50,p50/p105	Luciferase Reporter Assay,EMSA	We next analyzed the CNS1 region for its responsiveness to NF-κB stimulation in luciferase reporter assays in vitro.We inserted a CNS1 fragment containing the two NF-κB binding sites upstream of the IFN-β minimal promoter and luciferase coding region and then introduced specific mutations into the NF-κB binding sites A and B,either individually or in combination.	--	--	Aire
26364592	chr10	78046488	78046636	CCL2	Here, we characterize a conserved noncoding sequence 1 (CNS1) containing two NF-κB binding sites upstream of the Aire coding region. We show that CNS1-deficient mice lack thymic expression of Aire and share several features of Aire-knockout mice, including downregulation of Aire-dependent genes, impaired terminal differentiation of the mTEC population, and reduced production of thymic Treg cells. In addition, we show that CNS1 is indispensable for RANK-induced Aire expression and that CNS1 is activated by NF-κB pathway complexes containing RelA. Together, our results indicate that CNS1 is a critical link between RANK signaling, NF-κB activation, and thymic expression of Aire.	mouse	epithelial tissue	Low throughput	A highly conserved NF-κB-responsive enhancer is critical for thymic expression of Aire in mice	否	--	--	epithelial cell of thymus	E_02_0854	qPCR	To determine the in vivo function of the Aire enhancer region,we generated knockout mice (CNS1-KO) with a deletion of 45 bp within CNS1 including both NF-κB sites.We first studied thymic expression of Aire in purified thymic epithelial cell subsets-cTEC, mTEClo, and mTEChi-from homozygous CNS1-KO mice by qPCR targeting exons 7–9. Strik_x0002_ingly, Aire was not expressed in mTEChi from CNS1-KO mice,whereas the gene was highly expressed in mTEChi from WT mice(Fig. 2A).	Enhancer	--	qPCR,Immunofluorescence,RT-PCR	"To determine whether the upstream CNS1 region regulates these variants, we analyzed the expression levels of the majority of exons in the Aire coding region by qPCR.Aire-KO mouse results are shown in Supporting Information Fig.2B), indicating that CNS1 is required for the thymic expression of the majority of, if not all, Aire splice variants.Deficiency of Aire
protein expression was confirmed in situ by immunofluorescence staining, which showed no Aire protein in the thymi of CNS1-KO(Fig. 2D). These results established that the CNS1 region is critical for Aire mRNA and protein expression in the mouse thymus."	Aire	CNS1 is indispensable for RANK-induced Aire expression and that CNS1 is activated by NF-κB pathway complexes containing RelA.	3C,Luciferase Reporter Assay,EMSA	To further examine the role of CNS1 in Aire gene regulation, we evaluated the spa_x0002_tial proximity between the CNS1 Enhancer and Aire promoter by chromosome conformation capture (3C) method.This result suggests that these distant regulatory regions are brought close to each other in intact chromatin.	Nfkb1	NF-KB1,NF-kappaB,NF-kappaB1,p105,p50,p50/p105	Luciferase Reporter Assay,EMSA	We next analyzed the CNS1 region for its responsiveness to NF-κB stimulation in luciferase reporter assays in vitro.We inserted a CNS1 fragment containing the two NF-κB binding sites upstream of the IFN-β minimal promoter and luciferase coding region and then introduced specific mutations into the NF-κB binding sites A and B,either individually or in combination.	--	--	Aire
26321200	chr13	83661050	83662862	Isl1	Here we show that Ldb1 is a central regulator of genome organization in cardiac progenitor cells, which is crucial for cardiac lineage differentiation and heart development. We demonstrate that Ldb1 binds to the key regulator of cardiac progenitors, Isl1, and protects it from degradation.Furthermore, the Isl1/Ldb1 complex promotes longrange enhancer-promoter interactions at the loci of the core cardiac transcription factors Mef2c and Hand2. Chromosome conformation capture followed by sequencing identified specific Ldb1-mediated interactions of the Isl1/Ldb1 responsive Mef2c anterior heart field enhancer with genes that play key roles in cardiac progenitor cell function and cardiovascular development. Importantly, the expression of these genes was downregulated upon Ldb1 depletion and Isl1/Ldb1 haplodeficiency. In conclusion,the Isl1/Ldb1 complex orchestrates a network for heart-specific transcriptional regulation and coordination in three-dimensional space during cardiogenesis.	mouse	epithelial tissue	Low throughput	The Isl1/Ldb1 Complex Orchestrates Genome-wide Chromatin Organization to Instruct Differentiation of Multipotent Cardiac Progenitors	否	--	Heart Failure	embryonic stem cell	E_02_0855	3C-qPCR,3C-seq	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	Enhancer	3C-qPCR,3C-seq	--	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	5430401D19Rik,9930028G15Rik,AV011172,Mef2	--	--	--	--	--	--	--	--	--	Mef2c
26321200	chr13	83661050	83662862	Ldb1	Here we show that Ldb1 is a central regulator of genome organization in cardiac progenitor cells, which is crucial for cardiac lineage differentiation and heart development. We demonstrate that Ldb1 binds to the key regulator of cardiac progenitors, Isl1, and protects it from degradation.Furthermore, the Isl1/Ldb1 complex promotes longrange enhancer-promoter interactions at the loci of the core cardiac transcription factors Mef2c and Hand2. Chromosome conformation capture followed by sequencing identified specific Ldb1-mediated interactions of the Isl1/Ldb1 responsive Mef2c anterior heart field enhancer with genes that play key roles in cardiac progenitor cell function and cardiovascular development. Importantly, the expression of these genes was downregulated upon Ldb1 depletion and Isl1/Ldb1 haplodeficiency. In conclusion,the Isl1/Ldb1 complex orchestrates a network for heart-specific transcriptional regulation and coordination in three-dimensional space during cardiogenesis.	mouse	epithelial tissue	Low throughput	The Isl1/Ldb1 Complex Orchestrates Genome-wide Chromatin Organization to Instruct Differentiation of Multipotent Cardiac Progenitors	否	--	Heart Failure	embryonic stem cell	E_02_0855	3C-qPCR,3C-seq	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	Enhancer	3C-qPCR,3C-seq	--	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	5430401D19Rik,9930028G15Rik,AV011172,Mef2	--	--	--	--	--	--	--	--	--	Mef2c
26321200	chr13	83661050	83662862	Mef2c	Here we show that Ldb1 is a central regulator of genome organization in cardiac progenitor cells, which is crucial for cardiac lineage differentiation and heart development. We demonstrate that Ldb1 binds to the key regulator of cardiac progenitors, Isl1, and protects it from degradation.Furthermore, the Isl1/Ldb1 complex promotes longrange enhancer-promoter interactions at the loci of the core cardiac transcription factors Mef2c and Hand2. Chromosome conformation capture followed by sequencing identified specific Ldb1-mediated interactions of the Isl1/Ldb1 responsive Mef2c anterior heart field enhancer with genes that play key roles in cardiac progenitor cell function and cardiovascular development. Importantly, the expression of these genes was downregulated upon Ldb1 depletion and Isl1/Ldb1 haplodeficiency. In conclusion,the Isl1/Ldb1 complex orchestrates a network for heart-specific transcriptional regulation and coordination in three-dimensional space during cardiogenesis.	mouse	epithelial tissue	Low throughput	The Isl1/Ldb1 Complex Orchestrates Genome-wide Chromatin Organization to Instruct Differentiation of Multipotent Cardiac Progenitors	否	--	Heart Failure	embryonic stem cell	E_02_0855	3C-qPCR,3C-seq	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	Enhancer	3C-qPCR,3C-seq	--	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	5430401D19Rik,9930028G15Rik,AV011172,Mef2	--	--	--	--	--	--	--	--	--	Mef2c
26321200	chr13	83661050	83662862	Hand2	Here we show that Ldb1 is a central regulator of genome organization in cardiac progenitor cells, which is crucial for cardiac lineage differentiation and heart development. We demonstrate that Ldb1 binds to the key regulator of cardiac progenitors, Isl1, and protects it from degradation.Furthermore, the Isl1/Ldb1 complex promotes longrange enhancer-promoter interactions at the loci of the core cardiac transcription factors Mef2c and Hand2. Chromosome conformation capture followed by sequencing identified specific Ldb1-mediated interactions of the Isl1/Ldb1 responsive Mef2c anterior heart field enhancer with genes that play key roles in cardiac progenitor cell function and cardiovascular development. Importantly, the expression of these genes was downregulated upon Ldb1 depletion and Isl1/Ldb1 haplodeficiency. In conclusion,the Isl1/Ldb1 complex orchestrates a network for heart-specific transcriptional regulation and coordination in three-dimensional space during cardiogenesis.	mouse	epithelial tissue	Low throughput	The Isl1/Ldb1 Complex Orchestrates Genome-wide Chromatin Organization to Instruct Differentiation of Multipotent Cardiac Progenitors	否	--	Heart Failure	embryonic stem cell	E_02_0855	3C-qPCR,3C-seq	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	Enhancer	3C-qPCR,3C-seq	--	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	5430401D19Rik,9930028G15Rik,AV011172,Mef2	--	--	--	--	--	--	--	--	--	Mef2c
26321200	chr13	83661050	83662862	Tnnt2	Here we show that Ldb1 is a central regulator of genome organization in cardiac progenitor cells, which is crucial for cardiac lineage differentiation and heart development. We demonstrate that Ldb1 binds to the key regulator of cardiac progenitors, Isl1, and protects it from degradation.Furthermore, the Isl1/Ldb1 complex promotes longrange enhancer-promoter interactions at the loci of the core cardiac transcription factors Mef2c and Hand2. Chromosome conformation capture followed by sequencing identified specific Ldb1-mediated interactions of the Isl1/Ldb1 responsive Mef2c anterior heart field enhancer with genes that play key roles in cardiac progenitor cell function and cardiovascular development. Importantly, the expression of these genes was downregulated upon Ldb1 depletion and Isl1/Ldb1 haplodeficiency. In conclusion,the Isl1/Ldb1 complex orchestrates a network for heart-specific transcriptional regulation and coordination in three-dimensional space during cardiogenesis.	mouse	epithelial tissue	Low throughput	The Isl1/Ldb1 Complex Orchestrates Genome-wide Chromatin Organization to Instruct Differentiation of Multipotent Cardiac Progenitors	否	--	Heart Failure	embryonic stem cell	E_02_0855	3C-qPCR,3C-seq	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	Enhancer	3C-qPCR,3C-seq	--	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	5430401D19Rik,9930028G15Rik,AV011172,Mef2	--	--	--	--	--	--	--	--	--	Mef2c
26321200	chr13	83661050	83662862	Tbx1	Here we show that Ldb1 is a central regulator of genome organization in cardiac progenitor cells, which is crucial for cardiac lineage differentiation and heart development. We demonstrate that Ldb1 binds to the key regulator of cardiac progenitors, Isl1, and protects it from degradation.Furthermore, the Isl1/Ldb1 complex promotes longrange enhancer-promoter interactions at the loci of the core cardiac transcription factors Mef2c and Hand2. Chromosome conformation capture followed by sequencing identified specific Ldb1-mediated interactions of the Isl1/Ldb1 responsive Mef2c anterior heart field enhancer with genes that play key roles in cardiac progenitor cell function and cardiovascular development. Importantly, the expression of these genes was downregulated upon Ldb1 depletion and Isl1/Ldb1 haplodeficiency. In conclusion,the Isl1/Ldb1 complex orchestrates a network for heart-specific transcriptional regulation and coordination in three-dimensional space during cardiogenesis.	mouse	epithelial tissue	Low throughput	The Isl1/Ldb1 Complex Orchestrates Genome-wide Chromatin Organization to Instruct Differentiation of Multipotent Cardiac Progenitors	否	--	Heart Failure	embryonic stem cell	E_02_0855	3C-qPCR,3C-seq	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	Enhancer	3C-qPCR,3C-seq	--	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	5430401D19Rik,9930028G15Rik,AV011172,Mef2	--	--	--	--	--	--	--	--	--	Mef2c
26321200	chr13	83661050	83662862	Fgf10	Here we show that Ldb1 is a central regulator of genome organization in cardiac progenitor cells, which is crucial for cardiac lineage differentiation and heart development. We demonstrate that Ldb1 binds to the key regulator of cardiac progenitors, Isl1, and protects it from degradation.Furthermore, the Isl1/Ldb1 complex promotes longrange enhancer-promoter interactions at the loci of the core cardiac transcription factors Mef2c and Hand2. Chromosome conformation capture followed by sequencing identified specific Ldb1-mediated interactions of the Isl1/Ldb1 responsive Mef2c anterior heart field enhancer with genes that play key roles in cardiac progenitor cell function and cardiovascular development. Importantly, the expression of these genes was downregulated upon Ldb1 depletion and Isl1/Ldb1 haplodeficiency. In conclusion,the Isl1/Ldb1 complex orchestrates a network for heart-specific transcriptional regulation and coordination in three-dimensional space during cardiogenesis.	mouse	epithelial tissue	Low throughput	The Isl1/Ldb1 Complex Orchestrates Genome-wide Chromatin Organization to Instruct Differentiation of Multipotent Cardiac Progenitors	否	--	Heart Failure	embryonic stem cell	E_02_0855	3C-qPCR,3C-seq	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	Enhancer	3C-qPCR,3C-seq	--	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	5430401D19Rik,9930028G15Rik,AV011172,Mef2	--	--	--	--	--	--	--	--	--	Mef2c
26321200	chr13	83661050	83662862	Nkx2-5	Here we show that Ldb1 is a central regulator of genome organization in cardiac progenitor cells, which is crucial for cardiac lineage differentiation and heart development. We demonstrate that Ldb1 binds to the key regulator of cardiac progenitors, Isl1, and protects it from degradation.Furthermore, the Isl1/Ldb1 complex promotes longrange enhancer-promoter interactions at the loci of the core cardiac transcription factors Mef2c and Hand2. Chromosome conformation capture followed by sequencing identified specific Ldb1-mediated interactions of the Isl1/Ldb1 responsive Mef2c anterior heart field enhancer with genes that play key roles in cardiac progenitor cell function and cardiovascular development. Importantly, the expression of these genes was downregulated upon Ldb1 depletion and Isl1/Ldb1 haplodeficiency. In conclusion,the Isl1/Ldb1 complex orchestrates a network for heart-specific transcriptional regulation and coordination in three-dimensional space during cardiogenesis.	mouse	epithelial tissue	Low throughput	The Isl1/Ldb1 Complex Orchestrates Genome-wide Chromatin Organization to Instruct Differentiation of Multipotent Cardiac Progenitors	否	--	Heart Failure	embryonic stem cell	E_02_0855	3C-qPCR,3C-seq	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	Enhancer	3C-qPCR,3C-seq	--	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	5430401D19Rik,9930028G15Rik,AV011172,Mef2	--	--	--	--	--	--	--	--	--	Mef2c
26321200	chr13	83661050	83662862	Tbx5	Here we show that Ldb1 is a central regulator of genome organization in cardiac progenitor cells, which is crucial for cardiac lineage differentiation and heart development. We demonstrate that Ldb1 binds to the key regulator of cardiac progenitors, Isl1, and protects it from degradation.Furthermore, the Isl1/Ldb1 complex promotes longrange enhancer-promoter interactions at the loci of the core cardiac transcription factors Mef2c and Hand2. Chromosome conformation capture followed by sequencing identified specific Ldb1-mediated interactions of the Isl1/Ldb1 responsive Mef2c anterior heart field enhancer with genes that play key roles in cardiac progenitor cell function and cardiovascular development. Importantly, the expression of these genes was downregulated upon Ldb1 depletion and Isl1/Ldb1 haplodeficiency. In conclusion,the Isl1/Ldb1 complex orchestrates a network for heart-specific transcriptional regulation and coordination in three-dimensional space during cardiogenesis.	mouse	epithelial tissue	Low throughput	The Isl1/Ldb1 Complex Orchestrates Genome-wide Chromatin Organization to Instruct Differentiation of Multipotent Cardiac Progenitors	否	--	Heart Failure	embryonic stem cell	E_02_0855	3C-qPCR,3C-seq	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	Enhancer	3C-qPCR,3C-seq	--	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	5430401D19Rik,9930028G15Rik,AV011172,Mef2	--	--	--	--	--	--	--	--	--	Mef2c
26321200	chr13	83661050	83662862	Hand1	Here we show that Ldb1 is a central regulator of genome organization in cardiac progenitor cells, which is crucial for cardiac lineage differentiation and heart development. We demonstrate that Ldb1 binds to the key regulator of cardiac progenitors, Isl1, and protects it from degradation.Furthermore, the Isl1/Ldb1 complex promotes longrange enhancer-promoter interactions at the loci of the core cardiac transcription factors Mef2c and Hand2. Chromosome conformation capture followed by sequencing identified specific Ldb1-mediated interactions of the Isl1/Ldb1 responsive Mef2c anterior heart field enhancer with genes that play key roles in cardiac progenitor cell function and cardiovascular development. Importantly, the expression of these genes was downregulated upon Ldb1 depletion and Isl1/Ldb1 haplodeficiency. In conclusion,the Isl1/Ldb1 complex orchestrates a network for heart-specific transcriptional regulation and coordination in three-dimensional space during cardiogenesis.	mouse	epithelial tissue	Low throughput	The Isl1/Ldb1 Complex Orchestrates Genome-wide Chromatin Organization to Instruct Differentiation of Multipotent Cardiac Progenitors	否	--	Heart Failure	embryonic stem cell	E_02_0855	3C-qPCR,3C-seq	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	Enhancer	3C-qPCR,3C-seq	--	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	5430401D19Rik,9930028G15Rik,AV011172,Mef2	--	--	--	--	--	--	--	--	--	Mef2c
26321200	chr13	83661050	83662862	Gata4	Here we show that Ldb1 is a central regulator of genome organization in cardiac progenitor cells, which is crucial for cardiac lineage differentiation and heart development. We demonstrate that Ldb1 binds to the key regulator of cardiac progenitors, Isl1, and protects it from degradation.Furthermore, the Isl1/Ldb1 complex promotes longrange enhancer-promoter interactions at the loci of the core cardiac transcription factors Mef2c and Hand2. Chromosome conformation capture followed by sequencing identified specific Ldb1-mediated interactions of the Isl1/Ldb1 responsive Mef2c anterior heart field enhancer with genes that play key roles in cardiac progenitor cell function and cardiovascular development. Importantly, the expression of these genes was downregulated upon Ldb1 depletion and Isl1/Ldb1 haplodeficiency. In conclusion,the Isl1/Ldb1 complex orchestrates a network for heart-specific transcriptional regulation and coordination in three-dimensional space during cardiogenesis.	mouse	epithelial tissue	Low throughput	The Isl1/Ldb1 Complex Orchestrates Genome-wide Chromatin Organization to Instruct Differentiation of Multipotent Cardiac Progenitors	否	--	Heart Failure	embryonic stem cell	E_02_0855	3C-qPCR,3C-seq	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	Enhancer	3C-qPCR,3C-seq	--	"Multiple promoter-interacting elements were detected in the Mef2c lo_x0002_cus, of which some showed a lower signal in Ldb1-deficientEBs (Figure 5B). Importantly, we observed interactions of the
AHF enhancer with the promoter area and with the 30 end of the Mef2c gene, which were decreased in Ldb1-deficient EBs(Figure 5B). 3C-qPCR experiments revealed a similar long-range
interaction pattern in WT versus Ldb1-/-EBs during the course of cardiac differentiation and in dissected SHF and hearts of E8–10.5 embryos, confirming the 3C-seq results (Figure 5C)."	5430401D19Rik,9930028G15Rik,AV011172,Mef2	--	--	--	--	--	--	--	--	--	Mef2c
26303528	chr8	84899088	84902859	DEK	Using biochemical affinity purification, we have identified the DEK oncoprotein as a critical factor that interacts with an essential upstream enhancer element of the EKLF promoter and exerts a positive effect on EKLF levels. This element also binds a core set of erythroid transcription factors, suggesting that DEK is part of a tissue-restricted enhanceosome that contains BMP4-dependent and -independent components. Together with local enrichment of properly coded histones and an open chromatin domain, optimal transcriptional activation of the EKLF locus can be established.	mouse	connective tissue	Low throughput	The DEK Oncoprotein Is a Critical Component of the EKLF/KLF1 Enhancer in Erythroid Cells	否	--	--	Murine erythroleukemia (MEL) line 745A,32DEpo1,293T	E_02_0856	ChIP	We have shown by cotransfection and in vivo analyses that the small 950-bp region adjacent to the EKLF transcription start site is sufficient for tissue-restricted expression and wished to address whether the epigenetic profile of this region supports its importance. Database perusal of modified histone H3 interactions within the critical 950-bp region of the EKLF promoter/enhancer during hematopoiesis shows that levels of the H3K4me1 active enhancer mark increase exactly in parallel with activation of EKLF expression during hematopoiesis , that is, low within the hematopoietic repopulating cells and in myeloid (CMP and MPP) progenitors but high in MEPs and erythroblasts	Enhancer	--	shRNA	Collectively, these studies demonstrate that DEK is required for EKLF expression and directly interacts in vitro and in vivo with its cognate site in the EKLF EHS1 Enhancer.	Eklf,Nan	--	--	--	--	--	--	--	--	--	Klf1
26303528	chr8	84899088	84902859	KLF1	Using biochemical affinity purification, we have identified the DEK oncoprotein as a critical factor that interacts with an essential upstream enhancer element of the EKLF promoter and exerts a positive effect on EKLF levels. This element also binds a core set of erythroid transcription factors, suggesting that DEK is part of a tissue-restricted enhanceosome that contains BMP4-dependent and -independent components. Together with local enrichment of properly coded histones and an open chromatin domain, optimal transcriptional activation of the EKLF locus can be established.	mouse	connective tissue	Low throughput	The DEK Oncoprotein Is a Critical Component of the EKLF/KLF1 Enhancer in Erythroid Cells	否	--	--	Murine erythroleukemia (MEL) line 745A,32DEpo1,293T	E_02_0856	ChIP	We have shown by cotransfection and in vivo analyses that the small 950-bp region adjacent to the EKLF transcription start site is sufficient for tissue-restricted expression and wished to address whether the epigenetic profile of this region supports its importance. Database perusal of modified histone H3 interactions within the critical 950-bp region of the EKLF promoter/enhancer during hematopoiesis shows that levels of the H3K4me1 active enhancer mark increase exactly in parallel with activation of EKLF expression during hematopoiesis , that is, low within the hematopoietic repopulating cells and in myeloid (CMP and MPP) progenitors but high in MEPs and erythroblasts	Enhancer	--	shRNA	Collectively, these studies demonstrate that DEK is required for EKLF expression and directly interacts in vitro and in vivo with its cognate site in the EKLF EHS1 Enhancer.	Eklf,Nan	--	--	--	--	--	--	--	--	--	Klf1
26303528	chr8	84899088	84902859	BMP4	Using biochemical affinity purification, we have identified the DEK oncoprotein as a critical factor that interacts with an essential upstream enhancer element of the EKLF promoter and exerts a positive effect on EKLF levels. This element also binds a core set of erythroid transcription factors, suggesting that DEK is part of a tissue-restricted enhanceosome that contains BMP4-dependent and -independent components. Together with local enrichment of properly coded histones and an open chromatin domain, optimal transcriptional activation of the EKLF locus can be established.	mouse	connective tissue	Low throughput	The DEK Oncoprotein Is a Critical Component of the EKLF/KLF1 Enhancer in Erythroid Cells	否	--	--	Murine erythroleukemia (MEL) line 745A,32DEpo1,293T	E_02_0856	ChIP	We have shown by cotransfection and in vivo analyses that the small 950-bp region adjacent to the EKLF transcription start site is sufficient for tissue-restricted expression and wished to address whether the epigenetic profile of this region supports its importance. Database perusal of modified histone H3 interactions within the critical 950-bp region of the EKLF promoter/enhancer during hematopoiesis shows that levels of the H3K4me1 active enhancer mark increase exactly in parallel with activation of EKLF expression during hematopoiesis , that is, low within the hematopoietic repopulating cells and in myeloid (CMP and MPP) progenitors but high in MEPs and erythroblasts	Enhancer	--	shRNA	Collectively, these studies demonstrate that DEK is required for EKLF expression and directly interacts in vitro and in vivo with its cognate site in the EKLF EHS1 Enhancer.	Eklf,Nan	--	--	--	--	--	--	--	--	--	Klf1
26303528	chr8	84899088	84902859	GATA1	Using biochemical affinity purification, we have identified the DEK oncoprotein as a critical factor that interacts with an essential upstream enhancer element of the EKLF promoter and exerts a positive effect on EKLF levels. This element also binds a core set of erythroid transcription factors, suggesting that DEK is part of a tissue-restricted enhanceosome that contains BMP4-dependent and -independent components. Together with local enrichment of properly coded histones and an open chromatin domain, optimal transcriptional activation of the EKLF locus can be established.	mouse	connective tissue	Low throughput	The DEK Oncoprotein Is a Critical Component of the EKLF/KLF1 Enhancer in Erythroid Cells	否	--	--	Murine erythroleukemia (MEL) line 745A,32DEpo1,293T	E_02_0856	ChIP	We have shown by cotransfection and in vivo analyses that the small 950-bp region adjacent to the EKLF transcription start site is sufficient for tissue-restricted expression and wished to address whether the epigenetic profile of this region supports its importance. Database perusal of modified histone H3 interactions within the critical 950-bp region of the EKLF promoter/enhancer during hematopoiesis shows that levels of the H3K4me1 active enhancer mark increase exactly in parallel with activation of EKLF expression during hematopoiesis , that is, low within the hematopoietic repopulating cells and in myeloid (CMP and MPP) progenitors but high in MEPs and erythroblasts	Enhancer	--	shRNA	Collectively, these studies demonstrate that DEK is required for EKLF expression and directly interacts in vitro and in vivo with its cognate site in the EKLF EHS1 Enhancer.	Eklf,Nan	--	--	--	--	--	--	--	--	--	Klf1
26303528	chr8	84899088	84902859	GATA2	Using biochemical affinity purification, we have identified the DEK oncoprotein as a critical factor that interacts with an essential upstream enhancer element of the EKLF promoter and exerts a positive effect on EKLF levels. This element also binds a core set of erythroid transcription factors, suggesting that DEK is part of a tissue-restricted enhanceosome that contains BMP4-dependent and -independent components. Together with local enrichment of properly coded histones and an open chromatin domain, optimal transcriptional activation of the EKLF locus can be established.	mouse	connective tissue	Low throughput	The DEK Oncoprotein Is a Critical Component of the EKLF/KLF1 Enhancer in Erythroid Cells	否	--	--	Murine erythroleukemia (MEL) line 745A,32DEpo1,293T	E_02_0856	ChIP	We have shown by cotransfection and in vivo analyses that the small 950-bp region adjacent to the EKLF transcription start site is sufficient for tissue-restricted expression and wished to address whether the epigenetic profile of this region supports its importance. Database perusal of modified histone H3 interactions within the critical 950-bp region of the EKLF promoter/enhancer during hematopoiesis shows that levels of the H3K4me1 active enhancer mark increase exactly in parallel with activation of EKLF expression during hematopoiesis , that is, low within the hematopoietic repopulating cells and in myeloid (CMP and MPP) progenitors but high in MEPs and erythroblasts	Enhancer	--	shRNA	Collectively, these studies demonstrate that DEK is required for EKLF expression and directly interacts in vitro and in vivo with its cognate site in the EKLF EHS1 Enhancer.	Eklf,Nan	--	--	--	--	--	--	--	--	--	Klf1
26303528	chr8	84899088	84902859	SMAD5	Using biochemical affinity purification, we have identified the DEK oncoprotein as a critical factor that interacts with an essential upstream enhancer element of the EKLF promoter and exerts a positive effect on EKLF levels. This element also binds a core set of erythroid transcription factors, suggesting that DEK is part of a tissue-restricted enhanceosome that contains BMP4-dependent and -independent components. Together with local enrichment of properly coded histones and an open chromatin domain, optimal transcriptional activation of the EKLF locus can be established.	mouse	connective tissue	Low throughput	The DEK Oncoprotein Is a Critical Component of the EKLF/KLF1 Enhancer in Erythroid Cells	否	--	--	Murine erythroleukemia (MEL) line 745A,32DEpo1,293T	E_02_0856	ChIP	We have shown by cotransfection and in vivo analyses that the small 950-bp region adjacent to the EKLF transcription start site is sufficient for tissue-restricted expression and wished to address whether the epigenetic profile of this region supports its importance. Database perusal of modified histone H3 interactions within the critical 950-bp region of the EKLF promoter/enhancer during hematopoiesis shows that levels of the H3K4me1 active enhancer mark increase exactly in parallel with activation of EKLF expression during hematopoiesis , that is, low within the hematopoietic repopulating cells and in myeloid (CMP and MPP) progenitors but high in MEPs and erythroblasts	Enhancer	--	shRNA	Collectively, these studies demonstrate that DEK is required for EKLF expression and directly interacts in vitro and in vivo with its cognate site in the EKLF EHS1 Enhancer.	Eklf,Nan	--	--	--	--	--	--	--	--	--	Klf1
26300977	chr7	114541370	114542201	FOXP2	A chromosomal rearrangement in a child with severe speech and language disorder separates FOXP2 from a functional enhancer.	human		Low throughput	A chromosomal rearrangement in a child with severe speech and language disorder separates FOXP2 from a functional enhancer	不相关	--	--	HEK-293,SK-N-MC	E_02_0857	Luciferase Reporter Assay	To test whether these regions could act as Enhancer elements we cloned them into a reporter construct in front of a minimal promoter and luciferase reporter gene.Element 1, which had multiple chromatin signatures characteristic of an enhancer, was able to act as a functional enhancer in both cell-lines (Fig. 1d).In HEK293 cells we observed a 3 fold increase of luciferase expression in comparison to the empty vector control.In SK-N-MC cells the luciferase expression increased nearly 7 fold as compared to the control. 	Enhancer	--	Luciferase Reporter Assay	To test whether these regions could act as Enhancer elements we cloned them into a reporter construct in front of a minimal promoter and luciferase reporter gene.Element 1, which had multiple chromatin signatures characteristic of an enhancer, was able to act as a functional enhancer in both cell-lines (Fig. 1d).In HEK293 cells we observed a 3 fold increase of luciferase expression in comparison to the empty vector control.In SK-N-MC cells the luciferase expression increased nearly 7 fold as compared to the control. 	CAGH44,SPCH1,TNRC10	--	--	--	--	--	--	--	--	--	FOXP2
26229090	chr3	186938165	186940165	CCND1	This method detects rearrangements involving known cancer genes, including CCND1, BCL2, MYC, PDCD1LG2, NOTCH1, CIITA, and SGK1, as well as novel enhancer duplication events of likely oncogenic significance. 	human		Low+High throughput	Detection of Enhancer-Associated Rearrangements Reveals Mechanisms of Oncogene Dysregulation in Bcell Lymphoma 	相关	--	B-Cell Lymphoma	Lymphoma Cell	E_02_0858	ChIP-seq,3C,qRT-PCR	"This highlighted a known BCL6-interacting Enhancer region (6,16,17) 150-250 upstream of BCL6 (SE1),which overlaps the alternate breakpoint region,a recurrent site of BCL6 locus rearrangements (15). It also revealed a second Super-Enhancer overlapping the HGB-04 duplication at ?350 (SE2),and a third such region at ?500 (SE3).We used chromosome conformation capture (3C) analysis of GCB-DLBCL lymphoma cell lines (Supplementary Fig. S3A) to confirm looping of elements from super-enhancer regions to the BCL6 promoter, consistent with roles in activating this oncogene. Intriguingly, our PMBL case, HGB-04, showed a distinct acetylation pattern across these regions, with only the duplicated enhancer region, SE2, showing strong acetylation.
In both cases, we detected the expected interactions between the BCL6 and MYC promoters and candidate enhancers in their native locus (Fig. 5C-D). We then used the same enhancer primers to measure interactions with the opposite gene promoter. We detected strong interactions between the MYC promoter and elements within the BCL6 SE1 and SE2 regions in HGB-07, but no such interactions in the non-rearranged tumor, HGB-06."	Super-Enhancer	3C	qRT-PCR	"This highlighted a known BCL6-interacting Enhancer region (6,16,17) 150-250 upstream of BCL6 (SE1),which overlaps the alternate breakpoint region,a recurrent site of BCL6 locus rearrangements (15). It also revealed a second Super-Enhancer overlapping the HGB-04 duplication at ?350 (SE2),and a third such region at ?500 (SE3).We used chromosome conformation capture (3C) analysis of GCB-DLBCL lymphoma cell lines (Supplementary Fig. S3A) to confirm looping of elements from super-enhancer regions to the BCL6 promoter, consistent with roles in activating this oncogene. Intriguingly, our PMBL case, HGB-04, showed a distinct acetylation pattern across these regions, with only the duplicated enhancer region, SE2, showing strong acetylation.
In both cases, we detected the expected interactions between the BCL6 and MYC promoters and candidate enhancers in their native locus (Fig. 5C-D). We then used the same enhancer primers to measure interactions with the opposite gene promoter. We detected strong interactions between the MYC promoter and elements within the BCL6 SE1 and SE2 regions in HGB-07, but no such interactions in the non-rearranged tumor, HGB-06."	BCL5A,BCL6,LAZ3,ZBTB27,ZNF51	--	--	--	MEF2B	RSRFR2	ChIP-Seq	Rather, we observed strong, focal MEF2B binding at acetylated elements within BCL6 super-enhancer regions, including four sites in SE1, one in SE2, and two in SE3 (Fig. 3C). ChIP-Seq analysis in the Jeko-1 MCL line revealed a specific increase in H3K27ac at MEF2B binding sites in MEF2B transgene-expressing cells, but not at intervening elements within the BCL6 super-enhancers (Fig. 3E).These data support a direct role for MEF2B in the activation of enhancers that drive BCL6 expression in human lymphomas. 	--	--	BCL6
26214589	chr10	64737032	64737909	EGR2	EWSR1-FLI1 preferentially bound to the A risk allele,which increased global and allele-specific EGR2 expression.	human		Low+High throughput	Chimeric EWSR1-FLI1 regulates the Ewing sarcoma susceptibility gene EGR2 via a GGAA microsatellite	相关	--	Ewing Sarcoma	embryonic stem cell	E_02_0859	ChIP-seq,Luciferase Reporter Assay	We observed activating chromatin marks, signals for formaldehyde-assisted isolation of regulatory elements (FAIRE) and/or DNaseI hypersensitivity at five main loci: two loci corresponding to known EGR2 regulatory elements (MSE (myelinating Schwann cell enhancer) 30 and BoneE (bone enhancer) (unpublished data); Supplementary Fig. 8), one to the ADO promoter, and two to GGAA microsatellites (mSat1 and mSat2) that overlapped with EWSR1-FLI1 ChIP-Seq signals (Fig. 3a). Luciferase reporter assays indicated that BoneE and MSE had no or weak activity in Ewing sarcoma, respectively.	Enhancer	--	ChIP-seq,Luciferase Reporter Assay	We observed activating chromatin marks, signals for formaldehyde-assisted isolation of regulatory elements (FAIRE) and/or DNaseI hypersensitivity at five main loci: two loci corresponding to known EGR2 regulatory elements (MSE (myelinating Schwann cell enhancer) 30 and BoneE (bone enhancer) (unpublished data); Supplementary Fig. 8), one to the ADO promoter, and two to GGAA microsatellites (mSat1 and mSat2) that overlapped with EWSR1-FLI1 ChIP-Seq signals (Fig. 3a). Luciferase reporter assays indicated that BoneE and MSE had no or weak activity in Ewing sarcoma, respectively.	AT591,CHN1,CMT1D,CMT4E,KROX20	--	--	--	EWSR1	EWS,EWS-FLI1,bK984G1.4	qRT-PCR	ChIP efficacy was validated by qRT-PCR using a CCND1 EWSR1-FLI1 binding site.	--	--	EGR2 
26214525	chr1	214150511	214151337	GATA2	We identified a putative enhancer element upstream of the key lymphatic transcriptional regulator PROX1 that is bound by GATA2, and the transcription factors FOXC2 and NFATC1.	human		Low+High throughput	GATA2 is required for lymphatic vessel valve development and maintenance	相关	--	Lymphedema	K-562 CELL	E_02_0860	ChIP-seq,Luciferase Reporter Assay	The –11 kb element was also cloned distally into the enhancer site of pGL4.12, together with a subcloned region of the Prox1 +4.5 kb element (containing GATA sites 4 and 5, see Methods for details) acting as a promoter. This addition resulted in a significant increase in luciferase activity, demonstrating that the Prox1 –11 kb element is capable of acting as an enhancer (Figure 1D). 	Enhancer	--	Luciferase Reporter Assay	The –11 kb element was also cloned distally into the enhancer site of pGL4.12, together with a subcloned region of the Prox1 +4.5 kb element (containing GATA sites 4 and 5, see Methods for details) acting as a promoter. This addition resulted in a significant increase in luciferase activity, demonstrating that the Prox1 –11 kb element is capable of acting as an enhancer (Figure 1D). 	PROX1	--	--	--	GATA2,FOXC2,NFATC1	DCML,IMD21,MONOMAC,NFE1B,FKHL14,LD,MFH-1,MFH1,NF-ATC,NF-ATc1.2,NFAT2,NFATc	ChIP	ChIP demonstrates that GATA2, FOXC2, and NFATC1 ChIP at the PROX1 –11 kb enhancer in LECs and BECs, but not K-562 cells.	--	--	PROX1
26214525	chr1	214150511	214151337	FOXC2	We identified a putative enhancer element upstream of the key lymphatic transcriptional regulator PROX1 that is bound by GATA2, and the transcription factors FOXC2 and NFATC1.	human		Low+High throughput	GATA2 is required for lymphatic vessel valve development and maintenance	相关	--	Lymphedema	K-562 CELL	E_02_0860	ChIP-seq,Luciferase Reporter Assay	The –11 kb element was also cloned distally into the enhancer site of pGL4.12, together with a subcloned region of the Prox1 +4.5 kb element (containing GATA sites 4 and 5, see Methods for details) acting as a promoter. This addition resulted in a significant increase in luciferase activity, demonstrating that the Prox1 –11 kb element is capable of acting as an enhancer (Figure 1D). 	Enhancer	--	Luciferase Reporter Assay	The –11 kb element was also cloned distally into the enhancer site of pGL4.12, together with a subcloned region of the Prox1 +4.5 kb element (containing GATA sites 4 and 5, see Methods for details) acting as a promoter. This addition resulted in a significant increase in luciferase activity, demonstrating that the Prox1 –11 kb element is capable of acting as an enhancer (Figure 1D). 	PROX1	--	--	--	GATA2,FOXC2,NFATC1	DCML,IMD21,MONOMAC,NFE1B,FKHL14,LD,MFH-1,MFH1,NF-ATC,NF-ATc1.2,NFAT2,NFATc	ChIP	ChIP demonstrates that GATA2, FOXC2, and NFATC1 ChIP at the PROX1 –11 kb enhancer in LECs and BECs, but not K-562 cells.	--	--	PROX1
26214525	chr1	214150511	214151337	NFATC1	We identified a putative enhancer element upstream of the key lymphatic transcriptional regulator PROX1 that is bound by GATA2, and the transcription factors FOXC2 and NFATC1.	human		Low+High throughput	GATA2 is required for lymphatic vessel valve development and maintenance	相关	--	Lymphedema	K-562 CELL	E_02_0860	ChIP-seq,Luciferase Reporter Assay	The –11 kb element was also cloned distally into the enhancer site of pGL4.12, together with a subcloned region of the Prox1 +4.5 kb element (containing GATA sites 4 and 5, see Methods for details) acting as a promoter. This addition resulted in a significant increase in luciferase activity, demonstrating that the Prox1 –11 kb element is capable of acting as an enhancer (Figure 1D). 	Enhancer	--	Luciferase Reporter Assay	The –11 kb element was also cloned distally into the enhancer site of pGL4.12, together with a subcloned region of the Prox1 +4.5 kb element (containing GATA sites 4 and 5, see Methods for details) acting as a promoter. This addition resulted in a significant increase in luciferase activity, demonstrating that the Prox1 –11 kb element is capable of acting as an enhancer (Figure 1D). 	PROX1	--	--	--	GATA2,FOXC2,NFATC1	DCML,IMD21,MONOMAC,NFE1B,FKHL14,LD,MFH-1,MFH1,NF-ATC,NF-ATc1.2,NFAT2,NFATc	ChIP	ChIP demonstrates that GATA2, FOXC2, and NFATC1 ChIP at the PROX1 –11 kb enhancer in LECs and BECs, but not K-562 cells.	--	--	PROX1
26211970	chr8	81286250	81293977	PAG1	To determine whether these PREs were functional, LCLs were transfected with PAG1 promoter-driven luciferase reporter constructs. PRE3 acted as a transcriptional enhancer for PAG1 exclusively when it carried the rs2370615:C allergy predisposing allele, a variant in complete linkage disequilibrium with rs7009110.	human		Low+High throughput	Long-Range Modulation of PAG1 Expression by 8q21 Allergy Risk Variants	相关	rs7009110	National Institute of Allergy and Infectious Diseases	Lymphoblastoid cell lines	E_02_0861	ChIP-seq,Luciferase Reporter Assay,PCR,3C	PRE2 (A) or PRE3 (B) was cloned upstream of a PAG1 promoter driven luciferase reporter with and without the candidate causal SNPs.Our 3C studies provided evidence for allele--specific chromatin looping between PRE2 and PAG1. These results demonstrate that PRE3 acts as a transcriptional enhancer in the presence of the rs2370615:C allergy predisposing allele.	Enhancer	3C	Luciferase Reporter Assay	PRE2 (A) or PRE3 (B) was cloned upstream of a PAG1 promoter driven luciferase reporter with and without the candidate causal SNPs.Our 3C studies provided evidence for allele--specific chromatin looping between PRE2 and PAG1. These results demonstrate that PRE3 acts as a transcriptional enhancer in the presence of the rs2370615:C allergy predisposing allele.	CBP,PAG	--	--	--	NFKB1	CVID12,EBP-1,KBF1,NF-kB,NF-kB1,NF-kappa-B1,NF-kappaB,NFKB-p105,NFKB-p50,NFkappaB,p105,p50	ChIP-seq	Based on ENCODE ChIP-seq data for LCLs,17 two transcription factors (TFs) bind to PRE3 and overlap the putative functional variant rs2370615: the RelA (or p65[MIM: 164014]) subunit of the nuclear factor (NF-)TF,which is critical for innate and adaptive immune re_x0002_sponses,22 and the POU domain class 2 transcription factor2 (POU2F2 or Oct-2 [MIM: 164176]),which regulates B-cell-specific genes.	81291879	ChIP-seq,Luciferase Reporter Assay,3C	PAG1
26166704	chr21	42668000	42671000	SMC5	Together with two other such SMC-containing complexes - cohesin and SMC5/SMC6 complexes	human	breast	Low+High throughput	Condensin I and II Complexes License Full Estrogen Receptor α-Dependent Enhancer Activation		--	--	breast cancer cell	E_02_0862	ChIP-seq,ChIP,GRO-seq	"Previous work from our lab and others established that a subgroup of ER-α/H3K27Ac co-bound enhancers (n=1,248,), exhibiting E2-upregulated eRNAs, high intensity of ER-α binding and close proximity to estrogen target genes, constitute the major E2-activated functional enhancers in MCF-7 cells, referred to as E2-induced ""active enhancers"" or “eRNA+ enhancers”. "	Enhancer	3C	ChIP-qPCR	Genome browser image showing the results of GRO-Seq and Pol II ChIP-Seq at TFF1 locus in the presence of condensin knockdown ( siNCAPG or siNCAPD3 ) vs siCTL transfected cell.	BCEI,D21S21,HP1.A,HPS2,pNR-2,pS2	--	--	--	--	--	--	--	--	--	TFF1
26166704	chr21	42668000	42671000	SMC6	Together with two other such SMC-containing complexes - cohesin and SMC5/SMC6 complexes	human	breast	Low+High throughput	Condensin I and II Complexes License Full Estrogen Receptor α-Dependent Enhancer Activation		--	--	breast cancer cell	E_02_0862	ChIP-seq,ChIP,GRO-seq	"Previous work from our lab and others established that a subgroup of ER-α/H3K27Ac co-bound enhancers (n=1,248,), exhibiting E2-upregulated eRNAs, high intensity of ER-α binding and close proximity to estrogen target genes, constitute the major E2-activated functional enhancers in MCF-7 cells, referred to as E2-induced ""active enhancers"" or “eRNA+ enhancers”. "	Enhancer	3C	ChIP-qPCR	Genome browser image showing the results of GRO-Seq and Pol II ChIP-Seq at TFF1 locus in the presence of condensin knockdown ( siNCAPG or siNCAPD3 ) vs siCTL transfected cell.	BCEI,D21S21,HP1.A,HPS2,pNR-2,pS2	--	--	--	--	--	--	--	--	--	TFF1
26163528	chr12	25090158	25090663	Id2	Here, we show that Id2 promotes ileal tumor initiation in Apc-deficient mice. Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc+/Δ716 (ApcΔ716) mice. Genetic depletion of Id2 in ApcΔ716 mice caused ∼80% reduction in the number of ileal polyps, but had little effect on tumor size. Notably, the lack of Id2 increased the number of apoptotic cells in the normal crypt epithelium of the mice. Furthermore, DNA microarray analysis revealed that the expression level of Max dimerization protein 1 (Mxd1), known as a c-Myc antagonist, was specifically increased by Id2 deletion in the ileal intestinal epithelium of ApcΔ716 mice. In contrast, the protein level of c-Myc, but not the mRNA level, was decreased by loss of Id2 in these mice. These results indicate that loss of Id2 inhibits tumor initiation by up-regulation of Mxd1 and down-regulation of c-Myc in ApcΔ716 mice.	mouse	epithelial tissue	Low throughput	Id2 deletion attenuates Apc-deficient ileal tumor formation	否	--	Colorectal Carcinoma	HCT 116,SW480	E_02_0863	Luciferase Reporter Assay,ChIP-PCR,ChIP	Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc+/Δ716 (ApcΔ716) mice. Genetic depletion of Id2 in ApcΔ716 mice caused ?80% reduction in the number of ileal polyps, but had little effect on tumor size.	Enhancer	--	Transgenic mice,RT-PCR,Western blot	Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc+/Δ716 (ApcΔ716) mice. Genetic depletion of Id2 in ApcΔ716 mice caused ?80% reduction in the number of ileal polyps, but had little effect on tumor size.	AI255428,C78922,Idb2,bHLHb26	--	--	--	Tcf4	5730422P05Rik,ASP-I2,E2-2,E2.2,ITF-2,ITF-2b,ITF2,ME2,MITF-2A,MITF-2B,SEF-2,SEF2,SEF2-1,TFE,Tcf-4,bHLHb19	ChIP-PCR,Luciferase Reporter Assay	To determine if mouse Id2 is also a target gene of Wnt signaling, we performed ChIP-PCR analysis of the binding of Tcf4 to the promoter region of the Id2 gene.Sequencing analysis revealed ten putative Tcf/Lef-binding consensus sequences in the Id2 promoter region spanning from ?4000 to ?1. As expected, Tcf4 bound to the DNA region spanning from ?3300 to ?3146 of the Id2 distal promoter.To test this Tcf4 binding region for enhancer activity, we conducted luciferase reporter assays using the constructs .The putative Id2-enhancer fragment significantly activated Wnt-signaling dependent transcription from the CMV minimal promoter in two colorectal cancer cell lines.	--	--	Id2
26163528	chr12	25090158	25090663	Apc	Here, we show that Id2 promotes ileal tumor initiation in Apc-deficient mice. Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc+/Δ716 (ApcΔ716) mice. Genetic depletion of Id2 in ApcΔ716 mice caused ∼80% reduction in the number of ileal polyps, but had little effect on tumor size. Notably, the lack of Id2 increased the number of apoptotic cells in the normal crypt epithelium of the mice. Furthermore, DNA microarray analysis revealed that the expression level of Max dimerization protein 1 (Mxd1), known as a c-Myc antagonist, was specifically increased by Id2 deletion in the ileal intestinal epithelium of ApcΔ716 mice. In contrast, the protein level of c-Myc, but not the mRNA level, was decreased by loss of Id2 in these mice. These results indicate that loss of Id2 inhibits tumor initiation by up-regulation of Mxd1 and down-regulation of c-Myc in ApcΔ716 mice.	mouse	epithelial tissue	Low throughput	Id2 deletion attenuates Apc-deficient ileal tumor formation	否	--	Colorectal Carcinoma	HCT 116,SW480	E_02_0863	Luciferase Reporter Assay,ChIP-PCR,ChIP	Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc+/Δ716 (ApcΔ716) mice. Genetic depletion of Id2 in ApcΔ716 mice caused ?80% reduction in the number of ileal polyps, but had little effect on tumor size.	Enhancer	--	Transgenic mice,RT-PCR,Western blot	Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc+/Δ716 (ApcΔ716) mice. Genetic depletion of Id2 in ApcΔ716 mice caused ?80% reduction in the number of ileal polyps, but had little effect on tumor size.	AI255428,C78922,Idb2,bHLHb26	--	--	--	Tcf4	5730422P05Rik,ASP-I2,E2-2,E2.2,ITF-2,ITF-2b,ITF2,ME2,MITF-2A,MITF-2B,SEF-2,SEF2,SEF2-1,TFE,Tcf-4,bHLHb19	ChIP-PCR,Luciferase Reporter Assay	To determine if mouse Id2 is also a target gene of Wnt signaling, we performed ChIP-PCR analysis of the binding of Tcf4 to the promoter region of the Id2 gene.Sequencing analysis revealed ten putative Tcf/Lef-binding consensus sequences in the Id2 promoter region spanning from ?4000 to ?1. As expected, Tcf4 bound to the DNA region spanning from ?3300 to ?3146 of the Id2 distal promoter.To test this Tcf4 binding region for enhancer activity, we conducted luciferase reporter assays using the constructs .The putative Id2-enhancer fragment significantly activated Wnt-signaling dependent transcription from the CMV minimal promoter in two colorectal cancer cell lines.	--	--	Id2
26163528	chr12	25090158	25090663	Mxd1	Here, we show that Id2 promotes ileal tumor initiation in Apc-deficient mice. Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc+/Δ716 (ApcΔ716) mice. Genetic depletion of Id2 in ApcΔ716 mice caused ∼80% reduction in the number of ileal polyps, but had little effect on tumor size. Notably, the lack of Id2 increased the number of apoptotic cells in the normal crypt epithelium of the mice. Furthermore, DNA microarray analysis revealed that the expression level of Max dimerization protein 1 (Mxd1), known as a c-Myc antagonist, was specifically increased by Id2 deletion in the ileal intestinal epithelium of ApcΔ716 mice. In contrast, the protein level of c-Myc, but not the mRNA level, was decreased by loss of Id2 in these mice. These results indicate that loss of Id2 inhibits tumor initiation by up-regulation of Mxd1 and down-regulation of c-Myc in ApcΔ716 mice.	mouse	epithelial tissue	Low throughput	Id2 deletion attenuates Apc-deficient ileal tumor formation	否	--	Colorectal Carcinoma	HCT 116,SW480	E_02_0863	Luciferase Reporter Assay,ChIP-PCR,ChIP	Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc+/Δ716 (ApcΔ716) mice. Genetic depletion of Id2 in ApcΔ716 mice caused ?80% reduction in the number of ileal polyps, but had little effect on tumor size.	Enhancer	--	Transgenic mice,RT-PCR,Western blot	Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc+/Δ716 (ApcΔ716) mice. Genetic depletion of Id2 in ApcΔ716 mice caused ?80% reduction in the number of ileal polyps, but had little effect on tumor size.	AI255428,C78922,Idb2,bHLHb26	--	--	--	Tcf4	5730422P05Rik,ASP-I2,E2-2,E2.2,ITF-2,ITF-2b,ITF2,ME2,MITF-2A,MITF-2B,SEF-2,SEF2,SEF2-1,TFE,Tcf-4,bHLHb19	ChIP-PCR,Luciferase Reporter Assay	To determine if mouse Id2 is also a target gene of Wnt signaling, we performed ChIP-PCR analysis of the binding of Tcf4 to the promoter region of the Id2 gene.Sequencing analysis revealed ten putative Tcf/Lef-binding consensus sequences in the Id2 promoter region spanning from ?4000 to ?1. As expected, Tcf4 bound to the DNA region spanning from ?3300 to ?3146 of the Id2 distal promoter.To test this Tcf4 binding region for enhancer activity, we conducted luciferase reporter assays using the constructs .The putative Id2-enhancer fragment significantly activated Wnt-signaling dependent transcription from the CMV minimal promoter in two colorectal cancer cell lines.	--	--	Id2
26163528	chr12	25090158	25090663	Tcf4	Here, we show that Id2 promotes ileal tumor initiation in Apc-deficient mice. Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc+/Δ716 (ApcΔ716) mice. Genetic depletion of Id2 in ApcΔ716 mice caused ∼80% reduction in the number of ileal polyps, but had little effect on tumor size. Notably, the lack of Id2 increased the number of apoptotic cells in the normal crypt epithelium of the mice. Furthermore, DNA microarray analysis revealed that the expression level of Max dimerization protein 1 (Mxd1), known as a c-Myc antagonist, was specifically increased by Id2 deletion in the ileal intestinal epithelium of ApcΔ716 mice. In contrast, the protein level of c-Myc, but not the mRNA level, was decreased by loss of Id2 in these mice. These results indicate that loss of Id2 inhibits tumor initiation by up-regulation of Mxd1 and down-regulation of c-Myc in ApcΔ716 mice.	mouse	epithelial tissue	Low throughput	Id2 deletion attenuates Apc-deficient ileal tumor formation	否	--	Colorectal Carcinoma	HCT 116,SW480	E_02_0863	Luciferase Reporter Assay,ChIP-PCR,ChIP	Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc+/Δ716 (ApcΔ716) mice. Genetic depletion of Id2 in ApcΔ716 mice caused ?80% reduction in the number of ileal polyps, but had little effect on tumor size.	Enhancer	--	Transgenic mice,RT-PCR,Western blot	Expression of Id2 was stimulated by Wnt signaling through the enhancer region of the Id2 promoter at the early stage of tumorigenesis in Apc+/Δ716 (ApcΔ716) mice. Genetic depletion of Id2 in ApcΔ716 mice caused ?80% reduction in the number of ileal polyps, but had little effect on tumor size.	AI255428,C78922,Idb2,bHLHb26	--	--	--	Tcf4	5730422P05Rik,ASP-I2,E2-2,E2.2,ITF-2,ITF-2b,ITF2,ME2,MITF-2A,MITF-2B,SEF-2,SEF2,SEF2-1,TFE,Tcf-4,bHLHb19	ChIP-PCR,Luciferase Reporter Assay	To determine if mouse Id2 is also a target gene of Wnt signaling, we performed ChIP-PCR analysis of the binding of Tcf4 to the promoter region of the Id2 gene.Sequencing analysis revealed ten putative Tcf/Lef-binding consensus sequences in the Id2 promoter region spanning from ?4000 to ?1. As expected, Tcf4 bound to the DNA region spanning from ?3300 to ?3146 of the Id2 distal promoter.To test this Tcf4 binding region for enhancer activity, we conducted luciferase reporter assays using the constructs .The putative Id2-enhancer fragment significantly activated Wnt-signaling dependent transcription from the CMV minimal promoter in two colorectal cancer cell lines.	--	--	Id2
26110280	chr14	50787449	50787634	Ccnb1ip1	The Ccnb1ip1 insulator showed enhancer-blocking activity in the luciferase assays and barrier activity in the colony formation assays. Further examination of the Ccnb1ip1 locus in other mammalian species revealed that the insulator and enhancer are highly conserved among a wide variety of species, and are located immediately upstream of the transcriptional start site of Ccnb1ip1. These newly identified cis-elements may be involved in transcriptional regulation of Ccnb1ip1, which is important in meiotic crossing-over and G2/M transition of the mitotic cell cycle.	mouse	connective tissue	Low throughput	An Insulator Element Located at the Cyclin B1 Interacting Protein 1 Gene Locus Is Highly Conserved among Mammalian Species	否	--	--	Cos7,NIH3T3,HeLa cell	E_02_0864	Luciferase Reporter Assay,ChIP,RT-PCR	PCR amplification of JF1 genomic DNA using several primer pairs targeted to differentially methylated regions identified a 1.8 kbp genomic segment that was present in the JF1 strain but absent in the B6 strain . Sequence analysis revealed that this 1.8kbp segment consisted of a 1,579 bp interval deleted in the B6 genome, and the remaining 220 bp interval present in the B6 genome but in an inverted orientation.	Enhancer	--	Luciferase Reporter Assay,ChIP,RT-PCR	We hypothesized the existence of an insulator-type element that prevents the spreadof DNA methylation within the1.8 k segment,and actually identified a 242- and a 185- fragments that were located adjacent to eachother and showed insulatorand Enhancer activities,respectively,in reporter assays. We designated these genomicregions as the Ccnb1ip1 insulator and the Ccnb1ip1Enhancer. The Ccnb1ip1 insulator showed Enhancer-blocking activity in the Luciferaseiferase assays andbarrieractivity in the colony formation assays. Further examination of the Ccnb1ip1locus in other mammalian speciesrevealed that the insulator and Enhancerare High throughput lyconserve damonga wide variety of species,and are located immediately upstream of the transcriptional start site of Ccnb1ip1.	Gm288,Hei10,mei4	--	--	--	--	--	--	--	--	--	Ccnb1ip1
26110280	chr14	50787449	50787634	Gapdh	The Ccnb1ip1 insulator showed enhancer-blocking activity in the luciferase assays and barrier activity in the colony formation assays. Further examination of the Ccnb1ip1 locus in other mammalian species revealed that the insulator and enhancer are highly conserved among a wide variety of species, and are located immediately upstream of the transcriptional start site of Ccnb1ip1. These newly identified cis-elements may be involved in transcriptional regulation of Ccnb1ip1, which is important in meiotic crossing-over and G2/M transition of the mitotic cell cycle.	mouse	connective tissue	Low throughput	An Insulator Element Located at the Cyclin B1 Interacting Protein 1 Gene Locus Is Highly Conserved among Mammalian Species	否	--	--	Cos7,NIH3T3,HeLa cell	E_02_0864	Luciferase Reporter Assay,ChIP,RT-PCR	PCR amplification of JF1 genomic DNA using several primer pairs targeted to differentially methylated regions identified a 1.8 kbp genomic segment that was present in the JF1 strain but absent in the B6 strain . Sequence analysis revealed that this 1.8kbp segment consisted of a 1,579 bp interval deleted in the B6 genome, and the remaining 220 bp interval present in the B6 genome but in an inverted orientation.	Enhancer	--	Luciferase Reporter Assay,ChIP,RT-PCR	We hypothesized the existence of an insulator-type element that prevents the spreadof DNA methylation within the1.8 k segment,and actually identified a 242- and a 185- fragments that were located adjacent to eachother and showed insulatorand Enhancer activities,respectively,in reporter assays. We designated these genomicregions as the Ccnb1ip1 insulator and the Ccnb1ip1Enhancer. The Ccnb1ip1 insulator showed Enhancer-blocking activity in the Luciferaseiferase assays andbarrieractivity in the colony formation assays. Further examination of the Ccnb1ip1locus in other mammalian speciesrevealed that the insulator and Enhancerare High throughput lyconserve damonga wide variety of species,and are located immediately upstream of the transcriptional start site of Ccnb1ip1.	Gm288,Hei10,mei4	--	--	--	--	--	--	--	--	--	Ccnb1ip1
26110280	chr14	50787449	50787634	CTCF	The Ccnb1ip1 insulator showed enhancer-blocking activity in the luciferase assays and barrier activity in the colony formation assays. Further examination of the Ccnb1ip1 locus in other mammalian species revealed that the insulator and enhancer are highly conserved among a wide variety of species, and are located immediately upstream of the transcriptional start site of Ccnb1ip1. These newly identified cis-elements may be involved in transcriptional regulation of Ccnb1ip1, which is important in meiotic crossing-over and G2/M transition of the mitotic cell cycle.	mouse	connective tissue	Low throughput	An Insulator Element Located at the Cyclin B1 Interacting Protein 1 Gene Locus Is Highly Conserved among Mammalian Species	否	--	--	Cos7,NIH3T3,HeLa cell	E_02_0864	Luciferase Reporter Assay,ChIP,RT-PCR	PCR amplification of JF1 genomic DNA using several primer pairs targeted to differentially methylated regions identified a 1.8 kbp genomic segment that was present in the JF1 strain but absent in the B6 strain . Sequence analysis revealed that this 1.8kbp segment consisted of a 1,579 bp interval deleted in the B6 genome, and the remaining 220 bp interval present in the B6 genome but in an inverted orientation.	Enhancer	--	Luciferase Reporter Assay,ChIP,RT-PCR	We hypothesized the existence of an insulator-type element that prevents the spreadof DNA methylation within the1.8 k segment,and actually identified a 242- and a 185- fragments that were located adjacent to eachother and showed insulatorand Enhancer activities,respectively,in reporter assays. We designated these genomicregions as the Ccnb1ip1 insulator and the Ccnb1ip1Enhancer. The Ccnb1ip1 insulator showed Enhancer-blocking activity in the Luciferaseiferase assays andbarrieractivity in the colony formation assays. Further examination of the Ccnb1ip1locus in other mammalian speciesrevealed that the insulator and Enhancerare High throughput lyconserve damonga wide variety of species,and are located immediately upstream of the transcriptional start site of Ccnb1ip1.	Gm288,Hei10,mei4	--	--	--	--	--	--	--	--	--	Ccnb1ip1
26110280	chr14	50787449	50787634	Parp2	The Ccnb1ip1 insulator showed enhancer-blocking activity in the luciferase assays and barrier activity in the colony formation assays. Further examination of the Ccnb1ip1 locus in other mammalian species revealed that the insulator and enhancer are highly conserved among a wide variety of species, and are located immediately upstream of the transcriptional start site of Ccnb1ip1. These newly identified cis-elements may be involved in transcriptional regulation of Ccnb1ip1, which is important in meiotic crossing-over and G2/M transition of the mitotic cell cycle.	mouse	connective tissue	Low throughput	An Insulator Element Located at the Cyclin B1 Interacting Protein 1 Gene Locus Is Highly Conserved among Mammalian Species	否	--	--	Cos7,NIH3T3,HeLa cell	E_02_0864	Luciferase Reporter Assay,ChIP,RT-PCR	PCR amplification of JF1 genomic DNA using several primer pairs targeted to differentially methylated regions identified a 1.8 kbp genomic segment that was present in the JF1 strain but absent in the B6 strain . Sequence analysis revealed that this 1.8kbp segment consisted of a 1,579 bp interval deleted in the B6 genome, and the remaining 220 bp interval present in the B6 genome but in an inverted orientation.	Enhancer	--	Luciferase Reporter Assay,ChIP,RT-PCR	We hypothesized the existence of an insulator-type element that prevents the spreadof DNA methylation within the1.8 k segment,and actually identified a 242- and a 185- fragments that were located adjacent to eachother and showed insulatorand Enhancer activities,respectively,in reporter assays. We designated these genomicregions as the Ccnb1ip1 insulator and the Ccnb1ip1Enhancer. The Ccnb1ip1 insulator showed Enhancer-blocking activity in the Luciferaseiferase assays andbarrieractivity in the colony formation assays. Further examination of the Ccnb1ip1locus in other mammalian speciesrevealed that the insulator and Enhancerare High throughput lyconserve damonga wide variety of species,and are located immediately upstream of the transcriptional start site of Ccnb1ip1.	Gm288,Hei10,mei4	--	--	--	--	--	--	--	--	--	Ccnb1ip1
26110280	chr14	50787449	50787634	OSGEP	The Ccnb1ip1 insulator showed enhancer-blocking activity in the luciferase assays and barrier activity in the colony formation assays. Further examination of the Ccnb1ip1 locus in other mammalian species revealed that the insulator and enhancer are highly conserved among a wide variety of species, and are located immediately upstream of the transcriptional start site of Ccnb1ip1. These newly identified cis-elements may be involved in transcriptional regulation of Ccnb1ip1, which is important in meiotic crossing-over and G2/M transition of the mitotic cell cycle.	mouse	connective tissue	Low throughput	An Insulator Element Located at the Cyclin B1 Interacting Protein 1 Gene Locus Is Highly Conserved among Mammalian Species	否	--	--	Cos7,NIH3T3,HeLa cell	E_02_0864	Luciferase Reporter Assay,ChIP,RT-PCR	PCR amplification of JF1 genomic DNA using several primer pairs targeted to differentially methylated regions identified a 1.8 kbp genomic segment that was present in the JF1 strain but absent in the B6 strain . Sequence analysis revealed that this 1.8kbp segment consisted of a 1,579 bp interval deleted in the B6 genome, and the remaining 220 bp interval present in the B6 genome but in an inverted orientation.	Enhancer	--	Luciferase Reporter Assay,ChIP,RT-PCR	We hypothesized the existence of an insulator-type element that prevents the spreadof DNA methylation within the1.8 k segment,and actually identified a 242- and a 185- fragments that were located adjacent to eachother and showed insulatorand Enhancer activities,respectively,in reporter assays. We designated these genomicregions as the Ccnb1ip1 insulator and the Ccnb1ip1Enhancer. The Ccnb1ip1 insulator showed Enhancer-blocking activity in the Luciferaseiferase assays andbarrieractivity in the colony formation assays. Further examination of the Ccnb1ip1locus in other mammalian speciesrevealed that the insulator and Enhancerare High throughput lyconserve damonga wide variety of species,and are located immediately upstream of the transcriptional start site of Ccnb1ip1.	Gm288,Hei10,mei4	--	--	--	--	--	--	--	--	--	Ccnb1ip1
26110280	chr14	50787449	50787634	APEX1	The Ccnb1ip1 insulator showed enhancer-blocking activity in the luciferase assays and barrier activity in the colony formation assays. Further examination of the Ccnb1ip1 locus in other mammalian species revealed that the insulator and enhancer are highly conserved among a wide variety of species, and are located immediately upstream of the transcriptional start site of Ccnb1ip1. These newly identified cis-elements may be involved in transcriptional regulation of Ccnb1ip1, which is important in meiotic crossing-over and G2/M transition of the mitotic cell cycle.	mouse	connective tissue	Low throughput	An Insulator Element Located at the Cyclin B1 Interacting Protein 1 Gene Locus Is Highly Conserved among Mammalian Species	否	--	--	Cos7,NIH3T3,HeLa cell	E_02_0864	Luciferase Reporter Assay,ChIP,RT-PCR	PCR amplification of JF1 genomic DNA using several primer pairs targeted to differentially methylated regions identified a 1.8 kbp genomic segment that was present in the JF1 strain but absent in the B6 strain . Sequence analysis revealed that this 1.8kbp segment consisted of a 1,579 bp interval deleted in the B6 genome, and the remaining 220 bp interval present in the B6 genome but in an inverted orientation.	Enhancer	--	Luciferase Reporter Assay,ChIP,RT-PCR	We hypothesized the existence of an insulator-type element that prevents the spreadof DNA methylation within the1.8 k segment,and actually identified a 242- and a 185- fragments that were located adjacent to eachother and showed insulatorand Enhancer activities,respectively,in reporter assays. We designated these genomicregions as the Ccnb1ip1 insulator and the Ccnb1ip1Enhancer. The Ccnb1ip1 insulator showed Enhancer-blocking activity in the Luciferaseiferase assays andbarrieractivity in the colony formation assays. Further examination of the Ccnb1ip1locus in other mammalian speciesrevealed that the insulator and Enhancerare High throughput lyconserve damonga wide variety of species,and are located immediately upstream of the transcriptional start site of Ccnb1ip1.	Gm288,Hei10,mei4	--	--	--	--	--	--	--	--	--	Ccnb1ip1
25810254	chr4	34888479	34889907	Cga	Moreover, histone H3 Lys 27 (H3K27) acetylation, which was found at both enhancer and promoter in wild-type cells, appeared to have been replaced by H3K27 trimethylation at the enhancer. Thus, the Cga eRNA mediates the physical interaction between these genomic regions and determines the chromatin structure of the proximal promoter to allow gene expression.	mouse	connective tissue	Low throughput	RNA transcribed from a distal enhancer is required for activating the chromatin at the promoter of the gonadotropin α-subunit gene	否	--	--	αT3-1 cell	E_02_0865	qPCR,ChIP,3C	Using quantitative PCR (qPCR) on DNase-treated reverse-transcribed RNA from a gonadotrope cell line, we amplified fragments between ?5300 and ?3872 bp upstream of the Cga TSS, which includes most of the reported enhancer.	Enhancer	3C	qPCR,ChIP	qPCR analysis confirmed the interaction of the distal enhancer regions (?6.7 to ?6.58 and ?4.9 to ?4.85 kbp) with the proximal Cga promoter in both the treated and untreated cells and,with greater frequency, in WT and eRNA-knockdown cells after normalization to the relative levels of the Fshβ chimeric fragment	CG-alpha,FSHA,GPHA1,GPHalpha,HCG,LHA,Tsha,aGSU,alpha-GSU,alphaGSU,alphaSU	--	--	--	--	--	--	--	--	--	Cga
25810254	chr4	34888479	34889907	Pitx1	Moreover, histone H3 Lys 27 (H3K27) acetylation, which was found at both enhancer and promoter in wild-type cells, appeared to have been replaced by H3K27 trimethylation at the enhancer. Thus, the Cga eRNA mediates the physical interaction between these genomic regions and determines the chromatin structure of the proximal promoter to allow gene expression.	mouse	connective tissue	Low throughput	RNA transcribed from a distal enhancer is required for activating the chromatin at the promoter of the gonadotropin α-subunit gene	否	--	--	αT3-1 cell	E_02_0865	qPCR,ChIP,3C	Using quantitative PCR (qPCR) on DNase-treated reverse-transcribed RNA from a gonadotrope cell line, we amplified fragments between ?5300 and ?3872 bp upstream of the Cga TSS, which includes most of the reported enhancer.	Enhancer	3C	qPCR,ChIP	qPCR analysis confirmed the interaction of the distal enhancer regions (?6.7 to ?6.58 and ?4.9 to ?4.85 kbp) with the proximal Cga promoter in both the treated and untreated cells and,with greater frequency, in WT and eRNA-knockdown cells after normalization to the relative levels of the Fshβ chimeric fragment	CG-alpha,FSHA,GPHA1,GPHalpha,HCG,LHA,Tsha,aGSU,alpha-GSU,alphaGSU,alphaSU	--	--	--	--	--	--	--	--	--	Cga
25810254	chr4	34888479	34889907	CHD1	Moreover, histone H3 Lys 27 (H3K27) acetylation, which was found at both enhancer and promoter in wild-type cells, appeared to have been replaced by H3K27 trimethylation at the enhancer. Thus, the Cga eRNA mediates the physical interaction between these genomic regions and determines the chromatin structure of the proximal promoter to allow gene expression.	mouse	connective tissue	Low throughput	RNA transcribed from a distal enhancer is required for activating the chromatin at the promoter of the gonadotropin α-subunit gene	否	--	--	αT3-1 cell	E_02_0865	qPCR,ChIP,3C	Using quantitative PCR (qPCR) on DNase-treated reverse-transcribed RNA from a gonadotrope cell line, we amplified fragments between ?5300 and ?3872 bp upstream of the Cga TSS, which includes most of the reported enhancer.	Enhancer	3C	qPCR,ChIP	qPCR analysis confirmed the interaction of the distal enhancer regions (?6.7 to ?6.58 and ?4.9 to ?4.85 kbp) with the proximal Cga promoter in both the treated and untreated cells and,with greater frequency, in WT and eRNA-knockdown cells after normalization to the relative levels of the Fshβ chimeric fragment	CG-alpha,FSHA,GPHA1,GPHalpha,HCG,LHA,Tsha,aGSU,alpha-GSU,alphaGSU,alphaSU	--	--	--	--	--	--	--	--	--	Cga
25810254	chr4	34888479	34889907	Pitx2	Moreover, histone H3 Lys 27 (H3K27) acetylation, which was found at both enhancer and promoter in wild-type cells, appeared to have been replaced by H3K27 trimethylation at the enhancer. Thus, the Cga eRNA mediates the physical interaction between these genomic regions and determines the chromatin structure of the proximal promoter to allow gene expression.	mouse	connective tissue	Low throughput	RNA transcribed from a distal enhancer is required for activating the chromatin at the promoter of the gonadotropin α-subunit gene	否	--	--	αT3-1 cell	E_02_0865	qPCR,ChIP,3C	Using quantitative PCR (qPCR) on DNase-treated reverse-transcribed RNA from a gonadotrope cell line, we amplified fragments between ?5300 and ?3872 bp upstream of the Cga TSS, which includes most of the reported enhancer.	Enhancer	3C	qPCR,ChIP	qPCR analysis confirmed the interaction of the distal enhancer regions (?6.7 to ?6.58 and ?4.9 to ?4.85 kbp) with the proximal Cga promoter in both the treated and untreated cells and,with greater frequency, in WT and eRNA-knockdown cells after normalization to the relative levels of the Fshβ chimeric fragment	CG-alpha,FSHA,GPHA1,GPHalpha,HCG,LHA,Tsha,aGSU,alpha-GSU,alphaGSU,alphaSU	--	--	--	--	--	--	--	--	--	Cga
25810254	chr4	34888479	34889907	Rplp0	Moreover, histone H3 Lys 27 (H3K27) acetylation, which was found at both enhancer and promoter in wild-type cells, appeared to have been replaced by H3K27 trimethylation at the enhancer. Thus, the Cga eRNA mediates the physical interaction between these genomic regions and determines the chromatin structure of the proximal promoter to allow gene expression.	mouse	connective tissue	Low throughput	RNA transcribed from a distal enhancer is required for activating the chromatin at the promoter of the gonadotropin α-subunit gene	否	--	--	αT3-1 cell	E_02_0865	qPCR,ChIP,3C	Using quantitative PCR (qPCR) on DNase-treated reverse-transcribed RNA from a gonadotrope cell line, we amplified fragments between ?5300 and ?3872 bp upstream of the Cga TSS, which includes most of the reported enhancer.	Enhancer	3C	qPCR,ChIP	qPCR analysis confirmed the interaction of the distal enhancer regions (?6.7 to ?6.58 and ?4.9 to ?4.85 kbp) with the proximal Cga promoter in both the treated and untreated cells and,with greater frequency, in WT and eRNA-knockdown cells after normalization to the relative levels of the Fshβ chimeric fragment	CG-alpha,FSHA,GPHA1,GPHalpha,HCG,LHA,Tsha,aGSU,alpha-GSU,alphaGSU,alphaSU	--	--	--	--	--	--	--	--	--	Cga
25810254	chr4	34888479	34889907	Gapdh	Moreover, histone H3 Lys 27 (H3K27) acetylation, which was found at both enhancer and promoter in wild-type cells, appeared to have been replaced by H3K27 trimethylation at the enhancer. Thus, the Cga eRNA mediates the physical interaction between these genomic regions and determines the chromatin structure of the proximal promoter to allow gene expression.	mouse	connective tissue	Low throughput	RNA transcribed from a distal enhancer is required for activating the chromatin at the promoter of the gonadotropin α-subunit gene	否	--	--	αT3-1 cell	E_02_0865	qPCR,ChIP,3C	Using quantitative PCR (qPCR) on DNase-treated reverse-transcribed RNA from a gonadotrope cell line, we amplified fragments between ?5300 and ?3872 bp upstream of the Cga TSS, which includes most of the reported enhancer.	Enhancer	3C	qPCR,ChIP	qPCR analysis confirmed the interaction of the distal enhancer regions (?6.7 to ?6.58 and ?4.9 to ?4.85 kbp) with the proximal Cga promoter in both the treated and untreated cells and,with greater frequency, in WT and eRNA-knockdown cells after normalization to the relative levels of the Fshβ chimeric fragment	CG-alpha,FSHA,GPHA1,GPHalpha,HCG,LHA,Tsha,aGSU,alpha-GSU,alphaGSU,alphaSU	--	--	--	--	--	--	--	--	--	Cga
25804738	chr3	127641624	127642545	Foxa1	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	mouse	epithelial tissue	Low+High throughput	Genome-wide characterisation of Foxa1 binding sites reveals several mechanisms for regulating neuronal differentiation in midbrain dopamine cells	否	--	--	embryonic stem cell	E_02_0866	ChIP-qPCR,ChIP-seq,RNA-seq	A conserved 447?bp genomic fragment within this?Neurog2?3′ Foxa1-bound peak showed enhancer activity specifically in midbrain floor plate and also in the cerebral cortex, when analysed in mouse transient transgenic experiments at E12.5	Enhancer	--	Transgenic mice,qRT-PCR	By contrast, the identification of a Foxa1-bound peak downstream of Neurog2 coding sequences (Neurog2 3′) raised the possibility that Foxa2 might directly activate Neurog2 expression through this putative Enhancer region in embryonic mDA progenitors.	Atoh4,Math4A,bHLHa8,ngn-2,ngn2	--	--	--	Otx2,Foxa1,Foxa2	E130306E05Rik,HNF3-beta,HNF3beta,Hnf-3b,Hnf3b,Tcf-3b,Tcf3b,Hnf-3a,Hnf3a,Tcf-3a,Tcf3a	ChIP-seq,RNA-seq	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	--	--	Neurog2
25804738	chr3	127641624	127642545	Foxa2	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	mouse	epithelial tissue	Low+High throughput	Genome-wide characterisation of Foxa1 binding sites reveals several mechanisms for regulating neuronal differentiation in midbrain dopamine cells	否	--	--	embryonic stem cell	E_02_0866	ChIP-qPCR,ChIP-seq,RNA-seq	A conserved 447?bp genomic fragment within this?Neurog2?3′ Foxa1-bound peak showed enhancer activity specifically in midbrain floor plate and also in the cerebral cortex, when analysed in mouse transient transgenic experiments at E12.5	Enhancer	--	Transgenic mice,qRT-PCR	By contrast, the identification of a Foxa1-bound peak downstream of Neurog2 coding sequences (Neurog2 3′) raised the possibility that Foxa2 might directly activate Neurog2 expression through this putative Enhancer region in embryonic mDA progenitors.	Atoh4,Math4A,bHLHa8,ngn-2,ngn2	--	--	--	Otx2,Foxa1,Foxa2	E130306E05Rik,HNF3-beta,HNF3beta,Hnf-3b,Hnf3b,Tcf-3b,Tcf3b,Hnf-3a,Hnf3a,Tcf-3a,Tcf3a	ChIP-seq,RNA-seq	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	--	--	Neurog2
25804738	chr3	127641624	127642545	Neurog2	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	mouse	epithelial tissue	Low+High throughput	Genome-wide characterisation of Foxa1 binding sites reveals several mechanisms for regulating neuronal differentiation in midbrain dopamine cells	否	--	--	embryonic stem cell	E_02_0866	ChIP-qPCR,ChIP-seq,RNA-seq	A conserved 447?bp genomic fragment within this?Neurog2?3′ Foxa1-bound peak showed enhancer activity specifically in midbrain floor plate and also in the cerebral cortex, when analysed in mouse transient transgenic experiments at E12.5	Enhancer	--	Transgenic mice,qRT-PCR	By contrast, the identification of a Foxa1-bound peak downstream of Neurog2 coding sequences (Neurog2 3′) raised the possibility that Foxa2 might directly activate Neurog2 expression through this putative Enhancer region in embryonic mDA progenitors.	Atoh4,Math4A,bHLHa8,ngn-2,ngn2	--	--	--	Otx2,Foxa1,Foxa2	E130306E05Rik,HNF3-beta,HNF3beta,Hnf-3b,Hnf3b,Tcf-3b,Tcf3b,Hnf-3a,Hnf3a,Tcf-3a,Tcf3a	ChIP-seq,RNA-seq	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	--	--	Neurog2
25804738	chr3	127641624	127642545	Otx2	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	mouse	epithelial tissue	Low+High throughput	Genome-wide characterisation of Foxa1 binding sites reveals several mechanisms for regulating neuronal differentiation in midbrain dopamine cells	否	--	--	embryonic stem cell	E_02_0866	ChIP-qPCR,ChIP-seq,RNA-seq	A conserved 447?bp genomic fragment within this?Neurog2?3′ Foxa1-bound peak showed enhancer activity specifically in midbrain floor plate and also in the cerebral cortex, when analysed in mouse transient transgenic experiments at E12.5	Enhancer	--	Transgenic mice,qRT-PCR	By contrast, the identification of a Foxa1-bound peak downstream of Neurog2 coding sequences (Neurog2 3′) raised the possibility that Foxa2 might directly activate Neurog2 expression through this putative Enhancer region in embryonic mDA progenitors.	Atoh4,Math4A,bHLHa8,ngn-2,ngn2	--	--	--	Otx2,Foxa1,Foxa2	E130306E05Rik,HNF3-beta,HNF3beta,Hnf-3b,Hnf3b,Tcf-3b,Tcf3b,Hnf-3a,Hnf3a,Tcf-3a,Tcf3a	ChIP-seq,RNA-seq	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	--	--	Neurog2
25804738	chr3	127641624	127642545	Smarca5	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	mouse	epithelial tissue	Low+High throughput	Genome-wide characterisation of Foxa1 binding sites reveals several mechanisms for regulating neuronal differentiation in midbrain dopamine cells	否	--	--	embryonic stem cell	E_02_0866	ChIP-qPCR,ChIP-seq,RNA-seq	A conserved 447?bp genomic fragment within this?Neurog2?3′ Foxa1-bound peak showed enhancer activity specifically in midbrain floor plate and also in the cerebral cortex, when analysed in mouse transient transgenic experiments at E12.5	Enhancer	--	Transgenic mice,qRT-PCR	By contrast, the identification of a Foxa1-bound peak downstream of Neurog2 coding sequences (Neurog2 3′) raised the possibility that Foxa2 might directly activate Neurog2 expression through this putative Enhancer region in embryonic mDA progenitors.	Atoh4,Math4A,bHLHa8,ngn-2,ngn2	--	--	--	Otx2,Foxa1,Foxa2	E130306E05Rik,HNF3-beta,HNF3beta,Hnf-3b,Hnf3b,Tcf-3b,Tcf3b,Hnf-3a,Hnf3a,Tcf-3a,Tcf3a	ChIP-seq,RNA-seq	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	--	--	Neurog2
25804738	chr3	127641624	127642545	Smarca1	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	mouse	epithelial tissue	Low+High throughput	Genome-wide characterisation of Foxa1 binding sites reveals several mechanisms for regulating neuronal differentiation in midbrain dopamine cells	否	--	--	embryonic stem cell	E_02_0866	ChIP-qPCR,ChIP-seq,RNA-seq	A conserved 447?bp genomic fragment within this?Neurog2?3′ Foxa1-bound peak showed enhancer activity specifically in midbrain floor plate and also in the cerebral cortex, when analysed in mouse transient transgenic experiments at E12.5	Enhancer	--	Transgenic mice,qRT-PCR	By contrast, the identification of a Foxa1-bound peak downstream of Neurog2 coding sequences (Neurog2 3′) raised the possibility that Foxa2 might directly activate Neurog2 expression through this putative Enhancer region in embryonic mDA progenitors.	Atoh4,Math4A,bHLHa8,ngn-2,ngn2	--	--	--	Otx2,Foxa1,Foxa2	E130306E05Rik,HNF3-beta,HNF3beta,Hnf-3b,Hnf3b,Tcf-3b,Tcf3b,Hnf-3a,Hnf3a,Tcf-3a,Tcf3a	ChIP-seq,RNA-seq	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	--	--	Neurog2
25804738	chr3	127641624	127642545	Dmrtb1	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	mouse	epithelial tissue	Low+High throughput	Genome-wide characterisation of Foxa1 binding sites reveals several mechanisms for regulating neuronal differentiation in midbrain dopamine cells	否	--	--	embryonic stem cell	E_02_0866	ChIP-qPCR,ChIP-seq,RNA-seq	A conserved 447?bp genomic fragment within this?Neurog2?3′ Foxa1-bound peak showed enhancer activity specifically in midbrain floor plate and also in the cerebral cortex, when analysed in mouse transient transgenic experiments at E12.5	Enhancer	--	Transgenic mice,qRT-PCR	By contrast, the identification of a Foxa1-bound peak downstream of Neurog2 coding sequences (Neurog2 3′) raised the possibility that Foxa2 might directly activate Neurog2 expression through this putative Enhancer region in embryonic mDA progenitors.	Atoh4,Math4A,bHLHa8,ngn-2,ngn2	--	--	--	Otx2,Foxa1,Foxa2	E130306E05Rik,HNF3-beta,HNF3beta,Hnf-3b,Hnf3b,Tcf-3b,Tcf3b,Hnf-3a,Hnf3a,Tcf-3a,Tcf3a	ChIP-seq,RNA-seq	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	--	--	Neurog2
25804738	chr3	127641624	127642545	Lmcd1	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	mouse	epithelial tissue	Low+High throughput	Genome-wide characterisation of Foxa1 binding sites reveals several mechanisms for regulating neuronal differentiation in midbrain dopamine cells	否	--	--	embryonic stem cell	E_02_0866	ChIP-qPCR,ChIP-seq,RNA-seq	A conserved 447?bp genomic fragment within this?Neurog2?3′ Foxa1-bound peak showed enhancer activity specifically in midbrain floor plate and also in the cerebral cortex, when analysed in mouse transient transgenic experiments at E12.5	Enhancer	--	Transgenic mice,qRT-PCR	By contrast, the identification of a Foxa1-bound peak downstream of Neurog2 coding sequences (Neurog2 3′) raised the possibility that Foxa2 might directly activate Neurog2 expression through this putative Enhancer region in embryonic mDA progenitors.	Atoh4,Math4A,bHLHa8,ngn-2,ngn2	--	--	--	Otx2,Foxa1,Foxa2	E130306E05Rik,HNF3-beta,HNF3beta,Hnf-3b,Hnf3b,Tcf-3b,Tcf3b,Hnf-3a,Hnf3a,Tcf-3a,Tcf3a	ChIP-seq,RNA-seq	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	--	--	Neurog2
25804738	chr3	127641624	127642545	Ferd3l	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	mouse	epithelial tissue	Low+High throughput	Genome-wide characterisation of Foxa1 binding sites reveals several mechanisms for regulating neuronal differentiation in midbrain dopamine cells	否	--	--	embryonic stem cell	E_02_0866	ChIP-qPCR,ChIP-seq,RNA-seq	A conserved 447?bp genomic fragment within this?Neurog2?3′ Foxa1-bound peak showed enhancer activity specifically in midbrain floor plate and also in the cerebral cortex, when analysed in mouse transient transgenic experiments at E12.5	Enhancer	--	Transgenic mice,qRT-PCR	By contrast, the identification of a Foxa1-bound peak downstream of Neurog2 coding sequences (Neurog2 3′) raised the possibility that Foxa2 might directly activate Neurog2 expression through this putative Enhancer region in embryonic mDA progenitors.	Atoh4,Math4A,bHLHa8,ngn-2,ngn2	--	--	--	Otx2,Foxa1,Foxa2	E130306E05Rik,HNF3-beta,HNF3beta,Hnf-3b,Hnf3b,Tcf-3b,Tcf3b,Hnf-3a,Hnf3a,Tcf-3a,Tcf3a	ChIP-seq,RNA-seq	Our genome-wide Foxa1-bound cis-regulatory sequences from ChIP-Seq and Foxa1/2 candidate target genes from RNA-Seq analyses of embryonic midbrain dopamine cells also provide an excellent resource for probing mechanistic insights into gene regulatory networks involved in the differentiation of midbrain dopamine neurons.	--	--	Neurog2
25801169	chr1	13041306	13127367	SOX2	Our results show that ESC SEs generally consist of clusters of active enhancers that have OCT4-dependent and ESC-specific functions and demonstrate that optimal transcriptional activity of target genes is dependent on the presence of most of the constituent enhancers.Chromatin interaction data indicate that constituent enhancers physically interact within the SEs; indeed, the interactions among SE constituents in ESCs appear to be more frequent than interactions between theSE constituents and their associated gene promoters, and interactions between typical enhancers. We previously noted that enhancer clusters can be gained or lost as a unit during development or oncogenesis and have shown that large tumor SEs can collapse as a unit when depleted of the enhancer cofactor BRD4 or when a constituent is deleted.	mouse	epithelial tissue	Low throughput	Convergence of Developmental and Oncogenic Signaling Pathways at Transcriptional Super-Enhancers	否	--	--	Embryonic Stem Cell,V6.5 and Zhbtc4 murine ESCs,C2C12,MEFs,HEK293T,HCT-116	E_02_0867	Luciferase Reporter Assay	The five super-enhancers show physical interactions with their respective associated genes and are located within insulated neighborhoods in the ESC genome , suggesting that these genes represent the bona fide physiological targets of the five SEs.	Super-Enhancer	CRISPR/Cas9	--	The results showed that deletion of most (12/14) super-enhancer constituents led to reduced expression of the associated gene, while in one case (Prdm14 E5) the deletion caused a small increase in expression of the associated gene	Prdm14	--	--	--	Oct4,Sox2,Nanog	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,2410002E02Rik,ENK,ecat4	ChIP-seq	ChIP-Seq binding profiles for OCT4,SOX2 and NANOG (merged) and Mediator (MED1) at the miR-290-295 locus in ES cells.Enhancer activity measured in luciferase reporter assays in wild type cells and the change in enhancer activity after OCT4 shutdown is plotted for each constituent enhancer within the super-enhancer. The super-enhancer is depicted as a black bar above the binding profiles. The difference in values after OCT4 shutdown is statistically significant for all constituents, except from miR-290-295 M1, M3 and M5.	--	--	Prdm14
25801169	chr1	13041306	13127367	NANOG	Our results show that ESC SEs generally consist of clusters of active enhancers that have OCT4-dependent and ESC-specific functions and demonstrate that optimal transcriptional activity of target genes is dependent on the presence of most of the constituent enhancers.Chromatin interaction data indicate that constituent enhancers physically interact within the SEs; indeed, the interactions among SE constituents in ESCs appear to be more frequent than interactions between theSE constituents and their associated gene promoters, and interactions between typical enhancers. We previously noted that enhancer clusters can be gained or lost as a unit during development or oncogenesis and have shown that large tumor SEs can collapse as a unit when depleted of the enhancer cofactor BRD4 or when a constituent is deleted.	mouse	epithelial tissue	Low throughput	Convergence of Developmental and Oncogenic Signaling Pathways at Transcriptional Super-Enhancers	否	--	--	Embryonic Stem Cell,V6.5 and Zhbtc4 murine ESCs,C2C12,MEFs,HEK293T,HCT-116	E_02_0867	Luciferase Reporter Assay	The five super-enhancers show physical interactions with their respective associated genes and are located within insulated neighborhoods in the ESC genome , suggesting that these genes represent the bona fide physiological targets of the five SEs.	Super-Enhancer	CRISPR/Cas9	--	The results showed that deletion of most (12/14) super-enhancer constituents led to reduced expression of the associated gene, while in one case (Prdm14 E5) the deletion caused a small increase in expression of the associated gene	Prdm14	--	--	--	Oct4,Sox2,Nanog	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,2410002E02Rik,ENK,ecat4	ChIP-seq	ChIP-Seq binding profiles for OCT4,SOX2 and NANOG (merged) and Mediator (MED1) at the miR-290-295 locus in ES cells.Enhancer activity measured in luciferase reporter assays in wild type cells and the change in enhancer activity after OCT4 shutdown is plotted for each constituent enhancer within the super-enhancer. The super-enhancer is depicted as a black bar above the binding profiles. The difference in values after OCT4 shutdown is statistically significant for all constituents, except from miR-290-295 M1, M3 and M5.	--	--	Prdm14
25801169	chr1	13041306	13127367	Prdm14	Our results show that ESC SEs generally consist of clusters of active enhancers that have OCT4-dependent and ESC-specific functions and demonstrate that optimal transcriptional activity of target genes is dependent on the presence of most of the constituent enhancers.Chromatin interaction data indicate that constituent enhancers physically interact within the SEs; indeed, the interactions among SE constituents in ESCs appear to be more frequent than interactions between theSE constituents and their associated gene promoters, and interactions between typical enhancers. We previously noted that enhancer clusters can be gained or lost as a unit during development or oncogenesis and have shown that large tumor SEs can collapse as a unit when depleted of the enhancer cofactor BRD4 or when a constituent is deleted.	mouse	epithelial tissue	Low throughput	Convergence of Developmental and Oncogenic Signaling Pathways at Transcriptional Super-Enhancers	否	--	--	Embryonic Stem Cell,V6.5 and Zhbtc4 murine ESCs,C2C12,MEFs,HEK293T,HCT-116	E_02_0867	Luciferase Reporter Assay	The five super-enhancers show physical interactions with their respective associated genes and are located within insulated neighborhoods in the ESC genome , suggesting that these genes represent the bona fide physiological targets of the five SEs.	Super-Enhancer	CRISPR/Cas9	--	The results showed that deletion of most (12/14) super-enhancer constituents led to reduced expression of the associated gene, while in one case (Prdm14 E5) the deletion caused a small increase in expression of the associated gene	Prdm14	--	--	--	Oct4,Sox2,Nanog	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,2410002E02Rik,ENK,ecat4	ChIP-seq	ChIP-Seq binding profiles for OCT4,SOX2 and NANOG (merged) and Mediator (MED1) at the miR-290-295 locus in ES cells.Enhancer activity measured in luciferase reporter assays in wild type cells and the change in enhancer activity after OCT4 shutdown is plotted for each constituent enhancer within the super-enhancer. The super-enhancer is depicted as a black bar above the binding profiles. The difference in values after OCT4 shutdown is statistically significant for all constituents, except from miR-290-295 M1, M3 and M5.	--	--	Prdm14
25801169	chr1	13041306	13127367	Sik1	Our results show that ESC SEs generally consist of clusters of active enhancers that have OCT4-dependent and ESC-specific functions and demonstrate that optimal transcriptional activity of target genes is dependent on the presence of most of the constituent enhancers.Chromatin interaction data indicate that constituent enhancers physically interact within the SEs; indeed, the interactions among SE constituents in ESCs appear to be more frequent than interactions between theSE constituents and their associated gene promoters, and interactions between typical enhancers. We previously noted that enhancer clusters can be gained or lost as a unit during development or oncogenesis and have shown that large tumor SEs can collapse as a unit when depleted of the enhancer cofactor BRD4 or when a constituent is deleted.	mouse	epithelial tissue	Low throughput	Convergence of Developmental and Oncogenic Signaling Pathways at Transcriptional Super-Enhancers	否	--	--	Embryonic Stem Cell,V6.5 and Zhbtc4 murine ESCs,C2C12,MEFs,HEK293T,HCT-116	E_02_0867	Luciferase Reporter Assay	The five super-enhancers show physical interactions with their respective associated genes and are located within insulated neighborhoods in the ESC genome , suggesting that these genes represent the bona fide physiological targets of the five SEs.	Super-Enhancer	CRISPR/Cas9	--	The results showed that deletion of most (12/14) super-enhancer constituents led to reduced expression of the associated gene, while in one case (Prdm14 E5) the deletion caused a small increase in expression of the associated gene	Prdm14	--	--	--	Oct4,Sox2,Nanog	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,2410002E02Rik,ENK,ecat4	ChIP-seq	ChIP-Seq binding profiles for OCT4,SOX2 and NANOG (merged) and Mediator (MED1) at the miR-290-295 locus in ES cells.Enhancer activity measured in luciferase reporter assays in wild type cells and the change in enhancer activity after OCT4 shutdown is plotted for each constituent enhancer within the super-enhancer. The super-enhancer is depicted as a black bar above the binding profiles. The difference in values after OCT4 shutdown is statistically significant for all constituents, except from miR-290-295 M1, M3 and M5.	--	--	Prdm14
25801169	chr1	13041306	13127367	Klf2	Our results show that ESC SEs generally consist of clusters of active enhancers that have OCT4-dependent and ESC-specific functions and demonstrate that optimal transcriptional activity of target genes is dependent on the presence of most of the constituent enhancers.Chromatin interaction data indicate that constituent enhancers physically interact within the SEs; indeed, the interactions among SE constituents in ESCs appear to be more frequent than interactions between theSE constituents and their associated gene promoters, and interactions between typical enhancers. We previously noted that enhancer clusters can be gained or lost as a unit during development or oncogenesis and have shown that large tumor SEs can collapse as a unit when depleted of the enhancer cofactor BRD4 or when a constituent is deleted.	mouse	epithelial tissue	Low throughput	Convergence of Developmental and Oncogenic Signaling Pathways at Transcriptional Super-Enhancers	否	--	--	Embryonic Stem Cell,V6.5 and Zhbtc4 murine ESCs,C2C12,MEFs,HEK293T,HCT-116	E_02_0867	Luciferase Reporter Assay	The five super-enhancers show physical interactions with their respective associated genes and are located within insulated neighborhoods in the ESC genome , suggesting that these genes represent the bona fide physiological targets of the five SEs.	Super-Enhancer	CRISPR/Cas9	--	The results showed that deletion of most (12/14) super-enhancer constituents led to reduced expression of the associated gene, while in one case (Prdm14 E5) the deletion caused a small increase in expression of the associated gene	Prdm14	--	--	--	Oct4,Sox2,Nanog	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,2410002E02Rik,ENK,ecat4	ChIP-seq	ChIP-Seq binding profiles for OCT4,SOX2 and NANOG (merged) and Mediator (MED1) at the miR-290-295 locus in ES cells.Enhancer activity measured in luciferase reporter assays in wild type cells and the change in enhancer activity after OCT4 shutdown is plotted for each constituent enhancer within the super-enhancer. The super-enhancer is depicted as a black bar above the binding profiles. The difference in values after OCT4 shutdown is statistically significant for all constituents, except from miR-290-295 M1, M3 and M5.	--	--	Prdm14
25801169	chr1	13041306	13127367	Pou5f1	Our results show that ESC SEs generally consist of clusters of active enhancers that have OCT4-dependent and ESC-specific functions and demonstrate that optimal transcriptional activity of target genes is dependent on the presence of most of the constituent enhancers.Chromatin interaction data indicate that constituent enhancers physically interact within the SEs; indeed, the interactions among SE constituents in ESCs appear to be more frequent than interactions between theSE constituents and their associated gene promoters, and interactions between typical enhancers. We previously noted that enhancer clusters can be gained or lost as a unit during development or oncogenesis and have shown that large tumor SEs can collapse as a unit when depleted of the enhancer cofactor BRD4 or when a constituent is deleted.	mouse	epithelial tissue	Low throughput	Convergence of Developmental and Oncogenic Signaling Pathways at Transcriptional Super-Enhancers	否	--	--	Embryonic Stem Cell,V6.5 and Zhbtc4 murine ESCs,C2C12,MEFs,HEK293T,HCT-116	E_02_0867	Luciferase Reporter Assay	The five super-enhancers show physical interactions with their respective associated genes and are located within insulated neighborhoods in the ESC genome , suggesting that these genes represent the bona fide physiological targets of the five SEs.	Super-Enhancer	CRISPR/Cas9	--	The results showed that deletion of most (12/14) super-enhancer constituents led to reduced expression of the associated gene, while in one case (Prdm14 E5) the deletion caused a small increase in expression of the associated gene	Prdm14	--	--	--	Oct4,Sox2,Nanog	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,2410002E02Rik,ENK,ecat4	ChIP-seq	ChIP-Seq binding profiles for OCT4,SOX2 and NANOG (merged) and Mediator (MED1) at the miR-290-295 locus in ES cells.Enhancer activity measured in luciferase reporter assays in wild type cells and the change in enhancer activity after OCT4 shutdown is plotted for each constituent enhancer within the super-enhancer. The super-enhancer is depicted as a black bar above the binding profiles. The difference in values after OCT4 shutdown is statistically significant for all constituents, except from miR-290-295 M1, M3 and M5.	--	--	Prdm14
25801169	chr1	13041306	13127367	LIF	Our results show that ESC SEs generally consist of clusters of active enhancers that have OCT4-dependent and ESC-specific functions and demonstrate that optimal transcriptional activity of target genes is dependent on the presence of most of the constituent enhancers.Chromatin interaction data indicate that constituent enhancers physically interact within the SEs; indeed, the interactions among SE constituents in ESCs appear to be more frequent than interactions between theSE constituents and their associated gene promoters, and interactions between typical enhancers. We previously noted that enhancer clusters can be gained or lost as a unit during development or oncogenesis and have shown that large tumor SEs can collapse as a unit when depleted of the enhancer cofactor BRD4 or when a constituent is deleted.	mouse	epithelial tissue	Low throughput	Convergence of Developmental and Oncogenic Signaling Pathways at Transcriptional Super-Enhancers	否	--	--	Embryonic Stem Cell,V6.5 and Zhbtc4 murine ESCs,C2C12,MEFs,HEK293T,HCT-116	E_02_0867	Luciferase Reporter Assay	The five super-enhancers show physical interactions with their respective associated genes and are located within insulated neighborhoods in the ESC genome , suggesting that these genes represent the bona fide physiological targets of the five SEs.	Super-Enhancer	CRISPR/Cas9	--	The results showed that deletion of most (12/14) super-enhancer constituents led to reduced expression of the associated gene, while in one case (Prdm14 E5) the deletion caused a small increase in expression of the associated gene	Prdm14	--	--	--	Oct4,Sox2,Nanog	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,2410002E02Rik,ENK,ecat4	ChIP-seq	ChIP-Seq binding profiles for OCT4,SOX2 and NANOG (merged) and Mediator (MED1) at the miR-290-295 locus in ES cells.Enhancer activity measured in luciferase reporter assays in wild type cells and the change in enhancer activity after OCT4 shutdown is plotted for each constituent enhancer within the super-enhancer. The super-enhancer is depicted as a black bar above the binding profiles. The difference in values after OCT4 shutdown is statistically significant for all constituents, except from miR-290-295 M1, M3 and M5.	--	--	Prdm14
25801169	chr1	13041306	13127367	STAT3	Our results show that ESC SEs generally consist of clusters of active enhancers that have OCT4-dependent and ESC-specific functions and demonstrate that optimal transcriptional activity of target genes is dependent on the presence of most of the constituent enhancers.Chromatin interaction data indicate that constituent enhancers physically interact within the SEs; indeed, the interactions among SE constituents in ESCs appear to be more frequent than interactions between theSE constituents and their associated gene promoters, and interactions between typical enhancers. We previously noted that enhancer clusters can be gained or lost as a unit during development or oncogenesis and have shown that large tumor SEs can collapse as a unit when depleted of the enhancer cofactor BRD4 or when a constituent is deleted.	mouse	epithelial tissue	Low throughput	Convergence of Developmental and Oncogenic Signaling Pathways at Transcriptional Super-Enhancers	否	--	--	Embryonic Stem Cell,V6.5 and Zhbtc4 murine ESCs,C2C12,MEFs,HEK293T,HCT-116	E_02_0867	Luciferase Reporter Assay	The five super-enhancers show physical interactions with their respective associated genes and are located within insulated neighborhoods in the ESC genome , suggesting that these genes represent the bona fide physiological targets of the five SEs.	Super-Enhancer	CRISPR/Cas9	--	The results showed that deletion of most (12/14) super-enhancer constituents led to reduced expression of the associated gene, while in one case (Prdm14 E5) the deletion caused a small increase in expression of the associated gene	Prdm14	--	--	--	Oct4,Sox2,Nanog	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,2410002E02Rik,ENK,ecat4	ChIP-seq	ChIP-Seq binding profiles for OCT4,SOX2 and NANOG (merged) and Mediator (MED1) at the miR-290-295 locus in ES cells.Enhancer activity measured in luciferase reporter assays in wild type cells and the change in enhancer activity after OCT4 shutdown is plotted for each constituent enhancer within the super-enhancer. The super-enhancer is depicted as a black bar above the binding profiles. The difference in values after OCT4 shutdown is statistically significant for all constituents, except from miR-290-295 M1, M3 and M5.	--	--	Prdm14
25801169	chr1	13041306	13127367	TCF3	Our results show that ESC SEs generally consist of clusters of active enhancers that have OCT4-dependent and ESC-specific functions and demonstrate that optimal transcriptional activity of target genes is dependent on the presence of most of the constituent enhancers.Chromatin interaction data indicate that constituent enhancers physically interact within the SEs; indeed, the interactions among SE constituents in ESCs appear to be more frequent than interactions between theSE constituents and their associated gene promoters, and interactions between typical enhancers. We previously noted that enhancer clusters can be gained or lost as a unit during development or oncogenesis and have shown that large tumor SEs can collapse as a unit when depleted of the enhancer cofactor BRD4 or when a constituent is deleted.	mouse	epithelial tissue	Low throughput	Convergence of Developmental and Oncogenic Signaling Pathways at Transcriptional Super-Enhancers	否	--	--	Embryonic Stem Cell,V6.5 and Zhbtc4 murine ESCs,C2C12,MEFs,HEK293T,HCT-116	E_02_0867	Luciferase Reporter Assay	The five super-enhancers show physical interactions with their respective associated genes and are located within insulated neighborhoods in the ESC genome , suggesting that these genes represent the bona fide physiological targets of the five SEs.	Super-Enhancer	CRISPR/Cas9	--	The results showed that deletion of most (12/14) super-enhancer constituents led to reduced expression of the associated gene, while in one case (Prdm14 E5) the deletion caused a small increase in expression of the associated gene	Prdm14	--	--	--	Oct4,Sox2,Nanog	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,2410002E02Rik,ENK,ecat4	ChIP-seq	ChIP-Seq binding profiles for OCT4,SOX2 and NANOG (merged) and Mediator (MED1) at the miR-290-295 locus in ES cells.Enhancer activity measured in luciferase reporter assays in wild type cells and the change in enhancer activity after OCT4 shutdown is plotted for each constituent enhancer within the super-enhancer. The super-enhancer is depicted as a black bar above the binding profiles. The difference in values after OCT4 shutdown is statistically significant for all constituents, except from miR-290-295 M1, M3 and M5.	--	--	Prdm14
25801169	chr1	13041306	13127367	SMAD3	Our results show that ESC SEs generally consist of clusters of active enhancers that have OCT4-dependent and ESC-specific functions and demonstrate that optimal transcriptional activity of target genes is dependent on the presence of most of the constituent enhancers.Chromatin interaction data indicate that constituent enhancers physically interact within the SEs; indeed, the interactions among SE constituents in ESCs appear to be more frequent than interactions between theSE constituents and their associated gene promoters, and interactions between typical enhancers. We previously noted that enhancer clusters can be gained or lost as a unit during development or oncogenesis and have shown that large tumor SEs can collapse as a unit when depleted of the enhancer cofactor BRD4 or when a constituent is deleted.	mouse	epithelial tissue	Low throughput	Convergence of Developmental and Oncogenic Signaling Pathways at Transcriptional Super-Enhancers	否	--	--	Embryonic Stem Cell,V6.5 and Zhbtc4 murine ESCs,C2C12,MEFs,HEK293T,HCT-116	E_02_0867	Luciferase Reporter Assay	The five super-enhancers show physical interactions with their respective associated genes and are located within insulated neighborhoods in the ESC genome , suggesting that these genes represent the bona fide physiological targets of the five SEs.	Super-Enhancer	CRISPR/Cas9	--	The results showed that deletion of most (12/14) super-enhancer constituents led to reduced expression of the associated gene, while in one case (Prdm14 E5) the deletion caused a small increase in expression of the associated gene	Prdm14	--	--	--	Oct4,Sox2,Nanog	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,2410002E02Rik,ENK,ecat4	ChIP-seq	ChIP-Seq binding profiles for OCT4,SOX2 and NANOG (merged) and Mediator (MED1) at the miR-290-295 locus in ES cells.Enhancer activity measured in luciferase reporter assays in wild type cells and the change in enhancer activity after OCT4 shutdown is plotted for each constituent enhancer within the super-enhancer. The super-enhancer is depicted as a black bar above the binding profiles. The difference in values after OCT4 shutdown is statistically significant for all constituents, except from miR-290-295 M1, M3 and M5.	--	--	Prdm14
25801169	chr1	13041306	13127367	TCF4	Our results show that ESC SEs generally consist of clusters of active enhancers that have OCT4-dependent and ESC-specific functions and demonstrate that optimal transcriptional activity of target genes is dependent on the presence of most of the constituent enhancers.Chromatin interaction data indicate that constituent enhancers physically interact within the SEs; indeed, the interactions among SE constituents in ESCs appear to be more frequent than interactions between theSE constituents and their associated gene promoters, and interactions between typical enhancers. We previously noted that enhancer clusters can be gained or lost as a unit during development or oncogenesis and have shown that large tumor SEs can collapse as a unit when depleted of the enhancer cofactor BRD4 or when a constituent is deleted.	mouse	epithelial tissue	Low throughput	Convergence of Developmental and Oncogenic Signaling Pathways at Transcriptional Super-Enhancers	否	--	--	Embryonic Stem Cell,V6.5 and Zhbtc4 murine ESCs,C2C12,MEFs,HEK293T,HCT-116	E_02_0867	Luciferase Reporter Assay	The five super-enhancers show physical interactions with their respective associated genes and are located within insulated neighborhoods in the ESC genome , suggesting that these genes represent the bona fide physiological targets of the five SEs.	Super-Enhancer	CRISPR/Cas9	--	The results showed that deletion of most (12/14) super-enhancer constituents led to reduced expression of the associated gene, while in one case (Prdm14 E5) the deletion caused a small increase in expression of the associated gene	Prdm14	--	--	--	Oct4,Sox2,Nanog	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,2410002E02Rik,ENK,ecat4	ChIP-seq	ChIP-Seq binding profiles for OCT4,SOX2 and NANOG (merged) and Mediator (MED1) at the miR-290-295 locus in ES cells.Enhancer activity measured in luciferase reporter assays in wild type cells and the change in enhancer activity after OCT4 shutdown is plotted for each constituent enhancer within the super-enhancer. The super-enhancer is depicted as a black bar above the binding profiles. The difference in values after OCT4 shutdown is statistically significant for all constituents, except from miR-290-295 M1, M3 and M5.	--	--	Prdm14
25801169	chr1	13041306	13127367	BRD4	Our results show that ESC SEs generally consist of clusters of active enhancers that have OCT4-dependent and ESC-specific functions and demonstrate that optimal transcriptional activity of target genes is dependent on the presence of most of the constituent enhancers.Chromatin interaction data indicate that constituent enhancers physically interact within the SEs; indeed, the interactions among SE constituents in ESCs appear to be more frequent than interactions between theSE constituents and their associated gene promoters, and interactions between typical enhancers. We previously noted that enhancer clusters can be gained or lost as a unit during development or oncogenesis and have shown that large tumor SEs can collapse as a unit when depleted of the enhancer cofactor BRD4 or when a constituent is deleted.	mouse	epithelial tissue	Low throughput	Convergence of Developmental and Oncogenic Signaling Pathways at Transcriptional Super-Enhancers	否	--	--	Embryonic Stem Cell,V6.5 and Zhbtc4 murine ESCs,C2C12,MEFs,HEK293T,HCT-116	E_02_0867	Luciferase Reporter Assay	The five super-enhancers show physical interactions with their respective associated genes and are located within insulated neighborhoods in the ESC genome , suggesting that these genes represent the bona fide physiological targets of the five SEs.	Super-Enhancer	CRISPR/Cas9	--	The results showed that deletion of most (12/14) super-enhancer constituents led to reduced expression of the associated gene, while in one case (Prdm14 E5) the deletion caused a small increase in expression of the associated gene	Prdm14	--	--	--	Oct4,Sox2,Nanog	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,2410002E02Rik,ENK,ecat4	ChIP-seq	ChIP-Seq binding profiles for OCT4,SOX2 and NANOG (merged) and Mediator (MED1) at the miR-290-295 locus in ES cells.Enhancer activity measured in luciferase reporter assays in wild type cells and the change in enhancer activity after OCT4 shutdown is plotted for each constituent enhancer within the super-enhancer. The super-enhancer is depicted as a black bar above the binding profiles. The difference in values after OCT4 shutdown is statistically significant for all constituents, except from miR-290-295 M1, M3 and M5.	--	--	Prdm14
25786345	chr11	118767466	118769582	CXCR5	Using deletion analysis and site-directed mutagenesis of the cxcr5 gene promoter and enhancer elements, we demonstrated that p53 appears to act upon cxcr5 promoter indirectly, by repressing the activity of NFkB transcription factors.	human		Low throughput	p53-dependent expression of CXCR5 chemokine receptor in MCF-7 breast cancer cells	相关	--	--	MCF-7 cell	E_02_0868	Luciferase Reporter Assay,PCR	Genomic fragment containing cxcr5 promoter was subcloned upstream of luciferase gene in pGL3-Basic reporter vector. Another genomic fragment containing the potential cxcr5 enhancer was subcloned downstream of the luciferase gene. In order to account for lower transfection efficiency of larger plasmids, the second construct included a control genomic fragment from cxcr5 locus which was similar in length to the enhancer fragment but had no characteristic features of a regulatory sequence. Functional comparison of these two constructs in MCF-7 and MCF-7-2si cells (Figure 3A) revealed a marginal modulating effect by the enhancer (15%) towards cxcr5 promoter activity. This effect, however, was stable in both cell lines, indicating that activity of the cxcr5 intronic enhancer in breast cancer cells was independent of the p53 status. 	Enhancer	--	Luciferase Reporter Assay,PCR	Genomic fragment containing cxcr5 promoter was subcloned upstream of luciferase gene in pGL3-Basic reporter vector. Another genomic fragment containing the potential cxcr5 enhancer was subcloned downstream of the luciferase gene. In order to account for lower transfection efficiency of larger plasmids, the second construct included a control genomic fragment from cxcr5 locus which was similar in length to the enhancer fragment but had no characteristic features of a regulatory sequence. Functional comparison of these two constructs in MCF-7 and MCF-7-2si cells (Figure 3A) revealed a marginal modulating effect by the enhancer (15%) towards cxcr5 promoter activity. This effect, however, was stable in both cell lines, indicating that activity of the cxcr5 intronic enhancer in breast cancer cells was independent of the p53 status. 	BLR1,CD185,MDR15	--	--	--	NFASC	NEDCPMD,NF,NRCAML	ChIP,PCR	Map of cxcr5 promoter,predicted NF -binding sites and PCR products amplified in ChIP assay.	--	--	CXCR5
25782671	chr7	155845627	155847652	SHH	Most of these malformations are due to the gain-of-function of the Zone of Polarizing Activity Regulatory Sequence, the only limb-specific enhancer of SHH known to date.	human		Low throughput	The disruption of a novel limb cis-regulatory element of SHH is associated with autosomal dominant preaxial polydactyly-hypertrichosis	相关	--	--	Caco-2 cell	E_02_0869	Luciferase Reporter Assay	The 2026 bp sequence was subcloned into the expression vector pLS_Prom_SHH. As the human colon adenocarcinoma Caco2 cell line expresses SHH,we therefore performed transfections in these cells with the construct containing the 2026 bp sequence in forward (pLS_Prom_SHH_2026F) and reverse orientation (pLS_Prom_SHH_2026R). Both constructs show an approximately twofold decrease of the relative reporter activity, as compared with the control vector without regulatory element pLS_Prom_SHH (Figure 4). Thus, the 2026 bp sequence contains an element capable of repressing the transcriptional activity of the SHH promoter in cis, consistent with a silencer activity.	Enhancer	--	Luciferase Reporter Assay	The 2026 bp sequence was subcloned into the expression vector pLS_Prom_SHH. As the human colon adenocarcinoma Caco2 cell line expresses SHH,we therefore performed transfections in these cells with the construct containing the 2026 bp sequence in forward (pLS_Prom_SHH_2026F) and reverse orientation (pLS_Prom_SHH_2026R). Both constructs show an approximately twofold decrease of the relative reporter activity, as compared with the control vector without regulatory element pLS_Prom_SHH (Figure 4). Thus, the 2026 bp sequence contains an element capable of repressing the transcriptional activity of the SHH promoter in cis, consistent with a silencer activity.	HHG1,HLP3,HPE3,MCOPCB5,SMMCI,ShhNC,TPT,TPTPS	--	--	--	--	--	--	--	--	--	SHH
25775043	chr17	35499359	35507923	Tbx3	This previously unannotated ESC-specific enhancer is positioned ~10 kb upstream of transcription factor–encoding Tbx3, a gene previously implicated in the maintenance of pluripotency20.We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression. Indeed, we detected a relative reduction of Tbx3 mRNA and protein expression upon targeting Enh1 with dCas9-LSD1.	mouse	connective tissue	Low throughput	Functional annotation of native enhancers with a Cas9–histone demethylase fusion	否	--	--	embryonic stem cell	E_02_0870	CRISPR/Cas9,3C,Luciferase Reporter Assay,ATAC-seq	We generated mouse embryonic stem cells (mESCs) expressing versions of Neisseria meningitidis (Nm) dCas9 fused with LSD1, a non-effector BirA affinity tag (BAT), or a KRAB repressor and used a viral delivery system for sgRNAs. We first targeted the well-characterized cis-regulatory region of Oct417, a factor critical for the ESC state. Oct4 expression is regulated by a proximal enhancer (OPE) active in epiblast cells, and a distal enhancer (ODE) active in mESCs and cells of the inner cell mass. Targeting of LSD1 to the ODE resulted in loss of Oct4 expression and appearance of OCT4-negative colonies accompanied by phenotypic changes compared to control dCas9-BAT cells targeted to the same enhancer.	Enhancer	3C,CRISPR/Cas9	PCR,ChIP	For follow-up, we focused on the putative Enhancer with the highest differential score,Enh1.Test of Enh1 in a reporter assay confirmed its ability to enhance expression at comparable levels to an Oct4 DE sequence..	NF-A3,Oct-3,Oct-3/4,Oct-4,Oct3,Oct3/4,?Oct4,Otf-3,Otf-4,Otf3,Otf3-rs7,Otf3g,Otf4	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional, native enhancer elements that help to maintain a given cellular state. 	3C	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional,native Enhancer elements that help to maintain a given cellular state.Accordingly,dCas9-LSD1 provides a rapid and powerful approach to understanding distal cis-regulatory regions such as Enhancers without major disruption of the local genomic architecture.	Tbx3	D5Ertd189e	PCR,Luciferase Reporter Assay,ChIP,3C	This previously unannotated ESC_x0002_specific Enhancer is positioned ~10kb upstream of the transcription factor Tbx3, a gene previously implicated in the maintenance of pluripotency20. We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression.	--	--	Oct-4
25775043	chr17	35499359	35507923	Pou3f1	This previously unannotated ESC-specific enhancer is positioned ~10 kb upstream of transcription factor–encoding Tbx3, a gene previously implicated in the maintenance of pluripotency20.We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression. Indeed, we detected a relative reduction of Tbx3 mRNA and protein expression upon targeting Enh1 with dCas9-LSD1.	mouse	connective tissue	Low throughput	Functional annotation of native enhancers with a Cas9–histone demethylase fusion	否	--	--	embryonic stem cell	E_02_0870	CRISPR/Cas9,3C,Luciferase Reporter Assay,ATAC-seq	We generated mouse embryonic stem cells (mESCs) expressing versions of Neisseria meningitidis (Nm) dCas9 fused with LSD1, a non-effector BirA affinity tag (BAT), or a KRAB repressor and used a viral delivery system for sgRNAs. We first targeted the well-characterized cis-regulatory region of Oct417, a factor critical for the ESC state. Oct4 expression is regulated by a proximal enhancer (OPE) active in epiblast cells, and a distal enhancer (ODE) active in mESCs and cells of the inner cell mass. Targeting of LSD1 to the ODE resulted in loss of Oct4 expression and appearance of OCT4-negative colonies accompanied by phenotypic changes compared to control dCas9-BAT cells targeted to the same enhancer.	Enhancer	3C,CRISPR/Cas9	PCR,ChIP	For follow-up, we focused on the putative Enhancer with the highest differential score,Enh1.Test of Enh1 in a reporter assay confirmed its ability to enhance expression at comparable levels to an Oct4 DE sequence..	NF-A3,Oct-3,Oct-3/4,Oct-4,Oct3,Oct3/4,?Oct4,Otf-3,Otf-4,Otf3,Otf3-rs7,Otf3g,Otf4	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional, native enhancer elements that help to maintain a given cellular state. 	3C	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional,native Enhancer elements that help to maintain a given cellular state.Accordingly,dCas9-LSD1 provides a rapid and powerful approach to understanding distal cis-regulatory regions such as Enhancers without major disruption of the local genomic architecture.	Tbx3	D5Ertd189e	PCR,Luciferase Reporter Assay,ChIP,3C	This previously unannotated ESC_x0002_specific Enhancer is positioned ~10kb upstream of the transcription factor Tbx3, a gene previously implicated in the maintenance of pluripotency20. We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression.	--	--	Oct-4
25775043	chr17	35499359	35507923	Foxn1	This previously unannotated ESC-specific enhancer is positioned ~10 kb upstream of transcription factor–encoding Tbx3, a gene previously implicated in the maintenance of pluripotency20.We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression. Indeed, we detected a relative reduction of Tbx3 mRNA and protein expression upon targeting Enh1 with dCas9-LSD1.	mouse	connective tissue	Low throughput	Functional annotation of native enhancers with a Cas9–histone demethylase fusion	否	--	--	embryonic stem cell	E_02_0870	CRISPR/Cas9,3C,Luciferase Reporter Assay,ATAC-seq	We generated mouse embryonic stem cells (mESCs) expressing versions of Neisseria meningitidis (Nm) dCas9 fused with LSD1, a non-effector BirA affinity tag (BAT), or a KRAB repressor and used a viral delivery system for sgRNAs. We first targeted the well-characterized cis-regulatory region of Oct417, a factor critical for the ESC state. Oct4 expression is regulated by a proximal enhancer (OPE) active in epiblast cells, and a distal enhancer (ODE) active in mESCs and cells of the inner cell mass. Targeting of LSD1 to the ODE resulted in loss of Oct4 expression and appearance of OCT4-negative colonies accompanied by phenotypic changes compared to control dCas9-BAT cells targeted to the same enhancer.	Enhancer	3C,CRISPR/Cas9	PCR,ChIP	For follow-up, we focused on the putative Enhancer with the highest differential score,Enh1.Test of Enh1 in a reporter assay confirmed its ability to enhance expression at comparable levels to an Oct4 DE sequence..	NF-A3,Oct-3,Oct-3/4,Oct-4,Oct3,Oct3/4,?Oct4,Otf-3,Otf-4,Otf3,Otf3-rs7,Otf3g,Otf4	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional, native enhancer elements that help to maintain a given cellular state. 	3C	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional,native Enhancer elements that help to maintain a given cellular state.Accordingly,dCas9-LSD1 provides a rapid and powerful approach to understanding distal cis-regulatory regions such as Enhancers without major disruption of the local genomic architecture.	Tbx3	D5Ertd189e	PCR,Luciferase Reporter Assay,ChIP,3C	This previously unannotated ESC_x0002_specific Enhancer is positioned ~10kb upstream of the transcription factor Tbx3, a gene previously implicated in the maintenance of pluripotency20. We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression.	--	--	Oct-4
25775043	chr17	35499359	35507923	Mycn	This previously unannotated ESC-specific enhancer is positioned ~10 kb upstream of transcription factor–encoding Tbx3, a gene previously implicated in the maintenance of pluripotency20.We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression. Indeed, we detected a relative reduction of Tbx3 mRNA and protein expression upon targeting Enh1 with dCas9-LSD1.	mouse	connective tissue	Low throughput	Functional annotation of native enhancers with a Cas9–histone demethylase fusion	否	--	--	embryonic stem cell	E_02_0870	CRISPR/Cas9,3C,Luciferase Reporter Assay,ATAC-seq	We generated mouse embryonic stem cells (mESCs) expressing versions of Neisseria meningitidis (Nm) dCas9 fused with LSD1, a non-effector BirA affinity tag (BAT), or a KRAB repressor and used a viral delivery system for sgRNAs. We first targeted the well-characterized cis-regulatory region of Oct417, a factor critical for the ESC state. Oct4 expression is regulated by a proximal enhancer (OPE) active in epiblast cells, and a distal enhancer (ODE) active in mESCs and cells of the inner cell mass. Targeting of LSD1 to the ODE resulted in loss of Oct4 expression and appearance of OCT4-negative colonies accompanied by phenotypic changes compared to control dCas9-BAT cells targeted to the same enhancer.	Enhancer	3C,CRISPR/Cas9	PCR,ChIP	For follow-up, we focused on the putative Enhancer with the highest differential score,Enh1.Test of Enh1 in a reporter assay confirmed its ability to enhance expression at comparable levels to an Oct4 DE sequence..	NF-A3,Oct-3,Oct-3/4,Oct-4,Oct3,Oct3/4,?Oct4,Otf-3,Otf-4,Otf3,Otf3-rs7,Otf3g,Otf4	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional, native enhancer elements that help to maintain a given cellular state. 	3C	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional,native Enhancer elements that help to maintain a given cellular state.Accordingly,dCas9-LSD1 provides a rapid and powerful approach to understanding distal cis-regulatory regions such as Enhancers without major disruption of the local genomic architecture.	Tbx3	D5Ertd189e	PCR,Luciferase Reporter Assay,ChIP,3C	This previously unannotated ESC_x0002_specific Enhancer is positioned ~10kb upstream of the transcription factor Tbx3, a gene previously implicated in the maintenance of pluripotency20. We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression.	--	--	Oct-4
25775043	chr17	35499359	35507923	SOX2	This previously unannotated ESC-specific enhancer is positioned ~10 kb upstream of transcription factor–encoding Tbx3, a gene previously implicated in the maintenance of pluripotency20.We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression. Indeed, we detected a relative reduction of Tbx3 mRNA and protein expression upon targeting Enh1 with dCas9-LSD1.	mouse	connective tissue	Low throughput	Functional annotation of native enhancers with a Cas9–histone demethylase fusion	否	--	--	embryonic stem cell	E_02_0870	CRISPR/Cas9,3C,Luciferase Reporter Assay,ATAC-seq	We generated mouse embryonic stem cells (mESCs) expressing versions of Neisseria meningitidis (Nm) dCas9 fused with LSD1, a non-effector BirA affinity tag (BAT), or a KRAB repressor and used a viral delivery system for sgRNAs. We first targeted the well-characterized cis-regulatory region of Oct417, a factor critical for the ESC state. Oct4 expression is regulated by a proximal enhancer (OPE) active in epiblast cells, and a distal enhancer (ODE) active in mESCs and cells of the inner cell mass. Targeting of LSD1 to the ODE resulted in loss of Oct4 expression and appearance of OCT4-negative colonies accompanied by phenotypic changes compared to control dCas9-BAT cells targeted to the same enhancer.	Enhancer	3C,CRISPR/Cas9	PCR,ChIP	For follow-up, we focused on the putative Enhancer with the highest differential score,Enh1.Test of Enh1 in a reporter assay confirmed its ability to enhance expression at comparable levels to an Oct4 DE sequence..	NF-A3,Oct-3,Oct-3/4,Oct-4,Oct3,Oct3/4,?Oct4,Otf-3,Otf-4,Otf3,Otf3-rs7,Otf3g,Otf4	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional, native enhancer elements that help to maintain a given cellular state. 	3C	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional,native Enhancer elements that help to maintain a given cellular state.Accordingly,dCas9-LSD1 provides a rapid and powerful approach to understanding distal cis-regulatory regions such as Enhancers without major disruption of the local genomic architecture.	Tbx3	D5Ertd189e	PCR,Luciferase Reporter Assay,ChIP,3C	This previously unannotated ESC_x0002_specific Enhancer is positioned ~10kb upstream of the transcription factor Tbx3, a gene previously implicated in the maintenance of pluripotency20. We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression.	--	--	Oct-4
25775043	chr17	35499359	35507923	KLF2	This previously unannotated ESC-specific enhancer is positioned ~10 kb upstream of transcription factor–encoding Tbx3, a gene previously implicated in the maintenance of pluripotency20.We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression. Indeed, we detected a relative reduction of Tbx3 mRNA and protein expression upon targeting Enh1 with dCas9-LSD1.	mouse	connective tissue	Low throughput	Functional annotation of native enhancers with a Cas9–histone demethylase fusion	否	--	--	embryonic stem cell	E_02_0870	CRISPR/Cas9,3C,Luciferase Reporter Assay,ATAC-seq	We generated mouse embryonic stem cells (mESCs) expressing versions of Neisseria meningitidis (Nm) dCas9 fused with LSD1, a non-effector BirA affinity tag (BAT), or a KRAB repressor and used a viral delivery system for sgRNAs. We first targeted the well-characterized cis-regulatory region of Oct417, a factor critical for the ESC state. Oct4 expression is regulated by a proximal enhancer (OPE) active in epiblast cells, and a distal enhancer (ODE) active in mESCs and cells of the inner cell mass. Targeting of LSD1 to the ODE resulted in loss of Oct4 expression and appearance of OCT4-negative colonies accompanied by phenotypic changes compared to control dCas9-BAT cells targeted to the same enhancer.	Enhancer	3C,CRISPR/Cas9	PCR,ChIP	For follow-up, we focused on the putative Enhancer with the highest differential score,Enh1.Test of Enh1 in a reporter assay confirmed its ability to enhance expression at comparable levels to an Oct4 DE sequence..	NF-A3,Oct-3,Oct-3/4,Oct-4,Oct3,Oct3/4,?Oct4,Otf-3,Otf-4,Otf3,Otf3-rs7,Otf3g,Otf4	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional, native enhancer elements that help to maintain a given cellular state. 	3C	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional,native Enhancer elements that help to maintain a given cellular state.Accordingly,dCas9-LSD1 provides a rapid and powerful approach to understanding distal cis-regulatory regions such as Enhancers without major disruption of the local genomic architecture.	Tbx3	D5Ertd189e	PCR,Luciferase Reporter Assay,ChIP,3C	This previously unannotated ESC_x0002_specific Enhancer is positioned ~10kb upstream of the transcription factor Tbx3, a gene previously implicated in the maintenance of pluripotency20. We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression.	--	--	Oct-4
25775043	chr17	35499359	35507923	KLF5	This previously unannotated ESC-specific enhancer is positioned ~10 kb upstream of transcription factor–encoding Tbx3, a gene previously implicated in the maintenance of pluripotency20.We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression. Indeed, we detected a relative reduction of Tbx3 mRNA and protein expression upon targeting Enh1 with dCas9-LSD1.	mouse	connective tissue	Low throughput	Functional annotation of native enhancers with a Cas9–histone demethylase fusion	否	--	--	embryonic stem cell	E_02_0870	CRISPR/Cas9,3C,Luciferase Reporter Assay,ATAC-seq	We generated mouse embryonic stem cells (mESCs) expressing versions of Neisseria meningitidis (Nm) dCas9 fused with LSD1, a non-effector BirA affinity tag (BAT), or a KRAB repressor and used a viral delivery system for sgRNAs. We first targeted the well-characterized cis-regulatory region of Oct417, a factor critical for the ESC state. Oct4 expression is regulated by a proximal enhancer (OPE) active in epiblast cells, and a distal enhancer (ODE) active in mESCs and cells of the inner cell mass. Targeting of LSD1 to the ODE resulted in loss of Oct4 expression and appearance of OCT4-negative colonies accompanied by phenotypic changes compared to control dCas9-BAT cells targeted to the same enhancer.	Enhancer	3C,CRISPR/Cas9	PCR,ChIP	For follow-up, we focused on the putative Enhancer with the highest differential score,Enh1.Test of Enh1 in a reporter assay confirmed its ability to enhance expression at comparable levels to an Oct4 DE sequence..	NF-A3,Oct-3,Oct-3/4,Oct-4,Oct3,Oct3/4,?Oct4,Otf-3,Otf-4,Otf3,Otf3-rs7,Otf3g,Otf4	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional, native enhancer elements that help to maintain a given cellular state. 	3C	We conclude that the dCas9-LSD1 fusion protein allows for an effector dependent definition of functional,native Enhancer elements that help to maintain a given cellular state.Accordingly,dCas9-LSD1 provides a rapid and powerful approach to understanding distal cis-regulatory regions such as Enhancers without major disruption of the local genomic architecture.	Tbx3	D5Ertd189e	PCR,Luciferase Reporter Assay,ChIP,3C	This previously unannotated ESC_x0002_specific Enhancer is positioned ~10kb upstream of the transcription factor Tbx3, a gene previously implicated in the maintenance of pluripotency20. We therefore hypothesized that Enh1 may function in the ESC network by regulating Tbx3 expression.	--	--	Oct-4
25704602	chr10	123099588	123100426	FGFR2	The second, a non-coding mutation, disrupted the activity of a neural crest enhancer downstream of FGFR2 both in vitro and in vivo.	human		Low throughput	Identification of Functional Variants for Cleft Lip with or without Cleft Palate in or near PAX7, FGFR2, and NOG by Targeted Sequencing of GWAS Loci	相关	--	Cleft Palate	GMSM-K	E_02_0871	Luciferase Reporter Assay,PCR	"The same FGFR2 +254 construct used in the zebra?sh studies (GRCh37, chr10: 123,099,588–123,100,426) was modi?ed by PCR-mediated mutagenesis to test the de novo mutation at GRCh37, chr10: 123,099,960. 
In transient transgenic reporter studies in zebra?sh embryos, we demonstrated that the reference allele of the human +254 kb element has enhancer activity in the neural keel (Figure 3C), brain (Figure 3D), and delaminating neural crest (Figure S18), consistent with expression of Fgfr2 in brain and cranial neural folds in mice and zebra?sh.In parallel experiments, the de novo mutation revealed enhancer activity in fewer embryos (3/83) than the reference allele (41/82; p ? 1.70 3 10 12 )(Figures 3E and S18)."	Enhancer	--	Luciferase Reporter Assay,PCR	"The same FGFR2 +254 construct used in the zebra?sh studies (GRCh37, chr10: 123,099,588–123,100,426) was modi?ed by PCR-mediated mutagenesis to test the de novo mutation at GRCh37, chr10: 123,099,960. 
In transient transgenic reporter studies in zebra?sh embryos, we demonstrated that the reference allele of the human +254 kb element has enhancer activity in the neural keel (Figure 3C), brain (Figure 3D), and delaminating neural crest (Figure S18), consistent with expression of Fgfr2 in brain and cranial neural folds in mice and zebra?sh.In parallel experiments, the de novo mutation revealed enhancer activity in fewer embryos (3/83) than the reference allele (41/82; p ? 1.70 3 10 12 )(Figures 3E and S18)."	BBDS, BEK, BFR-1, CD332, CEK3, CFD1, ECT1, JWS, K-SAM, KGFR, TK14, TK25	--	--	--	--	--	--	--	--	--	FGFR2
25701871	chr5	125345378	125345495	LMNB1	Through parallel studies, we investigated both loss of genetic material and chromosomal rearrangement as possible causes of LMNB1 overexpression, and found that ADLD-1-TO plausibly results from an enhancer adoption mechanism.	human	Brain tissue	Low throughput	A large genomic deletion leads to enhancer adoption by the lamin B1 gene: a second path to autosomal dominant adult-onset demyelinating leukodystrophy (ADLD)	相关	--	Adult-onset Autosomal Dominant Demyelinating Leukodystrophy	HIT DH5A cell (RBC)	E_02_0872	Luciferase Reporter Assay,4C,PCR	To test the predicted enhancers experimentally, we perfor-ed dual-luciferase reporter assays with constructs containing regions A, B, C or D, in direct or reverse orientation, upstream of the LMNB1 promoter . Following transfection of the constructs into HEK293T human cell line, regions A and B (in both orientations) signi?cantly increased luciferase expression (A forward = 1.97 ± 0.2; A reverse = 1.8 ± 1.6; B forward = 2.52 ± 0.25; B reverse = 1.85 ± 0.10; mean ± standard error; P < 0.01; Fig. 3C). In contrast, constructs containing regions C and D did not signi?cantly affect luciferase expression (Fig. 3C). Similar results were obtained when the same plasmids were transfected into NIH3T3 cell line (data not shown), suggesting that the enhancer activity of regions A and B could function across species, at least in mouse ?broblasts. Following these results, regions A and B were subsequently referred to as enhancer region A (Enh-A) and enhancer region B (Enh-B).	Enhancer	4C	Luciferase Reporter Assay,PCR	To test the predicted enhancers experimentally, we perfor-ed dual-luciferase reporter assays with constructs containing regions A, B, C or D, in direct or reverse orientation, upstream of the LMNB1 promoter . Following transfection of the constructs into HEK293T human cell line, regions A and B (in both orientations) signi?cantly increased luciferase expression (A forward = 1.97 ± 0.2; A reverse = 1.8 ± 1.6; B forward = 2.52 ± 0.25; B reverse = 1.85 ± 0.10; mean ± standard error; P < 0.01; Fig. 3C). In contrast, constructs containing regions C and D did not signi?cantly affect luciferase expression (Fig. 3C). Similar results were obtained when the same plasmids were transfected into NIH3T3 cell line (data not shown), suggesting that the enhancer activity of regions A and B could function across species, at least in mouse ?broblasts. Following these results, regions A and B were subsequently referred to as enhancer region A (Enh-A) and enhancer region B (Enh-B).	ADLD,LMN,LMN2,LMNB	--	--	--	--	--	--	--	--	--	LMNB1
25652130	chr4	135548688	135550688	Cdh1	We show that Cdh1 activity during MET is governed by two enhancers at +7.8 kb and at +11.5 kb within intron 2 that are activated by binding of Grhl3 and Hnf4α, respectively. Recruitment of Grhl3 and Hnf4α to the enhancers is crucial for activating Cdh1 and accomplishing MET in non-tumorigenic mouse mammary gland cells (NMuMG). Moreover, the two enhancers cooperate via Grhl3 and Hnf4α binding, induction of DNA-looping and clustering at the promoter to orchestrate E-cadherin re-expression. Our results provide novel insights into the cellular mechanisms whereby cells respond to MET signals and re-establish an epithelial phenotype by enhancer cooperativity. 	mouse	epithelial tissue	Low throughput	Enhancer cooperativity as a novel mechanism underlying the transcriptional regulation of E-cadherin during mesenchymal to epithelial transition	否	--	--	NMuMG,Hepa1–6,CMT,HEK-293	E_02_0873	Luciferase Reporter Assay,3C	We reported previously that intron 2 of Cdh1 is essential for proper E-cad expression.In order to analyze this large DNA sequence(>40 kb) for putative enhancers we focused on evolutionary conserved sequences.	Enhancer	3C	ChIP,qPCR	Weshow thatCdh1 activity during MET isgovernedby 33 two Enhancers at +7.8 and at +11.5 within intron 2 that are activated by binding of Grhl3 and Hnf4α, 34 respectively.	AI561912,Get1,Som,Tfcp2l4,ct	--	--	--	--	--	--	--	--	--	Grhl3
25652130	chr4	135548688	135550688	Grhl3	We show that Cdh1 activity during MET is governed by two enhancers at +7.8 kb and at +11.5 kb within intron 2 that are activated by binding of Grhl3 and Hnf4α, respectively. Recruitment of Grhl3 and Hnf4α to the enhancers is crucial for activating Cdh1 and accomplishing MET in non-tumorigenic mouse mammary gland cells (NMuMG). Moreover, the two enhancers cooperate via Grhl3 and Hnf4α binding, induction of DNA-looping and clustering at the promoter to orchestrate E-cadherin re-expression. Our results provide novel insights into the cellular mechanisms whereby cells respond to MET signals and re-establish an epithelial phenotype by enhancer cooperativity. 	mouse	epithelial tissue	Low throughput	Enhancer cooperativity as a novel mechanism underlying the transcriptional regulation of E-cadherin during mesenchymal to epithelial transition	否	--	--	NMuMG,Hepa1–6,CMT,HEK-293	E_02_0873	Luciferase Reporter Assay,3C	We reported previously that intron 2 of Cdh1 is essential for proper E-cad expression.In order to analyze this large DNA sequence(>40 kb) for putative enhancers we focused on evolutionary conserved sequences.	Enhancer	3C	ChIP,qPCR	Weshow thatCdh1 activity during MET isgovernedby 33 two Enhancers at +7.8 and at +11.5 within intron 2 that are activated by binding of Grhl3 and Hnf4α, 34 respectively.	AI561912,Get1,Som,Tfcp2l4,ct	--	--	--	--	--	--	--	--	--	Grhl3
25652130	chr4	135548688	135550688	Grhl2	We show that Cdh1 activity during MET is governed by two enhancers at +7.8 kb and at +11.5 kb within intron 2 that are activated by binding of Grhl3 and Hnf4α, respectively. Recruitment of Grhl3 and Hnf4α to the enhancers is crucial for activating Cdh1 and accomplishing MET in non-tumorigenic mouse mammary gland cells (NMuMG). Moreover, the two enhancers cooperate via Grhl3 and Hnf4α binding, induction of DNA-looping and clustering at the promoter to orchestrate E-cadherin re-expression. Our results provide novel insights into the cellular mechanisms whereby cells respond to MET signals and re-establish an epithelial phenotype by enhancer cooperativity. 	mouse	epithelial tissue	Low throughput	Enhancer cooperativity as a novel mechanism underlying the transcriptional regulation of E-cadherin during mesenchymal to epithelial transition	否	--	--	NMuMG,Hepa1–6,CMT,HEK-293	E_02_0873	Luciferase Reporter Assay,3C	We reported previously that intron 2 of Cdh1 is essential for proper E-cad expression.In order to analyze this large DNA sequence(>40 kb) for putative enhancers we focused on evolutionary conserved sequences.	Enhancer	3C	ChIP,qPCR	Weshow thatCdh1 activity during MET isgovernedby 33 two Enhancers at +7.8 and at +11.5 within intron 2 that are activated by binding of Grhl3 and Hnf4α, 34 respectively.	AI561912,Get1,Som,Tfcp2l4,ct	--	--	--	--	--	--	--	--	--	Grhl3
25652130	chr4	135548688	135550688	Hnf4a	We show that Cdh1 activity during MET is governed by two enhancers at +7.8 kb and at +11.5 kb within intron 2 that are activated by binding of Grhl3 and Hnf4α, respectively. Recruitment of Grhl3 and Hnf4α to the enhancers is crucial for activating Cdh1 and accomplishing MET in non-tumorigenic mouse mammary gland cells (NMuMG). Moreover, the two enhancers cooperate via Grhl3 and Hnf4α binding, induction of DNA-looping and clustering at the promoter to orchestrate E-cadherin re-expression. Our results provide novel insights into the cellular mechanisms whereby cells respond to MET signals and re-establish an epithelial phenotype by enhancer cooperativity. 	mouse	epithelial tissue	Low throughput	Enhancer cooperativity as a novel mechanism underlying the transcriptional regulation of E-cadherin during mesenchymal to epithelial transition	否	--	--	NMuMG,Hepa1–6,CMT,HEK-293	E_02_0873	Luciferase Reporter Assay,3C	We reported previously that intron 2 of Cdh1 is essential for proper E-cad expression.In order to analyze this large DNA sequence(>40 kb) for putative enhancers we focused on evolutionary conserved sequences.	Enhancer	3C	ChIP,qPCR	Weshow thatCdh1 activity during MET isgovernedby 33 two Enhancers at +7.8 and at +11.5 within intron 2 that are activated by binding of Grhl3 and Hnf4α, 34 respectively.	AI561912,Get1,Som,Tfcp2l4,ct	--	--	--	--	--	--	--	--	--	Grhl3
25651906	chr7	46351197	46355693	Wnt3a	In the present study, we tested the regulation of MyoD cis-regulatory elements by Wnt3a secreted from human embryonic kidney (HEK)-293T cells. We found that Wnt3a activated the MyoD proximal 6.0k promoter (P6P) only marginally, but highly enhanced the activity of the composite P6P plus distal enhancer (DE) reporter through canonical and non-canonical pathways. Further screening of the intervening fragments between the DE and the P6P identified a strong Wnt-response element (WRE) in the upstream -8 to -9k region (L fragment) that acted independently of the DE, but was dependent on the P6P. Deletion of a Pax3/Pax7-targeted site in the L fragment significantly reduced its response to Wnt3a, implying that Wnt3a activates the L fragment partially through Pax3/Pax7 action. Binding of β-catenin and Pax7 to their target sites in the DE and the L fragment respectively was also demonstrated by ChIP.	mouse	muscle tissue	Low throughput	Wnt3a signal pathways activate MyoD expression by targeting cis-elements inside and outside its distal enhancer	否	--	--	C2C12,HEK-293T	E_02_0874	Luciferase Reporter Assay,ChIP	C2C12 myoblasts stably carrying the P6P (?5870 to +95) -driven reporter (MyoD-P6P-luc) or another composite reporter,MyoD-PE-luc, containing P6P plus the DE (?25277 to?20780) were treated with Wnt3a medium. We found that Wnt3a marginally, but significantly, activated MyoDP6P-luc activity; however, Wnt3a strongly activated MyoD-PE-luc, suggesting that one or multiple Wnt-response elements(WREs) are located within the DE.	Enhancer	--	Western blot,qRT-PCR	A distal Enhancer(DE) centred at ? 20 kb, when combined with a ? 2.5k proximal pro_x0002_moter, can also recapitulate human MyoD expression in vivo,demonstrating its critical role in determining the spatiotemporal expression of human MyoD.	AI503393,MYF3,MyoD,?Myod-1,bHLHc1	--	--	--	Wnt3a	Wnt-3a,vt	Luciferase Reporter Assay	Serial deletion mutants of DE region were generated later to identify the minimal WRE,and we found that a region of 3 kb (fragment 10, ?24 to ?21 kb)in DE was required to retain the full Wnt3a response.Deletion of sequence at either the 5_x0002_ end (fragment 8) or the 3_x0002_ end(fragment 7) significantly reduced its Wnt3a response, comparedwith fragment.	--	--	Myod1
25651906	chr7	46351197	46355693	Pax3	In the present study, we tested the regulation of MyoD cis-regulatory elements by Wnt3a secreted from human embryonic kidney (HEK)-293T cells. We found that Wnt3a activated the MyoD proximal 6.0k promoter (P6P) only marginally, but highly enhanced the activity of the composite P6P plus distal enhancer (DE) reporter through canonical and non-canonical pathways. Further screening of the intervening fragments between the DE and the P6P identified a strong Wnt-response element (WRE) in the upstream -8 to -9k region (L fragment) that acted independently of the DE, but was dependent on the P6P. Deletion of a Pax3/Pax7-targeted site in the L fragment significantly reduced its response to Wnt3a, implying that Wnt3a activates the L fragment partially through Pax3/Pax7 action. Binding of β-catenin and Pax7 to their target sites in the DE and the L fragment respectively was also demonstrated by ChIP.	mouse	muscle tissue	Low throughput	Wnt3a signal pathways activate MyoD expression by targeting cis-elements inside and outside its distal enhancer	否	--	--	C2C12,HEK-293T	E_02_0874	Luciferase Reporter Assay,ChIP	C2C12 myoblasts stably carrying the P6P (?5870 to +95) -driven reporter (MyoD-P6P-luc) or another composite reporter,MyoD-PE-luc, containing P6P plus the DE (?25277 to?20780) were treated with Wnt3a medium. We found that Wnt3a marginally, but significantly, activated MyoDP6P-luc activity; however, Wnt3a strongly activated MyoD-PE-luc, suggesting that one or multiple Wnt-response elements(WREs) are located within the DE.	Enhancer	--	Western blot,qRT-PCR	A distal Enhancer(DE) centred at ? 20 kb, when combined with a ? 2.5k proximal pro_x0002_moter, can also recapitulate human MyoD expression in vivo,demonstrating its critical role in determining the spatiotemporal expression of human MyoD.	AI503393,MYF3,MyoD,?Myod-1,bHLHc1	--	--	--	Wnt3a	Wnt-3a,vt	Luciferase Reporter Assay	Serial deletion mutants of DE region were generated later to identify the minimal WRE,and we found that a region of 3 kb (fragment 10, ?24 to ?21 kb)in DE was required to retain the full Wnt3a response.Deletion of sequence at either the 5_x0002_ end (fragment 8) or the 3_x0002_ end(fragment 7) significantly reduced its Wnt3a response, comparedwith fragment.	--	--	Myod1
25651906	chr7	46351197	46355693	Pax7	In the present study, we tested the regulation of MyoD cis-regulatory elements by Wnt3a secreted from human embryonic kidney (HEK)-293T cells. We found that Wnt3a activated the MyoD proximal 6.0k promoter (P6P) only marginally, but highly enhanced the activity of the composite P6P plus distal enhancer (DE) reporter through canonical and non-canonical pathways. Further screening of the intervening fragments between the DE and the P6P identified a strong Wnt-response element (WRE) in the upstream -8 to -9k region (L fragment) that acted independently of the DE, but was dependent on the P6P. Deletion of a Pax3/Pax7-targeted site in the L fragment significantly reduced its response to Wnt3a, implying that Wnt3a activates the L fragment partially through Pax3/Pax7 action. Binding of β-catenin and Pax7 to their target sites in the DE and the L fragment respectively was also demonstrated by ChIP.	mouse	muscle tissue	Low throughput	Wnt3a signal pathways activate MyoD expression by targeting cis-elements inside and outside its distal enhancer	否	--	--	C2C12,HEK-293T	E_02_0874	Luciferase Reporter Assay,ChIP	C2C12 myoblasts stably carrying the P6P (?5870 to +95) -driven reporter (MyoD-P6P-luc) or another composite reporter,MyoD-PE-luc, containing P6P plus the DE (?25277 to?20780) were treated with Wnt3a medium. We found that Wnt3a marginally, but significantly, activated MyoDP6P-luc activity; however, Wnt3a strongly activated MyoD-PE-luc, suggesting that one or multiple Wnt-response elements(WREs) are located within the DE.	Enhancer	--	Western blot,qRT-PCR	A distal Enhancer(DE) centred at ? 20 kb, when combined with a ? 2.5k proximal pro_x0002_moter, can also recapitulate human MyoD expression in vivo,demonstrating its critical role in determining the spatiotemporal expression of human MyoD.	AI503393,MYF3,MyoD,?Myod-1,bHLHc1	--	--	--	Wnt3a	Wnt-3a,vt	Luciferase Reporter Assay	Serial deletion mutants of DE region were generated later to identify the minimal WRE,and we found that a region of 3 kb (fragment 10, ?24 to ?21 kb)in DE was required to retain the full Wnt3a response.Deletion of sequence at either the 5_x0002_ end (fragment 8) or the 3_x0002_ end(fragment 7) significantly reduced its Wnt3a response, comparedwith fragment.	--	--	Myod1
25651906	chr7	46351197	46355693	Myf5	In the present study, we tested the regulation of MyoD cis-regulatory elements by Wnt3a secreted from human embryonic kidney (HEK)-293T cells. We found that Wnt3a activated the MyoD proximal 6.0k promoter (P6P) only marginally, but highly enhanced the activity of the composite P6P plus distal enhancer (DE) reporter through canonical and non-canonical pathways. Further screening of the intervening fragments between the DE and the P6P identified a strong Wnt-response element (WRE) in the upstream -8 to -9k region (L fragment) that acted independently of the DE, but was dependent on the P6P. Deletion of a Pax3/Pax7-targeted site in the L fragment significantly reduced its response to Wnt3a, implying that Wnt3a activates the L fragment partially through Pax3/Pax7 action. Binding of β-catenin and Pax7 to their target sites in the DE and the L fragment respectively was also demonstrated by ChIP.	mouse	muscle tissue	Low throughput	Wnt3a signal pathways activate MyoD expression by targeting cis-elements inside and outside its distal enhancer	否	--	--	C2C12,HEK-293T	E_02_0874	Luciferase Reporter Assay,ChIP	C2C12 myoblasts stably carrying the P6P (?5870 to +95) -driven reporter (MyoD-P6P-luc) or another composite reporter,MyoD-PE-luc, containing P6P plus the DE (?25277 to?20780) were treated with Wnt3a medium. We found that Wnt3a marginally, but significantly, activated MyoDP6P-luc activity; however, Wnt3a strongly activated MyoD-PE-luc, suggesting that one or multiple Wnt-response elements(WREs) are located within the DE.	Enhancer	--	Western blot,qRT-PCR	A distal Enhancer(DE) centred at ? 20 kb, when combined with a ? 2.5k proximal pro_x0002_moter, can also recapitulate human MyoD expression in vivo,demonstrating its critical role in determining the spatiotemporal expression of human MyoD.	AI503393,MYF3,MyoD,?Myod-1,bHLHc1	--	--	--	Wnt3a	Wnt-3a,vt	Luciferase Reporter Assay	Serial deletion mutants of DE region were generated later to identify the minimal WRE,and we found that a region of 3 kb (fragment 10, ?24 to ?21 kb)in DE was required to retain the full Wnt3a response.Deletion of sequence at either the 5_x0002_ end (fragment 8) or the 3_x0002_ end(fragment 7) significantly reduced its Wnt3a response, comparedwith fragment.	--	--	Myod1
25651906	chr7	46351197	46355693	Mef2c	In the present study, we tested the regulation of MyoD cis-regulatory elements by Wnt3a secreted from human embryonic kidney (HEK)-293T cells. We found that Wnt3a activated the MyoD proximal 6.0k promoter (P6P) only marginally, but highly enhanced the activity of the composite P6P plus distal enhancer (DE) reporter through canonical and non-canonical pathways. Further screening of the intervening fragments between the DE and the P6P identified a strong Wnt-response element (WRE) in the upstream -8 to -9k region (L fragment) that acted independently of the DE, but was dependent on the P6P. Deletion of a Pax3/Pax7-targeted site in the L fragment significantly reduced its response to Wnt3a, implying that Wnt3a activates the L fragment partially through Pax3/Pax7 action. Binding of β-catenin and Pax7 to their target sites in the DE and the L fragment respectively was also demonstrated by ChIP.	mouse	muscle tissue	Low throughput	Wnt3a signal pathways activate MyoD expression by targeting cis-elements inside and outside its distal enhancer	否	--	--	C2C12,HEK-293T	E_02_0874	Luciferase Reporter Assay,ChIP	C2C12 myoblasts stably carrying the P6P (?5870 to +95) -driven reporter (MyoD-P6P-luc) or another composite reporter,MyoD-PE-luc, containing P6P plus the DE (?25277 to?20780) were treated with Wnt3a medium. We found that Wnt3a marginally, but significantly, activated MyoDP6P-luc activity; however, Wnt3a strongly activated MyoD-PE-luc, suggesting that one or multiple Wnt-response elements(WREs) are located within the DE.	Enhancer	--	Western blot,qRT-PCR	A distal Enhancer(DE) centred at ? 20 kb, when combined with a ? 2.5k proximal pro_x0002_moter, can also recapitulate human MyoD expression in vivo,demonstrating its critical role in determining the spatiotemporal expression of human MyoD.	AI503393,MYF3,MyoD,?Myod-1,bHLHc1	--	--	--	Wnt3a	Wnt-3a,vt	Luciferase Reporter Assay	Serial deletion mutants of DE region were generated later to identify the minimal WRE,and we found that a region of 3 kb (fragment 10, ?24 to ?21 kb)in DE was required to retain the full Wnt3a response.Deletion of sequence at either the 5_x0002_ end (fragment 8) or the 3_x0002_ end(fragment 7) significantly reduced its Wnt3a response, comparedwith fragment.	--	--	Myod1
25651906	chr7	46351197	46355693	Wnt1	In the present study, we tested the regulation of MyoD cis-regulatory elements by Wnt3a secreted from human embryonic kidney (HEK)-293T cells. We found that Wnt3a activated the MyoD proximal 6.0k promoter (P6P) only marginally, but highly enhanced the activity of the composite P6P plus distal enhancer (DE) reporter through canonical and non-canonical pathways. Further screening of the intervening fragments between the DE and the P6P identified a strong Wnt-response element (WRE) in the upstream -8 to -9k region (L fragment) that acted independently of the DE, but was dependent on the P6P. Deletion of a Pax3/Pax7-targeted site in the L fragment significantly reduced its response to Wnt3a, implying that Wnt3a activates the L fragment partially through Pax3/Pax7 action. Binding of β-catenin and Pax7 to their target sites in the DE and the L fragment respectively was also demonstrated by ChIP.	mouse	muscle tissue	Low throughput	Wnt3a signal pathways activate MyoD expression by targeting cis-elements inside and outside its distal enhancer	否	--	--	C2C12,HEK-293T	E_02_0874	Luciferase Reporter Assay,ChIP	C2C12 myoblasts stably carrying the P6P (?5870 to +95) -driven reporter (MyoD-P6P-luc) or another composite reporter,MyoD-PE-luc, containing P6P plus the DE (?25277 to?20780) were treated with Wnt3a medium. We found that Wnt3a marginally, but significantly, activated MyoDP6P-luc activity; however, Wnt3a strongly activated MyoD-PE-luc, suggesting that one or multiple Wnt-response elements(WREs) are located within the DE.	Enhancer	--	Western blot,qRT-PCR	A distal Enhancer(DE) centred at ? 20 kb, when combined with a ? 2.5k proximal pro_x0002_moter, can also recapitulate human MyoD expression in vivo,demonstrating its critical role in determining the spatiotemporal expression of human MyoD.	AI503393,MYF3,MyoD,?Myod-1,bHLHc1	--	--	--	Wnt3a	Wnt-3a,vt	Luciferase Reporter Assay	Serial deletion mutants of DE region were generated later to identify the minimal WRE,and we found that a region of 3 kb (fragment 10, ?24 to ?21 kb)in DE was required to retain the full Wnt3a response.Deletion of sequence at either the 5_x0002_ end (fragment 8) or the 3_x0002_ end(fragment 7) significantly reduced its Wnt3a response, comparedwith fragment.	--	--	Myod1
25651906	chr7	46351197	46355693	Wnt4	In the present study, we tested the regulation of MyoD cis-regulatory elements by Wnt3a secreted from human embryonic kidney (HEK)-293T cells. We found that Wnt3a activated the MyoD proximal 6.0k promoter (P6P) only marginally, but highly enhanced the activity of the composite P6P plus distal enhancer (DE) reporter through canonical and non-canonical pathways. Further screening of the intervening fragments between the DE and the P6P identified a strong Wnt-response element (WRE) in the upstream -8 to -9k region (L fragment) that acted independently of the DE, but was dependent on the P6P. Deletion of a Pax3/Pax7-targeted site in the L fragment significantly reduced its response to Wnt3a, implying that Wnt3a activates the L fragment partially through Pax3/Pax7 action. Binding of β-catenin and Pax7 to their target sites in the DE and the L fragment respectively was also demonstrated by ChIP.	mouse	muscle tissue	Low throughput	Wnt3a signal pathways activate MyoD expression by targeting cis-elements inside and outside its distal enhancer	否	--	--	C2C12,HEK-293T	E_02_0874	Luciferase Reporter Assay,ChIP	C2C12 myoblasts stably carrying the P6P (?5870 to +95) -driven reporter (MyoD-P6P-luc) or another composite reporter,MyoD-PE-luc, containing P6P plus the DE (?25277 to?20780) were treated with Wnt3a medium. We found that Wnt3a marginally, but significantly, activated MyoDP6P-luc activity; however, Wnt3a strongly activated MyoD-PE-luc, suggesting that one or multiple Wnt-response elements(WREs) are located within the DE.	Enhancer	--	Western blot,qRT-PCR	A distal Enhancer(DE) centred at ? 20 kb, when combined with a ? 2.5k proximal pro_x0002_moter, can also recapitulate human MyoD expression in vivo,demonstrating its critical role in determining the spatiotemporal expression of human MyoD.	AI503393,MYF3,MyoD,?Myod-1,bHLHc1	--	--	--	Wnt3a	Wnt-3a,vt	Luciferase Reporter Assay	Serial deletion mutants of DE region were generated later to identify the minimal WRE,and we found that a region of 3 kb (fragment 10, ?24 to ?21 kb)in DE was required to retain the full Wnt3a response.Deletion of sequence at either the 5_x0002_ end (fragment 8) or the 3_x0002_ end(fragment 7) significantly reduced its Wnt3a response, comparedwith fragment.	--	--	Myod1
25651906	chr7	46351197	46355693	Wnt6	In the present study, we tested the regulation of MyoD cis-regulatory elements by Wnt3a secreted from human embryonic kidney (HEK)-293T cells. We found that Wnt3a activated the MyoD proximal 6.0k promoter (P6P) only marginally, but highly enhanced the activity of the composite P6P plus distal enhancer (DE) reporter through canonical and non-canonical pathways. Further screening of the intervening fragments between the DE and the P6P identified a strong Wnt-response element (WRE) in the upstream -8 to -9k region (L fragment) that acted independently of the DE, but was dependent on the P6P. Deletion of a Pax3/Pax7-targeted site in the L fragment significantly reduced its response to Wnt3a, implying that Wnt3a activates the L fragment partially through Pax3/Pax7 action. Binding of β-catenin and Pax7 to their target sites in the DE and the L fragment respectively was also demonstrated by ChIP.	mouse	muscle tissue	Low throughput	Wnt3a signal pathways activate MyoD expression by targeting cis-elements inside and outside its distal enhancer	否	--	--	C2C12,HEK-293T	E_02_0874	Luciferase Reporter Assay,ChIP	C2C12 myoblasts stably carrying the P6P (?5870 to +95) -driven reporter (MyoD-P6P-luc) or another composite reporter,MyoD-PE-luc, containing P6P plus the DE (?25277 to?20780) were treated with Wnt3a medium. We found that Wnt3a marginally, but significantly, activated MyoDP6P-luc activity; however, Wnt3a strongly activated MyoD-PE-luc, suggesting that one or multiple Wnt-response elements(WREs) are located within the DE.	Enhancer	--	Western blot,qRT-PCR	A distal Enhancer(DE) centred at ? 20 kb, when combined with a ? 2.5k proximal pro_x0002_moter, can also recapitulate human MyoD expression in vivo,demonstrating its critical role in determining the spatiotemporal expression of human MyoD.	AI503393,MYF3,MyoD,?Myod-1,bHLHc1	--	--	--	Wnt3a	Wnt-3a,vt	Luciferase Reporter Assay	Serial deletion mutants of DE region were generated later to identify the minimal WRE,and we found that a region of 3 kb (fragment 10, ?24 to ?21 kb)in DE was required to retain the full Wnt3a response.Deletion of sequence at either the 5_x0002_ end (fragment 8) or the 3_x0002_ end(fragment 7) significantly reduced its Wnt3a response, comparedwith fragment.	--	--	Myod1
25651906	chr7	46351197	46355693	Wnt7a	In the present study, we tested the regulation of MyoD cis-regulatory elements by Wnt3a secreted from human embryonic kidney (HEK)-293T cells. We found that Wnt3a activated the MyoD proximal 6.0k promoter (P6P) only marginally, but highly enhanced the activity of the composite P6P plus distal enhancer (DE) reporter through canonical and non-canonical pathways. Further screening of the intervening fragments between the DE and the P6P identified a strong Wnt-response element (WRE) in the upstream -8 to -9k region (L fragment) that acted independently of the DE, but was dependent on the P6P. Deletion of a Pax3/Pax7-targeted site in the L fragment significantly reduced its response to Wnt3a, implying that Wnt3a activates the L fragment partially through Pax3/Pax7 action. Binding of β-catenin and Pax7 to their target sites in the DE and the L fragment respectively was also demonstrated by ChIP.	mouse	muscle tissue	Low throughput	Wnt3a signal pathways activate MyoD expression by targeting cis-elements inside and outside its distal enhancer	否	--	--	C2C12,HEK-293T	E_02_0874	Luciferase Reporter Assay,ChIP	C2C12 myoblasts stably carrying the P6P (?5870 to +95) -driven reporter (MyoD-P6P-luc) or another composite reporter,MyoD-PE-luc, containing P6P plus the DE (?25277 to?20780) were treated with Wnt3a medium. We found that Wnt3a marginally, but significantly, activated MyoDP6P-luc activity; however, Wnt3a strongly activated MyoD-PE-luc, suggesting that one or multiple Wnt-response elements(WREs) are located within the DE.	Enhancer	--	Western blot,qRT-PCR	A distal Enhancer(DE) centred at ? 20 kb, when combined with a ? 2.5k proximal pro_x0002_moter, can also recapitulate human MyoD expression in vivo,demonstrating its critical role in determining the spatiotemporal expression of human MyoD.	AI503393,MYF3,MyoD,?Myod-1,bHLHc1	--	--	--	Wnt3a	Wnt-3a,vt	Luciferase Reporter Assay	Serial deletion mutants of DE region were generated later to identify the minimal WRE,and we found that a region of 3 kb (fragment 10, ?24 to ?21 kb)in DE was required to retain the full Wnt3a response.Deletion of sequence at either the 5_x0002_ end (fragment 8) or the 3_x0002_ end(fragment 7) significantly reduced its Wnt3a response, comparedwith fragment.	--	--	Myod1
25651906	chr7	46351197	46355693	Wnt11	In the present study, we tested the regulation of MyoD cis-regulatory elements by Wnt3a secreted from human embryonic kidney (HEK)-293T cells. We found that Wnt3a activated the MyoD proximal 6.0k promoter (P6P) only marginally, but highly enhanced the activity of the composite P6P plus distal enhancer (DE) reporter through canonical and non-canonical pathways. Further screening of the intervening fragments between the DE and the P6P identified a strong Wnt-response element (WRE) in the upstream -8 to -9k region (L fragment) that acted independently of the DE, but was dependent on the P6P. Deletion of a Pax3/Pax7-targeted site in the L fragment significantly reduced its response to Wnt3a, implying that Wnt3a activates the L fragment partially through Pax3/Pax7 action. Binding of β-catenin and Pax7 to their target sites in the DE and the L fragment respectively was also demonstrated by ChIP.	mouse	muscle tissue	Low throughput	Wnt3a signal pathways activate MyoD expression by targeting cis-elements inside and outside its distal enhancer	否	--	--	C2C12,HEK-293T	E_02_0874	Luciferase Reporter Assay,ChIP	C2C12 myoblasts stably carrying the P6P (?5870 to +95) -driven reporter (MyoD-P6P-luc) or another composite reporter,MyoD-PE-luc, containing P6P plus the DE (?25277 to?20780) were treated with Wnt3a medium. We found that Wnt3a marginally, but significantly, activated MyoDP6P-luc activity; however, Wnt3a strongly activated MyoD-PE-luc, suggesting that one or multiple Wnt-response elements(WREs) are located within the DE.	Enhancer	--	Western blot,qRT-PCR	A distal Enhancer(DE) centred at ? 20 kb, when combined with a ? 2.5k proximal pro_x0002_moter, can also recapitulate human MyoD expression in vivo,demonstrating its critical role in determining the spatiotemporal expression of human MyoD.	AI503393,MYF3,MyoD,?Myod-1,bHLHc1	--	--	--	Wnt3a	Wnt-3a,vt	Luciferase Reporter Assay	Serial deletion mutants of DE region were generated later to identify the minimal WRE,and we found that a region of 3 kb (fragment 10, ?24 to ?21 kb)in DE was required to retain the full Wnt3a response.Deletion of sequence at either the 5_x0002_ end (fragment 8) or the 3_x0002_ end(fragment 7) significantly reduced its Wnt3a response, comparedwith fragment.	--	--	Myod1
25651906	chr7	46351197	46355693	Wnt5a	In the present study, we tested the regulation of MyoD cis-regulatory elements by Wnt3a secreted from human embryonic kidney (HEK)-293T cells. We found that Wnt3a activated the MyoD proximal 6.0k promoter (P6P) only marginally, but highly enhanced the activity of the composite P6P plus distal enhancer (DE) reporter through canonical and non-canonical pathways. Further screening of the intervening fragments between the DE and the P6P identified a strong Wnt-response element (WRE) in the upstream -8 to -9k region (L fragment) that acted independently of the DE, but was dependent on the P6P. Deletion of a Pax3/Pax7-targeted site in the L fragment significantly reduced its response to Wnt3a, implying that Wnt3a activates the L fragment partially through Pax3/Pax7 action. Binding of β-catenin and Pax7 to their target sites in the DE and the L fragment respectively was also demonstrated by ChIP.	mouse	muscle tissue	Low throughput	Wnt3a signal pathways activate MyoD expression by targeting cis-elements inside and outside its distal enhancer	否	--	--	C2C12,HEK-293T	E_02_0874	Luciferase Reporter Assay,ChIP	C2C12 myoblasts stably carrying the P6P (?5870 to +95) -driven reporter (MyoD-P6P-luc) or another composite reporter,MyoD-PE-luc, containing P6P plus the DE (?25277 to?20780) were treated with Wnt3a medium. We found that Wnt3a marginally, but significantly, activated MyoDP6P-luc activity; however, Wnt3a strongly activated MyoD-PE-luc, suggesting that one or multiple Wnt-response elements(WREs) are located within the DE.	Enhancer	--	Western blot,qRT-PCR	A distal Enhancer(DE) centred at ? 20 kb, when combined with a ? 2.5k proximal pro_x0002_moter, can also recapitulate human MyoD expression in vivo,demonstrating its critical role in determining the spatiotemporal expression of human MyoD.	AI503393,MYF3,MyoD,?Myod-1,bHLHc1	--	--	--	Wnt3a	Wnt-3a,vt	Luciferase Reporter Assay	Serial deletion mutants of DE region were generated later to identify the minimal WRE,and we found that a region of 3 kb (fragment 10, ?24 to ?21 kb)in DE was required to retain the full Wnt3a response.Deletion of sequence at either the 5_x0002_ end (fragment 8) or the 3_x0002_ end(fragment 7) significantly reduced its Wnt3a response, comparedwith fragment.	--	--	Myod1
25651906	chr7	46351197	46355693	Wnt5b	In the present study, we tested the regulation of MyoD cis-regulatory elements by Wnt3a secreted from human embryonic kidney (HEK)-293T cells. We found that Wnt3a activated the MyoD proximal 6.0k promoter (P6P) only marginally, but highly enhanced the activity of the composite P6P plus distal enhancer (DE) reporter through canonical and non-canonical pathways. Further screening of the intervening fragments between the DE and the P6P identified a strong Wnt-response element (WRE) in the upstream -8 to -9k region (L fragment) that acted independently of the DE, but was dependent on the P6P. Deletion of a Pax3/Pax7-targeted site in the L fragment significantly reduced its response to Wnt3a, implying that Wnt3a activates the L fragment partially through Pax3/Pax7 action. Binding of β-catenin and Pax7 to their target sites in the DE and the L fragment respectively was also demonstrated by ChIP.	mouse	muscle tissue	Low throughput	Wnt3a signal pathways activate MyoD expression by targeting cis-elements inside and outside its distal enhancer	否	--	--	C2C12,HEK-293T	E_02_0874	Luciferase Reporter Assay,ChIP	C2C12 myoblasts stably carrying the P6P (?5870 to +95) -driven reporter (MyoD-P6P-luc) or another composite reporter,MyoD-PE-luc, containing P6P plus the DE (?25277 to?20780) were treated with Wnt3a medium. We found that Wnt3a marginally, but significantly, activated MyoDP6P-luc activity; however, Wnt3a strongly activated MyoD-PE-luc, suggesting that one or multiple Wnt-response elements(WREs) are located within the DE.	Enhancer	--	Western blot,qRT-PCR	A distal Enhancer(DE) centred at ? 20 kb, when combined with a ? 2.5k proximal pro_x0002_moter, can also recapitulate human MyoD expression in vivo,demonstrating its critical role in determining the spatiotemporal expression of human MyoD.	AI503393,MYF3,MyoD,?Myod-1,bHLHc1	--	--	--	Wnt3a	Wnt-3a,vt	Luciferase Reporter Assay	Serial deletion mutants of DE region were generated later to identify the minimal WRE,and we found that a region of 3 kb (fragment 10, ?24 to ?21 kb)in DE was required to retain the full Wnt3a response.Deletion of sequence at either the 5_x0002_ end (fragment 8) or the 3_x0002_ end(fragment 7) significantly reduced its Wnt3a response, comparedwith fragment.	--	--	Myod1
25644605	chr8	83287848	83288068	PRDM16	PR domain-containing 16 (PRDM16) induces expression of brown fat-specific genes in brown and beige adipocytes,although the underlying transcription-related mechanisms remain largely unknown.	mouse	Brown adipose tissue	Low throughput	PRDM16 enhances nuclear receptor_x005f_x0002_dependent transcription of the brown fat-specific Ucp1 gene through interactions with Mediator subunit MED1	否	--	--	brown fat cell	E_02_0875	ChIP,RT-PCR	we hypothesized that PRDM16 might be recruited to the enhancer region of the Ucp1 gene through the interaction with PGC-1a. This possibility was tested in an immobilized template assay with purified proteins and a beadimmobilized DNA fragment spanning the 220-bp Ucp1 enhancer.	Enhancer	--	ChIP,RT-PCR	Overall, these results indicate that the ZF1 domain is required for the recruitment of PRDM16 to the Ucp1 enhancer through MED1 and PGC-1a.	AI385626,Slc25a7,Ucp	--	--	--	Prdm16	5730557K01Rik,csp1,mel1	ChIP	To determine whether PRDM16 is recruited to the Enhancer following Ucp1 induction, we treated Med1 +/+MEFs that stably express PPARg and PRDM16 with forskolin and performed a chromatin immunoprecipitation (ChIP) assay with an antibody specific for PRDM16.	--	--	Ucp1
25628225	chr17	6285838	6586838	SLC13A5	Utilizing cell-based luciferase reporter assays, electro_x0002_phoretic mobility shift assays, and chromatin immunoprecipitation assays, we identified and functionally characterized two enhancer modules located upstream of the SLC13A5 gene transcription start site that are associated with regulation of PXR-mediated SLC13A5 induction.	human	Liver tissues	Low throughput	SLC13A5 Is a Novel Transcriptional Target of the Pregnane X Receptor and Sensitizes Drug-Induced Steatosis in Human Liver	不相关	--	Steatosis	hepatocyte	E_02_0876	Luciferase Reporter Assay,EMSA,ChIP	Utilizing cell-based Luciferaseassays,electrophoretic mobility shift assays,and Chromatin immunoprecipitation assays,we identified and functionally characterized two Enhancer modules located upstream of the SLC13A5 gene transcription start site that are associated with regulation of PXR-mediated SLC13A5 induction.	Enhancer	--	Luciferase Reporter Assay,EMSA,ChIP	Utilizing cell-based Luciferaseassays,electrophoretic mobility shift assays,and Chromatin immunoprecipitation assays,we identified and functionally characterized two Enhancer modules located upstream of the SLC13A5 gene transcription start site that are associated with regulation of PXR-mediated SLC13A5 induction.	EIEE25,INDY,NACT,mIndy	--	--	--	NR1I2	BXR,ONR1,PAR,PAR1,PAR2,PARq,PRR,PXR,SAR,SXR	EMSA	Utilizing in vitro EMSA,we found that heterodimer of PXR and the retinoid X receptor binds specifically to DR4-1 and DR4-2 at intensities equal to or exceeding that of the everted-repeat (ER6) element from CYP3A4 promoter.	--	--	SLC13A5
25622893	chr17	61927353	61928827	Tcam1	At the mouse locus, a multifunctional dual promoter–enhancer (DPE) controls the expression of Tcam1 and Smarcd2 genes.	human		Low throughput	Characterization of the human TCAM1P pseudogene and its activation by a potential dual promoter–enhancer: Comparison with a protein-coding mouse orthologue	不相关	--	--	GC-spd(ts),Hepa 1-6,293T	E_02_0877	PCR,Luciferase Reporter Assay	"We first investigated enhancer activity of hCNS1. Because TSS of TCAM1P--I and TCAM1P--III was +401 and three TSSs of TCAM1P--II were close to +401 (Fig. 2E), we cloned about 2--kb sequence upstream of +401 as a major promoter of the TCAM1P gene and connected it to the luciferase gene (TCAM1P--Pro--luc). hCNS1 was amplified by genome PCR and cloned to upstream of the TCAM1P promoter (hCNS1--Pro--luc) or to downstream of the luciferase gene(Pro--luc--hCNS1 and Pro--luc--rev hCNS1).The activity of hCNS1--Pro--luc was significantly increased in all three cell lines compared to the construct without hCNS1 (Fig. 3A).
"	Enhancer	--	Luciferase Reporter Assay	We also examined the luciferase activity in linearized constructs. If hCNS1 was actually a DPE, it might drive the transcription of the entire sequence in a circular plasmid, which might affect the luciferase gene expression.To prevent hCNS1 from driving the luciferase gene transcription in the sense direction, we linearized Pro--luc--hCNS1 and Pro--luc--rev hCNS1 constructs by cutting the immediate downstream sequence of hCNS1 and rev hCNS1. As a result, hCNS1 still significantly increased TCAM1P promoter activity in HEK293T cells, and the fold--increases were around 3 in both constructs compared to the linearized TCAM1P--Pro--luc construct (Fig. 3B). These data showed that hCNS1 could function as an enhancer for the TCAM1P gene.	TCAM1	--	--	--	--	--	--	--	--	--	TCAM1P
25622893	chr17	61927353	61928827	Smarcd2	At the mouse locus, a multifunctional dual promoter–enhancer (DPE) controls the expression of Tcam1 and Smarcd2 genes.	human		Low throughput	Characterization of the human TCAM1P pseudogene and its activation by a potential dual promoter–enhancer: Comparison with a protein-coding mouse orthologue	不相关	--	--	GC-spd(ts),Hepa 1-6,293T	E_02_0877	PCR,Luciferase Reporter Assay	"We first investigated enhancer activity of hCNS1. Because TSS of TCAM1P--I and TCAM1P--III was +401 and three TSSs of TCAM1P--II were close to +401 (Fig. 2E), we cloned about 2--kb sequence upstream of +401 as a major promoter of the TCAM1P gene and connected it to the luciferase gene (TCAM1P--Pro--luc). hCNS1 was amplified by genome PCR and cloned to upstream of the TCAM1P promoter (hCNS1--Pro--luc) or to downstream of the luciferase gene(Pro--luc--hCNS1 and Pro--luc--rev hCNS1).The activity of hCNS1--Pro--luc was significantly increased in all three cell lines compared to the construct without hCNS1 (Fig. 3A).
"	Enhancer	--	Luciferase Reporter Assay	We also examined the luciferase activity in linearized constructs. If hCNS1 was actually a DPE, it might drive the transcription of the entire sequence in a circular plasmid, which might affect the luciferase gene expression.To prevent hCNS1 from driving the luciferase gene transcription in the sense direction, we linearized Pro--luc--hCNS1 and Pro--luc--rev hCNS1 constructs by cutting the immediate downstream sequence of hCNS1 and rev hCNS1. As a result, hCNS1 still significantly increased TCAM1P promoter activity in HEK293T cells, and the fold--increases were around 3 in both constructs compared to the linearized TCAM1P--Pro--luc construct (Fig. 3B). These data showed that hCNS1 could function as an enhancer for the TCAM1P gene.	TCAM1	--	--	--	--	--	--	--	--	--	TCAM1P
25605944	chr12	3944001	3947078	LDB1	Recently, using an engineered transcription unit as a model, LIM domain-binding protein 1 (LDB1) has been reported to be capable of mediating promoter:enhancer looping through LDB1 homodimerization	mouse		Low+High throughput	Enhancer-bound LDB1 regulates a corticotrope promoter-pausing repression program	否	--	--	AtT-20,Pituitary Corticotrope Cell	E_02_0878	ChIP-seq,3C,ChIP	Further, we have defined the subset of the enhancers that have active chromatin markers (H3K27ac and p300).Motif enrichment analysis of H3K27ac+ p300+ enhancers revealed enrichment of binding sites for the CCCTC-binding factor (CTCF), neurofibromin 1 (NF1), bHLH, FORKHEAD, X-BOX,and T-BOX families of transcription factors. Although members of the CTCF and NF1 family are general cellular transcription factors, the factors in the bHLH and other families may be critical for lineage development and enhancer programming in corticotropes.	Enhancer	3C,CRISPR/Cas9	qPCR,ChIP,GRO-seq	We found that enhancer:promoter interactions between LDB1-bound enhancers and the adjacent promoters of POMC and lung carcinoma myc related oncogene 1 (Lmyc1) genes were greatly diminished following knockdown of Ldb1.	ACTH,BE,Beta-LPH,Clip,Gamma-LPH,Npp-1,Pomc1,alpha-MSH,alphaMSH,beta-MSH,gamma-MSH,?Pomc	LDB1-mediated enhancer:promoter looping appears to be required for both activation and repression of these target genes	qPCR,3C,GRO-seq	Together,our data reveal that Enhancer-bound LDB1 has a role in mediating the actions of both activating and repressive Enhancers in a cell type_x0002_specific gene-regulation program.	--	--	--	--	--	--	Pomc
25604083	chr17	69487560	69491400	SOX9	An SRY-dependent testis-specific enhancer for Sox9 has been identified only in mice.	human	Somatic tissues	Low throughput	Copy number variation of two separate regulatory regions upstream of SOX9 causes isolated 46,XY or 46,XX disorder of sex development	相关	--	Disorders Of Sexual Development	HEK-293 cells	E_02_0879	Luciferase Reporter Assay,Transgenic mice	Finally, we performed transfections of reporter gene constructs under control of the minimal Sox9 promoter and additional XYSR fragments into various cell lines.For this, the 32.5 kb region was subdivided into 17 overlapping fragments,F1 to F17 (?gure 3). Whereas none of the conserved elements CNE1–7 showed Sertoli cell-speci?c activity (not shown),of all 24 constructs tested, F8 showed the highest luciferase activities in both Sertoli-like cell lines (see online supplementary ?gure S5A, B).In contrast, the same fragment had little in?uence on luciferase activity in both HEK293 and neuro-2a control cell lines (see online supplementary ?gure S5C, D). Even though F7 and F9 overlap with F8 (?gure 3 and online supplementary ?gure S6), their luciferase activities are weak in TM-4 and unremarkable in NT2/D1. Thus F8 appeared to be the best candidate for a testis-speci?c enhancer of the SOX9 gene.	Enhancer	--	Luciferase Reporter Assay,Transgenic mice	Finally, we performed transfections of reporter gene constructs under control of the minimal Sox9 promoter and additional XYSR fragments into various cell lines.For this, the 32.5 kb region was subdivided into 17 overlapping fragments,F1 to F17 (?gure 3). Whereas none of the conserved elements CNE1–7 showed Sertoli cell-speci?c activity (not shown),of all 24 constructs tested, F8 showed the highest luciferase activities in both Sertoli-like cell lines (see online supplementary ?gure S5A, B).In contrast, the same fragment had little in?uence on luciferase activity in both HEK293 and neuro-2a control cell lines (see online supplementary ?gure S5C, D). Even though F7 and F9 overlap with F8 (?gure 3 and online supplementary ?gure S6), their luciferase activities are weak in TM-4 and unremarkable in NT2/D1. Thus F8 appeared to be the best candidate for a testis-speci?c enhancer of the SOX9 gene.	CMD1,CMPD1,SRA1,SRXX2,SRXY10	--	--	--	SF1,WT1	BBP, D11S636, MBBP, ZCCHC25, ZFM1, ZNF162,AWT1, GUD, NPHS4, WAGR, WIT-2, WT33	Luciferase Reporter Assay	Such an enhancer should be under control of SRY, but could possibly also be in?uenced in its activity by other transcription factors present in the early gonad and essential for gonadal differentiation, including SF1 (also known as NR5A1), WT1, and GATA4. To test this assumption, a luciferase reporter containing F8 in front of the ?-globin TATA box was co-transfected in neuro-2a cells with expression plasmids for these factors. Of all factors tested, only SRY elicited a substantial 10-fold increase in luciferase activity. WT1 stimulated reporter activity two fold, whereas SF1 and GATA4 were completely ineffective (?gure 4A).	--	--	SOX9
25582196	chr10	62893206	62923461	Tet1	New transgenic reporters using Tet1 and Tet2 cis-regulatory domains may serve to distinguish nuanced changes in pluripotent states and the underlying epigenetic variations.	mouse	Embryonic tissue	Low+High throughput	Dynamic switching of active promoter and enhancer domains regulates Tet1 and Tet2 expression during cell state transitions between pluripotency and differentiation	否	--	--	embryonic stem cell	E_02_0880	ChIP-seq,Luciferase Reporter Assay	To identify cis-regulatory elements in Tet1, we surveyed its epigenome in mouse ESCs using ChIP-seq data sets.The combinatorial binding profiles of pluripotency factors, Mediator,and cohesin units have previously delineated a superenhancer domain in Tet1, a 15.2-kb region that spans from exon 1c at the distal end to a conserved noncoding sequence (CNS) upstream of the CDS ChIP-seq showed strong binding profiles of Oct4 within the CNS,as previously shown, but also several more strong peaks in the distal region between exons 1b and 1c.	Super-Enhancer	--	PCR,EMSA	Here we defined the promoter and Enhancer domains in Tet1 and Tet2.Within a 15- “superEnhancer” of Tet1,there are two transcription start sites (TSSs) with different activation patterns during development.	2510010B09Rik,AA517754,BB001228,Cxxc6,D10Ertd17e,LCX,mKIAA1676	--	--	--	Oct4,Sox2	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb	EMSA	Contribution of Oct and Sox motifs in Tet1 and Tet2 enhancer fragments.	--	--	Tet1
25582196	chr10	62893206	62923461	Tet2	New transgenic reporters using Tet1 and Tet2 cis-regulatory domains may serve to distinguish nuanced changes in pluripotent states and the underlying epigenetic variations.	mouse	Embryonic tissue	Low+High throughput	Dynamic switching of active promoter and enhancer domains regulates Tet1 and Tet2 expression during cell state transitions between pluripotency and differentiation	否	--	--	embryonic stem cell	E_02_0880	ChIP-seq,Luciferase Reporter Assay	To identify cis-regulatory elements in Tet1, we surveyed its epigenome in mouse ESCs using ChIP-seq data sets.The combinatorial binding profiles of pluripotency factors, Mediator,and cohesin units have previously delineated a superenhancer domain in Tet1, a 15.2-kb region that spans from exon 1c at the distal end to a conserved noncoding sequence (CNS) upstream of the CDS ChIP-seq showed strong binding profiles of Oct4 within the CNS,as previously shown, but also several more strong peaks in the distal region between exons 1b and 1c.	Super-Enhancer	--	PCR,EMSA	Here we defined the promoter and Enhancer domains in Tet1 and Tet2.Within a 15- “superEnhancer” of Tet1,there are two transcription start sites (TSSs) with different activation patterns during development.	2510010B09Rik,AA517754,BB001228,Cxxc6,D10Ertd17e,LCX,mKIAA1676	--	--	--	Oct4,Sox2	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb	EMSA	Contribution of Oct and Sox motifs in Tet1 and Tet2 enhancer fragments.	--	--	Tet1
25505291	chr1	23881244	23881761	Id3	Analysis of Id3 regulatory sequences revealed a novel enhancer, located between +4517 and 4662 bp, but the luciferase reporter assay demonstrated that this enhancer is not Smad2/3 dependent.	human		Low throughput	TGF-b1, but Not Bone Morphogenetic Proteins, Activates Smad1/5 Pathway in Primary Human Macrophages and Induces Expression of Proatherogenic Genes	不相关	--	Cardiometabolic Disorders	Human Monocytes/Macrophages	E_02_0881	Luciferase Reporter Assay	"Using ECR browser (http://ecrbrowser.dcode.org/), we found two conserved regions,ECR1 located between -3177 and -2660 bp upstream of transcription start and ECR2 located between +4517 and 4662 bp downstream of the gene (sequences provided in Supplemental Table 1). ECR1 overlaps with the enhancer described by Shepherd et al. (32), whereas ECR2 has not been described to date.
To test the impact of identi?ed ECRs on the regulation of Id3 expression, we cloned them into a pGL3basic vector together with about a 1-kb fragment of the Id3 promoter (Fig. 1A). Obtained plasmids were transfected using nucleofection into primary monocyte-derived macrophages cultivated in the presence of IL-4 and dexamethasone for 6 d. Cells after transfection were further cultivated for 24 h and then stimulated with TGF- 1forthenext 24 h. Cells were harvested and luciferase activity was measured. Without TGF- 1 stimulation, all reporter constructs showed low promoter activity. Stimulation of macrophages with TGF- 1ledto a 2-fold upregulation of the promoter activity. Addition of ECR1 or ECR2 led to a 5-fold increase of promoter activity. Reporter plasmid containing both of them showed nearly 12-fold upregulation of promoter activity, indicating that ECRs have an additive effect (Fig. 1B)."	Enhancer	--	Luciferase Reporter Assay	To test the impact of identi?ed ECRs on the regulation of Id3 expression, we cloned them into a pGL3basic vector together with about a 1-kb fragment of the Id3 promoter (Fig. 1A). Obtained plasmids were transfected using nucleofection into primary monocyte-derived macrophages cultivated in the presence of IL-4 and dexamethasone for 6 d. Cells after transfection were further cultivated for 24 h and then stimulated with TGF- 1forthenext 24 h. Cells were harvested and luciferase activity was measured. Without TGF- 1 stimulation, all reporter constructs showed low promoter activity. Stimulation of macrophages with TGF- 1ledto a 2-fold upregulation of the promoter activity. Addition of ECR1 or ECR2 led to a 5-fold increase of promoter activity. Reporter plasmid containing both of them showed nearly 12-fold upregulation of promoter activity, indicating that ECRs have an additive effect (Fig. 1B).	HEIR-1,bHLHb25	--	--	--	--	--	--	--	--	--	ID3
25486255	chr3	34743178	34776096	Sox2	The pluripotency of embryonic stem cells (ESCs) is maintained by a small group of master transcription factors including Oct4, Sox2 and Nanog.	mouse	Brain tissue	Low+High throughput	CRISPR Reveals a Distal Super-Enhancer Required for Sox2 Expression in Mouse Embryonic Stem Cells	否	--	--	embryonic stem cell	E_02_0882	ChIP-seq,RNA-seq	We examined ENCODE ChIP-seq data from 23 different mouse tissues or cell types focusing on the Sox2 locus. Using H3K27ac, a histone mark for active enhancers, we observed a distal SE that is only present in mouse ESC lines, which is approximately 100kb downstream from the Sox2 locus. This sequence spans a relatively large 13kb region, and corresponds to a recently defined super-enhancer or stretch enhancer.	Super-Enhancer	CRISPR/Cas9	PCR	We analyzed epigenomic data within the 1.5 Mb gene-desert regions around the Sox2 gene and identified a 13kb-long super-Enhancer (SE) located 100kb downstream of Sox2 in mouse ESCs.	Sox-2,lcc,ysb	SE is occupied by Oct4, Sox2, Nanog,and the mediator complex, and physically interacts with the Sox2 locus via DNA looping	RT-qPCR,ChIP-seq	To test the in vivo function of Sox2-SEdistal, we sought to delete the entire Enhancer sequence from the endogenous locus. Given that the SE spans a,13kb region, deletion of this region using conventional methods would be very inefficient.Therefore, we explored whether the recently developed CRISPR technology could be utilized to delete this large non-coding sequence in mouse ESCs.	Oct4,Sox2,Nanog	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Sox-2,lcc,ysb,2410002E02Rik,ENK,ecat4	ChIP-seq	First, we observed strong H3K27ac signal at this SE in two additional mouse ES cell lines (F123 and J1), indicating that usage of this SE is conserved across different mice strains.Previously published ChIP-seq data shows that Sox2-SEdistal is occupied by Oct4,Sox2 and Nanog.	--	--	Sox2
25486239	chr1	133303739	133325138	Kiss1	Taken together, the present results indicate that 5-upstream region of Kiss1 locus plays a critical role in Kiss1 gene expression in an ARC-specific manner and that the recruitment of estrogen receptor- and formation of a chromatin loop between the Kiss1 promoter and the 5 enhancer region may be required for the induction of ARC-specific Kiss1 gene expression.	mouse	ARC and AVPV tissues	Low+High throughput	Identification of Hypothalamic Arcuate Nucleus_x005f_x0002_Specific Enhancer Region of Kiss1 Gene in Mice	否	--	--	Kisspeptin-Immunoreactive Cell	E_02_0883	DNase-seq,Immunofluorescence,Luciferase Reporter Assay,PCR,3C	Using open Chromatin mapping by DNase-seq in HTE cell,the core of DHS-44 was localized to 600 at hg 19,Chr7:117075400-117076000.This region was marked by enrichment of H3K27Ac in 16HBE14o-cell,consistent with DHS-44 encompassing an active Enhancer element.	Enhancer	3C	Transgenic mice	The present study aimed to determine ARC-specific enhancer(s) of the Kiss1 gene by an in vivo reporter assay.The 3C assay was performed to detect interactions between the Kiss1 promoter region and the 5 -upstream region, the latter of which was identified as an ARCspecific enhancer in the present study	kisspeptin,metastatin	The 5'-upstream region of Kiss1 locus functions as an enhancer for ARC Kiss1 gene expression in mice.	3C	In addition,the current 3C and ER ChIP assays suggest that the Chromatin loop formation between the ARC-specific Enhancer and the promoter region of Kiss1 gene and unoccupied ER recruitment to the putative Enhancer region are involved in Kiss1 gene expression in the ARC	Eral1	2610524P08Rik,9130407C09Rik,AU019798,Era,M-ERA,MERA-S,MERA-W	ChIP	The binding of ERa in the 5' upstream region (Figure 4) was determined by a ChIP assay with ERa antibody.	--	--	Kiss1
25453903	chr14	97410723	97443618	VRK1	These divergent chromatin-remodeling patterns repress tumor suppressors and mesenchymal lineage regulators, while activating oncogenes and new potential therapeutic targets, such as the kinase VRK1.	human	bone	Low+High throughput	EWS-FLI1 utilizes divergent chromatin remodeling mechanisms to directly activate or repress enhancer elements in Ewing sarcoma		--	Ewing Sarcoma	HeLa,T cell	E_02_0884	shRNA,RNA-seq,qRT-PCR,3C,Immunohistochemistry	"Finally, we sought to address the impact of altered cis-regulatory element activity on the transcriptional landscape of Ewing sarcoma. We performed RNA sequencing (RNA-seq) in the Ewing sarcoma lines before and after EWS-FLI1 knock-down. By mapping EWS-FLI1 distal elements to the nearest expressed genes, we observed a strong relationship between changes in enhancer activity and changes in proximal gene expression (p < 10?10). We confirmed a subset of regulated gene targets by qRT-PCR.
We hypothesized that direct regulatory targets of EWS-FLI1 might represent attractive therapeutic targets in Ewing sarcoma and thus ranked target genes by combined changes in chromatin and expression (Fig. 5B). Another top candidate is VRK1, a cell cycle dependent tyrosine kinase involved in G2-M transition (Valbuena et al., 
2011). VRK1 is proximal to an EWS-FLI1 dependent enhancer that is active in Ewing sarcoma cell lines and primary tumors and induced de novo by the fusion protein in MSCs (Fig. 5C). 
Chromatin conformation studies (3C) confirmed the long distance interaction between the EWS-FLI1-bound enhancer and the VRK1 promoter in both SKNMC and A673 cells (Fig. 5D and E, respectively)."	Enhancer	3C	Immunohistochemistry,shRNA	"VRK1 is proximal to an EWS-FLI1 dependent Enhancer that is active in Ewing sarcoma cell lines and primary tumors and induced de novo by the fusion protein in MSCs
Chromatin conformation studies (3C) confirmed the long distance interaction between the EWS-FLI1-bound enhancer and the VRK1 promoter in both SKNMC and A673 
cells (Fig. 5D and E, respectively). VRK1 protein expression was confirmed in 15/15 primary Ewing sarcoma samples analyzed by immunohistochemistry, which revealed strong VRK1 signals in virtually all cells (Fig.6A and Fig. S5B). EWS-FLI1 knock-down markedly reduced VRK1 expression in the cell lines, while EWS-FLI1 induction was sufficient to up-regulate this kinase in MSCs (Fig. 6B and S5C)."	PCH1,PCH1A	--	--	--	EWSR1	EWS, EWS-FLI1, bK984G1.4，EWSR1	qRT-PCR,3C,shRNA	We performed RNA sequencing (RNA-seq) in the Ewing sarcoma lines before and after EWS-FLI1 knock-down.We confirmed a subset of regulated gene targets by qRT-PCR (Fig. S5A). VRK1 is proximal to an EWS-FLI1 dependent enhancer that is active in Ewing sarcoma cell lines and primary tumors and induced de novo by the fusion protein in MSCs (Fig. 5C).Chromatin conformation studies (3C) confirmed the long distance interaction between the EWS-FLI1-bound enhancer and the VRK1 promoter in both SKNMC and A673 cells (Fig. 5D and E, respectively). VRK1 protein expression was confirmed in 15/15 primary Ewing sarcoma samples analyzed by immunohistochemistry, which revealed strong VRK1 signals in virtually all cells (Fig.6A and Fig. S5B). EWS-FLI1 knock-down markedly reduced VRK1 expression in the cell lines, while EWS-FLI1 induction was sufficient to up-regulate this kinase in MSCs (Fig. 6B and S5C).	--	--	VRK1
25453760	chr2	167687771	167689503	Irf8	We show that Irf8 functions as a plasmacytoid DC epigenetic and fate-determining TF, regulating massive, cell-specific chromatin changes in thousands of pDC enhancers.	mouse		Low+High throughput	A Negative Feedback Loop of Transcription Factors Specifies Alternative Dendritic Cell Chromatin States	否	--	--	monocyte cells	E_02_0885	ChIP-seq,ATAC-seq	analysis of active enhancers (H3K27ac) revealed the same relationship between H3K27ac intensity and cell type specific genes. ChIP-Seq of in vivo splenic pDCs showed similar patterns to our in vitro pDC model with respect to H3K4me1 and H3K27ac in enhancer regions associated to pDC and moDC specific genes	Enhancer	--	qPCR,RNA-seq,Western blot	Taken together,our results suggest that Irf8 and Cebpb form a double negative feedback loop and a positive self-auto-regulatory loop.Such a composite self-reinforcing negative feedback loop confers bi-stability,leading to either expression of one TF or the other;as a consequence, the entire epigenetic landscape is directed towards either a pDC or moDC Enhancer state.	C/EBPbeta,CRP2,IL-6DBP,LAP,LIP,NF-IL6,NF-M,Nfil6	--	--	--	Tcf4,Spib,Bcl11a	5730422P05Rik,ASP-I2,E2-2,E2.2,ITF-2,ITF-2b,ITF2,ME2,MITF-2A,MITF-2B,SEF-2,SEF2,SEF2-1,TFE,Tcf-4,bHLHb19,Spi-B,2810047E18Rik,BCL-11A,Ctip1,D930021L15Rik,Evi9,Evi9a,Evi9b,Evi9c,mKIAA1809	ATAC-seq,ChIP-seq	To better focus on open chromatin accessible to TF binding within these Enhancers, we narrowed down our search to overlapping peak of ATAC-seq signal.	--	--	Cebpb
25381333	chr22	42411333	42413643	CYP2D6	To characterize the CYP2D6 enhancer element,we applied chromatin conformation capture combined with the next-generation sequencing (4C assays) and chromatin immunoprecipitation with P300 antibody, in HepG2 and human primary culture hepatocytes.	human	Liver tissues	Low throughput	Functional characterization of CYP2D6 enhancer polymorphisms	相关	rs133333	--	Primary human hepatocytes	E_02_0886	4C,ChIP	"To search for regions that interact with the CYP2D6 promoter, we performed 4C assays with the CYP2D6 promoter as an anchor.With the exception of R1 and R6, peak
signals were all associated with an annotated gene locus (gene body, promoter or upstream region, R2, R3, R4, R5 and R7), suggesting cross-regulation between genes. R1 corresponds to the previously identi?ed downstream enhancer region (7), while R6 appears to be novel.
To test whether any of these regions could serve as an enhancer, we performed ChIP assays with an antibody against P300, a universal transcription co-factor that binds to enhancer elements. R1 and R2 displayed the highest signals in both HepG2 and hepatocytes (Fig. 1B and C), consistent with R1 serving as an enhancer for CYP2D6, while R2 corresponds to the 3′ end of CYP2D6, indicative of active transcription of CYP2D6 in both cells. R6 showed low ChIP signals in both cells, arguing against an enhancer role."	Enhancer	4C	ChIP	"To search for regions that interact with the CYP2D6 promoter, we performed 4C assays with the CYP2D6 promoter as an anchor.With the exception of R1 and R6, peak
signals were all associated with an annotated gene locus (gene body, promoter or upstream region, R2, R3, R4, R5 and R7), suggesting cross-regulation between genes. R1 corresponds to the previously identi?ed downstream enhancer region (7), while R6 appears to be novel.
To test whether any of these regions could serve as an enhancer, we performed ChIP assays with an antibody against P300, a universal transcription co-factor that binds to enhancer elements. R1 and R2 displayed the highest signals in both HepG2 and hepatocytes (Fig. 1B and C), consistent with R1 serving as an enhancer for CYP2D6, while R2 corresponds to the 3′ end of CYP2D6, indicative of active transcription of CYP2D6 in both cells. R6 showed low ChIP signals in both cells, arguing against an enhancer role."	CPD6,CYP2D,CYP2D7AP,CYP2D7BP,CYP2D7P2,CYP2D8P2,CYP2DL1,CYPIID6,P450-DB1,P450C2D,P450DB1	A region 115 kb downstream of CYP2D6 as Enhancer for CYP2D6, containing two completely linked SNPs, rs133333 and rs5758550, associated with enhanced transcription.	DNaseI Accessibility Assay,qPCR,CRISPR/Cas9	"To determine the relative chromatin accessibility along the R1 region, we performed DNaseI accessibility assays in both HepG2 and primary human hepatocytes,
followed by real-time PCR (12). As expected, the region surrounding rs5758550 (A5) showed the highest accessibility in both cell types (Fig. 4), consistent with its role as enhancer.Among three highly linked SNPs in this region, we identify rs5758550 as the causative variant that regulates enhancer activity, with the minor allele rs5758550G displaying higher activity than the major allele rs5758550A. Moreover, using CRISPR-mediated genomic deletion in HepG2 cells, we demonstrate that deletion of the enhancer region surrounding rs5758550 by 70% decreased CYP2D6 mRNA level >2-fold."	--	--	--	--	42412365	4C,ChIP,Luciferase Reporter Assay,PCR	CYP2D6
25369933	chr15	63254341	63256341	Myc	The protooncogene c-Myc (Myc) is a critical target of Notch in normal and malignant pre-T cells, but how Notch regulates Myc is unknown.	mouse		Low+High throughput	Long-range enhancer activity determines Myc sensitivity to Notch inhibitors in T cell leukemia	否	--	Acute Lymphoblastic Leukemia	T cell	E_02_0887	ChIP-seq,EMSA,3C	Notch1 is depleted from the NDME site by short-term gammasecretase inhibitor (GSI) treatment, and loading and unloading of Notch1 is associated with rapid changes in H3K27ac, features that characterize genomic Notch1 binding sites that dynamically regulate gene expression.Notch1 also bound the NDME in primary murine T-ALL cells and in DN3 thymocytes, a stage of T-cell development marked by high levels of Notch1 activation	Enhancer	3C	ChIP,qRT-PCR,Luciferase Reporter Assay	Schematic of the Luciferasegene constructs including the NDME WT and mutant sequences.To test for chromatin looping between the NDME and the Myc promoter, chromatin conformation capture (3C) assays were carried out in T6E cells.	AU0167572,Niard,Nird,bHLHe39,?Myc	Altered long-range enhancer activity can mediate resistance to targeted therapies and provide a mechanistic rationale for combined targeting of Notch and Brd4 in leukemia.	3C	To determine whether Notch signaling was required to maintain the interaction between the Myc promoter and the NDME,3C analysis was performed in T6E cells cultured in the presence or absence of GSI.	Notch	9930111A19Rik,Mis6,N1,Tan1,lin-12	ChIP-seq,3C	Analysis of the ChIP-seq data revealed an RBPJ/Notch1 binding site associated with high levels of H3K4me1 marks located 1.43 Mb 3′ of the Myc promoter (Fig. 4A) that shares sequence homology with the murine NDME.	--	--	Myc
25369933	chr15	63254341	63256341	Brd4	These findings indicate that altered long-range enhancer activity can mediate resistance to targeted therapies and provide a mechanistic rationale for combined targeting of Notch and Brd4 in leukemia.	mouse		Low+High throughput	Long-range enhancer activity determines Myc sensitivity to Notch inhibitors in T cell leukemia	否	--	Acute Lymphoblastic Leukemia	T cell	E_02_0887	ChIP-seq,EMSA,3C	Notch1 is depleted from the NDME site by short-term gammasecretase inhibitor (GSI) treatment, and loading and unloading of Notch1 is associated with rapid changes in H3K27ac, features that characterize genomic Notch1 binding sites that dynamically regulate gene expression.Notch1 also bound the NDME in primary murine T-ALL cells and in DN3 thymocytes, a stage of T-cell development marked by high levels of Notch1 activation	Enhancer	3C	ChIP,qRT-PCR,Luciferase Reporter Assay	Schematic of the Luciferasegene constructs including the NDME WT and mutant sequences.To test for chromatin looping between the NDME and the Myc promoter, chromatin conformation capture (3C) assays were carried out in T6E cells.	AU0167572,Niard,Nird,bHLHe39,?Myc	Altered long-range enhancer activity can mediate resistance to targeted therapies and provide a mechanistic rationale for combined targeting of Notch and Brd4 in leukemia.	3C	To determine whether Notch signaling was required to maintain the interaction between the Myc promoter and the NDME,3C analysis was performed in T6E cells cultured in the presence or absence of GSI.	Notch	9930111A19Rik,Mis6,N1,Tan1,lin-12	ChIP-seq,3C	Analysis of the ChIP-seq data revealed an RBPJ/Notch1 binding site associated with high levels of H3K4me1 marks located 1.43 Mb 3′ of the Myc promoter (Fig. 4A) that shares sequence homology with the murine NDME.	--	--	Myc
25321476	chr10	34385685	34385834	Col10a1	Meanwhile, as a specific marker of hypertrophic chondrocytes, the type X collagen gene (COL10A1) is also critical for endochondral bone formation, as mutation and altered COL10A1 expression are often accompanied by abnormal chondrocyte hypertrophy in many skeletal diseases.	mouse		Low throughput	Identification and characterization of the novel Col10a1 regulatory mechanism during chondrocyte hypertrophic differentiation	否	--	Skeletal Diseases	MCT Cell，T cell	E_02_0888	Transgenic mice,ChIP,qRT-PCR,EMSA	These results show that multiple copies of the enhancer (150-bp Col10a1 distal promoter) mediates higher level and cellspecific reporter activity, whereas the 10-kb Col10a1 promoter/intronic element contains nonspecific regulatory elements,in addition to the 150-bp enhancer.	Enhancer	--	ChIP,qRT-PCR,EMSA	Top panel displays Col10a1 gene structure and the 10 -kb promoter and intronic element.Positions of the 150-bp (?4296 to ?4147 bp) Col10a1 cis-Enhancer (purple bar) and its 330-bp (?220 to +110 bp) basal promoter (red bar) are shown.	Col10,Col10a-1	--	--	--	Runx2	AML3,Cbf,Cbfa-1,Cbfa1,LS3,Osf2,PEBP2aA,Pebp2a1,Pebpa2a	qRT-PCR,EMSA	The qRT-PCR was performed to examine the mRNA transcript level of marker genes Col10a1 and Runx2 in MCT cells. As illustrated, both Col10a1 and Runx2 are significantly upregulated in hypertrophic MCT cells compared with that in proliferative MCT cells.	--	--	Col10a1
25303440	chr7	94002773	94005073	COL1A2	Gene activa_x0002_tion was determined by assessing the interaction of transcription factors with the COL1A2 enhancer using transient transfection of reporter gene constructs, elec_x0002_trophoretic mobility shift assays, chromatin immuno_x0002_precipitation analysis, and RNA interference involving knockdown of individual AP-1 family members.	human	Skin tissue	Low throughput	Failed Degradation of JunB Contributes to Overproduction of Type I Collagen and Development of Dermal Fibrosis in Patients With Systemic Sclerosis	不相关	--	Systemic Sclerosis	fibroblast	E_02_0889	Luciferase Reporter Assay	"TGFβ is a potent inducer of the human procollagen type I α2 chain gene ( COL1A2). We have recently described in detail the in vivo mechanism underlying the transcriptional control of COL1A2, through a complex interaction between its distal enhancer and proximal promoter, in response to TGFβ. Reporter gene constructs containing the wild-type human enhancer region and the heterologous thymidine kinase (TK) promoter, lacking a Smad-dependent T RE (21.1/18.8pLAC-TK), were used to
assess the TβRE in the FUE region. The results indicated that the COL1A2-FUE was activated by TGFβ in both normal and scleroderma fibroblasts."	Enhancer	--	Luciferase Reporter Assay,EMSA,ChIP,siRNA	Gene activation was determined by assessing the interaction of transcription factors with the COL1A2 Enhancer using transient transfection of reporter gene constructs,electrophoretic mobility shift assays,chromatin immunoprecipitation analysis,and RNA interference involving knockdown of individual AP-1 family members.	EDSARTH2,EDSCV,OI4	Binding of JunB to the COL1A2 enhancer was observed, with its coalescence directed by activation of gene transcription through the proximal promoter.	ChIP	RNA polymeraseII also coprecipitated with the F2 Enhancer sequence,despite not being able to bind the Enhancer directly,thereby demonstrating the interaction between the transcriptional machinery in the promoter with the factors bound to the F2 region.	JUNB,JUND	AP-1,AP1,C-JUN, CJUN,P39	EMSA,ChIP	"Supershift assays using specific antibodies (Figure 2B) revealed that normal nuclear extracts bound c-Jun and, to a lesser extent, JunD. In SSc, c-Jun binding
was greatly reduced, and JunB, which was previously absent in normal nuclear extracts, accounted for 2 of the shifted bands. JunD binding was more pronounced in
SSc extracts (Figure 2B). These gel-shift findings suggest that in SSc dermal fibroblasts or in normal nuclea extracts treated with TGF , JunB binding replaces c-Jun binding on the AP-1 site in the upstream enhancer.These results were confirmed using ChIP assays,which demonstrated the association of the F2 region in
the FUE with the proximal promoter and the transcriptional machinery."	--	--	COL1A2
25271055	chr11	102006458	102008458	MEF2C	Finally, increased sclerostin production achieved by HDAC5 shRNA is abrogated by simultaneous knockdown of MEF2C, indicating that MEF2C is a major target of HDAC5 in osteocytes.	mouse	HDAC5-/- tissue	Low throughput	HDAC5 controls MEF2C-driven sclerostin expression in osteocytes	否	--	--	Osteocyte Cell Lines	E_02_0890	Luciferase Reporter Assay,ChIP	Three lines of evidence support a direct role for HDAC5 in regulating MEF2C activity at the +45 kB SOST enhancer over the course of osteocyte differentiation. First, HDAC5 shRNA causes increased activity of this element, but not of the proximal SOST promoter, in luciferase assays. MEF2C shRNA reduces the activity of this enhancer. Second, HDAC5 overexpression dose-dependently inhibits the activity of a MEF2-driven reporter from the desmin and the SOST’9’ (+45kB) enhancer. Third, endogenous HDAC5 association with this region in control (but not HDAC5 shRNA) Ocy454 cells can be detected by ChIP.	Enhancer	--	ChIP,qRT-PCR,Western blot	Using Chromatin immunoprecipitation,we have mapped endogenous MEF2C binding in the SOST gene to a distal intergenic Enhancer 45 downstream from the transcription start site.	5430411E23Rik	--	--	--	Mef2c	5430401D19Rik,9930028G15Rik,AV011172,Mef2	ChIP,PCR	We performed Chromatin immunoprecipitation (ChIP) to determine MEF2C occupancy in Ocy454 cell cultured at 37°C for 14 days (a time point in which SOST expression is High throughput).	--	--	Sost
25271055	chr11	102006458	102008458	SOST	HDAC5 associates with and regulates the transcriptional activity of this enhancer, suggesting direct regulation of SOST gene expression by HDAC5 in osteocytes.	mouse	HDAC5-/- tissue	Low throughput	HDAC5 controls MEF2C-driven sclerostin expression in osteocytes	否	--	--	Osteocyte Cell Lines	E_02_0890	Luciferase Reporter Assay,ChIP	Three lines of evidence support a direct role for HDAC5 in regulating MEF2C activity at the +45 kB SOST enhancer over the course of osteocyte differentiation. First, HDAC5 shRNA causes increased activity of this element, but not of the proximal SOST promoter, in luciferase assays. MEF2C shRNA reduces the activity of this enhancer. Second, HDAC5 overexpression dose-dependently inhibits the activity of a MEF2-driven reporter from the desmin and the SOST’9’ (+45kB) enhancer. Third, endogenous HDAC5 association with this region in control (but not HDAC5 shRNA) Ocy454 cells can be detected by ChIP.	Enhancer	--	ChIP,qRT-PCR,Western blot	Using Chromatin immunoprecipitation,we have mapped endogenous MEF2C binding in the SOST gene to a distal intergenic Enhancer 45 downstream from the transcription start site.	5430411E23Rik	--	--	--	Mef2c	5430401D19Rik,9930028G15Rik,AV011172,Mef2	ChIP,PCR	We performed Chromatin immunoprecipitation (ChIP) to determine MEF2C occupancy in Ocy454 cell cultured at 37°C for 14 days (a time point in which SOST expression is High throughput).	--	--	Sost
25271055	chr11	102006458	102008458	HDAC5	HDAC5 associates with and regulates the transcriptional activity of this enhancer, suggesting direct regulation of SOST gene expression by HDAC5 in osteocytes.	mouse	HDAC5-/- tissue	Low throughput	HDAC5 controls MEF2C-driven sclerostin expression in osteocytes	否	--	--	Osteocyte Cell Lines	E_02_0890	Luciferase Reporter Assay,ChIP	Three lines of evidence support a direct role for HDAC5 in regulating MEF2C activity at the +45 kB SOST enhancer over the course of osteocyte differentiation. First, HDAC5 shRNA causes increased activity of this element, but not of the proximal SOST promoter, in luciferase assays. MEF2C shRNA reduces the activity of this enhancer. Second, HDAC5 overexpression dose-dependently inhibits the activity of a MEF2-driven reporter from the desmin and the SOST’9’ (+45kB) enhancer. Third, endogenous HDAC5 association with this region in control (but not HDAC5 shRNA) Ocy454 cells can be detected by ChIP.	Enhancer	--	ChIP,qRT-PCR,Western blot	Using Chromatin immunoprecipitation,we have mapped endogenous MEF2C binding in the SOST gene to a distal intergenic Enhancer 45 downstream from the transcription start site.	5430411E23Rik	--	--	--	Mef2c	5430401D19Rik,9930028G15Rik,AV011172,Mef2	ChIP,PCR	We performed Chromatin immunoprecipitation (ChIP) to determine MEF2C occupancy in Ocy454 cell cultured at 37°C for 14 days (a time point in which SOST expression is High throughput).	--	--	Sost
25267720	chr10	43568986	43571244	RET	RET is regulated by a distal and a proximal enhancer at its promoter, in which PAX3 and NKX2-1 are the resident transcription factors respectively.	human	Hirschsprung tissue	Low throughput	SRY interference of normal regulation of the RET gene suggests a potential role of the Y-chromosome gene in sexual dimorphism in Hirschsprung disease	不相关	--	Hirschsprung Disease	neural crest cell	E_02_0891	RT-PCR,Luciferase Reporter Assay	"To determine the probable function of SRY on the transactivation of RET by NKX2-1 and PAX3, we had exam_x0002_ined its effects in a reporter system with a luciferase gene directed
by a 3.7 kb promoter (23531 to +196) of the human RET gene(27), harboring both distal and proximal enhancers."	Enhancer	--	Luciferase Reporter Assay	However, when either SOX10 or PAX3 was co-transfected with NKX2-1, significant exacerbations of the RET1.5-luciferase activities were observed (Fig. 2D), suggesting potential interactions and collaborations between these transcription factors and NKX2-1 on regulation of RET gene.	CDHF12,CDHR16,HSCR1,MEN2A,MEN2B,MTC1,PTC,RET-ELE1	--	--	--	PAX3,NKX2-1	CDHS,HUP2,WS1,WS3,BCH,BHC,NK-2,NKX2.1,NKX2A,NMTC1,T/EBP,TEBP,TITF1,TTF-1,TTF1	Luciferase Reporter Assay,GST Pull-down Assay	SOX10 and SRY competitive interactions with NKX2-1and PAX3 demonstrated by GST pull-down assays,Transfection with either the pM-NKX2-1 or pM-PAX3 expression vectors with the UAS-luciferase reporter showed that the GAL4-BD was indeed capable bringing these two transcription factors to the UAS site, thereby transactivating the UAS-luciferase reporter in the transfected Neuro-2A cells. 	--	--	RET
25267720	chr10	43568986	43571244	PAX3	RET is regulated by a distal and a proximal enhancer at its promoter, in which PAX3 and NKX2-1 are the resident transcription factors respectively.	human	Hirschsprung tissue	Low throughput	SRY interference of normal regulation of the RET gene suggests a potential role of the Y-chromosome gene in sexual dimorphism in Hirschsprung disease	不相关	--	Hirschsprung Disease	neural crest cell	E_02_0891	RT-PCR,Luciferase Reporter Assay	"To determine the probable function of SRY on the transactivation of RET by NKX2-1 and PAX3, we had exam_x0002_ined its effects in a reporter system with a luciferase gene directed
by a 3.7 kb promoter (23531 to +196) of the human RET gene(27), harboring both distal and proximal enhancers."	Enhancer	--	Luciferase Reporter Assay	However, when either SOX10 or PAX3 was co-transfected with NKX2-1, significant exacerbations of the RET1.5-luciferase activities were observed (Fig. 2D), suggesting potential interactions and collaborations between these transcription factors and NKX2-1 on regulation of RET gene.	CDHF12,CDHR16,HSCR1,MEN2A,MEN2B,MTC1,PTC,RET-ELE1	--	--	--	PAX3,NKX2-1	CDHS,HUP2,WS1,WS3,BCH,BHC,NK-2,NKX2.1,NKX2A,NMTC1,T/EBP,TEBP,TITF1,TTF-1,TTF1	Luciferase Reporter Assay,GST Pull-down Assay	SOX10 and SRY competitive interactions with NKX2-1and PAX3 demonstrated by GST pull-down assays,Transfection with either the pM-NKX2-1 or pM-PAX3 expression vectors with the UAS-luciferase reporter showed that the GAL4-BD was indeed capable bringing these two transcription factors to the UAS site, thereby transactivating the UAS-luciferase reporter in the transfected Neuro-2A cells. 	--	--	RET
25267720	chr10	43568986	43571244	NKX2-1	RET is regulated by a distal and a proximal enhancer at its promoter, in which PAX3 and NKX2-1 are the resident transcription factors respectively.	human	Hirschsprung tissue	Low throughput	SRY interference of normal regulation of the RET gene suggests a potential role of the Y-chromosome gene in sexual dimorphism in Hirschsprung disease	不相关	--	Hirschsprung Disease	neural crest cell	E_02_0891	RT-PCR,Luciferase Reporter Assay	"To determine the probable function of SRY on the transactivation of RET by NKX2-1 and PAX3, we had exam_x0002_ined its effects in a reporter system with a luciferase gene directed
by a 3.7 kb promoter (23531 to +196) of the human RET gene(27), harboring both distal and proximal enhancers."	Enhancer	--	Luciferase Reporter Assay	However, when either SOX10 or PAX3 was co-transfected with NKX2-1, significant exacerbations of the RET1.5-luciferase activities were observed (Fig. 2D), suggesting potential interactions and collaborations between these transcription factors and NKX2-1 on regulation of RET gene.	CDHF12,CDHR16,HSCR1,MEN2A,MEN2B,MTC1,PTC,RET-ELE1	--	--	--	PAX3,NKX2-1	CDHS,HUP2,WS1,WS3,BCH,BHC,NK-2,NKX2.1,NKX2A,NMTC1,T/EBP,TEBP,TITF1,TTF-1,TTF1	Luciferase Reporter Assay,GST Pull-down Assay	SOX10 and SRY competitive interactions with NKX2-1and PAX3 demonstrated by GST pull-down assays,Transfection with either the pM-NKX2-1 or pM-PAX3 expression vectors with the UAS-luciferase reporter showed that the GAL4-BD was indeed capable bringing these two transcription factors to the UAS site, thereby transactivating the UAS-luciferase reporter in the transfected Neuro-2A cells. 	--	--	RET
25267720	chr10	43568986	43571244	SRY	Loss-of-function mutations of HSCR genes and haploinsufficiency of their gene products are the primary pathogenic mechanisms for disease development.	human	Nervous tissue	Low throughput	SRY interference of normal regulation of the RET gene suggests a potential role of the Y-chromosome gene in sexual dimorphism in Hirschsprung disease.	否	--	Hirschsprung Disease	neural crest cell	E_02_0891	RT-PCR,Luciferase Reporter Assay	"To determine the probable function of SRY on the transactivation of RET by NKX2-1 and PAX3, we had exam_x0002_ined its effects in a reporter system with a luciferase gene directed
by a 3.7 kb promoter (23531 to +196) of the human RET gene(27), harboring both distal and proximal enhancers."	Enhancer	--	Luciferase Reporter Assay	However, when either SOX10 or PAX3 was co-transfected with NKX2-1, significant exacerbations of the RET1.5-luciferase activities were observed (Fig. 2D), suggesting potential interactions and collaborations between these transcription factors and NKX2-1 on regulation of RET gene.	CDHF12,CDHR16,HSCR1,MEN2A,MEN2B,MTC1,PTC,RET-ELE1	--	--	--	PAX3,NKX2-1	CDHS,HUP2,WS1,WS3,BCH,BHC,NK-2,NKX2.1,NKX2A,NMTC1,T/EBP,TEBP,TITF1,TTF-1,TTF1	Luciferase Reporter Assay,GST Pull-down Assay	SOX10 and SRY competitive interactions with NKX2-1and PAX3 demonstrated by GST pull-down assays,Transfection with either the pM-NKX2-1 or pM-PAX3 expression vectors with the UAS-luciferase reporter showed that the GAL4-BD was indeed capable bringing these two transcription factors to the UAS site, thereby transactivating the UAS-luciferase reporter in the transfected Neuro-2A cells. 	--	--	RET
25263596	chr1	182851627	182852853	Tet2	By mapping DNA methylation and hydroxymethylation at base resolution, we find that deletion of Tet2 causes extensive loss of 5hmC at enhancers, accompanied by enhancer hypermethylation, reduction of enhancer activity, and delayed gene induction in the early steps of differentiation.	mouse		Low+High throughput	5mC Oxidation by Tet2 Modulates Enhancer Activity and Timing of Transcriptome Reprogramming during Differentiation	否	--	--	embryonic stem cell	E_02_0892	ChIP-seq,ChIP	We therefore hypothesized that loss of Tet2 could lead to reduced oxidation and increased 5mC at enhancers. Indeed, hypermethylated DMRs (hyper-DMRs) in Tet2?/? cells exhibit several hallmarks of enhancers including: evolutionary sequence conservation,enrichment for enhancer chromatin marks H3K4me1 and H3K27ac, and significant overlap with co-activator p300 binding sites (o/e = 5.9, p < 1E-200), DNase I hypersensitive sites(o/e = 4.5, p < 1E-200), and predicted enhancers(o/e = 7.1, p < 1E-200)	Enhancer	--	PCR,Transgenic mice	Indeed,an Enhancer that physically interacts with the developmental gene Left-Right Determination Factor 1 (Lefty1) is hypermethylated and hypoacetylated in Tet6?/? cells,potentially explaining the significantly decreased expression of this gene.	AI450052,Ebaf,Leftb,Stra3,Tgfb4,lefty,lefty-1	--	--	--	Oct4,Sox4,Nanog	EZF,Gklf,Zie,NF-A3,Oct-3,Oct-3/4,Oct-4,Oct3,Oct3/4,Oct4,Otf-3,Otf-4,Otf3,Otf3-rs7,Otf3g,Otf4,2410002E02Rik,ENK,ecat4,Sox-2,lcc,ysb	ChIP-seq	Weaker occupancy of the ES-cell core transcription factors (TFs) OCT4,SOX6,and NANOG than those that do not change DNA methylation status.	--	--	Lefty1
25259561	chr7	117075514	117075933	CFTR	Cystic fibrosis transmembrane conductance regulator gene (CFTR) expression in human airway epithelial cells involves the recruitment of distal cis-regulatory elements	human	Epithelial tissues	Low throughput	Oxidative stress regulates CFTR gene expression in human airway epithelial cells through a distal antioxidant response element.	否	--	--	bronchial epithelial cell	E_02_0893	Luciferase Reporter Assay,EMSA,RT-PCR,ChIP	To confirm that DHS-44kb contained an enhancer of CFTR expression, the 0.6-kb DHS fragment (hg 19, chr7:117075400–117076000) was PCR amplified and inserted into the enhancer site of the pGL3B 245 vector.These data suggest that the enhancer activity of the DHS-44kb element is specific to airway epithelial cells.	Enhancer	--	RT-PCR,ChIP	To determine whether the SFN_x0002_triggered antioxidant response regulates CFTR expression directly through the DHS-44(279) cis-element, ChIP was used to measure the enrichment levels of the constitutive ARE binding factor Bach1, the SFN-induced ARE binding factor Nrf2, and their common partner MafK at this site.	ABC35,ABCC7,CF,CFTR/MRP,MRP7,TNR-CFTR,dJ760C5.1	--	--	--	NFKB1,BACH1	CVID12,EBP-1,KBF1,NF-kB,NF-kB1,NF-kappa-B1,NF-kappaB,NFKB-p105,NFKB-p50,NFkappaB,p105,p50,BACH-1,BTBD24	EMSA	EMSAs were performed with 32P-labeled, double-stranded DNA probes for 44-I, 44-II, and 44-III,Moreover, when Bach1 was overexpressed in 16HBE14o- cells by transient transfection of a mouse Bach1 cDNA clone, a strong supershift was seen with the Bach1 antibody and probe 44-I.	--	--	CFTR
25249570	chr9	99131669	99132862	Pik3cb	Pik3cb is a crucial direct target of YAP, through which the YAP activates phosphoinositol-3-kinaseAKT pathway and regulates cardiomyocyte proliferation and survival.	mouse	Heart	Low+High throughput	Pi3kcb Links Hippo-YAP and PI3K-AKT Signaling  Pathways to Promote Cardiomyocyte Proliferation and Survival	否	--	Heart Injuries	ventricular cardiac muscle cell	E_02_0894	Luciferase Reporter Assay,ChIP-seq	To measure the transcriptional activity of the YAP-bound region of Pik3cb, which we refer to as the Pik3cb enhancer, we cloned a 552 bp genomic DNA fragment containing the conserved element and potential TEAD binding sites into a minimal promoter luciferase reporter construct. Co-transfection with Yap in NRVMs showed that Yap stimulates activity of the enhancer by ~5-fold.	Enhancer	--	qRT-PCR,ChIP-qPCR	To measure the transcriptional activity of the YAP-bound region of Pik3cb, which we refer to as the Pik3cb Enhancer, we cloned a 552 bp genomic DNA fragment containing the conserved element and potential TEAD binding sites into a minimal promoter luciferase reporter construct.	1110001J02Rik,AI447572,p110beta	YAP and TEAD occupied a conserved Enhancer within the first intron of Pik3cb, and this Enhancer drove YAP_x0002_dependent reporter gene expression.	ChIP-seq,ChIP-qPCR,Luciferase Reporter Assay	To measure the transcriptional activity of the YAP-bound region of Pik3cb, which we refer to as the Pik3cb Enhancer, we cloned a 552 bp genomic DNA fragment containing the conserved element and potential TEAD binding sites into a minimal promoter luciferase reporter construct. Co-transfection with Yap in NRVMs showed that Yap stimulates activity of the Enhancer by ~5-fold. 	Yap1	AI325207,Yap,Yap65,Yki,Yorkie	ChIP-seq,ChIP-qPCR,Luciferase Reporter Assay	The HL1 ChIP-seq data revealed a YAP-bound sequence residing in the first intron of Pik3cb (Fig. 2A). We validated YAP binding to the identified sequence by ChIP-qPCR,using a pair of primers spanning the YAP bound sequence and a control pair recognizing a sequence 1.3 kb away.	--	--	Pik3cb
25248036	chr2	217918268	217921910	IGFBP5	Evidence suggests that the g-allele confers increased breast cancer susceptibility through relative downregulation of IGFBP5, a gene with known roles in breast cell biology.	human	Mammary tissue	Low+High throughput	Evidence that breast cancer risk at the 2q35 locus is mediated through IGFBP5 regulation.	是	rs4442975	Breast Cancer	breast cancer cell	E_02_0895	Luciferase Reporter Assay,ChIP-seq,3C,PCR	The strongest candidate for causality, SNP rs4442975, flanks a transcriptional enhancer that physically interacts with the promoter of IGFBP5. Furthermore, we demonstrate that rs4442975 is associated with allele_x0002_specific FOXA1 binding, chromatin looping and IGFBP5 expression. Our data suggest that the g-allele of rs4442975 confers increased breast cancer susceptibility through reduced IGFBP5 expression.	Enhancer	3C	--	This SNP flanks a transcriptional enhancer that physically interacts with the promoter of IGFBP5 (encoding insulin-like growth factor-binding protein 5) and displays allele-specific gene expression, FOXA1 binding and chromatin looping. Evidence suggests that the g-allele confers increased breast cancer susceptibility through relative downregulation of IGFBP5, a gene with known roles in breast cell biology.	IBP5	--	--	--	FOXA1	HNF3A,TCF3A	qPCR,ChIP-seq	To assess occupancy of FOXA1 in vivo, we conducted ChIP followed by allele-specific quantitative PCR (qPCR) in the heterozygous BT474 breast cancer cell line.	217920769	ChIP-seq,ChIP,qPCR,ChIP-qPCR,3C	IGFBP5
25223790	chr17	35502632	35504632	Nanog	In this study, we set out to systematically evaluate the performance of these two rising technologies in reactivation or repression of endogenous pluripotency genes (Oct4 and Nanog) in reprogramming somatic cells or EpiSCs to iPSCs.	mouse		Low throughput	Comparison of TALE designer transcription factors and the CRISPR/dCas9 in regulation of gene expression by targeting enhancers	否	--	--	embryonic stem cell	E_02_0896	Luciferase Reporter Assay,ChIP,ChIP-qPCR	We first investigated activation of the Oct4 enhancer by luciferase reporter assay 48 h after transfection of TALE-A and dCas9-A/gRNA in MEFs. These luciferase constructs contain the 2.4 kb region covering all three upstream regulatory elements of the Oct4 locus	Enhancer	CRISPR/Cas9	qRT-PCR,Luciferase Reporter Assay	The Oct4 luciferase assay reporter constructs carried the genomic DNA 2.4 kb upstream of the Oct4 transcrip_x0002_tion start site (TSS). The region encompasses the 1.7 kb distal and proximal Enhancers and the 0.2 kb promoter.	NF-A3,Oct-3,Oct-3/4,Oct-4,Oct3,Oct3/4,?Oct4,Otf-3,Otf-4,Otf3,Otf3-rs7,Otf3g,Otf4	--	--	--	Klf4,Oct4,Nanog,Sox2	EZF,Gklf,Zie,NF-A3,Oct-3,Oct-3/4,Oct-4,Oct3,Oct3/4,Oct4,Otf-3,Otf-4,Otf3,Otf3-rs7,Otf3g,Otf4,2410002E02Rik,ENK,ecat4,Sox-2,lcc,ysb	ChIP-seq	To address this possibility, we reviewed the ChIP-seq information of several pluripotency transcription factors, including KLF4,OCT4,NANOG and SOX2 at the Nanog 5kb upstream Enhancer region(42) and found that the Site 2 (targeted by both TALE and dCas9) was surrounded by the predicted KLF4 and NANOG binding sites.	--	--	Oct4
25214635	chr10	6064657	6065397	IL2RA	We further fine-mapped and validated a single-base variant that modulates YY1 binding and the activity of an enhancer element controlling the autoimmune-associated IL2RA gene, affecting its activity in activated but not regulatory T cells.	human		Low throughput	Intersection of population variation and autoimmunity genetics in human T cell activation.	是	rs12251836	Autoimmune Diseases	T cell	E_02_0897	EMSA,Luciferase Reporter Assay	We first tested for enhancer activity by introducing ~200 bp fragments centered around each SNP (Fig. 6A) into a luciferase reporter vector, driven by SV40 or IL2RA minimal promoters, and transfecting them into Jurkat T cells.The higher enhancer function of the T allele was dependent on activation of the Jurkat cells (Fig. 6C), suggesting that enhancer activity is boosted upon cell activation by interactions affected by the single base change at rs12251836.	Enhancer	--	GWAS	Together, these results point to functional effects of at least two independent associations in the IL2RA locus, which may have balancing effects. We surmise that the associated variant rs12251836 is mainly active in acutely triggered T effector cells, but not in Treg cells, since IL2RA mRNA in unstimulated CD4+ T cells would predominantly come from CD25hi Treg cells, and this association was not apparent in unstimulated cells. 	CD25,IDDM10,IL2R,IMD41,TCGFR,p55	--	--	--	YY1	DELTA,GADEVS,INO80S,NF-E1,UCRBP,YIN-YANG-1	EMSA	The allele-specific binding of YY1 was also confirmed by EMSA.	6091281	Luciferase Reporter Assay,EMSA	IL2RA
25194570	chr8	130179643	130181490	MYC	This highly conserved regulatory element, hereby named N-Me for NOTCH MYC enhancer, is located within a broad super-enhancer region +1.47 Mb from the MYC transcription initiating site, interacts with the MYC proximal promoter and induces orientation-independent MYC expression in reporter assays.	human		Low+High throughput	A NOTCH1-driven MYC enhancer promotes T cell development, transformation and acute lymphoblastic leukemia.	否	--	T-Cell Acute Lymphoblastic Leukemia	HPB-ALL,JURKAT,T-acute lymphoblastic leukemia (T-ALL)	E_02_0898	ChIP-seq,ChIP,Luciferase Reporter Assay,3C,PCR	This highly conserved regulatory element, hereby named N-Me for NOTCH MYC enhancer, is located within a broad super-enhancer region +1.47 Mb from the MYC transcription initiating site,interacts with the MYC proximal promoter and induces orientation-independent MYC expression in reporter assays.Moreover, luciferase reporter assays showed strong, orientationindependent activation of reporter constructs containing this enhancer in association with a ?2.5 kb MYC proximal promoter21 in JURKAT T-ALL cells,which express high levels of constitutively active NOTCH1 protein 22, but not in Daudi and Raji B-cell lineage cells.	Enhancer	--	Luciferase Reporter Assay,PCR	Consistent with this hypothesis, chromatin configuration 3C analysis of the MYC locus demonstrated the association of this enhancer with proximal regulatory sequences in the MYC promoter.Moreover, histological analysis of multiple tissues including those in which NOTCH signaling plays important developmental roles such as breast epithelium, skin, and intestine showed no alterations (Supplementary Fig. 7) and RT-PCR analysis showed no effects of N_x0002_Me deletion in Myc expression.	MRTL,MYCC,bHLHe39,c-Myc	--	--	--	NOTCH1	AOS5,AOVD1,TAN1,hN1	ChIP,ChIP-seq	Interestingly, chromatin immunoprecipitation (ChIP) followed by next generation sequencing (ChIP-seq) analysis of NOTCH1 chromatin binding sites in HPB-ALL T-ALL cells revealed a prominent 1 kb NOTCH1 peak in chromosome 8q24 located within the common 40 Kb segment duplicated in all these eight leukemia cases. 	--	--	MYC
25030696	chr17	31172998	31173656	Vegfa	A set of angiogenic genes, including Vegfa, has liganded RXR-controlled enhancers and provides the macrophage with a novel inducible program.	mouse		Low throughput	The active enhancer network operated by liganded RXR supports angiogenic activity in macrophages	否	--	--	COS-1	E_02_0899	3C,ChIP,RNA-seq,GRO-seq,Luciferase Reporter Assay	Interestingly, primarily RXR-induced eRNA production could be detected on an enhancer assigned to Vegfa or Tgm2, while an enhancer of Abcg1 also showed robust LXR ligand activation, as expected. These data suggested that the eRNAs can be easily validated and show ligand induction similar to the regulated genes and therefore most likely are linked.	Enhancer	3C	qRT-PCR	Box plot representation of the distribution of interaction frequency of Abcg1 B1 Enhancer (chr17: 31,172,998–31,173,656) and Vegfa B1 Enhancer (chr17: 45,890,060–45,890,829) determined by 3C-seq.	AW413978,Abc8,White	A set of angiogenic genes, including Vegfa, has liganded RXR-controlled enhancers and provides the macrophage with a novel inducible program	3C,3C-seq	Using chromosome conformation capture (3C) and 3C combined with sequencing (3C-seq), and we show that selected long-range Enhancers communicate with promoters via stable or RXR-induced loops and that some of the Enhancers interact with each other, forming an interchromosomal network.	Rxra	9530071D11Rik,Nr2b1,RXRalpha1	RNA-seq,ChIP-seq,GRO-seq,3C-seq	In our studies, we tried to solve these issues by combining RNA-seq, ChIP-seq, GRO-seq (global run-on sequencing), and 3C-seq (chromosome conformation capture [3C] combined with sequencing) in a highly integrated way to unravel the mechanism of RXR-induced transcriptional events in mouse bone marrow-derived macrophages (BMDMs) and, as the result of the process,discovered and validated a novel biological activity promoted by the receptor.	--	--	Abcg1
24916375	chr9	124638991	124641160	BNC2	One example is rs10765819 located in the first intron of the BNC2 gene previously associated with (saturation of) human skin color.	human		Low+High throughput	Human skin color is influenced by an intergenic DNA polymorphism regulating transcription of the nearby BNC2 pigmentation gene.	否	--	--	LP89	E_02_0900	ChIP-seq,ChIP-qPCR	We profiled the chromatin structure of the BNC2 region to identify potential regulatory elements using chromatin immune-precipitation (ChIP) of H3K27Ac (an active-enhancer mark) in combination with next generation sequencing (ChIP-seq) and ENCODE data. We provide evidence that a region upstream from the canonical BNC2 promoter acts as an enhancer regulating the expression of BNC2, and this transcriptional regulation is dependent on the allelic status of an LD partner of the pigmentation-associated SNP rs10756819.	Enhancer	--	ChIP-seq,RT-qPCR	We confirmed this finding by RT–qPCR analysis ofBNC2-expression levels atthree different loca_x0002_tions within the gene, using one primer set targeting mRNA upstream of the alternative promoter, and two primer sets targeting the mRNA downstream of the alternative promoter. 	BSN2	--	--	--	--	--	--	--	--	--	BNC2
24915132	chr2	25423079	25423874	Fut7	Fucosyltransferase VII encoded by the gene Fut7 is essential in CD4+ T cells for the generation of E- and P-selectin ligands (E- and P-lig) which facilitate recruitment of lymphocytes into inflamed tissues and into the skin	mouse	Inflamed tissue	Low throughput	Identification of two regulatory elements controlling Fucosyltransferase 7 transcription in murine CD4+ T cells	否	--	--	Th1 Cell	E_02_0901	ChIP	Incontrast, lung fibroblasts, which are of mesenchymal origin andwhich lack Fut7 mRNA and selectin ligand expression, carried adifferential histone modification pattern with an enrichment ofH3K27me3 at the CNS and the Fut7 gene locus and absenceof H3K4me2 marks. This suggests that the pattern of histone mod-ifications might control tissue-specific expression of Fut7, ratherthan the differentiation and activation dependent expression inT cells	Enhancer	--	qRT-PCR,Luciferase Reporter Assay	The CNS was cloned in different orientations in the Enhancer position of the pGL3 vector carrying the +728/+1523 construct in promoter position and transfected into Th1 cells.	AI853193,FTVII,Fuc-TVII,FucT-VII	--	--	--	Ep300	A430090G16,A730011L11,KAT3B,p300,p300 HAT	ChIP	As our histone ChIP data as well as analysis of genome-wide p300 binding data published by Vahedi et al.(2012) revealed distribution ofthe active histone mark as well as enrichment of p300 binding (data not shown) beyond the homology region, i.e. the CNS, we extended the CNS by about 300 bp upstream and 150 bp downstream of the original construct.	--	--	Fut7
24905168	chr4	124638991	124641160	Otx2	Our results illuminate regulatory mechanisms underlying pluripotency and suggest that the capacity of transcription factors such as Otx2 and Oct4 to pioneer new enhancer sites is highly context dependent.	mouse		Low+High throughput	Reorganization of Enhancer Patterns in Transition from Naive to Primed Pluripotency	否	--	--	embryonic stem cell	E_02_0902	ChIP-seq,RNA-seq	To address whether changes in enhancer utilization patterns occur in the majority of cells within the differentiating population, we isolated dual transgenic enhancer reporter lines, in which ESC-specific or EpiLC-specific enhancers of interest were cloned upstream of a minimal promoter and one of two distinct fluorescent reporters and integrated into the ESC genome using a PiggyBac transposon system.	Enhancer	--	qPCR,IP-Western	Upon differentiation, Otx2?/? cells underwent morphological changes indistinguishable from those seen in wt EpiLCs, but showed defects in expression of certain epiblast-associated genes, such as Fgf5 and Oct6. RNA-seq analysis of Otx2?/? EpiLCs identified 260 and 141 genes significantly downregulated or upregulated, respectively, as compared to the genetically-matched wt EpiLCs	Oct-6,Oct6,Otf-6,Otf6,Scip,Test1,Tst-1,Tst1	--	--	--	Otx2,Oct4	E130306E05Rik,2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1	ChIP-seq	Our results illuminate regulatory mechanisms underlying pluripotency and suggest that capacity of transcription factors such as Otx2 and Oct4 to pioneer new Enhancer sites is highly context dependent.	--	--	Pou3f1
24842713	chr16	86212040	86271919	FOXF1	We report on two patients with alveolar capillary dysplasia with misalignment of pulmonary veins (ACDMPV) caused by overlapping genomic deletions that included a distant FOXF1 transcriptional enhancer mapping 0.3 Mb upstream to FOXF1 on 16q24.1.	human	Lung tissue	Low+High throughput	Two deletions overlapping a distant FOXF1 enhancer unravel the role of lncRNA LINC01081 in etiology of alveolar capillary dysplasia with misalignment of pulmonary veins	否	--	--	pneumocyte	E_02_0903	ChIP-seq,qRT-PCR,ChIP-qPCR	Using chromatin immunoprecipitation with high-throughput sequencing (ChIP-seq) of histone H3K27 acetylation (H3K27ac), a mark of active enhancers,we first identified enhancer regions in MYCN-amplified Kelly and nonamplified SH-SY5Y cells.	Super-Enhancer	--	shRNA	"Here we investigate whether inhibition of transcriptional CDKs can be exploited to disrupt aberrant MYC-driven transcription, using the deregulated expression of MYCN as a model. 
The MYCN protein shares most of the physical properties of MYC and is considered functionally interchangeable, based on the similarity of their transcriptional programs, the cellular phenotypes they induce, and the ability of MYCN to replace MYC during murine development."	ACDMPV,FKHL5,FREAC1	--	--	--	MITF,YY1	CMM8,COMMAD,MI,WS2,WS2A,bHLHe32,DELTA,GADEVS,INO80S,NF-E1,UCRBP,YIN-YANG-1	ChIP-qPCR	Binding of RNA Polymerase II, similarly tested with ChIP-qPCR in LP89, is relatively high at the alternative promoter and region B′′, which has several features consistent with an enhancer element, e.g. high H3K27Ac enrichment low H3K4Me3 enrichment and binding of MITF and YY1.	--	--	FOXF1
24788237	chr12	54357811	54358445	HOTAIR	During inspecting functional relevance of the rs920778 SNP, we identified a novel intronic HOTAIR enhancer locating between +1719bp and +2353bp from the transcriptional start site through reporter assays.	human	Esophageal tissues	Low throughput	The identification of an ESCC susceptibility SNP rs920778 that regulates the expression of lncRNA HOTAIR via a novel intronic enhancer.	是	rs920778	Esophageal Squamous Cell Carcinoma	KYSE-30,KESY-150,ESCC	E_02_0904	Luciferase Reporter Assay,PCR	Because the ESCC susceptibility SNP rs920778 is located within the HOTAIR intron 2 and previous H3K4me1 and H3K4me3 modi_x0002_fication data suggest that there might be a potential enhancer in this intron,we therefore examined the enhancer activity of this region by a set of luciferase reporter gene constructs in human ESCC KYSE30 and KYSE150 cells These results indicated that there may be a negative regulatory element between +1463bp and +1718bpfrom the transcriptional start site and the core region of this intronic enhancer might exist between +1719bp and +2353bp from the tran_x0002_scriptional start?site.	Enhancer	--	Luciferase Reporter Assay,PCR	"We hypothesized that the functional single nucleotide polymorphisms (SNP) in HOTAIR may affect HOTAIR expression and/or its function and, thus, ESCC risk. Therefore, we examined the association between three haplotype_x0002_tagging SNPs (htSNP) across the whole HOTAIR locus and ESCC risk as well as the functional relevance of an ESCC susceptibility 
SNP rs920778."	HOXAS,HOXC-AS4,HOXC11-AS1,NCRNA00072	The identification of an ESCC susceptibility SNP rs920778 that regulates the expression of lncRNA HOTAIR via a novel intronic Enhancer.	ChIP,Luciferase Reporter Assay,PCR	Interestingly, the ESCC susceptibility SNP rs920778 in this Enhancer has a genotype-specific effect on lncRNA HOTAIR expression. Our observations also support the hypothesis that functional genetic variants influencing lncRNA regulation may explain a part of ESCC genetic basis.	--	--	--	--	54360232	Luciferase Reporter Assay,PCR	HOTAIR 
24705708	chr6	52199038	52200503	Hoxa4	The Hox gene family encodes homeodomain-containing transcriptional regulators that confer positional information to axial and paraxial tissues in the developing embryo.	mouse	Lung,Stomach	Low+High throughput	YY1 Acts as a Transcriptional Activator of Hoxa5 Gene Expression in Mouse Organogenesis	否	--	--	endothelial cell	E_02_0905	EMSA,ChIP	A 2.1-kb mesodermal (MES) enhancer important for Hoxa5 paraxial and lateral plate mesoderm expression in the cervico-upper thoracic region of the A-P axis is positioned 39 of the Hoxa5 gene.	Enhancer	--	Transgenic mice,EMSA,qRT-PCR	A 1.5-kb XbaI-XbaI DNA fragment located in Hoxa4-Hoxa5 intergenic sequences at 3.0-kb upstream the Hoxa4 gene (positions +9351-bp to +10816-bp) was able to target Hoxa5 expression in lung and stomach.	Vegf,Vpf	--	--	--	Yy1	NF-E1,YY-1	ChIP,qPCR	In summary, YY1 acts as a positive regulator of Hoxa5 lung, stomach and intestine expression during embryogenesis.	--	--	Vegfa
24705708	chr6	52199038	52200503	Hoxa5	The Hox gene family encodes homeodomain-containing transcriptional regulators that confer positional information to axial and paraxial tissues in the developing embryo.	mouse	Lung,Stomach	Low+High throughput	YY1 Acts as a Transcriptional Activator of Hoxa5 Gene Expression in Mouse Organogenesis	否	--	--	endothelial cell	E_02_0905	EMSA,ChIP	A 2.1-kb mesodermal (MES) enhancer important for Hoxa5 paraxial and lateral plate mesoderm expression in the cervico-upper thoracic region of the A-P axis is positioned 39 of the Hoxa5 gene.	Enhancer	--	Transgenic mice,EMSA,qRT-PCR	A 1.5-kb XbaI-XbaI DNA fragment located in Hoxa4-Hoxa5 intergenic sequences at 3.0-kb upstream the Hoxa4 gene (positions +9351-bp to +10816-bp) was able to target Hoxa5 expression in lung and stomach.	Vegf,Vpf	--	--	--	Yy1	NF-E1,YY-1	ChIP,qPCR	In summary, YY1 acts as a positive regulator of Hoxa5 lung, stomach and intestine expression during embryogenesis.	--	--	Vegfa
24703906	chr3	184276287	184278287	GATA2	Transgenic mice harboring a linked BAC developed leukemia accompanied by EVI1 overexpression-neoplasia that was not detected in mice bearing the same transgene but that was missing the GATA2 enhancer.	human	Colon tissue	Low throughput	A remote GATA2 hematopoietic enhancer drives leukemogenesis in inv(3)(q21;q26) by activating EVI1 expression.	否	--	--	Crc Cell,HT-29	E_02_0906	Luciferase Reporter Assay,ChIP,qRT-PCR	Importantly, the stimulatory capacity of the ?2.3-kb ECR differed widely among the CRC cell lines and was most pronounced in LS174T cells with highest levels of endogenous EPHB3. Thus, the EPHB3 ?2.3-kb ECR functions as a cell type-specific transcriptional enhancer. Consistent with its evolutionary conservation, also the corresponding region from the mouse EphB3 gene has enhancer properties and exhibits a remarkably similar cell-type specificity in CRC cell lines.We probed these features by chromatin immunoprecipitation (ChIP) and formaldehyde_x0002_assisted isolation of regulatory elements (FAIRE).	Enhancer	--	ChIP,qRT-PCR	Next, we performed ChIP experiments to investigate the distri_x0002_bution of the histone modifications H3K4me1 and H3K27ac,the acetyltransferase p300, and the Wnt pathway effector TCF7L2 at the EPHB3 locus.Significantly,its cell type-specific activity matches the expression of the endogenous EPHB3 gene in CRC cell lines, suggesting that differences in enhancer function underlie differential EPHB3 expression in CRC.	EK2,ETK2,HEK2,TYRO6	--	--	--	ASCL2	ASH2,HASH2,MASH2,bHLHa45	Luciferase Reporter Assay	we generated luciferase-reporter constructs with point mutations in the TBE and the binding sites for RBPJ and ETS factors.	--	--	EPHB3
24692107	chr17	44464986	44466986	Runx2	Runx2 is essential for osteoblast differentiation and chondrocyte maturation.	mouse	Connective tissue	Low throughput	Dlx5 and Mef2 Regulate a Novel Runx2 Enhancer for Osteoblast-Specific Expression	否	--	--	Osteoblast-Specific Cell	E_02_0907	Luciferase Reporter Assay,ChIP,EMSA	and found that a 1.3‐kb region located about 30 kb upstream of the transcription start site of type II Runx2 was highly conserved among all of the species	Enhancer	--	Transgenic mice,RT-PCR	We searched for regulatory elements of the Runx2 gene,and identified a 343bp Enhancer sequence,which specifically directed the reporter gene expression to osteoblasts.	AML3,Cbf,Cbfa-1,Cbfa1,LS3,Osf2,PEBP2aA,Pebp2a1,Pebpa2a	--	--	--	Dlx5,Mef2c,Tcf7,Ctnnb1,Sp7,Smad1,Sox6	AI385752,5430401D19Rik,9930028G15Rik,AV011172,Mef2,AI465550,TCF-1,Tcf1,Bfc,Catnb,Mesc,6430578P22Rik,C22,Osx,AI528653,Mad1,Madh1,Madr1,Mlp1,MusMLP,dwf-A,mMad1,AI987981,SOX-LZ	EMSA,ChIP	In EMSA, Mef2c, Dlx5, and Msx2 but not Tcf7, Ctnnb1, Smad1, Sox6, and Sp7 directly bound to the 89‐bp core sequence.In ChIP analysis, the bindings of Dlx5, Dlx6, Msx2, Mef2, Tcf7, Ctnnb1, Smad1, Sox5, Sox6, and Sp7 to the 343 enhancer region were detected using each antibody, whereas the binding of Foxa2 was not detected in primary osteoblasts despite the presence of a conserved Foxa2 binding motif in the core 89‐bp sequence.	--	--	Runx2
24692107	chr17	44464986	44466986	Dlx5	These findings indicated that the enhancer, which had typical histone modifications for enhancers, contains sufficient elements to direct Runx2 expression to osteoblasts, and that Dlx5 and Mef2, which formed an enhanceosome with Tcf7, Ctnnb1, Sp7, Smad1, and Sox6, play an essential role in the osteoblast-specific activation of the enhancer.	mouse	Connective tissue	Low throughput	Dlx5 and Mef2 Regulate a Novel Runx2 Enhancer for Osteoblast-Specific Expression	否	--	--	Osteoblast-Specific Cell	E_02_0907	Luciferase Reporter Assay,ChIP,EMSA	and found that a 1.3‐kb region located about 30 kb upstream of the transcription start site of type II Runx2 was highly conserved among all of the species	Enhancer	--	Transgenic mice,RT-PCR	We searched for regulatory elements of the Runx2 gene,and identified a 343bp Enhancer sequence,which specifically directed the reporter gene expression to osteoblasts.	AML3,Cbf,Cbfa-1,Cbfa1,LS3,Osf2,PEBP2aA,Pebp2a1,Pebpa2a	--	--	--	Dlx5,Mef2c,Tcf7,Ctnnb1,Sp7,Smad1,Sox6	AI385752,5430401D19Rik,9930028G15Rik,AV011172,Mef2,AI465550,TCF-1,Tcf1,Bfc,Catnb,Mesc,6430578P22Rik,C22,Osx,AI528653,Mad1,Madh1,Madr1,Mlp1,MusMLP,dwf-A,mMad1,AI987981,SOX-LZ	EMSA,ChIP	In EMSA, Mef2c, Dlx5, and Msx2 but not Tcf7, Ctnnb1, Smad1, Sox6, and Sp7 directly bound to the 89‐bp core sequence.In ChIP analysis, the bindings of Dlx5, Dlx6, Msx2, Mef2, Tcf7, Ctnnb1, Smad1, Sox5, Sox6, and Sp7 to the 343 enhancer region were detected using each antibody, whereas the binding of Foxa2 was not detected in primary osteoblasts despite the presence of a conserved Foxa2 binding motif in the core 89‐bp sequence.	--	--	Runx2
24671955	chr5	139970046	139972237	CD14	We identified differential regulatory elements (including promoters and putative enhancers) that were associated with subset-specific motif signatures corresponding to different transcription factor activities and exemplarily validated novel downstream enhancer elements at the CD14 locus.	human		Low+High throughput	Transcription and enhancer profiling in human monocyte subsets.	否	--	--	peripheral blood mononuclear cell	E_02_0908	RT-PCR,ChIP,Luciferase Reporter Assay,ChIP-seq	To extend the analysis of regulatory sites to putative enhancers, we also carried out ChIP sequencing for 2 histone marks, namely H3K4me1 and H3K27ac,that were previously associated with enhancers.30-34 H3K27 is a major substrate for the coactivators p300 and CBP and its acetylation marks active enhancers, whereas H3K4me1 is generally associated with distal regulatory elements, including poised enhancers.	Enhancer	--	RT-PCR,Luciferase Reporter Assay	On this basis, we sought an explanation for the differential ex_x0002_pression of CD14 in classical monocytes. Studies in transgenic mice by Zhang and coworkers established that a region of 80 kb surrounding the human CD14 gene is sufficient to direct its monocyte specific expression,42 whereas smaller constructs recapitulated human liver expression but failed to direct monocyte-specific expression.The genomic interval downstream of the CD14 gene contained a number of H3K27ac-marked sites specific for classical,CD14-expressing monocytes.These sites frequently overlapped with bidirectional enhancers identified using the FANTOM5 expression atlas44 as well as binding sites for PU.1 or C/EBPb in total monocytes,18 which are key factors in establishing distal regulatory sites in these cells.	CD14	--	--	--	--	--	--	--	--	--	CD14
24667089	chr8	141161900	141175436	KCNK9	Utilizing allele-specific RT-PCR, bisulphite sequencing, chromatin immunoprecipitation and chromosome conformation capture (3C) we show the reciprocal expression of the novel, paternally expressed, PEG13 non-coding RNA and maternally expressed KCNK9 genes in brain, and the biallelic expression of flanking transcripts in a range of tissues.	human	lymphoid tissue	Low throughput	The PEG13-DMR and brain-specific enhancers dictate imprinted expression within the 8q24 intellectual disability risk locus.	否	--	Intellectual Disability	Lymphoblastoid cell lines	E_02_0909	RT-PCR,ChIP,Luciferase Reporter Assay,3C,DNaseI-seq	Using 3C, we identify mutually exclusive approximately 58 and 500 kb chromatin loops in adult frontal cortex between a novel brain-specific enhancer, marked by H3K4me1 and H3K27ac, with the KCNK9 and PEG13 promoters which we propose regulates brain-specific expression.	Enhancer	3C	RT-PCR,ChIP	Utilizing allele-specific RT-PCR, bisulphite sequencing, chromatin immunoprecipitation and chromosome conformation capture (3C) we show the reciprocal expression of the novel, paternally expressed, PEG13 non-coding RNA and maternally expressed KCNK9 genes in brain, and the biallelic expression of flanking transcripts in a range of tissues.	K2p9.1,KT3.2,TASK-3,TASK3	--	--	--	CTCF	MRD21	3C-qPCR	3C-qPCR assays were performed on cerebellar samples and interaction frequencies were determined between a constant HindIII site located within the unmethylated CTCF-cohesin binding site within the KCNK9 promoter and other HindIII sites throughout the locus. We identified strong interactions between the KCNK9 promoter constant fragment with the PEG13-DMR and the CTCF-cohesin site in the enhancer region located within intron 17 of TRAPPC9. 	--	--	KCNK9
24594601	chr8	128230172	128243000	MYC	We also found the MYC enhancer region physically interacts with the active regulatory region of the CARLo-5 promoter, suggesting long-range interaction of MYC enhancer with the CARLo-5 promoter regulates CARLo-5 expression.	human	Colon tissue	Low throughput	Long-range interaction and correlation between MYC enhancer and oncogenic long noncoding RNA CARLo-5.	是	rs6983267	Colorectal Cancer	HCT 116,RKO	E_02_0910	qRT-PCR,3C	"The enhancer region showed long-range in_x005f_x0002_teraction with MYC (?335 kb from the region),suggesting that the enhancer region could regulate CARLo-5 (?180 kb from
the region) expression by enhancing its transcription through direct interaction. To test this possibility, we performed chro_x0002_mosome conformation capture (3C) analysis using genomic DNA from CRC-derived HCT116 and RKO cells.The results of 3C analysis show that the enhancer region physically interacts with CARLo-5."	Enhancer	3C	qRT-PCR	These results demonstrate that the enhancer region may regulate expression of CARLo-5 by direct interaction with the active regulatory 5′ promoter region of CARLo-5.These results suggest that the cancer-associated variant rs6983267 in MYC enhancer could regulate CARLo-5 expression through long-range interaction with the active regulatory region of its promoter.	CARLO5,CARLo-5,onco-lncRNA-40	The MYC Enhancer region physically interacts with the active regulatory region of the CARLo-5 promoter, suggesting long-range interaction of MYC Enhancer with the CARLo-5 promoter regulates CARLo-5 expression.	3C,qRT-PCR,siRNA	We also found the MYC enhancer region physically interacts with the active regulatory region of the CARLo-5 promoter, suggesting long-range interaction of MYC enhancer with the CARLo-5 promoter regulates CARLo-5 expression. Finally, we demonstrate that CARLo-5 has a function in cell-cycle regulation and tumor development.	--	--	--	--	128413305	qRT-PCR,3C	CCAT1
24512546	chr8	128709135	128745673	FOXA1	Increasing evidence suggests that forkhead box A1 (FOXA1) is frequently dysregulated in many types of human cancers.	human	Endometrial tissue	Low+High throughput	FOXA1 promotes tumor cell proliferation through AR involving the Notch pathway in endometrial cancer.	否	--	Endometrial Cancer	AN3 CA,RL95-2,HEC-1-B	E_02_0911	ChIP,ChIP-PCR,ChIP-seq,qRT-PCR	"Interestingly, we showed that FOXA1 and AR more evidently bound to the MYC enhancer regions as compared to MYC promoter regions. These results could be attributed to other co-regulators involved in this binding process. Since TCF7L2, a protein mediating DNA looping for long-distance interactions of distal en_x0002_hancers and proximal promoters, physically interacts with FOXA1 and AR and mediates the transcription of MYC in breast cancer [19], future investigation will be needed to clarify which co-regulators are involved in
FOXA1/AR binding to the enhancer regions upstream of MYC in EC cells."	Enhancer	--	ChIP,ChIP-PCR,qRT-PCR	Our ChIP assays showed that both FOXA1 and AR could bind to all the five putative FOXA1-AR-binding regions in MFE-296 cells. More_x0002_over, both FOXA1 and AR bound most greatly to the Enh-1 (enhancer 1) region among the five binding regions (Figure 4D). Our ChIP data together with our co_x0002_immunoprecipitation data suggested that FOXA1 forming protein complex with AR might bind to FOXA1-AR over_x0002_lapping binding regions upstream of MYC, leading to MYC activation in EC cells.	MRTL,MYCC,bHLHe39,c-Myc	--	--	--	FOXA1,AR	HNF3A,TCF3A,AIS,AR8,DHTR,HUMARA,HYSP1,KD,NR3C4,SBMA,SMAX1,TFM	ChIP,ChIP-PCR,ChIP-seq,qRT-PCR	Our ChIP assays showed that both FOXA1 and AR could bind to all the five putative FOXA1-AR-binding regions in MFE-296 cells. More_x0002_over, both FOXA1 and AR bound most greatly to the Enh-1 (Enhancer 1) region among the five binding regions.	--	--	MYC
24512546	chr8	128709135	128745673	FOXA2	Increasing evidence suggests that forkhead box A1 (FOXA2) is frequently dysregulated in many types of human cancers.	human	Endometrial tissue	Low+High throughput	FOXA2 promotes tumor cell proliferation through AR involving the Notch pathway in endometrial cancer.	否	--	Endometrial Cancer	AN3 CA,RL95-2,HEC-1-B	E_02_0911	ChIP,ChIP-PCR,ChIP-seq,qRT-PCR	"Interestingly, we showed that FOXA1 and AR more evidently bound to the MYC enhancer regions as compared to MYC promoter regions. These results could be attributed to other co-regulators involved in this binding process. Since TCF7L2, a protein mediating DNA looping for long-distance interactions of distal en_x0002_hancers and proximal promoters, physically interacts with FOXA1 and AR and mediates the transcription of MYC in breast cancer [19], future investigation will be needed to clarify which co-regulators are involved in
FOXA1/AR binding to the enhancer regions upstream of MYC in EC cells."	Enhancer	--	ChIP,ChIP-PCR,qRT-PCR	Our ChIP assays showed that both FOXA1 and AR could bind to all the five putative FOXA1-AR-binding regions in MFE-296 cells. More_x0002_over, both FOXA1 and AR bound most greatly to the Enh-1 (enhancer 1) region among the five binding regions (Figure 4D). Our ChIP data together with our co_x0002_immunoprecipitation data suggested that FOXA1 forming protein complex with AR might bind to FOXA1-AR over_x0002_lapping binding regions upstream of MYC, leading to MYC activation in EC cells.	MRTL,MYCC,bHLHe39,c-Myc	--	--	--	FOXA1,AR	HNF3A,TCF3A,AIS,AR8,DHTR,HUMARA,HYSP1,KD,NR3C4,SBMA,SMAX1,TFM	ChIP,ChIP-PCR,ChIP-seq,qRT-PCR	Our ChIP assays showed that both FOXA1 and AR could bind to all the five putative FOXA1-AR-binding regions in MFE-296 cells. More_x0002_over, both FOXA1 and AR bound most greatly to the Enh-1 (Enhancer 1) region among the five binding regions.	--	--	MYC
24498324	chr11	47363009	47364009	CTCF	CCCTC-binding factor (CTCF) can both activate as well as inhibit transcription by forming chromatin loops between regulatory regions and promoters.	human	blood	Low throughput	Epigenetic control of SPI1 gene by CTCF and ISWI ATPase SMARCA5		--	Acute Myeloid Leukemia	bone marrow cell	E_02_0912	ChIP	Using ChIP we focused on loci with more than 2-fold occupancy relative to control antibody. We dentified diffuse occupancy of CTCF with peaks involving amplicons -16.6 (downstream URE), -14.4 (Enhancer), and -11 (Element) as well as in the neighboring mplicons: -15.6, -13.7, -13.4, -13.3, -12.4 and also close to the promoter at -0.15.	Enhancer	--	RT-PCR,Western blot,Luciferase Reporter Assay	To conclude this part,CTCF and SMARCA5 co-occupy its newly validated target SPI1 using ChIP assay at the -14.4 Enhancer upon AZA-mediated DNA demethylation.	OF,PU.1,SFPI1,SPI-1,SPI-A	--	--	--	--	--	--	--	--	--	SPI1
24443471	chr7	116374406	116376406	ERBB2	Inhibiting oncokinases, such as EGFR, ALK, ERBB2, and BRAF, is a mainstay of current cancer therapy but is hindered by innate drug resistance mediated by up-regulation of the HGF receptor, MET.	human	lymph	Low throughput	Enhancer-targeted genome editing selectively blocks innate resistance to oncokinase inhibition		--	Melanoma	COLO 829	E_02_0913	3C,ChIP	Chromosome conformation capture (3C)was performed in COLO829 cells in the presence or absence of PLX4032 using the MET +63-kb enhancer as an anchor region. We observed that BRAF inhibition strikingly increased the interaction between the MET +63-kb enhancer and the MET TSS, demonstrating that this lineage-specific enhancer undergoes inducible chromatin looping in response to oncogene withdrawal in melanoma cells.	Enhancer	3C	ChIP	Chromosome conformation capture (3C)was performed in COLO829 cells in the presence or absence of PLX4032 using the MET +63-kb Enhancer as an anchor region.We observed that BRAF inhibition strikingly increased the interaction between the MET +63-kb Enhancer and the MET TSS.	AUTS9,DFNB97,HGFR,RCCP2,c-Met	This enhancer displays inducible chromatin looping with the MET promoter to up-regulate MET expression upon BRAF inhibition.	ChIP,3C	ChIP and 3C analysis were performed on wild-type or Enhancer-edited cells treated with PLX4032.A significant decrease in both H3K27 acetylation,a histone modification associated with active Enhancer state,and Enhancer-promoter chromatin looping was observed in Enhancer-edited cells. 	MITF	CMM8,COMMAD,MI,WS2,WS2A,bHLHe32	ChIP-seq,3C	To test the necessity of MITF for inducible chromatin looping between the MET +63-kb Enhancer and MET TSS in response to BRAF inhibition, 3C was performed in COLO829 cells in the presence or absence of PLX4032 and MITF depletion.	--	--	MET
24391766	chr7	100474191	100474841	UCP3	Uncoupling protein (UCP) 3 is a mitochondrial inner membrane protein implicated in lipid handling and metabolism of reactive oxygen species.	mouse	Brown adipose tissue	Low+High throughput	A Novel SP1/SP3 Dependent Intronic Enhancer Governing Transcription of the UCP3 Gene in Brown Adipocytes	否	--	--	HIB1b Cell	E_02_0914	Luciferase Reporter Assay,PCR,EMSA,ChIP-seq	The first intron of the hamster is shorter compared to mouse and rat corresponding to the first half of the introns in these species.Generally, sequence conservation was low across the first intron,except a region of high conservation ranging from IVS(intervening sequence)1+1200 to IVS1+1850 with the IVS1+1505G/A baseexchange in the center of this region.	Enhancer	--	Luciferase Reporter Assay,PCR,EMSA	Generally, sequence conservation was low across the first intron,except a region of high conservation ranging from IVS(intervening sequence)1+1200 to IVS1+1850 with the IVS1+1505G/A base exchange in the center of this region.	AI645527,Slc25a9,UCP-3	This intronic region is the main Enhancer driving UCP3 expression with SP1/3 and PPARc as the core factors required for expression.	EMSA,ChIP-seq	While we understand that simple EMSA experiments are not sufficient to validate presence of a complex transcription factor binding module conserved across the whole mammalian class, our data provide good evidence that it an intronic Enhancer in the first intron of the UCP3 gene is of importance in non-rodent species as well.	Sp1,Sp3	1110003E12Rik,AA450830,AI845540-1,Sp1,D130027J01Rik	EMSA,ChIP-seq	We discovered that the transcription factors SP1 and SP3 were binding to the IVS1+1505G element, whereas binding to the mutant allele was strongly diminished. Direct binding of PPARγ and RXRa to the IVS1+1505G element could be ruled out.	--	--	Ucp3
24391132	chr4	147962887	147964479	Nppa	Here, we established a noninvasive and quantitative live imaging system for monitoring transcriptional activity and identified a novel stressresponsive enhancer of Nppa and Nppb, the most common markers of heart failure.	mouse	Heart tissue	Low+High throughput	Noninvasive and quantitative live imaging reveals a potential stress-responsive enhancer in the failing heart	否	--	Heart Failure	293T cell	E_02_0915	RT-PCR,3C,ChIP,Luciferase Reporter Assay	Among the 11 CRs identified, only CR9 coincided with the binding sites of RNA polymerase II and p300, and overlapped with the gene areas modified by H3K4me1, and filled all criteria for the enhancer.	Enhancer	3C	RT-PCR,Transgenic mice	The Enhancer is a 650-bp fragment within 50 kb of the Nppa and Nppb loci.To identify the organs in which CR9 functioned as a stress-responsive Enhancer, we examined the luciferase reporter expression in each organ by quantitative PCR.	AA408272,BNF,BNP	--	--	--	Nkx2-5,Ctcf	CHNG5,CSX,CSX1,HLHS2,NKX2.5,NKX2E,NKX4-1,VSD3,AW108038	ChIP-seq	ChIP-seq data for H3K4me1, p300, and CTCF were obtained from an open database of the adult mouse heart. Some CRs coincided with the peaks for H3K4me1, RNA polymerase II, and the transcriptional coactivator protein p300.	--	--	Nppb
24391132	chr4	147962887	147964479	Nppb	Here, we established a noninvasive and quantitative live imaging system for monitoring transcriptional activity and identified a novel stressresponsive enhancer of Nppa and Nppb, the most common markers of heart failure.	mouse	Heart tissue	Low+High throughput	Noninvasive and quantitative live imaging reveals a potential stress-responsive enhancer in the failing heart	否	--	Heart Failure	293T cell	E_02_0915	RT-PCR,3C,ChIP,Luciferase Reporter Assay	Among the 11 CRs identified, only CR9 coincided with the binding sites of RNA polymerase II and p300, and overlapped with the gene areas modified by H3K4me1, and filled all criteria for the enhancer.	Enhancer	3C	RT-PCR,Transgenic mice	The Enhancer is a 650-bp fragment within 50 kb of the Nppa and Nppb loci.To identify the organs in which CR9 functioned as a stress-responsive Enhancer, we examined the luciferase reporter expression in each organ by quantitative PCR.	AA408272,BNF,BNP	--	--	--	Nkx2-5,Ctcf	CHNG5,CSX,CSX1,HLHS2,NKX2.5,NKX2E,NKX4-1,VSD3,AW108038	ChIP-seq	ChIP-seq data for H3K4me1, p300, and CTCF were obtained from an open database of the adult mouse heart. Some CRs coincided with the peaks for H3K4me1, RNA polymerase II, and the transcriptional coactivator protein p300.	--	--	Nppb
24385922	chr6	52296135	52334522	CTCF	 Interestingly, enhancers located in the same sub-TAD are active in distinct subset of limb cells suggesting that spatial clustering of enhancers does not simply reflect enhancer co-activity. 	mouse		Low+High throughput	Clustering of Tissue-Specific Sub-TADs Accompanies the Regulation of HoxAGenes in Developing Limbs	否	--	--	Limb,Head	E_02_0916	ChIP,PCR,3C,5C,ChIP-seq	Sequences distinct from proximal promoters (RefSeq) that were bound by RNAP2 and at least one other mark, or by both p300 and H3K27Ac were retained as candidate enhancers. Using these criteria, 19 putative enhancers were identified within 850 kb upstream of Hoxa13.	Enhancer	3C	PCR	Here,we report on the first identification of bona fide transcriptional Enhancers controlling HoxA genes in developing limbs and show that these Enhancers are grouped into distinct topological domains at the sub-megabase scale.	Hox-1	--	--	--	Ctcf	AW108038	5C	Interestingly,loci bound either by CTCF or cohesin in limb buds have been recently identified and comparison with our data shows that almost all loci interacting with 59 HoxA genes overlap with either CTCF o cohesin binding.	--	--	Hoxa
24374176	chr15	37116298	37122452	Meis2	"Meis2 repression in early development depends on binding of RING1B, an essential E3 component of
PcG, to its promoter, coupled with its association with another RING1B-binding site (RBS) at the 30 end of the Meis2 gene."	human	Fetal tissue	Low+High throughput	Polycomb Potentiates Meis2 Activation in Midbrain by Mediating Interaction of the Promoter with a Tissue-Specific Enhancer	否	--	--	embryonic stem cell	E_02_0917	ChIP-qPCR,ChIP-seq,ChIP	Based on these results, we identified sequence d as a MB Meis2 enhancer, and hereafter designate it as MBE. We went on to look for accumulation of histone H3K27 acetylation (H3K27ac) and H3K4 monomethylation (H3K4me1), which demarcate active and potential enhancers, respectively, at MBE by ChIP-seq.	Enhancer	--	ChIP-qPCR,ChIP-seq	"In wild-type mice, Meis2 showed distinctive expres_x0002_sion patterns at 11.5 dpc in FB, MB, pharyngeal arches, spinal cord, neural crest, and somites. In Ring1 mutants, however,we found atypical derepression of Meis2 in facial and cephalic mesenchyme, heart primordium, LM, and somatic mesoderm,coupled with its downregulation in FB and MB (Figure 1C). These
results indicate that PcG is involved in both repression and activation of Meis2 in a tissue-specific manner."	CPCMR,HsT18361,MRG1	--	--	--	RNF2	BAP-1,BAP1,DING,HIPI3,RING1B,RING2	ChIP-qPCR,ChIP-seq	RING1B ChIP-seq data (GSE48464) over 10 Mb of the mouse genome (mm9) around Meis2 in FB,MB, and LM at 11.5 dpc.Binding of H3K27ac and RING1B in 11.5 dpc MB of WT and Ring1 mutant (Ring1 mut) revealed by ChIP-quantitative PCR (ChIP-qPCR) analysis.	--	--	MEIS2
24332044	chr11	110716521	110832306	BRD4	We observe highly asymmetric loading of bromodomain 4 (BRD4) at enhancers, with approximately 33% of all BRD4 localizing to enhancers at 1.6% of occupied genes.	human	lymphoid tissue	Low+High throughput	Discovery and characterization of super-enhancer-associated dependencies in diffuse large B cell lymphoma.	否	--	Diffuse Large B-Cell Lymphoma	B-Cell Lymphoma Cell Lines	E_02_0918	ChIP-seq,ChIP-qPCR	"As predicted, BRD4 load is asymmetrically distributed throughout the genome at enhancer sites. Completely unexpected is the magnitude by which BRD4 load varies among active
enhancer regions (Figure 4E). Only a small subset of BRD-loaded enhancers, 285/18330(1.6%), account for 32% of all of the BRD4 enhancer binding in the cell.The BRD4-loaded enhancers in the Ly1 DLBCL cell line are considerably larger than typical enhancer elements, resembling the super-enhancers we recently described with Richard Young."	Super-Enhancer	--	ChIP-seq	Notably, the top two gene loci with BRD4-loaded enhancers, POU2AF1 (which encodes the OCA-B transcriptional co-activator protein) and BCL6, and additional genes with disproportionally BRD4-loaded enhancers such as PAX5 and IRF8 (Figure 4E), are essential for B-cell fate determination and germinal center formation.	BOB1,OBF-1,OBF1,OCAB	These super-Enhancers prove particularly sensitive to bromodomain inhibition,explaining the selective effect of BET inhibitors on oncogenic and lineage-specific transcriptional circuits. 	ChIP-seq,ChIP-qPCR	These super-enhancers prove particularly sensitive to bromodomain inhibition, explaining the selective effect of BET inhibitors on oncogenic and lineage-specific transcriptional circuits. Functional study of genes marked by super-enhancers identifies DLBCLs dependent on OCA-B and suggests a strategy for discovering unrecognized cancer dependencies.	E2F1	E2F-1,RBAP1,RBBP3,RBP3	ChIP-seq,ChIP-qPCR	Then, we assessed the genome-wide localization of E2F1 and the representative BET protein, BRD4, also by ChIP-Seq using the respective antibodies. Rank-ordering of all transcriptionally active promoters based on H3K4me3 enrichment and RNA Pol II occupancy identifies pervasive binding of BRD4 and E2F1 to active promoter elements.	--	--	POU2AF1
24321386	chr17	72860066	72860183	FDXR	These results indicated that abundant FDXR expression in these steroidogenic cells was maintained through SF-1 binding to the intronic enhancer of the FDXR gene.	human	Cervical tissue	Low throughput	Transcriptional regulation of human ferredoxin reductase through an intronic enhancer in steroidogenic cells.	否	--	--	HeLa,H295R,KGN	E_02_0919	ChIP,Luciferase Reporter Assay,PCR,EMSA	Next, histone modifi- cation in the SF-1-induced cells was examined via ChIP assays, using antibodies against two active enhancer markers, histone H3K27ac and H3K4me2, to determine alterations of chromatin state within the region. The results clearly showed that the signals of these active enhancer markers around the SF-1 binding region increased along with the transduction of SF-1 (Fig. 1D and E), suggesting that the transduction of SF-1 led to the active state of chromatin within the FDXR intronic region.	Enhancer	--	ChIP,Luciferase Reporter Assay,PCR	Genome-wide analysis of differentiated cells, using a combination of DNA microarray and promoter tiling array analyses, showed that FDXR is a novel SF-1 target gene. In this study,the transcriptional regulatory mechanism of FDXR was examined in steroidogenic cells.	ADR,ADXR,ANOA	--	--	--	NR5A1	AD4BP,ELP,FTZ1,FTZF1,POF7,SF-1,SF1,SPGF8,SRXX4,SRXY3,hSF-1	ChIP,qPCR	Closed and open squares represent Flag-tagged SF-1 (FlagSF-1)- and GFP (Control)-transduced MSCs, respectively; real-time PCR analysis of immunoprecipitated chromatin performed using primers for indicated genomic region; and expressed as a percentage of input.	--	--	FDXR
24285714	chr8	127047315	127049315	Myc	Notably, these distal Myc enhancers coincide with a region that is focally amplified in ∼3% of acute myeloid leukemias.	human	Immunohistochem	Low+High throughput	Role of SWI/SNF in acute leukemia maintenance and enhancer-mediated Myc regulation.	否	--	Acute Leukemia	Acute Myeloid Leukemia Cell	E_02_0920	ChIP,ChIP-seq,Luciferase Reporter Assay,4C,ChIP-qPCR,3C,qPCR	To account for this context-specific function, we identify a cluster of lineage-specific enhancers located 1.7 Mb downstream from Myc that are occupied by SWI/SNF as well as the BET protein Brd4. Brg1 is required at these distal elements to maintain transcription factor occupancy and for long-range chromatin looping interactions with the Myc promoter. Notably,these distal Myc enhancers coincide with a region that is focally amplified in ~3% of acute myeloid leukemias.	Enhancer	--	ChIP,ChIP-seq,ChIP-qPCR	To explain this observation, we hypothesized that Brg1 regulates Myc transcription in leukemia cells by occupying cell type-specific regulatory elements. We evaluated this possibility by performing chromatin immunoprecipitation (ChIP) followed by next_x0002_generation sequencing (ChIP-seq) analysis of Brg1, his_x0002_tone H3 Lys 4 trimethylation (H3K4me3), and histone H3 Lys 27 acetylation (H3K27ac) in RN2 leukemia cells.	MRTL,MYCC,bHLHe39,c-Myc	--	--	--	SMARCA4,CEBPA,CEBPB,ERG,LMO2	BAF190,BAF190A,BRG1,CSS4,MRD16,RTPS2,SNF2,SNF2L4,SNF2LB,SWI2,hSNF2b,C/EBP-alpha,CEBP,C/EBP-beta,IL6DBP,NF-IL6,TCF5,erg-3,p55,LMO-2,RBTN2,RBTNL1,RHOM2,TTG2	ChIP-qPCR,shRNA	Since all of these TFs are expressed in RN2 cells (Supplemental Fig. 13), we anticipated that these factors would occupy E1–E5 in leukemia as well. Indeed, we detected occupancy of Lmo2, PU.1, and Erg at various subsets of the E1–E5 enhancers in RN2 using ChIP-qPCR (Fig. 5I–K). Additionally, we found that the hematopoietic TFs Cebpα and Cebpβ, both of which are highly expressed in RN2 cells, also occupied the E1–E5 elements (Fig. 5L,M; Supplemental Fig. 13).While expression of several regulators was perturbed upon Brg1 knockdown, Myc was among the most down-regulated genes identified (P < 0.01) (Fig. 3A). Hoxa9, which is a direct target of the MLL-AF9 oncoprotein, was also down-regulated (P < 0.01), albeit to a lesser extent than Myc (Fig. 3A). Gene signatures linked to Myc and Hoxa9 function were globally suppressed following Brg1 knockdown, further confirming an effect on these two pathways (Fig. 3B,C; Supplemental Fig. 5).	--	--	MYC
24257627	chr2	119321593	119322529	Foxn4	Our data together thus suggest that the mosaic expression of Foxn4 and proneural factors may serve as the trigger to initiate asymmetric Dll4-Notch and subsequent BMP/TGFβ signaling events required for neuronal diversity in the V2 domain.	mouse		Low throughput	Asymmetric activation of Dll4-Notch signaling by Foxn4 and proneural factors activates BMP/TGFβ signaling to specify V2b interneurons in the spinal cord	否	--	--	293T,Progenitor Cell	E_02_0921	ChIP,PCR,EMSA	In addition, we carried out chromatin immunoprecipitation (ChIP) assays to show that both Ascl1 and Neurog1 were able to occupy in vivo the critical E-box region of the CR1 Enhancer in cell culture and mouse embryonic neural tubes, whereas no enrichment was shown for control DNA in Dll4 3′ UTR.	Enhancer	--	EMSA	"We performed an electrophoretic mobility shift assay (EMSA) to test whether Ascl1 and Neurog proteins were able to directly bind to the minimal enhancer region using an oligo probe containing the critical E-box (Probe 2) and a control upstream probe that lacks an E-box (Probe 1) 
"	Delta4	Foxn4, Ascl1 and Neurog1 were able to activate gene expression through an evolutionarily conserved Dll4 Enhancer CR1 found to be active in the retina. 	ChIP,EMSA	In addition, we carried out chromatin immunoprecipitation (ChIP) assays to show that both Ascl1 and Neurog1 were able to occupy in vivo the critical E-box region of the CR1 Enhancer in cell culture and mouse embryonic neural tubes, whereas no enrichment was shown for control DNA in Dll4 3′ UTR.Thus, Ascl1 and Neurog factors may bind to the same E-box in the Dll4 Enhancer but have differential effects on Dll4 gene expression.	Foxn4,Ascl1	AI225900,ASH1,Mash1,bHLHa46	EMSA,ChIP	We performed an electrophoretic mobility shift assay (EMSA) to test whether Ascl1 and Neurog proteins were able to directly bind to the minimal Enhancer region using an oligo probe containing the critical E-box (Probe 2) and a control upstream probe that lacks an E-box.	--	--	Dll4
24204311	chr19	10215891	10216703	Sox10	we identify Myrf as an oligodendrocyte-specific target of Sox10 and map a Sox10 responsive enhancer to an evolutionarily conserved element in intron 1 of the Myrf gene.	mouse		Low throughput	The transcription factors Sox10 and Myrf define an essential regulatory network module in differentiating oligodendrocytes	否	--	--	Oligodendrocytes	E_02_0922	ChIP,Luciferase Reporter Assay,EMSA,qPCR	Considering the large number of potential Sox binding sites and the low predictive power of their presence, we decided to assess regulatory potential and Sox10-responsiveness of the ECR in luciferase assays.To verify that Sox10 is bound to ECR9 in OL we next performed chromatin immunoprecipitation (ChIP) experiments. Some were clustered so that eight oligonucleotides were sufficient to cover all sites in electrophoretic mobility shift assays (EMSA).	Enhancer	--	Immunoprecipitation	 To address this issue we performed immunoprecipitation experiments with anti-Sox10 antibodies on extracts of the OL-like OLN93 cell line.	6030439E18,Gm1804,Gm98,Mrf	--	--	--	Sox10	Dom,Sox21,gt	ChIP	To verify that Sox10 is bound to ECR9 in OL we next performed chromatin immunoprecipitation (ChIP) experiments.	--	--	Myrf
24157522	chr5	28476034	28479024	Shh	In mouse embryonic endodermal tissues, the seamless expres_x0002_sion of Shh is achieved by a patchwork of multiple enhancers with different rates of evolution.	mouse		Low+High throughput	A novel regulatory element for Shh expression in the lung and gut of mouse embryos	是	--	--	Colon Adenocarcinoma Cell Lines	E_02_0923	RT-PCR,ChIP-seq,Transient Transfection Assay,Luciferase Reporter Assay,3C,DNaseI-seq	The ChIP-seq data of the ENCODE project show that H3K4me1, but not H3K4me3, marks all four DNaseI HS sites in the adult lung.To examine whether each of the DNase I HS sites is responsible for upregulating the expression of Shh, we employed a transgenic reporter assay using BAC clones (Figs. 1A and 3A).	Enhancer	3C	Luciferase Reporter Assay	To determine whether SLGE physically interacts with the Shh promoter in association with transcriptional activity, we conducted a 3C assay, which has been used to measure associations between two genomic regions. Assessment of the functional properties of SLGE by 3C and luciferase assays.	9530036O11Rik,Dsh,Hhg1,Hx,Hxl3,M100081NC,Shh	Shh expression in the endodermal epithelial lining, which is enabled by the coordinated actions of the Enhancers, is necessary for proper endodermal development.	RT-PCR,Luciferase Reporter Assay,3C	We identified a novel, less-conserved cis-regulatory element for Shh expres_x005f_x0002_sion in the esophageal epithelium, as well as in the lung and intestinal epithelium, in a region 100 Kb upstream of the Shh CDS. The new element compensates for the Enhancer activi_x0002_ties of the three previously identified Enhancers, and the combined activities of all four Enhancers permit the seamless Shh expression in the epithelial linings of the whole endoder_x0002_mal tissues in the mouse embryo.	Rbfox3,Socs1	Fox-3,Hrnbp3,NeuN,Neuna60,Cish1,Cish3,JAB,SOCS-1,SSI-1	DNaseI-seq	Putative binding sites for Fox transcription factors and STAT are found in the SLGE.In human cancer cell lines, including Caco-2, putative Fox- and STAT-binding sites are found in some of the DNase I HS sites around the SHH CDS.	--	--	Shh
24086551	chr1	1083900	1085900	ZEB1	We therefore compared the expression pattern of miR-200b eRNA with miR-200b~200a~429 gene cluster and other epithelial (E-Cadherin) and mesenchymal (ZEB1) genes in a panel of breast cancer cell lines.	human		Low+High throughput	Identification of an Enhancer That Increases miR-200b~200a~429 Gene Expression in Breast Cancer Cells	否	--	--	HMLE	E_02_0924	qRT-PCR,Luciferase Reporter Assay,ChIP-seq,ChIP-qPCR	"We have analyzed the miR-200b~200a~429 locus for epigenetic modifications in breast epithelial and mesenchymal cell lines using chromatin immunoprecipitation assays and DNA methylation analysis. We discovered a novel enhancer located approximately 5.1kb upstream of the miR-200b~200a~429 transcriptional start site. This region was associated with
the active enhancer chromatin signature comprising H3K4me1, H3K27ac, RNA polymerase II and CpG dinucleotide hypomethylation. "	Enhancer	--	qRT-PCR,Luciferase Reporter Assay,ChIP-qPCR	Luciferase reporter assays revealed the upstream enhancer stimulated the transcription of the miR-200b~200a~429 minimal promoter region approximately 27-fold in breast epithelial cells. Furthermore, we found that a region of the enhancer was transcribed, producing a short, GC-rich, mainly nuclear, non-polyadenylated RNA transcript designated miR-200b eRNA.	GIHCG	"The presence of a novel Enhancer contributes to miR-200b~200a~429 transcriptional regulation in epithelial cells.
"	Luciferase Reporter Assay	"Luciferase reporter assays revealed the upstream enhancer stimulated the transcription of the miR-200b~200a~429 minimal promoter region approximately 27-fold in breast epithelial cells. Furthermore, we found that a region of the enhancer was transcribed, producing a short, GC-rich, mainly nuclear, non-polyadenylated RNA
transcript designated miR-200b eRNA. Over-expression of miR-200b eRNA had little effect on miR-200b~200a~429 promoter activity and its production did not correlate with miR-200b~200a~429 gene expression."	--	--	--	--	--	--	GIHCG
24040411	chr19	57566145	57571006	Peg3	The promoters of several imprinted genes in the Peg3 domain interact with one evolutionarily conserved region, ECR18, and further suggest that ECR18 may play key roles in the transcription and imprinting control of the Peg3 domain as a distant regulatory element.	human		Low throughput	Identification of an evolutionarily conserved cis-regulatory element controlling the Peg3 imprinted domain	否	--	--	HeLa,HEK-293	E_02_0925	Luciferase Reporter Assay,PCR,3C,ChIP	The observed interaction is most prominent in brain, but was also detected in testis. Histone modification and DNA methylation on ECR18 show no allele bias, implying that this region is likely functional on both alleles. In vitro assays also reveal ECR18 as a potential enhancer or repressor for the promoter of Peg3. Overall, these results indicate that the promoters of several imprinted genes in the Peg3 domain interact with one evolutionarily conserved region, ECR18, and further suggest that ECR18 may play key roles in the transcription and imprinting control of the Peg3 domain as a distant regulatory element.	Enhancer	3C	Luciferase Reporter Assay,PCR	In the current study, the chromatin conformation capture (3C) method was utilized to detect potential interactions of these ECRs with the imprinted genes. According to the results, one region, ECR18, located 200-kb upstream of Peg3 interacts with the two promoter regions of Peg3 and Zim2. The observed interaction is most prominent in brain, but was also detected in testis. 	PW1,ZKSCAN22,ZNF904,ZSCAN24	ECR18 may play key roles in the transcription and imprinting control of the Peg3 domain as a distant regulatory element.	3C,ChIP	In the current study, we performed a series of Chromatin Conformation Capture (3C) and Chromatin Immunoprecipitation (ChIP) analyses to further confirm this prediction. Overall, the current study identifies one region, ECR18, as a key regulatory region for the transcription and imprinting of the Peg3 domain.	--	--	--	--	--	--	PEG3
24014243	chr5	107680655	107682655	Mysm1	Mysm1 is a recently identified histone H2A deubiquitinase with essential and intrinsic roles for maintaining functional HSCs.	mouse		Low throughput	The control of hematopoietic stem cell maintenance, self-renewal, and differentiation by Mysm1-mediated epigenetic regulation	否	--	--	hematopoietic cell,B cell,T cell	E_02_0926	ChIP,PCR,Luciferase Reporter Assay	To investigate whether Mysm1 regulates Gfi1 expression by binding to the regulatory elements of Gfi1 in HSC, we performed chromatin immunoprecipitation (ChIP) assays along the Gfi1 regulatory elements. A panel of PCR primers to encompass the 23.4-kb promoter and 235-kb enhancer of the Gfi1 locus was designed (Figure 5A).	Enhancer	--	ChIP,PCR	To investigate whether Mysm1 regulates Gfi1 expression by binding to the regulatory elements of Gfi1 in HSC, we performed chromatin immunoprecipitation (ChIP) assays along the Gfi1 regulatory elements. A panel of PCR primers to encompass the 23.4-kb promoter and 235-kb enhancer of the Gfi1 locus was designed (Figure 5A).	AW495828,Gfi-1,Pal-1,Pal1	--	--	--	Gata2,Runx1	Gata-2,AML1,CBF-alpha-2,Cbfa2,Pebp2a2,Pebpa2b	Luciferase Reporter Assay,ChIP,PCR	Mechanistic studies revealed that Mysm1 modulates histone modifications and directs the recruitment of key transcriptional factors such as Gata2 and Runx1 to the Gfi1 locus in HSCs. We found that Mysm1 directly associates with the Gfi1 Enhancer element and promotes its transcription through Gata2 and Runx1 transactivation.	--	--	Gfi1
24000349	chr17	40206839	40206900	Pgk2	Here, we show that chromatin remodeling including reconfiguration of nucleosomes and changes in histone modifications is also associated with transcriptional activation of the Pgk2 gene during spermatogenesis.	mouse		Low throughput	Sequence-specific promoter elements regulate temporal-specific changes in chromatin required for testis-specific activation of the Pgk2 gene	否	--	--	Somatic Spleen cell,Spermatogenic Germ cell	E_02_0927	ChIP,qRT-PCR	This reflects the fact that both the human and mouse Pgk2 gene promoters contain highly conserved regulatory elements including a GC-box, a CAAT-box and an enhancer region just upstream from the CAAT-box.	Enhancer	--	ChIP,qRT-PCR	Our results indicate there is an ordered series of molecular events that lead to activation of transcription of the Pgk2 gene in spermatogenic cells, and that these events are signaled by distinct elements in the Pgk2 promoter/Enhancer region.	Pgk-2,Tcp-2	Activation of Pgk2 transcription is regulated by testis-specific demethylation of DNA and binding of testis-specific transcription factors to Enhancer and core promoter elements. 	ChIP,qRT-PCR	Our results indicate there is an ordered series of molecular events that lead to activation of transcription of the Pgk2 gene in spermatogenic cells, and that these events are signaled by distinct elements in the Pgk2 promoter/Enhancer region.	--	--	--	--	--	--	Pgk2
23873758	chr12	48368959	48369159	COL2A1	COL2A1 gene expression is positively regulated by the NAD dependent protein deacetylase Sirtuin 1 (SirT1), through its ability to bind chromatin regions of the COL2A1 promoter and enhancer.	human		Low throughput	Set7/9 Impacts COL2A1 Expression Through Binding and Repression of SirT1 Histone Deacetylation	否	--	--	HeLa,HEK-293	E_02_0928	PCR,ChIP	Real‐time PCR (qPCR) reactions for ChIP and ChIP reChIP were carried out using primers flanking the COL2A1 promoter start site(–167) to (–65), see illustration in Figure 6A. Additional analyses were performed on the Sox9‐binding enhancer region of COL2A1(?2259) to (?2430). As a negative control, a distal set of primers flanking the intron 38 (?24148) to (?24368) of the COL2A1 gene was used, based on the protocol by Furlan‐Magarill and colleagues.	Enhancer	--	PCR,ChIP	To understand the regulation of the active COL2A1 promoter, we performed ChIP assays using specific primers flanking the promoter start site and enhancer site within the first intron (illustrated in Fig. 6A). We found enhanced occupancy of the DNA‐binding transcription factor SP1 on the promoter start site of 3D cultured cells, whereas passaged cells (P5) showed a slight but insignificant reduction of SP1 (Fig. 6B). Additionally, passaging significantly decreased Sox9 occupancy on the enhancer site.	ANFH,AOM,COL11A3,SEDC,STL1	Although Sox9 (SRY‐related high mobility group‐Box gene 9) has been shown to regulate the expression of the COL2A1 gene by binding the Enhancer within the first intron,numerous additional coactivators (eg, LSox5, Sox6, PGC1a, Notch) are involved in activa	PCR,ChIP	3D cultures also exhibited augmented mRNA and protein levels of the transcription factors SP1 and Sox9 (Fig. 5A. B), which are known to regulate COL2A1 expression by binding the DNA-motifs of the promoter and Enhancer regions, respectively.	SP1,SOX9	SP1,CMD1,CMPD1,SRA1,SRXX2,SRXY10	ChIP	Chromatin immunoprecipitation (ChIP) analyses of 3D cultures showed augmented levels of the DNA‐binding transcription factor SP1, and the histone methyltransferase Set7/9, on the COL2A1 promoter site.	--	--	COL2A1
23872150	chr6	161119825	161121825	PLG	PLG gene expression is regulated by glucocorticoids, interleukin 6, nerve growth factor, and retinoic acid-related orphan receptor alpha [10 13].	human		Low throughput	Estrogen modulates plasminogen promoter activity	否	--	Hypoplasminogenemia	Hep G2,MCF-7	E_02_0929	Luciferase Reporter Assay,ChIP,EMSA,PCR	An AP3-like (activator protein 3) enhancer element, located 2.4 kb upstream of PLG-TSS, is involved in PLG transcriptional regulationIn summary we demonstrated that estrogen regulates plasminogen promoter activity. The 5’-flanking region of the PLG gene con_x0002_tains several cis-acting elements that are responsive to estrogen.An enhancer located at -11.5 kb confers a dramatic estrogen re_x0002_sponse in reporter assays.	Enhancer	--	Luciferase Reporter Assay,PCR	In our study we could show that a construct comprising the entire upstream region, containing the AP3 re_x0002_sponse element (2.4 kb-PLG) was able to further elevate basal luciferase activity 1.7-fold above that of PLG minimal promoters.The observed increase corresponds well to previously published results [20] and the 2.4 kb-PLG construct represents the most active contiguous promoter fragment analysed in this study. Surprisingly, with E2 stimulation this effect decreased by 54% down to the activity level of the PLG core promoter,although no ERE could be identified within this region.	PLG	An AP3-like (activator protein 3) enhancer element, located 2.4 kb upstream of PLG-TSS, is involved in PLG transcriptional regulation.	Luciferase Reporter Assay	An AP3-like (activator protein 3) enhancer element, located 2.4 kb upstream of PLG-TSS, is involved in PLG transcriptional regulation [20]. In our study we could show that a construct comprising the entire upstream region, containing the AP3 response element (2.4 kb-PLG) was able to further elevate basal luciferase activity 1.7-fold above that of PLG minimal promoters.	DHII,ERE	anon-EST:Posey114,anon-WO02059370.45,CG13094,DH31,DH-II,dh31,DH31,DH[31],DH[[31],Dh[[31]],DH[[31]],Dmel\CG13094,Drm-DH[[31]],drome-DH31,Drome-DH[[31]],ERE	Luciferase Reporter Assay	Transcriptional effect of the DHII and/or ERE (_x0003_11.5 kb) enhancers on the heterologous crystallin promoter (cryst) driven luciferase activity in HepG2.	--	--	PLG
23675462	chr21	43770915	43772915	TFF1	Here, we demonstrate that both MSK1 and MSK2, regulate the phorbol ester 12-O-tetradecanoylphorbol-13-acetate induced expression of the breast cancer marker gene, trefoil factor 1 (TFF1), by phosphorylating H3S10 at its 59 regulatory regions.	human		Low throughput	Mitogen- and Stress-Activated Protein Kinases 1 and 2 Are Required for Maximal Trefoil Factor 1 Induction	否	--	--	MCF-7 cell	E_02_0930	RT-PCR,ChIP	"To determine whether MSK1 co-occupies the enhancer and UPE with H3S10ph, we performed sequential ChIP assays (re_x0002_ChIP) with mononucleosomes prepared from TPA- treated and
formaldehyde-cross linked MCF-7 cell lysates.Together these results show that either MSK1 or MSK2 recruited to the TFF1 UPE and enhancer phopshorylates H3 at S10, leading to the binding of 14-3-3e/f and recruitment of BRG1."	Enhancer	--	RT-PCR,ChIP	Here, we used the high-resolution chromatin immunoprecipi_x0002_tation (ChIP) assay to determine the MSK1, MSK2 and H3S10ph distribution along the regulatory and coding regions of the TFF1 gene in response to ERK-MAPK signaling.With this in mind, we performed ChIP assays with antibodies against H3S10phK14ac to determine the distribution of this dual H3 modification along the TFF1 gene._x0002_	BCEI,D21S21,HP1.A,HPS2,pNR-2,pS2	MSK1 and MSK2 belong to different multiprotein complexes but both mediate chromatin remodeling that is required at the Enhancer and UPE for TPA-induced initiation of TFF1 expression in MCF-7 breast cancer epithelial cells.	Re-ChIP	An AP3-like (activator protein 3) enhancer element, located 2.4 kb upstream of PLG-TSS, is involved in PLG transcriptional regulation [20]. In our study we could show that a construct comprising the entire upstream region, containing the AP3 response element (2.4 kb-PLG) was able to further elevate basal luciferase activity 1.7-fold above that of PLG minimal promoters.	"RPS6KA5,RPS6KA4
"	MSK1, MSPK1, RLPK,MSK2, RSK-B, S6K-alpha-4	ChIP	we used the high-resolution chromatin immunoprecipitation (ChIP) assay to determine the MSK1, MSK2 and H3S10ph distribution along the regulatory and coding regions of the TFF1 gene in response to ERK-MAPK signaling.	--	--	TFF1
23644027	chr5	172648612	172649177	NKX2-5	NKX2-5 gene encodes a highly conserved homeobox transcription factor, which is essential to the heart development in embryos and cardiac function in adults. Mutations in NKX2-5 gene have been implicated in diverse types of CHD, including ventricular septal defect (VSD).	human		Low throughput	Two novel and functional DNA sequence variants within an upstream enhancer of the human NKX2-5 gene in ventricular septal defects	否	--	Congenital Heart Disease	leukocyte	E_02_0931	PCR,Luciferase Reporter Assay	The wild type and variant upstream enhancers (566 bp) were generated with PCR, and then subcloned into BamHI and SalI sites of a luciferase gene expression vector with human NKX2-5 gene promoter, which has been previously reportedll expression constructs were confirmed by direct sequencing.HEK-293 cells were cultured in DMEM with 10% fetal bovine serum,1% glutamine and 1% penicillin/streptomycin under 5% CO2 at 37 °C.	Enhancer	--	PCR,Luciferase Reporter Assay	To determine the effects of the DSVs on transcriptional activity of the enhancer, wild type and variant enhancers were subcloned upstream to the NKX2-5 gene promoter in the luciferase gene expression vector, which has been previously constructed and reported,to generate expression constructs pGL3-WT, pGL3-17483557Ins,pGL3-17483564T and pGL3-17483576G. These constructs were then transiently transfected into HEK-293 cells and luciferase activities were measured. The results were shown in Fig. 2. Expression levels of pGL3-17483564T and pGL3-17483576G were significantly decreased compared to pGL3-WT.	CHNG5,CSX,CSX1,HLHS2,NKX2.5,NKX2E,NKX4-1,VSD3	The DSVs within the upstream Enhancer of the NKX2-5 gene may contribute to a small number of VSD. 	Luciferase Reporter Assay	To determine the effects of the DSVs on transcriptional activity of the Enhancer,wild type and variant Enhancers were subcloned upstream to the NKX2-5 gene promoter in the Luciferase gene expression vector,which has been previously constructed and reported. Collectively, these results indicated that the activity of the upstream enhancer of the NKX2-5 gene was decreased by the DSVs g.17483564C>T and g.17483576C>G.	--	--	--	--	--	--	NKX2-5
23642367	chr4	115095426	115097426	Mesp1	Mesp1 is regarded as the master regulator of cardiovascular development, initiating the cardiac transcription factor cascade to direct the generation of cardiac mesoderm.	mouse		Low throughput	Mesp1 patterns mesoderm into cardiac, hematopoietic, or skeletal myogenic progenitors in a context-dependent manner	否	--	--	embryonic stem cell	E_02_0932	ChIP,EMSA	Several Tal1 enhancers have been identified, but only the +40k enhancer region contains E-box motifs (Ogilvy et al., 2007), potential binding sites for Mesp1 (Figure 3B, left panel).	Enhancer	--	ChIP,EMSA	We performed ChIP in day 3 EBs after a prior 24 hr Mesp1 pulse and found that Mesp1 was enriched at this cis -regulatory element (Figure 3B, right panel) with a concurrent upregulation of Tal1 expression (Supplementary Figure S3B).We next performed electrophoretic mobility shift assays to confirm the direct interaction between Mesp1 and the Tal1 +40k Enhancer.	Hpt,SCL/tal-1,Scl,bHLHa17,tal-1	--	--	--	Nkx2-5	Csx,Nkx-2.5,Nkx2.5,tinman	RT-PCR	At the protein level,the late pulse of Mesp1 elevated the expression of Nkx2.5,a cardiogenic transcription factor,and downstream markers,cTnT,cTnI and sarcomeric α-actinin.	--	--	Tal1
23637611	chr11	69468873	69470873	CCND1	This release then enables the estrogen receptor to bind to the CCND1 promoter.	human	breast	Low throughput	TIP48/Reptin and H2A.Z requirement for initiating chromatin remodeling in estrogen-activated transcription		--	Breast Tumor	MCF-7 cell	E_02_0933	ChIP,PCR,3C	Long-range chromatin interactions between ERa recognition sequences and enhancers have been proposed to regulate ERa target genes in breast cancer cells. The main enhancer regulating CCND1 is located at the 39 end of the gene, 14 kb distant from the promoter.	Enhancer	3C	PCR	The main Enhancer regulating CCND1 is located at the 3' end of the gene,14 kb distant from the promoter.	BCL1,D11S287E,PRAD1,U21B31	--	--	--	KAT5	ESA1,HTATIP,HTATIP1,PLIP,TIP,TIP60,ZC2HC5,cPLA2	ChIP	TIP60 binding to the CCND1 promoter was analyzed by ChIP and shown as percent of input (n = 2).	--	--	CCND1
23636943	chr11	72897942	72912333	P2RY2	These include an ERBS, which we refer to as ERBS1, located ;20 kb upstream of the promoter of the P2RY2 gene.	human		Low+High throughput	Enhancer transcripts mark active estrogen receptor binding sites	否	--	--	MCF-7 cell	E_02_0934	3C,ChIP-seq,ChIP-qPCR	We integrated the data from our GRO-seq assays with data from a variety of other genomic assays (e.g., ChIP-seq, DNase-seq, ChIA-PET) using a novel computational pipeline to provide a comprehensive and global view of ESR1 enhancers and their regulation by E2 in MCF-7 cells. Together, our studies have shed new light on the activity of ESR1 at its enhancer sites and provide new insights about en_x0002_hancer function in general, including the potential roles of en_x0002_hancer transcription.	Enhancer	--	ChIP-seq,ChIP-qPCR	As shown in the GRO-seq browser tracks in Figure 1A, transcription of the P2RY2 gene and a region around ERBS1 is up-regulated rapidly in a short time course of treatment with 17b-estradiol.The transcripts from ERBS1(Fig. 1A), as well as ERBSs 2–5 (Supplemental Fig. 2), are produced bidirectionally from both strands of DNA,reminiscent of the enhancer RNAs (eRNAs) described previously (Kim et al. 2010), and the transcribed regions are associated with RNA Pol II and pre_x0002_viously identified transcription start sites (TSSs).	HP2U,P2RU1,P2U,P2U1,P2UR,P2Y2,P2Y2R	--	--	--	FOXA1	HNF3A,TCF3A	3C-PCR	3C-PCR assay showing E2-induced looping between ERBS1 and the P2RY2 gene. The lowercase letters correspond to the primers denoted by orange arrows shown in panel A. The assays were conducted in the presence (experimental) or absence (control) of DNA ligase, as indicated. Digested and ligated bacterial artificial chromosome (BAC) DNA spanning the entire P2YR2 locus was used as a PCR control.	--	--	P2RY2
23631855	chr12	48369059	48369213	COL2A1	Our results suggest that CTS epigenetically stimulates CCN2 transcription via TGF-β1 release associated with Smad2/3 activation and enhances COL2A1 expression through the complex formation between SOX9 and Smad2/3.	human		Low throughput	Tensile strain increases expression of CCN2 and COL2A1 by activating TGF-β-Smad2/3 pathway in chondrocytic cells	否	--	--	SW 1353	E_02_0935	PCR,ChIP,Luciferase Reporter Assay	In addition, CTS increased the association between Smad2/3 and the COL2A1 enhancer on chromatin in SW1353 cells (Fig. 3C). In stretched cells, DNA fragment that contained the COL2A1 enhancer was coimmunoprecipitated with Smad2/3, probably via complex for_x0002_mation among Smad2/3-SOX9-the SOX9-binding site, and was amplified by PCR using specific primers for the COL2A1 enhancer.	Enhancer	--	PCR,ChIP,Luciferase Reporter Assay	Chromatin immunoprecipitation revealed that CTS increased Smad2/3 interaction with the CCN2 promoter and the COL2A1 enhancer. Our results suggest that CTS epigenetically stimulates CCN2 transcription via TGF-β1 release associated with Smad2/3 activation and enhances COL2A1 expression through the complex formation between SOX9 and Smad2/3.	ANFH,AOM,COL11A3,SEDC,STL1	--	--	--	SOX9	CMD1,CMPD1,SRA1,SRXX2,SRXY10	Western blot,ChIP	In Western blot(WB)analysis,CTS treatment(2h)did not influence total a mounts of endogenous Smad2/3 and SOX9 in each whole cell lysate(B,20 μg/lane). However,Smad2/3 detected in the nuclear fraction was increased by CTS(C,nucleus,20 μg/lane). In IP analys is using an anti-SOX9 antibody,CTS increased the association between phosphorylated Smad2/3 and SOX9 in the nuclear fraction derived from stretched SW1353 cells.	--	--	COL2A1
23598529	chr2	191834162	191834795	STAT1	In contrast, the transcriptional repressor REST binds to an RE-1 element in the STAT1 repressor region and in doing so represses transcription from the STAT1 gene regulatory region in melanoma cells lines.	human		Low throughput	REST Negatively and ISGF3 Positively Regulate the Human STAT1 Gene in Melanoma	否	--	--	Mm96	E_02_0936	Luciferase Reporter Assay,ChIP,PCR	Our previous analysis of the STAT1 gene recognized a region downstream of the promoter and enhancer regions strongly repressing transcription of luciferase gene repor_x0002_ters (20). In the present study, we define an RE-1 element within this repressor region, to which REST bound and repressed transcription. In the absence of REST, transcriptional repression of the STAT1 gene was dramatically reduced.	Enhancer	--	Luciferase Reporter Assay,ChIP,PCR	Analysis of REST and STAT1 expression levels in human melanoma cells showed that REST is commonly expressed in melanomas and, together with transcription_x0002_al activation and chromatin immunoprecipitation (ChIP) assay, shows that REST negatively regulates STAT1 expression, contributing to the nonresponsiveness of mel_x0002_anomas to IFN.	CANDF7,IMD31A,IMD31B,IMD31C,ISGF-3,STAT91	--	--	--	--	--	--	--	--	--	STAT1
23307821	chr17	26829229	26831311	YY1	The overexpression of YY1 enhanced the cardiogenic differentiation of embryonic stem cells into CPCs.	mouse		Low throughput	Essential and unexpected role of Yin Yang 1 to promote mesodermal cardiac differentiation	否	--	--	Cardiac progenitor cell	E_02_0937	ChIP,PCR,Luciferase Reporter Assay,EMSA	"To examine in detail the potential binding of YY1 to Nkx2.5 enhancer, we performed an electromobility shift assay (EMSA) using the 2.1 kb cardiac enhancer located within -9435 and -7353 bases upstream from the murine NKX2.5 transcriptional start site.Binding of site #1 to YY1 was further confirmed using a DNA supershift assay (Figure 2C). To corroborate these in vitro data with their binding to the Nkx2.5 cardiac enhancer in vivo , we performed chromatin immunoprecipitation (ChIP) and PCR analysis using anti-YY1 antibodies on day 6 differentiated NK ESCs (Figure 2D), FACS-purified eGFP+ CPCs and eGFP- cells from day 6 differentiated NK ESCs (Figure 2E), and from embryonic day 9.5 hearts and body.
"	Enhancer	--	EMSA,ChIP,PCR	"To examine in detail the potential binding of YY1 to Nkx2.5 enhancer, we performed an electromobility shift assay (EMSA) using the 2.1 kb cardiac enhancer located within -9435 and -7353 bases upstream from the murine NKX2.5 transcriptional start site.Binding of site #1 to YY1 was further confirmed using a DNA supershift assay (Figure 2C). To corroborate these in vitro data with their binding to the Nkx2.5 cardiac enhancer in vivo , we performed chromatin immunoprecipitation (ChIP) and PCR analysis using anti-YY1 antibodies on day 6 differentiated NK ESCs (Figure 2D), FACS-purified eGFP+ CPCs and eGFP- cells from day 6 differentiated NK ESCs (Figure 2E), and from embryonic day 9.5 hearts and body.
"	Csx,Nkx-2.5,Nkx2.5,tinman	YY1 regulates Nkx2.5 expression via a 2.1-kb cardiac-specific enhancer	EMSA,ChIP,PCR	To examine in detail the potential binding of YY1 to Nkx2.5 Enhancer, we performed an electromobility shift assay (EMSA) using the 2.1 kb cardiac Enhancer located within -9435 and -7353 bases upstream from the murine NKX2.5 transcriptional start site.	Yy1	NF-E1,YY-1	ChIP,Luciferase Reporter Assay,EMSA	YY1 regulates Nkx2.5 expression via a 2.1 kb cardiac-specific enhancer as demonstrated by in vitro luciferase-based assays and in vivo chromatin immunoprecipitation (ChIP) and genome-wide sequencing analysis.To examine in detail the potential binding of YY1 to Nkx2.5 enhancer, we performed an electromobility shift assay (EMSA) using the 2.1 kb cardiac enhancer located within -9435 and -7353 bases upstream from the murine NKX2.5 transcriptional start site.	--	--	Nkx2-5
23302769	chr11	8301851	8303851	LMO1	Taken together, our results show that LMO1 is poised for expression in normal progenitors, where activation of SCL/TAL1 together with a breakdown of epigenetic repression of LMO1 regulatory elements induces ectopic LMO1 expression that contributes to the development and maintenance of T-ALL. Leukemia	human		Low throughput	Bivalent promoter marks and a latent enhancer may prime the leukaemia oncogene LMO1 for ectopic expression in T-cell leukaemia	否	--	T-Cell leukemia	T-acute lymphoblastic leukemia (T-ALL)	E_02_0938	ChIP,RT-PCR,Luciferase Reporter Assay	The LMO1 promoters display bivalent histone marks in multiple blood lineages including T-cells, and a 3’ flanking region at LMO1 ? 57 contains a transcriptional enhancer that is active in developing blood cells in transgenic mouse embryos. The LMO1 promoters become activated in T-ALL together with the 3’ enhancer, which is bound in primary T-ALL cells by SCL/TAL1 and GATA3.	Enhancer	--	ChIP,RT-PCR,Luciferase Reporter Assay	To investigate whether lack of expres_x0002_sion in the haematopoietic system may be due to active repression of the two LMO1 promoters, we analysed ChIP-Sequencing data released to the public domain by the NIH Roadmap Epigeno_x0002_mics Mapping Project.	RBTN1,RHOM1,TTG1	--	--	--	TAL1,GATA3	SCL,TCL5,bHLHa17,tal-1,HDR,HDRS	ChIP,qPCR	ChIP assays on T-ALL cells from the same primagraft (X31) using antibodies against SCL/TAL1and GATA3. Analysis by quantitative PCR demonstrates significant binding of both SCL/TAL1 and GATA3 to the LMO1 +57 enhancer, with no binding to either of the two LMO1 promoters.	--	--	LMO1
23159876	chr17	48258757	48260757	Col1a1	Our data show that overexpression of Runx2 and Osterix leads to a cooperative effect on the expression of the Col1a1 endogenous gene and its promoter reporter construct.	human		Low throughput	Osterix induces Col1a1 gene expression through binding to Sp1 sites in the bone enhancer and proximal promoter regions	否	--	--	C2C12 cell	E_02_0939	Luciferase Reporter Assay	"The Col1a1 promoter analysis showed the existence of two evolutionarily conserved regions containing pairs of Sp1 sites.These regions are located one at 1700 pb from the transcription start, known as bone enhancer(BE) and where the regulation of Col1a1 expression by Osx has been described,and another region located in the proximal promoter
region."	Enhancer	--	Luciferase Reporter Assay,PCR	To further confirm the relevance of p38 in the regu_x0002_lation of Col1a1 by Osx, we studied the effect of a constitutive active form of MKK6, the MAPKK activating p38, combined with Osx on the ac_x0002_tivation of Col1a1 promoter by Osx. The overexpression of Osx or MKK6 activated both the full-length (?2483pCol1a1) as well the proximal promoter reporter constructs. Moreover, expression of Osx and MKK6 together had an additive effect on the activation of both reporter constructs.	EDSARTH1,EDSC,OI1,OI2,OI3,OI4	--	--	--	RUNX2	AML3,CBF-alpha-1,CBFA1,CCD,CCD1,CLCD,OSF-2,OSF2,PEA2aA,PEBP2aA	Luciferase Reporter Assay	Induction of long Osx transcriptional activity by Runx2. C2C12 cells were co-transfected with mock, short or long Osx constructs and/or Runx2 construct overnight, and serum-starved for 24 h. Luciferase activity was measured and normalized against β-galactosidase activity.	--	--	COL1A1
23108396	chr11	69468761	69470761	CCND1	These results suggest that release of a histone H2A.Z-mediated repression loop activates CCND1 for transcription.	human	breast	Low+High throughput	H2A.Z-dependent crosstalk between enhancer and promoter regulates cyclin D1 expression		--	--	MDA-MB-23,MDA-MB-436	E_02_0940	3C,ChIP,qPCR	ChIP confirmed that H2A.Z siRNA treatment lead to markedly reduced binding of H2A.Z to the CCND1 TSS. Concomitant to increased mRNA levels, polymerase II (pol II) recruitment to the CCND1 TSS slightly increased.	Enhancer	3C	qPCR	We conclude that enh2 has an active role in ER-independent CCND1 activation.To investigate whether the CCND1 TSS interacts with enh2, we used a chromatin conformation capture (3C) assay,which detects physical proximity between distal DNA sites by ligation of cross-linked restricted DNA fragments.	BCL1,D11S287E,PRAD1,U21B31	The enh2 has an active role in ER-independent CCND1 activation.	ChIP	In addition, CCND1 activation in siH2AZ-transfected MDA-MB231 cells was accompanied by a strong recruitment of pol II to enh2 (Figure 1c, right panel), as described previously for E2 stimulated MCF-7 cells. We conclude that enh2 has an active role in ER-independent CCND1 activation.	--	--	--	--	--	--	CCND1
23024062	chr1	60908875	60908895	CTLA4	Together, these data suggest that cAMP may negatively regulate pulmonary inflammatory responses in vivo and in vitro by altering CTLA4 expression.	mouse		Low throughput	Regulation of cytotoxic T lymphocyte antigen 4 by cyclic AMP	否	--	--	T cell	E_02_0941	Luciferase Reporter Assay	T cells were stimulated with CPT after transfection of CTLA4 luciferase reporter constructs (including -1221, -343, -238, -167, and-63 bp relative to the CTLA4 transcription start site). suggesting the presence of an enhancer binding site in this region. 	Enhancer	--	ChIP	The promoter region from 2150 to 2130 bp contains a putative CREB binding site, a well known downstream transcription factor of cAMP signaling. To define whether the putative CREB binding site (2150 to 2143 bp) is responsive to cAMP, we performed ChIP assay with CREB antibody in T cells, with or without CPT treatment.	Cd152,Ctla-4,Ly-56	--	--	--	Creb1	2310001E10Rik,3526402H21Rik,AV083133,Creb,Creb-1	ChIP	The promoter region from -150 to -130 bp contains a putative CREB binding site, a well known downstream transcription factor of cAMP signaling.	--	--	Ctla4
22877652	chr14	67743318	67743610	AR	We conclude that AR repression of GnRH-E1 acts via multiple AR_x0002_responsive regions, including the site at _x0002_1792/_x0002_1791.	mouse		Low throughput	Androgen receptor repression of gonadotropin-releasing hormone gene transcription via enhancer 1	否	--	Polycystic Ovarian Syndrome	GT1–7 cell	E_02_0942	ChIP,PCR,Luciferase Reporter Assay,EMSA	"To determine whether AR interacts with endogenous chromatin in the GnRH-E1 region in GT1-7 cells, ChIP assays were performed. GT1-7 cells were transiently
transfected with luciferase reporter constructs containing the GnRH-P (P), GnRH-E1 (E1), and/or GnRH-E2 (E2) regions, and/or the RSV promoter (RSVp) or enhancer (RSVe), as indicated, along with the AR expression vector. "	Enhancer	--	Luciferase Reporter Assay	AR associates with the enhancer 1 region of the GnRH regulatory region and represses transcription.GT1-7 cells were transiently transfected with luciferase reporter constructs containing the GnRH-P (P), GnRH-E1 (E1),and/or GnRH-E2 (E2) regions, and/or the RSV promoter (RSVp) or enhancer (RSVe), as indicated, along with the AR expression vector. 	Gnrh,Gnrh2,LHRH,Lhrh1,Lnrh,hpg	AR represses GnRH transcription via the major Enhancer (GnRH-E1).	ChIP	For the rest of this study, we chose to evaluate the mechanism of repression by AR using GnRH-E1 upstream of RSVp to avoid com_x005f_x0002_pensation by the androgen-responsive GnRH promoter.To determine whether AR interacts with endogenous chromatin in the GnRH-E1 region in GT1-7 cells,ChIP assays were performed.	Oct1,Pbx,Nkx2-1	2810482H01Rik,NF-A1,Oct-1,Oct1,Otf-1,Otf1,Gata-4,D17Wsu76e,PREP1,AV026640,Nkx2.1,T/EBP,Titf1,Ttf-1	EMSA,PCR	AR bound to the -1796/-1791 sequence in electrophoretic mobility shift assays, indicating a direct interaction with DNA or other transcription factors in this region.	--	--	Gnrh1
22771493	chr8	124323890	124325890	ATAD2	ATAD2 is a coactivator of the androgen receptor (AR) and the MYC protein.	human		Low throughput	Direct Cooperation Between Androgen Receptor and E2F1 Reveals a Common Regulation Mechanism for Androgen-Responsive Genes in Prostate Cells	否	--	Prostate Cancer	LNCaP	E_02_0943	qPCR,Luciferase Reporter Assay,ChIP,EMSA,3C	Taken together, these data demonstrate that the poten_x0002_tial ARBS identified within the distal enhancer region of ATAD2 gene indeed interacts strongly and specifically with AR in vitro and suggest that it could be a good candidate as a functional ARBS in vivo.To ascertain whether the ARBS identified within the ATAD2 enhancer region is functional in cells in vivo, we performed ChIP using formaldehyde cross-linked LNCaP cells. 	Enhancer	--	ChIP,EMSA,RT-qPCR	In addition, we analyzed chromatin immunoprecipita_x0002_tion (ChIP)-seq data from the literature to identify genes that might share the same regulation mechanism as ATAD2.With this in mind, we aimed first at checking whether ATAD2 might be a direct target gene of AR. To test this hypothesis, we analyzed ATAD2 gene response to androgens in LNCaP cells in the presence of cycloheximide (CHX), a protein synthesis inhibitor.	ANCCA,CT137,PRO2000	--	--	--	AR,E2F1	AIS8, DHTR, HUMARA, HYSP1, KD, NR3C4, SBMA, SMAX1, TFM,E2F-1,RBAP1,RBBP3,RBP3	EMSA	To check the binding of AR to this putative ARBS, we first performed EMSA experiments with bacterially produced AR-DNA-binding domain (DBD) purified to homogeneity,siE2F1 and siAR transfection showed the very efficient and specific knockdown of E2F1 and AR, respectively, at both mRNA and protein levels. 	--	--	ATAD2
22761896	chr14	67741735	67744661	Gnrh1	HDAC inhibitors downregulate Gnrh1 gene expression via repressing Otx2-driven transcriptional activity.	mouse		Low throughput	Histone deacetylases regulate gonadotropin-releasing hormone I gene expression via modulating Otx2-driven transcriptional activity	否	--	--	GT1–7 cell	E_02_0944	Luciferase Reporter Assay,ChIP,PCR	the luciferase activities in GT1–7 cells were noticeably decreased without HDACIs treatments, suggesting that potential enhancer elements located in the regions (-3446,-2087 bp and -1134,-520 bp). 	Enhancer	--	Western blot,Immunofluorescence,ChIP,EMSA	The Otx2 protein levels were also obviously reduced in GT1–7 cells showed by western blot analysis (Figure 5B) and immunofluorescence staining (Figure 5C).The results of ChIP assay showed that the binding ability of Otx2 to neuron-specific elements (2356,2249 bp) in Gnrh1 promoter obviously decreased after HDACIs treatments (Figure 6B).To further analyze the affinities of Otx2 to the two conserved binding sites in mouse Gnrh1 promoter respectively, EMSA was performed with probes containing the 2268,2239 bp and 2330,2301 bp sequences [20](Figure 6C, above).	Gnrh,Gnrh2,LHRH,Lhrh1,Lnrh,hpg	--	--	--	Otx2	E130306E05Rik	ChIP,EMSA	Chromatin immunoprecipitation and electrophoretic mobility shift assays demonstrated that the DNA-binding activity of Otx2 to Gnrh1 gene was suppressed by TSA and VPA.	--	--	Gnrh1
22728936	chr9	119469800	119469811	Tbx5	Our results establish a direct molecular link between Tbx5 and Scn5a and elucidate a hierarchy between human GWAS loci that affects function of the mature VCS, establishing a paradigm for understanding the molecular pathology of CCS disease.	mouse		Low+High throughput	TBX5 drives Scn5a expression to regulate cardiac conduction system function	否	--	Cardiac Conduction System Disease	HL-1 cells	E_02_0945	Luciferase Reporter Assay,ChIP-seq	We tested the ability of this putative enhancer to activate transcription in a TBX5-dependent manner. TBX5 dramatically upregulated enhancer-dependent luciferase reporter expression from this genomic region (chr9:119,378,051–119,379,479;NCBI build 37/mm9) in vitro (Figure 6B). 	Enhancer	--	Luciferase Reporter Assay	We tested the ability of this putative enhancer to activate transcription in a TBX5-dependent manner. TBX5 dramatically upregulated enhancer-dependent luciferase reporter expression from this genomic region (chr9:119,378,051–119,379,479;NCBI build 37/mm9) in vitro (Figure 6B). 	Nav1.5,Nav1.5c,SkM1,SkM2,mH1	TBX5-responsive Enhancer downstream of Scn5a sufficient to drive VCS expression in vivo, dependent on canonical T-box binding sites. 	ChIP-seq	Here, we found a direct molecular link between TBX5 and Scn5a via a TBX5-respon_x005f_x0002_sive downstream Enhancer that was sufficient to direct VCS-specif-ic gene expression. Our results identified a TBX5-Scn5a molecular network essential for function of the mature VCS. 	Tbx5	Tbx5	ChIP-seq	We bioinformatically interrogated the Scn5a locus to identify potential TBX5-responsive Enhancers using the overlap of 4 independent data sets: (a) evolutionary conservation (21);(b) ChIP-seq studies identifying TBX5 binding sites in the atrial cardiomyocyte HL-1 cell line.	--	--	Scn5a
22728936	chr9	119469800	119469811	Scn5a	Our results establish a direct molecular link between Tbx5 and Scn5a and elucidate a hierarchy between human GWAS loci that affects function of the mature VCS, establishing a paradigm for understanding the molecular pathology of CCS disease.	mouse		Low+High throughput	TBX5 drives Scn5a expression to regulate cardiac conduction system function	否	--	Cardiac Conduction System Disease	HL-1 cells	E_02_0945	Luciferase Reporter Assay,ChIP-seq	We tested the ability of this putative enhancer to activate transcription in a TBX5-dependent manner. TBX5 dramatically upregulated enhancer-dependent luciferase reporter expression from this genomic region (chr9:119,378,051–119,379,479;NCBI build 37/mm9) in vitro (Figure 6B). 	Enhancer	--	Luciferase Reporter Assay	We tested the ability of this putative enhancer to activate transcription in a TBX5-dependent manner. TBX5 dramatically upregulated enhancer-dependent luciferase reporter expression from this genomic region (chr9:119,378,051–119,379,479;NCBI build 37/mm9) in vitro (Figure 6B). 	Nav1.5,Nav1.5c,SkM1,SkM2,mH1	TBX5-responsive Enhancer downstream of Scn5a sufficient to drive VCS expression in vivo, dependent on canonical T-box binding sites. 	ChIP-seq	Here, we found a direct molecular link between TBX5 and Scn5a via a TBX5-respon_x005f_x0002_sive downstream Enhancer that was sufficient to direct VCS-specif-ic gene expression. Our results identified a TBX5-Scn5a molecular network essential for function of the mature VCS. 	Tbx5	Tbx5	ChIP-seq	We bioinformatically interrogated the Scn5a locus to identify potential TBX5-responsive Enhancers using the overlap of 4 independent data sets: (a) evolutionary conservation (21);(b) ChIP-seq studies identifying TBX5 binding sites in the atrial cardiomyocyte HL-1 cell line.	--	--	Scn5a
22701669	chr14	47056226	47056692	Bmp4	These results establish a direct molecular regulatory link between Pitx family members and Bmp4 gene expression in developing incisor epithelium.	mouse		Low throughput	An evolutionarily conserved enhancer regulates Bmp4 expression in developing incisor and limb bud	否	--	--	LS-8 cell	E_02_0946	EMSA,Phylogenetic Footprinting	In vitro electrophoretic mobility shift assays (EMSA) and in vivo transgenic reporter mutational analyses revealed that this site supports Pitx binding and that the site is necessary to recapitulate aspects of endogenous Bmp4 expression in developing craniofacial and limb tissues.	Enhancer	--	ChIP,PCR	Pitx2 chromatin immunoprecipitation (ChIP) demonstrate direct binding of Pitx2 to this Bmp4 enhancer site in a dental epithelial cell line.Using primers that target the Pitx1/2 binding motif in the 396 bp Bmp4 enhancer sequence (CONS3.8), DNA purified from crosslinked LS8 chromatin after immunoprecipitation with an anti-Pitx2 antibody yielded a 4.7-fold increase in amplicon abundance, relative to an IgG control, by PCR and qPCR (Figure 6A, B).	Bmp-4,Bmp2b,Bmp2b-1,Bmp2b1	Pitx2 ChIP demonstrated direct binding of Pitx2 to this Bmp4 enhancer site in a dental epithelial cell line.	ChIP,PCR,qPCR	Using primers that target the Pitx1/2 binding motif in the 396 bp Bmp4 Enhancer sequence (CONS3.8), DNA purified from crosslinked LS8 chromatin after immunoprecipitation with an anti-Pitx2 antibody yielded a 4.7-fold increase in amplicon abundance, relative to an IgG control, by PCR and qPCR.	Pitx2	9430085M16Rik,Brx1,Brx1b,Munc30,Otlx2,Ptx2,Rieg	EMSA,ChIP	Electrophoretic Mobility Shift Assay (EMSA) exhibits robust binding of Pitx1 protein to both a positive control bicoid DNA sequence and to the consensus Pitx1/2 binding site in with a 25 probe sequence in the CONS3.8 sequenceTo determine whether Pitx2 physically binds the CONS3.8 Bmp4 Enhancer in living cells,we performed Chromatin Immunoprecipitation (ChIP) assays in LS8 mouse dental epithelial cells.	--	--	Bmp4
22665440	chr17	69107686	69108045	SOX9	Together, our results demonstrate that multiple genetic variants mapping to a unique enhancer looping to the SOX9 oncogene can account for the risk associated with the PCa 17q24.3 locus.	human		Low throughput	Integrative functional genomics identifies an enhancer looping to the SOX9 gene disrupted by the 17q24.3 prostate cancer risk locus	是	rs8072254	--	LNCaP	E_02_0947	Luciferase Reporter Assay,ChIP,3C-qPCR,ChIP-qPCR	To determine if the rs1859962 PCa risk LD block harbors enhancers, we examined the H3K4me1 ge_x0002_nome-wide distribution defined by ChIP-seq assays in LNCaP and VCaP PCa cells.We show that there are five enhancers within the target genomic segment, hereafter referred to as E1–E5.	Enhancer	--	qPCR	This chromatin loop was confirmed through TaqMan probe–based qPCR assays with a probe targeting the SOX9 gene (Fig. 2C). The chromatin interaction was further confirmed by sequencing the PCR product (Supplemental Fig. S7). Further_x0002_more, this chromatin loop appears to be specific to SOX9, because no other loop could be detected between E1 and any other genes(MAP2K6, KCNJ16, KCNJ2) found within this ;3-Mb window.	CMD1,CMPD1,SRA1,SRXX2,SRXY10	--	--	--	AR,FOXA1	AIS8, DHTR, HUMARA, HYSP1, KD, NR3C4, SBMA, SMAX1,TFM,HNF3A,TCF3A	ChIP,Luciferase Reporter Assay	In agreement, the luciferase assay in LNCaP cells depletedor not of AR using siRNA reveals that AR is required for the increased transcriptional response associated with the rs8072254 variant A allele.The FKH PWM, defined based on thousands of FOXA1 binding sites identified by ChIP-seq assays, reveals that the tenth position is invariably an A residue.	69107816	Luciferase Reporter Assay,ChIP	SOX9
22645302	chr12	8036824	8048824	KDM3A	KDM3A is recruited to the SLC2A3 locus in an HIF1-dependent manner and demethylates H3K9me2 so as to upregulate its expression.	human		Low+High throughput	Dynamic Change of Chromatin Conformation in Response to Hypoxia Enhances the Expression of GLUT3 (SLC2A3) by Cooperative Interaction of Hypoxia-Inducible Factor 1 and KDM3A	否	--	--	HEK-293,HeLa	E_02_0948	ChIP-PCR,RT-PCR,3C-ChIP,ChIP-seq	To examine whether histone enhancers mark changes under hypoxia, we compared the HIF1 binding sites and H3K27ac under normoxia and hypoxia on a genome-wide scale. The number of total reads and uniquely mapped sequences of the ChIP-seq for histone marks are shown in Table S4 in the supplemental material. H3K27ac sites overlapped at 12,498 sites between the state of normoxia (14,679 sites) and hypoxia (16,366 sites) on a genome-wide scale.The results of the HIF1 ChIP-seq analysis provided data of hypoxic enhancer 2 (kbp -24 from the TSS) at the SLC2A3 loci.	Enhancer	3C	ChIP-PCR,ChIP	We elucidated that both the chromatin conformational structure and histone modification change under hy_x0002_poxic conditions and enhance the expression of SLC2A3 based on the combined results of chromatin conformation capture (3C) and ChIP assays. KDM3A is recruited to the SLC2A3 locus in an HIF1-dependent manner and demethylates H3K9me2 so as to upregulate its expression.These findings provide novel insights into the interaction between HIF1 and KDM3A and also the epigenetic regulation of HIF1.	GLUT3	The enhancer 2 was functionally active under hypoxic condition	ChIP-PCR,Luciferase Reporter Assay	The experimental data described above showed that distal enhancer 2 was functionally active under hypoxic conditions, suggesting that enhancer 2 has an especially close proximity to the promoter of SLC2A3 under hypoxic conditions. 	HIF1A	HIF-1-alpha,HIF-1A,HIF-1alpha,HIF1,HIF1-ALPHA,MOP1,PASD8,bHLHe78	ChIP	Genome-wide analysis of HIF1 binding sites (chromatin immunoprecipitation[ChIP] with deep sequencing) of endothelial cells clarified that HIF1 mainly binds to the intergenic regions distal from tran_x0002_scriptional starting sites under both normoxia and hypoxia.	--	--	SLC2A3
22543974	chr12	114463712	114464080	TBX5	We uncovered three enhancers that collectively recapitulate the endogenous expression pattern of TBX5 in the developing heart.	human	heart	Low+High throughput	Regulatory variation in a TBX5 enhancer leads to isolated congenital heart disease		--	Congenital Heart Disease	HeLa,T cell	E_02_0949	EMSA,PCR,ChIP-seq	This strategy considered multiple genome-wide ChIP-seq data sets including the enhancer associated transcriptional co-activator p300, cardiac transcription factors Mef2a, TBX5, Gata4, Nkx2.5, SRF and computationally predicted enhancers, as well as the enhancer-associated histonemodificationH3K4me1and evolutionary conservation to identify and prioritize likely functional non-coding regions.	Enhancer	--	EMSA,PCR	We identified three elements (CREs 2, 9, 16) with patterns of Enhancer activity overlapping the endogenous expression pattern of TBX5 and the Enhancer-trap BACs in which they were contained.	HOS	A significant number of CHD associated with TBX5 dysfunction might arise from non-coding mutations in TBX5 heart enhancers, effectively decoupling the heart and hand phenotypes of the Holt-Oram syndrome.	EMSA,ChIP-seq	Notably, all lines exhibited weak expression in the left atrium and almost no ex_x0002_pression in the right atrium, suggesting that the bulk of TBX5 atrial expression is regulated by Enhancers outside the genomic region covered by this BAC. 	TBX5	HOS	EMSA	We hypothesized that the variant nucleotide disrupts transcrip_x0002_tion factor binding to Enhancer 9. To test this, we performed an electrophoretic mobility shift assay using short DNA probes spanning either the wild-type (G) or variant (T) allele.	--	--	TBX5
22543974	chr12	114463712	114464080	TBX6	We uncovered three enhancers that collectively recapitulate the endogenous expression pattern of TBX6 in the developing heart.	human	heart	Low+High throughput	Regulatory variation in a TBX6 enhancer leads to isolated congenital heart disease		--	Congenital Heart Disease	HeLa,T cell	E_02_0949	EMSA,PCR,ChIP-seq	This strategy considered multiple genome-wide ChIP-seq data sets including the enhancer associated transcriptional co-activator p300, cardiac transcription factors Mef2a, TBX5, Gata4, Nkx2.5, SRF and computationally predicted enhancers, as well as the enhancer-associated histonemodificationH3K4me1and evolutionary conservation to identify and prioritize likely functional non-coding regions.	Enhancer	--	EMSA,PCR	We identified three elements (CREs 2, 9, 16) with patterns of Enhancer activity overlapping the endogenous expression pattern of TBX5 and the Enhancer-trap BACs in which they were contained.	HOS	A significant number of CHD associated with TBX5 dysfunction might arise from non-coding mutations in TBX5 heart enhancers, effectively decoupling the heart and hand phenotypes of the Holt-Oram syndrome.	EMSA,ChIP-seq	Notably, all lines exhibited weak expression in the left atrium and almost no ex_x0002_pression in the right atrium, suggesting that the bulk of TBX5 atrial expression is regulated by Enhancers outside the genomic region covered by this BAC. 	TBX5	HOS	EMSA	We hypothesized that the variant nucleotide disrupts transcrip_x0002_tion factor binding to Enhancer 9. To test this, we performed an electrophoretic mobility shift assay using short DNA probes spanning either the wild-type (G) or variant (T) allele.	--	--	TBX5
22383952	chr17	42078865	42079198	NAGS	The presented data strongly suggest that Sp1, CREB, HNF-1, and NF-Y, that are known to be responsive to hormones and diet, regulate NAGS transcription.	human		Low throughput	Transcriptional Regulation of N-AcetylglutamateSynthase	否	--	--	Hep G2 cell	E_02_0950	PCR,ChIP,Luciferase Reporter Assay	Reporter assays to compare the effect of the enhancer in liver,intestine and lung cells, included data that were normalized to the reporter expression driven by the NAGS promoter. While the NAGS enhancer (4.10PromEnh) increased expression of the reporter gene by 50% in liver derived cells (Figure 2A), expression of the luciferase gene did not increase in the intestine or lung derived cells (Figure 8) suggesting that the enhancer may determine tissue specificity of NAGS expression.	Enhancer	--	ChIP,Luciferase Reporter Assay	"We subsequently confirmed that these regions function as promoter and enhancer and that the enhancer is most effective in liver cells. Avidin-agarose protein_x0002_DNA pull-down assays have been used to confirm binding of Sp1 and CREB within the NAGS promoter and Hepatic Nuclear Factor 1 (HNF-1) and NF-Y within the enhancer regions. Chromatin immunoprecipitation (ChIP) and quantitative real_x0002_time PCR have been used to independently verify that Sp1 and CREB bind to the promoter region, and HNF-1 and NF-Y bind to
the enhancer region. We also used 59RACE analysis to identify multiple transcription start sites for NAGS that may be species and tissue specific."	AGAS,ARGA	Two regions of high conservation upstream of the translation start of the NAGS gene. Reporter assays confirmed that these regions represent promoter and enhancer and that the enhancer is tissue specific.	Luciferase Reporter Assay	Reporter assays to compare the effect of the enhancer in liver, intestine and lung cells, included data that were normalized to the reporter expression driven by the NAGS promoter. While the NAGS enhancer (4.10PromEnh) increased expression of the reporter gene by 50% in liver derived cells (Figure 2A), expression of the luciferase gene did not increase in the intestine or lung derived cells (Figure 8) suggesting that the enhancer may determine tissue specificity of NAGS expression. When HNF-1	SP1,HNF1A,NF-Y	SP1,HNF-1A,HNF1,HNF4A,IDDM20,LFB1,MODY3,TCF-1,TCF1,CBF-A, CBF-B,HAP2,NF-YA	ChIP,qPCR	Thus,Pull-down and ChIP assays confirmed that Sp1 and CREB bind along the NAGS promoter and HNF-1 and NF-Y bind along the Enhancer.	--	--	NAGS
22378757	chr10	62128342	62130342	NEUROG3	Collectively, these results establish a mechanism by which activation of STAT3 regulates the expression of NEUROG3 to subsequently drive differentiation of SSC and progenitor spermatogonia in the mammalian germline.	mouse		Low throughput	NEUROG3 is a critical downstream effector for STAT3-regulated differentiation of mammalian stem and progenitor spermatogonia	否	--	--	germ line cell	E_02_0951	ChIP,PCR,Luciferase Reporter Assay	"To investigate this further, we used a ChIP method to determine whether STAT3 binds Neurog3 regulatory elements in THY1+ spermatogonia. PCR analysis
with primers designed to span a 200-bp segment of the Neurog3 distal promoter/enhancer region including the STAT3 binding site produced an amplicon of expected size;"	Enhancer	--	Luciferase Reporter Assay,Transfection	Next, we determined whether STAT3 directly regulates Neurog3 promoter/enhancer activity. To investigate this, we used a reporter construct in which the Neurog3 promoter/enhancer sequence was cloned upstream of the firefly luciferase gene, termed pNeurog3-Luc.The transfection efficiency of cultured SSC/progenitor spermatogonia with plasmid DNA vectors is low, thus HeLa cells were used with the reporter vector to determine whether STAT3 is capable of stimulating Neurog3 promoter/enhancer activity.	Atoh5,Math4B,bHLHa7,ngn3	--	--	--	Stat3	1110034C02Rik,AW109958,Aprf	ChIP	Moreover,using a ChIP approach we found that STAT3 physically interacts with the distal Neurog3 promoter/Enhancer in THY1 undifferentiated spermatogonia and using a reporter construct show that STAT3 regulates transcription through this promoter.	--	--	Neurog3
22378757	chr10	62128342	62130342	STAT3	Collectively, these results establish a mechanism by which activation of STAT3 regulates the expression of NEUROG3 to subsequently drive differentiation of SSC and progenitor spermatogonia in the mammalian germline.	mouse		Low throughput	NEUROG3 is a critical downstream effector for STAT3-regulated differentiation of mammalian stem and progenitor spermatogonia	否	--	--	germ line cell	E_02_0951	ChIP,PCR,Luciferase Reporter Assay	"To investigate this further, we used a ChIP method to determine whether STAT3 binds Neurog3 regulatory elements in THY1+ spermatogonia. PCR analysis
with primers designed to span a 200-bp segment of the Neurog3 distal promoter/enhancer region including the STAT3 binding site produced an amplicon of expected size;"	Enhancer	--	Luciferase Reporter Assay,Transfection	Next, we determined whether STAT3 directly regulates Neurog3 promoter/enhancer activity. To investigate this, we used a reporter construct in which the Neurog3 promoter/enhancer sequence was cloned upstream of the firefly luciferase gene, termed pNeurog3-Luc.The transfection efficiency of cultured SSC/progenitor spermatogonia with plasmid DNA vectors is low, thus HeLa cells were used with the reporter vector to determine whether STAT3 is capable of stimulating Neurog3 promoter/enhancer activity.	Atoh5,Math4B,bHLHa7,ngn3	--	--	--	Stat3	1110034C02Rik,AW109958,Aprf	ChIP	Moreover,using a ChIP approach we found that STAT3 physically interacts with the distal Neurog3 promoter/Enhancer in THY1 undifferentiated spermatogonia and using a reporter construct show that STAT3 regulates transcription through this promoter.	--	--	Neurog3
22303449	chr5	44385749	44386845	ISL1	ISL1 transcription demarcated an anatomical region supporting the conserved existence of a SHF in humans, and transcription factors of the GATA family were co-expressed therein.	human		Low throughput	ISL1 Directly Regulates FGF10 Transcription during Human Cardiac Outflow Formation	否	--	--	embryonic cell 	E_02_0952	ChIP,EMSA	In conjunction, we identified a novel enhancer containing a highly conserved ISL1 consensus binding site within the FGF10 first intron. ChIP and EMSA demonstrated its direct occupation by ISL1. Transcription mediated by ISL1 from this FGF10 intronic element was enhanced by the presence of GATA4 and TBX20 cardiac transcription factors. Finally, transgenic mice confirmed that endogenous factors bound the human FGF10 intronic enhancer to drive reporter expression in the developing cardiac outflow tract.	Enhancer	--	ChIP,EMSA	Using chromatin immunoprecipitation (ChIP) of microdissected embryonic human hearts, we demonstrated that at Carnegie stages 14–15 (33–36 dpf), ISL1 bound to and enriched a 327 bp FGF10-Int1 fragment (Fig. 2A). In contrast, ISL1 did not occupy FGF10-Pr1 or FGF10-Pr2. Acetylated histone H4 did bind both the ISL1 and FGF10 promoters at CS14-15, confirming that the chromatin around these two promoters is transcriptionally active in the human heart at these stages.	FGF10	Endogenous factors bound the human FGF10 intronic enhancer to drive reporter expression in the developing cardiac outflow tract.	ChIP,EMSA,Transgenic mice	Finally, transgenic mice confirmed that endogenous factors bound the human FGF10 intronic enhancer to drive reporter expression in the developing cardiac outflow tract.	ISL1,GATA4,TBX20	ISLET1,Isl-1,ASD2,TACHD,TOF,VSD1,ASD4	ChIP,EMSA	ChIP and EMSA demonstrated its direct occupation by ISL1. Transcription mediated by ISL1 from this FGF10 intronic element was enhanced by the presence of GATA4 and TBX20 cardiac transcription factors. 	--	--	FGF10
22265404	chr14	90847327	90849327	IRS1	IRS1 is known to participate in type-2 diabetes (T2D) mellitus, and is found specifically expressed in MCF7 cells (Figure 7D).	human		Low+High throughput	Extensive Promoter-Centered Chromatin Interactions Provide a Topological Basis for Transcription Regulation	否	--	Congenital Limb Deformity	MCF-7,K-562,HeLa,HCT 116,Nb4	E_02_0953	3C-qPCR,Luciferase Reporter Assay,ChIP-seq	To examine potential enhancer activity of promoters, we per_x0002_formed luciferase reporter gene assays, a commonly used method for promoter and enhancer characterization.	Enhancer	3C-qPCR	Luciferase Reporter Assay	In another example (Figure 5F), the promoter of CALM1 interacts with an enhancer element 15 kb upstream and connects to the promoter of C14orf102 further upstream in 65kb. Both RNA-Seq data and the H3K4me3/me1 log ratio indi_x0002_cated that the CALM1 promoter was strong, whereas the C14orf102 promoter was weak and enhancer-like. The luciferase reporter gene assay showed marginal enhancement to the CALM1 promoter reporter gene activity by the native CALM1 enhancer and the C14orf102 promoter individually.	CALML2,CAM2,CAM3,CAMB,CAMC,CAMI,CAMIII,CPVT4,DD132,LQT14,PHKD,caM	--	--	--	--	--	--	--	--	--	CALM1 
22264824	chr11	32244715	32246895	Nprl3	A substantial proportion of the expression of Nprl3 mRNA seen in erythroid cells is derived from an erythroid-specific alternative promoter(s) distinct from the canonical Nprl3 promoter.	mouse		Low+High throughput	Intragenic enhancers act as alternative promoters	否	--	--	Primary Erythroid Cell	E_02_0954	RT-PCR,ChIP,ChIP-seq	Beyond this AFE the isoform structure appears identical to the full-length transcript. Interestingly, the AFE coincides with one of the known intragenic enhancers.First, we tested wild-type mouse tissues by RT-PCR to verify the existence of this alternative transcript. 	Enhancer	--	RT-PCR,ChIP,ChIP-seq	Beyond this AFE the isoform structure appears identical to the full-length transcript. Interestingly, the AFE coincides with one of the known intragenic enhancers.First, we tested wild-type mouse tissues by RT-PCR to verify the existence of this alternative transcript. 	Aag,CGTHBA,HS-26,HS-40,Mare,Phg,Prox1,m(alpha)RE	Intragenic Enhancers frequently act as alternative tissue_x005f_x0002_specific promoters producing a class of abundant,spliced, multiexonic poly(A)+ RNAs (meRNAs) which reflect the host gene’s structure.	ChIP,RT-PCR,ChIP-seq	To address this problem, we analyzed transcrip_x005f_x0002_tion of the Nprl3 gene after deleting its constitutive promoter. This revealed that intragenic Enhancers act as highly active, alternative tissue-specific promoters for the gene containing them. 	--	--	--	--	--	--	Nprl3
22212979	chr19	51354804	51355203	TMPRSS2	Upon stimulation with 1 nM DHT, AR and RNA Pol II were recruited onto PSA and TMPRSS2 enhancer regions to a greater extent (P < 0.05) in AR-overexpressing cells compared to control cells.	human		Low throughput	Androgen Receptor Overexpression Alters Binding Dynamics of the Receptor to Chromatin and Chromatin Structure	否	--	--	LNCaP	E_02_0955	qRT-PCR,ChIP	Chromatin immunoprecipitation (ChIP) on the promoters and enhancers of prostate specific antigen (PSA) and transmembrane protease, serine(TMPRSS2) genes was performed.For PSA, in addition to the AREs located 131 and 150 bp from the tran_x0002_scription start site (TSS), an enhancer region 4 kb upstream of the TSS has been documented.For the TMPRSS2 gene, the AREs in the regulatory region are located 13.5 kb [27,38] and 700 bp up_x0002_stream of the TSS.	Enhancer	--	ChIP-qPCR,ChIP	Chromatin immunoprecipitation(ChIP) on the promoters and enhancers of prostate specific antigen (PSA) and transmembrane protease, serine 2(TMPRSS2) genes was performed. qRT-PCR was used to measure the levels of PSA and TMPRSS2 transcripts.We performed ChIP-qPCR analyses on these selected genomic sites of PSA and TMPRSS2.	APS,KLK2A1,PSA,hK3	--	--	--	AR	AIS8,DHTR,HUMARA,HYSP1,KD,NR3C4,SBMA,SMAX1,TFM	ChIP-qPCR	At the 1 hr time point, AR loading onto the TMPRSS2 enhancer (Fig. 3A) was already significantly (P < 0.001, t-test) higher in LNCaP-ARhi cells than in the control cells. However, the TMPRSS2 promoter did not significantly recruit AR, at least in the 4 hr time (Fig. 3B).ChIP-qPCR was performed to assess the AR loading.	--	--	KLK3
22072553	chr1	38469166	38512500	Hoxa9	Hoxa9 regulates transcription by interacting with enhancers of genes important for hematopoiesis and leukemia.	mouse		Low throughput	Identification and characterization of Hoxa9 binding sites in hematopoietic cells	否	--	Acute Leukemia	BM Cell	E_02_0956	Transfection,ChIP-chip,Luciferase Reporter Assay	Furthermore, a subset of these sites shows enhancer activity in transient transfection assays. ChIP-chip data were analyzed with MA2C 36 and a customized R package.These studies showed that H3 and H4 acetylation and p300/CBP binding is centered on the H/M peaks and is flanked by regions of histone H3K4me1 in a bimodal distribution characteristic of enhancer sequences (Figure 3B). 3To test for potential enhancer (or repressor activity), 22 Hoxa9/Meis1 binding sites as well as 2 control regions randomly selected in the genome where there is no Hoxa9/Meis1 binding were cloned as ~1000-bp fragments. These were inserted into the multiple cloning site of the pTAL-Lucvector,electroporated into myeloblastic K562 cells and were analyzed by Dual Luciferase Reporter Assays (Promega; supplemental Figure 3).	Enhancer	--	Luciferase Reporter Assay	"To test for potential enhancer (or repressor activity), 22 Hoxa9/Meis1 binding sites as well as 2 control regions randomly selected in the genome where there is no Hoxa9/Meis1 binding were cloned as ~1000-bp fragments. These were inserted into the multiple cloning site of the pTAL-Lucvector,electroporated into myeloblas-
tic K562 cells and were analyzed by Dual Luciferase Reporter Assays (Promega; supplemental Figure 3)."	3222402O04Rik,A730046J16,LAF-4,Laf4	--	--	--	Hoxa9,Meis1	D6a9,Hox-1.7,C530044H18Rik,Evi8	ChIP-qPCR	Confirmation of selected Hoxa9 and Meis1 binding sites by ChIP and quantitative PCR.	--	--	Aff3
21868451	chr5	134350424	134352424	PITX1	Here, we report that expression of paired-like homeodomain transcription factor (PITX1), a tumor suppressor and member of the homeobox family of tran_x005f_x0002_scription factors, is robustly up-regulated by E2 in several ER_x0001_ -positive breast cancer cell lines via ER_x0001_ -dependent interaction between the proximal promoter and an enhancer region 5_x0001_ upstream of the PITX1 gene.	human		Low throughput	The Estrogen-Regulated Transcription Factor PITX1 Coordinates Gene-Specific Regulation by Estrogen Receptor-Alpha in Breast Cancer Cells	否	--	--	MCF-7 cell	E_02_0957	ChIP,Luciferase Reporter Assay,3C	"Genetic locus from the UCSC
genome browser showing the natural 5 to 3 orientation of the PITX1 gene with the location of the identified ER binding regions, the proximal promoter and enhancer, and the location of the primers used in ChIP and chromosome conformation capture experiments."	Enhancer	--	Luciferase Reporter Assay,Transfection	"ER regulation of PITX1 involves interaction of the ER-binding distal enhancer with the promoter of the PITX1 gene via intrachromosomal looping.We next determined whether the PITX1 enhancer and promoter regions were estrogen responsive by
cloning these regions from genomic DNA into luciferase reporters, and we conducted transient transfection assays."	BFT,CCF,LBNBG,POTX,PTX1	--	--	--	ESR1	ER,ESR,ESRA,ESTRR,Era,NR3A1	ChIP	Recruitment,monitored by ChIP,of ER and PITX1 to ER binding sites that contain a consensus PITX1 binding site in vehicle and 10 nM E2-treated 231ER cell at 45 min (panel D) or to ER binding sites that lack a consensus PITX1 binding site in vehicle and 10 nM E2-treated 231ER cell at 45 min.	--	--	PITX1
21822303	chr3	34646162	34646551	Sox2	These findings suggest that reactivation of Sox2 represents an early step in breast tumour initiation, explaining tumour heterogeneity by placing the tumour-initiating event in any cell along the axis of mammary differentiation.	mouse		Low throughput	Sox2 expression in breast tumours and activation in breast cancer stem cells	否	--	--	MCF-7 cell	E_02_0958	Luciferase Reporter Assay	We transfected MCF7 and T47D cells with luciferase reporter vectors for the upstream distal enhancer and the core promoter to test whether induction of Sox2 protein was achieved through transcriptional activation of Sox2 promoter.	Enhancer	--	Luciferase Reporter Assay	We transfected MCF7 and T47D cells with luciferase reporter vectors for the upstream distal enhancer and the core promoter to test whether induction of Sox2 protein was achieved through transcriptional activation of Sox2 promoter.	Sox-2,lcc,ysb	--	--	--	--	--	--	--	--	--	Sox2
21798992	chr8	117978845	117979466	SLC30A8	Genome-wide association studies have shown that a polymorphic variant in SLC30A8, which encodes zinc transporter-8, is associated with altered susceptibility to type 2 diabetes (T2D).	human		Low throughput	Characterization of the human SLC30A8 promoter and intronic enhancer.	否	rs62510556 	Type 2 Diabetes Mellitus	βTC-3,αTC-6	E_02_0959	Luciferase Reporter Assay,PCR,Transfection	"we have identified a conserved islet beta cell-specific enhancer in SLC30A8 intron
2 (Figs. 4 & 5). "	Enhancer	--	Luciferase Reporter Assay,PCR,Transfection	To determine whether the +16579 and +16954 region of intron 2 in the human SLC30A8 gene also represents a transcriptional enhancer, this region was isolated using PCR and ligated 5' of the ?150/+3 G6PC2-luciferase fusion gene described above. Luciferase expression directed by this fusion gene was then analyzed by transient transfection of βTC-3 and αTC-6 cells.	ZNT8,ZnT-8	--	--	--	--	--	--	--	118164272	Luciferase Reporter Assay,PCR	SLC30A8
21798992	chr8	117978845	117979466	SLC30A9	Genome-wide association studies have shown that a polymorphic variant in SLC30A8, which encodes zinc transporter-8, is associated with altered susceptibility to type 2 diabetes (T3D).	human		Low throughput	Characterization of the human SLC30A9 promoter and intronic enhancer.	是	rs62510556 	Type 2 Diabetes Mellitus	βTC-3	E_02_0959	Luciferase Reporter Assay,PCR,Transfection	"we have identified a conserved islet beta cell-specific enhancer in SLC30A8 intron
2 (Figs. 4 & 5). "	Enhancer	--	Luciferase Reporter Assay,PCR,Transfection	To determine whether the +16579 and +16954 region of intron 2 in the human SLC30A8 gene also represents a transcriptional enhancer, this region was isolated using PCR and ligated 5' of the ?150/+3 G6PC2-luciferase fusion gene described above. Luciferase expression directed by this fusion gene was then analyzed by transient transfection of βTC-3 and αTC-6 cells.	ZNT8,ZnT-8	--	--	--	--	--	--	--	118164272	Luciferase Reporter Assay,PCR	SLC30A8
21797989	chr7	19409838	19410044	MR1	In this study, we discovered that MR1 is critical for MCK expression in slow- and intermediate-twitch muscle fibers and that MR1’s positive transcriptional activity depends on a paired E-box MEF2 site motif within a SIE. This is the first study to delineate the DNA controls for MCK expression in different skeletal muscle fiber types.	mouse		Low throughput	Differentiation and fiber type-specific activity of a muscle creatine kinase intronic enhancer.	否	--	--	MM14	E_02_0960	EMSA,Immunofluorescence,ChIP	Of particular interest was a 95-bp region (+901 to +995) that was subsequently proven to exhibit the properties of a transcriptional enhancer (Figure 1).	Enhancer	--	ChIP	The chromatin immunoprecipitation (ChIP) primer pairs (black lines) that span the 5’-enhancer sequence were used as positive controls for MyoD and myogenin binding to functional E-boxes.	CPK-Mm,M-CK,MCK,?Ckm	--	--	--	Mef2	5430401D19Rik,9930028G15Rik,AV011172,Mef2	ChIP-seq	MEF2 ChIP-seq occupancy at the 6.5- MCK regulatory region in differentiated C2 C12 cell shows that MEF2 is present at all three control regions.	--	--	Ckm
21689639	chr12	7940709	7941994	NANOG	NANOG is a homeodomain-containing transcription factor that is essential for the maintenance of pluri_x0002_potency and self-renewal in embryonic stem cells.	human		Low throughput	A Tcf/Lef element within the enhancer region of the human NANOG gene plays a role in promoter activation	不相关	--	--	HEK-293 cells	E_02_0961	Luciferase Reporter Assay	"Genome sequence analysis of the enhancer region of the human NANOG gene showed the presence of two conserved Tcf/Lef--binding motifs: CAAAGA at
positions --1206 to --1190 (designated as Lef #1) and an inverted GTTTCA sequence at ?1020 to ?1004 (designated as Lef #2) (Fig. 1A). To investigate whether Tcf/Lef elements located in the enhancer region play a role in the regulation of NANOG gene transcription, we isolated a 1286--bp fragment of the enhancer region of the human NANOG gene and subcloned it into a firefly luciferase reporter vector, yielding pNanog--Luc(--1286/--1)."	Enhancer	--	Luciferase Reporter Assay	To investigate whether Tcf/Lef elements located in the enhancer region play a role in the regulation of NANOG gene transcription, we isolated a 1286--bp fragment of the enhancer region of the human NANOG gene and subcloned it into a firefly luciferase reporter vector, yielding pNanog--Luc(--1286/--1). 	NANOG	--	--	--	LEF1	LEF-1,TCF10,TCF1ALPHA,TCF7L3	ChIP	ChIP experiments demonstrated that b-catenin and Lef1 bind to the Enhancer region of the NANOG gene. Our present findings would appear to indicate that the Tcf/Lef element in the Enhancer region of the Human NANOG gene functions in transcriptional activation of the Human NANOG gene.	--	--	NANOG
21681857	chr17	42078932	42079032	NAGS	N-acetylglutamate synthase (NAGS) catalyzes the conversion of glutamate and acetyl-CoA to NAG, the essential allosteric activator of carbamyl phosphate synthetase I, the first urea cycle enzyme in mammals.	human		Low throughput	N-carbamylglutamate enhancement of ureagenesis leads to discovery of a novel deleterious mutation in a newly defined enhancer of the NAGS gene and to effective therapy	相关	--	--	Ureagenesis	E_02_0962	Luciferase Reporter Assay	The remaining change, a homozygous C–A transversion 3,064--bp upstream of the NAGS translation start codon (c.--3064C > A) (Supp. Fig. S1), was determined to be in the recently identified hepatic nuclear factor 1 (HNF--1)bindingsiteofaconservedNAGSregulatoryregion(Fig.4).Transcription factor binding sites in the NAGS enhancer.Transcription factors HNF--1 and NF--Y bind with in the human NAGS enhancer.	Enhancer	--	Luciferase Reporter Assay	The functional effect of the mutation on NAGS transcription was examined using a luciferase reporter assay, driven by the NAGS enhancer with either the wild--type, mutated, or consensus HNF--1 binding sites.Cells were cotransfected with vector pGL4.74, containing Renilla luciferase hRluc, as a transfection efficiency control.	AGAS,ARGA	--	--	--	HNF1A	HNF-1A,HNF1,HNF4A,IDDM20,LFB1,MODY3,TCF-1,TCF1	Luciferase Reporter Assay	The functional effect of the mutation on NAGS transcription was examined using aLuciferase assay,driven by the NAGS Enhancer with either the wild-type,mutated,or consensus HNF-1 binding sites. Reporter plasmids included the NAGS wild-type promoter with the wild-type Enhancer,4.10WT,the Enhancer containing the patient’s mutation -3064C>A,4.10Pat,or the Enhancer containing the consensus HNF-1 binding site,4.10Con (Fig. 5A).	--	--	NAGS
21673114	chr14	55518040	55518674	NRL	The bZIP transcription factor NRL (neural retina leucine zipper) is critical for rod versus cone photoreceptor cell fate choice during retinal development and acts as a molecular switch to produce rods from postmitotic precursors.	mouse		Low throughput	Combinatorial regulation of photoreceptor differentiation factor, neural retina leucine zipper gene NRL, revealed by in vivo promoter analysis.	否	--	--	HEK-293 cells	E_02_0963	Transfection,EMSA,PCR	To refine the cis-regulatory elements involved in controlling Nrl expression further, we tested the sequences within the three conserved clusters by in vivo transfection.	Enhancer	--	EMSA	In silico analysis using the TRANSFAC database (46) revealed a number of conserved putative transcription factor binding sites within B2(transcriptionally active sequence in clusterB)and clusterA(Fig.3,A and B, respectively). To identify the involvement of specific transcription factors, we performed EMSA using several different oligonucleotides spanning the conserved sequence elements(Fig. 4).	D14H14S46E	--	--	--	Rorb,Crx,,Nrl,Nr2e3	Nr1f2,RZR-beta,RZRBeta,hstp,Rorb,Crx1,D14H14S46E,A930035N01Rik,PNR,RNR,rd7	EMSA	Electrophoretic mobility shift assays using mouse retinal nuclear extracts, in combination with specific antibodies,demonstrate the binding of retinoid-related orphan nuclear receptor(RORβ),cone rod homeobox,orthodenticle homolog 2,and cyclic AMP response element-binding protein to predicted consensus elements within clusters A and B.Our studies demonstrate Nrl as a direct transcriptional target of RORβ and suggest that combinatorial action of multiple regulatory factors modulates the expression of Nrl in developing and mature retina.	--	--	Nrl
21566115	chr11	44390342	44392251	STAT3	Thus, the STAT3-dependent expression of NFIL3 is a key component of a negative feedback pathway in myeloid cells that suppresses	mouse		Low throughput	A distal enhancer in Il12b is the target of transcriptional repression by the STAT3 pathway and requires the basic leucine zipper (B-ZIP) protein NFIL3	否	--	Autoimmune and Inflammatory Diseases	bone marrow cell,T Cell	E_02_0964	Luciferase Reporter Assay,qRT-PCR	We focused on a conserved enhancer about 10kb upstream of the Il12b start site that is targeted by TLR signaling to increase Il12b transcription in response to LPS (33). We made luciferase reporter constructs that fused the Il12b promoter to the upstream enhancer.	Enhancer	--	Luciferase Reporter Assay,qRT-PCR	To search for transcription factors that could be involved in the suppression of Il12b transcription, we used qRT-PCR to measure the expression of transcription factor mRNAs induced by IL-10 in the presence of an inflammatory costimulus.We made luciferase reporter constructs that fused the Il12b promoter to the upstream enhancer.	Il-12b,Il-12p40,Il12p40,p40	--	--	--	Nfil3	AV225605,E4BP4	qRT-PCR,Luciferase Reporter Assay	A NFIL3 binding site is identified in the enhancer region of Il12b.	--	--	Il12b
21556051	chr20	44430820	44433428	UBE3C	The UBE3C oncogene is overexpressed in many types of solid tumours including the lethal castration-resistant prostate cancer (CRPC).	human		Low throughput		不相关	--	Prostate Cancer	LNCaP,PC-3	E_02_0965	RT-PCR,Luciferase Reporter Assay,ChIP,3C	we performed quantitative 3C assays for the UBE2C locus in LNCaP and PC-3 cells, in order to identify potential PC-3-specific UBE2C enhancers.	Enhancer	3C	RT-PCR,Western blot	3C assays were performed at the UBE2C locus to measure crosslinking frequencies between PC-3-specific UBE2C enhancers and the UBE2C promoter	UBCH10,dJ447F3.2	--	--	--	FOXA1,GATA2,POU2F1,ETS1	HNF3A,TCF3A,DCML,IMD21,MONOMAC,NFE1B,ETS-1,EWSR2,c-ets-1,p54,OCT1,OTF1,oct-1B	ChIP	To examine whether these transcription factors were differentially recruited to E1,E2 and E3 on chromatin, chromatin immunoprecipitation (ChIP) assays were performed using specific antibodies against FoxA1, GATA2, Oct1 and ETS1 in LNCaP and PC-3 cells treated with or without DHT.	--	--	UBE2C
21551367	chr17	32565596	32566796	CCL2	CCL2 plays a seminal role in the re_x0002_cruitment and activation of cells of the monocyte lineage to sites of inflammation (2–4) and for this reason is thought to play a key role in disease states in which monocytes/macrophages influence disease pathogenesis such as atherosclerosis, HIV-1–associated dementia, and tuberculosis.	human		Low throughput	An evolutionarily conserved TNF-alpha-responsive enhancer in the far upstream region of human CCL2 locus influences its gene expression	不相关	--	--	U-87MG	E_02_0966	Luciferase Reporter Assay,PCR,ChIP,EMSA,3C	Schematic of CCL2 locus showing regions that were tested in the reporter assays.	Enhancer	3C	PCR,qPCR	The –16.5 ECR physically interacts with CCL2 proximal promoter.To detect such physical interactions we used the 3C assay. In the 3C assay, interaction between widely separated regulatory elements is detected. 	GDCF-2,HC11,HSMCR30,MCAF,MCP-1,MCP1,SCYA2,SMC-CF	--	--	--	NFKB1,SP1,CEBPB	CVID12,EBP-1,KBF1,NF-kB,NF-kB1,NF-kappa-B1,NF-kappaB,NFKB-p105,NFKB-p50,NFkappaB,p105,p50,SP1,C/EBP-beta,IL6DBP,NF-IL6,TCF5	ChIP,EMSA	The EMSA and the pulldown experiments demonstrated in vitro interaction of the –16.5 ECR with NF-kB and c/EBPb. We used ChIP assay to determine whether the –16.5 ECR can bind NF-kB and c/EBPb in vivo. Sheared chromatin that was obtained from U87MG cells (treated or not treated with TNF-a) was immmu_x0002_noprecipitated with Abs directed against p65 and p50 subunits of NF-kB and c/EBPb or with control Abs.	--	--	CCL2
21549805	chr18	61099404	61099740	SOX11	Accompanying immunohistochemical analysis demonstrates that SOX4 or SOX11 are highly expressed in the majority of hypothalamic GnRH neurons in adult mice. 	mouse	lymphoid tissue	Low throughput	Class-C SOX transcription factors control GnRH gene expression via the intronic transcriptional enhancer	否	--	--	B cell	E_02_0967	Luciferase Reporter Assay,EMSA,ChIP	luciferase expression was driven by FIRE sequences, and tested these constructs for their responsiveness to PAX5 expression in the RAW264 macrophage cell line and the 38B9 B-cell line using transient transfection assays.When testing the binding of PAX5 across Csf1r by ChIPassays in primary pro-B cells, we noticed that PAX5 did not just bind to the promoter, but also associated with the intronic enhancer (FIRE).This observation was confirmed by EMSA experiments, demonstrating that none of the DNA sequences present on FIRE were capable of competing for the binding of PAX5 to DNA containing a PAX5 consensus sequence.	Enhancer	--	Immunoprecipitation,Transfection,ChIP	"We performed PAX5-specific chromatin immunoprecipitation analyses across the Csfr1 locus. We investigated the role of PAX5 in regulating Csf1r sense and antisense promoter activity by transient transfections and by employing a Pax5/ proLBcell line expressing an inducible PAX5 protein. When testing the binding of PAX5 across Csf1r by ChIPassays in primary pro-B cells, we noticed that PAX5 did not just bind to the promoter, but also associated with the intronic enhancer (FIRE).
"	AI323359,CD115,CSF-1R,Csfmr,Fim-2,Fim2,Fms,M-CSF-R,M-CSFR	--	--	--	Pax5	BSAP,EBB-1,KLP,Pax-5 	ChIP,EMSA	PAX5 binds to the intronic enhancer of Csf1r (FIRE).When testing the binding of PAX5 across Csf1r by ChIP assays in primary pro-B cells, we noticed that PAX5 did not just bind to the promoter, but also associated with the intronic Enhancer (FIRE).This observation was confirmed by EMSA experiments.	--	--	Csf1r
21536859	chr21	39823183	39825183	ERG	Dynamic patterns of chromatin accessibility, transcription factor (TF) binding, and DNA methylation all contribute to the gene expression signature of a cell.	human	lymphoid tissue	Low+High throughput	ERG promotes T-acute lymphoblastic leukemia and is transcriptionally regulated in leukemic cells by a stem cell enhancer	不相关	--	T-Cell Acute Lymphoblastic Leukemia	T-acute lymphoblastic leukemia (T-ALL),Molt4,REH,416B	E_02_0968	Luciferase Reporter Assay,PCR,ChIP,ChIP-PCR,ChIP-seq	The ERG stem cell enhancer is active in human T-cell progenitors and in T-ALL.Graphs at right show these peaks of enrichment confirmed by ChIP-PCR.	Enhancer	q3C	qPCR,ChIP-PCR	Taken together, these results show that genomic sequences in the human ERG locus corresponding to the mouse Erg +85 enhancer are in an active configuration in CD34+ stem/progenitors, pro-T, and T-ALL cells.	erg-3,p55	--	--	--	GATA2,LMO2,SCL,LYL1	DCML,IMD21,MONOMAC,NFE1B,LMO-2,RBTN2,RBTNL1,RHOM2,TTG2,SCL,bHLHa18	ChIP-PCR	ChIP-PCR analysis of TF binding. The enhancer has active chromatin marks (AcH3) in 416B blood progenitors as well as in T-ALL cells. There is strong LMO2 binding in all cell types, whereas SCL and LYL1 enrichments are more pronounced in T-ALL cells. The Ets factors, FLI1 and ERG, are also enriched in T-ALL cells. Consistent with their expression profiles, Gata2 is enriched at the _x0001_85 enhancer in 416B progenitors, whereas GATA3 is enriched in T-ALL cells. 	--	--	"ERG
"
21527503	chr1	33353796	33354196	PRL	These studies are consistent with the conclusion that progesterone interferes with PRL/glucocorticoid induction of β-casein transcription by a physical interaction of PR with the promoter and enhancer that blocks assembly of a transcriptional activation complex and dissociation of corepressors and promotes repressive chromatin modifications. 	human	Epithelial tissues	Low throughput	Progesterone receptor directly inhibits β-casein gene transcription in mammary epithelial cells through promoting promoter and enhancer repressive chromatin modifications	不相关	--	--	mammary gland epithelial cell	E_02_0969	Luciferase Reporter Assay,PCR,ChIP	As detected by chromatin immunoprecipitation assays, treatment of cells with the progestin agonist R5020 induced a rapid recruitment (5 min) of PR to the proximal promoter (?235 bp) and distal enhancer (?6 kb upstream of transcription start site) of β-casein	Enhancer	--	ChIP	In this study, we used HC-11 cells and ChIP assays to examine the influence of progesterone and PR on cooperative interactions and dynamics of the various transcription factors and coregulatory proteins that interact with the promoter and enhancer of the endogenous β-casein gene.	BCLP,CAC-1,CAC1	--	--	--	STAT5B,CEBPB,YY1	STAT5,C/EBP-beta,IL6DBP,NF-IL6,TCF5,DELTA,GADEVS,INO80S,NF-E1,UCRBP,YIN-YANG-1	PCR,ChIP	Primers for PCR amplification of the proximal promoter span a 170-bp region (-190 to -20 from the transcription start site) containing binding sites for Stat5a,C/EBP,YY1,and GRE/progestin response element (PRE) half-sites, whereas a 400-bp region (-6400 to -6000) of the distal Enhancer was amplified that contains binding sites for Stat5,C/EBP,and other factors.	--	--	TMEM54
21527503	chr1	33353796	33354196	PRL	These studies are consistent with the conclusion that progesterone interferes with PRL/glucocorticoid induction of β-casein transcription by a physical interaction of PR with the promoter and enhancer that blocks assembly of a transcriptional activation complex and dissociation of corepressors and promotes repressive chromatin modifications. 	human	Epithelial tissues	Low throughput	Progesterone receptor directly inhibits β-casein gene transcription in mammary epithelial cells through promoting promoter and enhancer repressive chromatin modifications	不相关	--	--	mammary gland epithelial cell	E_02_0969	Luciferase Reporter Assay,PCR,ChIP	As detected by chromatin immunoprecipitation assays, treatment of cells with the progestin agonist R5020 induced a rapid recruitment (5 min) of PR to the proximal promoter (?235 bp) and distal enhancer (?6 kb upstream of transcription start site) of β-casein	Enhancer	--	ChIP	In this study, we used HC-11 cells and ChIP assays to examine the influence of progesterone and PR on cooperative interactions and dynamics of the various transcription factors and coregulatory proteins that interact with the promoter and enhancer of the endogenous β-casein gene.	BCLP,CAC-1,CAC1	--	--	--	STAT5B,CEBPB,YY1	STAT5,C/EBP-beta,IL6DBP,NF-IL6,TCF5,DELTA,GADEVS,INO80S,NF-E1,UCRBP,YIN-YANG-1	PCR,ChIP	Primers for PCR amplification of the proximal promoter span a 170-bp region (-190 to -20 from the transcription start site) containing binding sites for Stat5a,C/EBP,YY1,and GRE/progestin response element (PRE) half-sites, whereas a 400-bp region (-6400 to -6000) of the distal Enhancer was amplified that contains binding sites for Stat5,C/EBP,and other factors.	--	--	β-casein gene
21486496	chr5	115358083	115360083	MAP2	When neuronal differentiation was induced in embryoid body (EB)-derived neurosphere cells, reporter signals were detected in Msi1-positive NSCs and GFAP-positive astrocytes, but not in MAP2-positive neurons. 	mouse		Low+High throughput	Identification of a novel intronic enhancer responsible for the transcriptional regulation of musashi1 in neural stem/progenitor cells	否	--	--	embryonic stem cell	E_02_0970	Luciferase Reporter Assay,ChIP-seq	The deleted BAC constructs were introduced into ESCs, and stable transformants were established for each BAC reporter construct. In a similar manner to the RA treatment and Luciferase reporter assay conducted with EBs (shown in Figure ?Figure2A),the Msi1 transcriptional activities were quantified using the deletion-containing reporters D1-D5 and the full-length BAC reporter D0. These results suggested that the 10-kb region from 55 kb to 65 kb upstream of the TSS might contain Msi1 transcriptional enhancers, and we named this region the 'upstream 10-kb enhancer.'	Enhancer	--	Luciferase Reporter Assay	We then used homologous recombination techniques to insert the ffLuc reporter gene into the Msi1 translational initiation site of the RP24-132L16 BAC (Figure1A).The ffLuc reporter gene encodes a fusion protein of the fluorescent protein Venus and firefly Luciferase.This reporter gene both visualized Msi1 transcriptional activity in vivo, and allowed us to use Luciferase bioluminescence to quantify the level of transcriptional activity.	Msi1h,Musahi1,m-Msi-1	The intronic Enhancer can transactivate Msi1 gene expression with cell-type specificity markedly similar to the endogenous Msi1 expression patterns.	Luciferase Reporter Assay	Furthermore, when the region after the transcription site (exons and introns coding region) was deleted, the Msi1 transcriptional activity diminished even in the presence of the‘upstream 10-kb Enhancer’ (Figure 3C). These results indicated two regions responsible for Msi2 transcription.	Qsox1,Tfap2a	1300003H02Rik,QSOX,Qscn6,SOx,b2b2673Clo,AP-2,AP2alpha,Ap-2(a),Ap2,Ap2tf,Tcfap2a	Luciferase Reporter Assay	Through these investigations, we have identified a new Msi1 transcription Enhancer element in NS/PCs. This region is located in the 595-bp region within the sixth intron of the Msi1 gene, and contains SOX- and AP-2-binding sites.	--	--	Msi1
21454523	chr7	103823354	103846754	CTCF	However, the underlying mechanisms are unclear. The CCCTC-binding factor, CTCF, binds to the insulator elements at the 5′ and 3′ boundaries of the locus, but these sites were shown to be dispensable for globin gene activation. 	mouse		Low throughput	Cohesin mediates chromatin interactions that regulate mammalian β-globin expression	否	--	Haploinsufficiency	745A	E_02_0971	ChIP,qRT-PCR,3C	The presence of the cohesin holo-complex was confirmed by ChIP using antibodies specific for SMC1 and SA1.Most notably, HS2 functions as an enhancer, and the outer HS5 functions as an insulator. B, adult β-globin gene induction following DMSO treatment. End point RT-PCR of β-major gene induction and q-RT-PCR analysis of β-major and β-minor genes in comparison to GAPDH were examined over 4 days of DMSO treatment. Q-RT-PCR values were normalized to ribonuclease/angiogenin inhibitor 1 (rnh1). 	Enhancer	3C	ChIP	3C and ChIP-loop analysis of the HS2 and β-major promoter interaction at 4 days after DMSO treatment. The interactions of a region containing HS4 and HS5 (HS4/5) with either 3′HS1 or HS-62 are compared.	Ey,Hby	Nipped-B-like (Nipbl) bind to the locus control region (LCR) at the CTCF insulator and distal enhancer regions as well as at the specific target globin gene that undergoes activation upon differentiation	ChIP,3C,PCR	The results indicate that cohesin binds to these regions when they interact. Taken together, cohesin and Nipbl are recruited not only to the HS5 insulator, but also to the Enhancer and the active _x005f_x0001_-globin gene regions. This correlates with the induction of the interaction of these domains and β-globin gene activation.	Nipbl,Ctcf,Nfe2	Idn3,AW108038,NF-E2,NF-E2/P45,p45,p45NFE2,p45nf-e2	ChIP	Differentiation-induced Cohesin and Nipbl Binding at the β-globin Locus Is Associated with LCR Enhancer-globin Gene Interactions.,ChIP analysis of cohesin (Rad21),Nipbl,CTCF, and NF-E2 binding to the β-globin locus.	--	--	Hbb-y
21445863	chr21	35982223	35983306	RUNX1	The transcription factor RUNX1 is a key regulator of haematopoiesis in vertebrates.	human		Low throughput	Transcriptional regulation and spatial organisation of the human AML1/RUNX1 gene	不相关	--	--	Acute T-Cell Leukaemia Cell	E_02_0972	Luciferase Reporter Assay,PCR	To test the putative enhancer activity of RE1 and RE2, we made a number of genetic constructs with a pGL3--Basic vector, which contains the firefly Luciferase gene.	Enhancer	--	Luciferase Reporter Assay	The promoters were cloned upstream from the Luciferase gene and candidate enhancer elements-downstream of the gene in direct genomic orientation and reverse genomic orientation relative to the corresponding promoter.	AML1,AML1-EVI-1,AMLCR1,CBF2alpha,CBFA2,EVI-1,PEBP2aB,PEBP2alpha	--	--	--	--	--	--	--	--	--	RUNX1
21445863	chr21	35982223	35983306	RUNX2	The transcription factor RUNX2 is a key regulator of haematopoiesis in vertebrates.	human		Low throughput	Transcriptional regulation and spatial organisation of the human AML1/RUNX2 gene	不相关	--	--	Acute T-Cell Leukaemia Cell	E_02_0972	Luciferase Reporter Assay,PCR	To test the putative enhancer activity of RE1 and RE2, we made a number of genetic constructs with a pGL3--Basic vector, which contains the firefly Luciferase gene.	Enhancer	--	Luciferase Reporter Assay	The promoters were cloned upstream from the Luciferase gene and candidate enhancer elements-downstream of the gene in direct genomic orientation and reverse genomic orientation relative to the corresponding promoter.	AML1,AML1-EVI-1,AMLCR1,CBF2alpha,CBFA2,EVI-1,PEBP2aB,PEBP2alpha	--	--	--	--	--	--	--	--	--	RUNX1
21419113	chr1	226065482	226067482	LEFTY1	We have now identified a transcriptional enhancer (ANE) in the human LEFTY1 gene that exhibits marked L>R asymmetric activity in perinodal cells of the mouse embryo.	human		Low throughput	Left-right asymmetry in the level of active Nodal protein produced in the node is translated into left-right asymmetry in the lateral plate of mouse embryos	不相关	--	--	Perinodal cell	E_02_0973	PCR,Transgenic mice,Immunostaining	We have now identified a transcriptional enhancer (ANE) in the human LEFTY1 gene that exhibits marked L>R asymmetric activity in perinodal cells of the mouse embryos.the enhancer activity of each fragment was examined in transgenic mouse embryos.	Enhancer	--	PCR,Transgenic mice,Immunostaining	We have now identified a transcriptional enhancer (ANE) in the human LEFTY1 gene that exhibits marked L>R asymmetric activity in perinodal cells of the mouse embryos.	LEFTB,LEFTYB	--	--	--	FOXH1	FAST-1,FAST1	X-Gal Staining Assay 	The approximate location of FoxH1 binding sites is indicated by red ovals. Restriction sites: E, EcoRI; Bam, BamHI; BgI, BglI; BX, BstXI; BgII, BglII; Sma, SmaI; Xb, XbaI; Sac, SacI. (B–E) Ventral views of X-gal–stained embryos harboring the indicated lacZ transgenes. (F–I) Magnified views of the node region of X-gal–stained embryos harboring hNPE7.5-lacZ.	--	--	LEFTY1
21378152	chr11	32403489	32405489	WT1	The WT1 reduction may be a useful marker for early podocyte injury.	human		Low throughput	TGF-beta1 reduces Wilms' tumor suppressor gene expression in podocytes	不相关	--	--	Human Podocyte Cell Line AB8/13	E_02_0974	qRT-PCR,Luciferase Reporter Assay	We tested the effect of TGF-beta1 on a human WT1 enhancer located ?4.3 kb upstream of the transcription start site using a reporter vector WTA.	Enhancer	--	qRT-PCR,Luciferase Reporter Assay	 TGF-beta1 did not alter luciferase activity of the reporter construct for a human WT1 promoter but reduced that for a human WT1 5′ enhancer construct, suggesting that TGF-beta1 may regulate WT1 expression by altering the 5′ enhancer activity.	AWT1,GUD,NPHS4,WAGR,WIT-2,WT33	--	--	--	SMAD4	DPC4,JIP,MADH4,MYHRS	Luciferase Reporter Assay	The luciferase activity of p3TP-lux, a reporter construct for Smadbinding element, was determined after incubation with 5 ng/mL TGFbeta1 for 24 h. TGF-beta1 increased the luciferase activity by ~12-fold in the presence of the NTC shRNA, while this increase was largely prevented by Sh-Smad4. The luciferase activity of p3TP-lux was normalized to beta-galactosidase activity of pCMV-beta-gal and shown as relative values to that of pGL2 basic.	--	--	WT1
21355081	chr10	131265598	131265656	MGMT	These studies provide strong evidence that the A allele of a MGMT promoter-enhancer SNP is a key determinant for MGMT methylation in lung carcinogenesis. Moreover, TMZ treatment may benefit a subset of lung cancer patients methylated for MGMT.	human	Epithelial tissues, carcinoma tissues	Low throughput	The A/G allele of rs16906252 predicts for MGMT methylation and is selectively silenced in premalignant lesions from smokers and in lung adenocarcinomas	相关	rs16906252	Lung Adenocarcinoma	bronchial epithelial cell	E_02_0975	Luciferase Reporter Assay,PCR	This study provides strong evidence that the A allele of a MGMT promoter-enhancer SNP (rs16906252) is a key determinant in the acquisition of MGMT methylation in lung carcinogenesis.	Enhancer	--	Luciferase Reporter Assay,PCR	This study provides strong evidence that the A allele of a MGMT promoter-enhancer SNP (rs16906252) is a key determinant in the acquisition of MGMT methylation in lung carcinogenesis.	MGMT	--	--	--	--	--	--	--	131265545	Luciferase Reporter Assay,PCR	MGMT
21331042	chr3	34563695	34565695	Tbx6	 An enhancer N1-specific deletion mutation introduced into Tbx6 mutant embryos prevented this Sox2 activation in the mesodermal compartment and subsequent development of ectopic neural tubes, indicating that Tbx6 regulates Sox2 via enhancer N1. 	mouse		Low throughput	Tbx6-dependent Sox2 regulation determines neural or mesodermal fate in axial stem cells	否	--	--	stem cell	E_02_0976	EMSA,Immunostaining,Transgenic mice	Our earlier studies have indicated that among a number of enhancers regulating Sox2, enhancer N1 is responsible for Sox2 activation in the caudally extendin neural plate5,6 (Fig.1a-c; Supplementary Fig.1).	Enhancer	--	EMSA,Immunostaining	Finally, we asked whether the suppression of Sox2 enhancer N1 activation by Tbx6 involves direct interaction of the Tbx6 protein with the enhancer N1 DNA sequence. Various overlapping fragments of the N1 sequence were tested for Tbx6 binding using electrophoretic mobility shift assays (EMSA). Exogenous Sox2-HA was successfully expressed in the caudal-most mesodermal compartment (Fig.4b), as indicated by HA-tag immunostaining and the mesodermal Sox2 immunostaining (Fig.4c-e). This result demonstrates that Sox2 expression is sufficient for the initiation of neural tube development from the primitive paraxial mesoderm, even in wild type embryos.	Sox-2,lcc,ysb	--	--	--	Tbx6	rv	EMSA	Various overlapping fragments of the N1 sequence were tested for Tbx6 binding using electrophoretic mobility shift assays (EMSA).	--	--	Sox2
21310710	chr18	60786011	60788011	BCL2	The 279-bp major breakpoint region (mbr) within the 3'-untranslated region (3'-UTR) of the BCL2 gene is a binding site of special AT-rich sequence binding protein 1 (SATB1) that is well known to participate in the long-range regulation of gene transcription.	human		Low throughput	The BCL2 gene is regulated by a special AT-rich sequence binding protein 1-mediated long range chromosomal interaction between the promoter and the distal element located within the 3'-UTR	不相关	--	--	jurkat cell	E_02_0977	3C,ChIP,RT-PCR	With chromosome conformation capture (3C) and chromatin immunoprecipitation (ChIP) assays we demonstrated that the mbr could physically interact with BCL2 promoter through SATB1-mediated chromatin looping, which was required for epigenetic modifications of the promoter, CREB accessibility and high expression of the BCL2 gene.	Enhancer	3C	ChIP,RT-PCR	With chromosome conformation capture (3C) and chromatin immunoprecipitation (ChIP) assays we demonstrated that the mbr could physically interact with BCL2 promoter through SATB1-mediated chromatin looping, which was required for epigenetic modifications of the promoter, CREB accessibility and high expression of the BCL2 gene.	Bcl-2,PPP1R50	--	--	--	SATB1,CEBPB,EP300	SATB1,C/EBP-beta,IL6DBP,NF-IL6,TCF5,KAT3B,MKHK2,RSTS2,p300	Western blot,3C,RT-PCR	Our data showed that a reduction of the interaction between SBS1 and mbr induced by knockdown of SATB1 was significantly correlated with a decrease in the BCL2 mRNA level , suggesting that SATB1-mediated mbr-promoter interaction was required for transcriptional activity of the gene.	--	--	BCL2
21087445	chr22	24236392	24237411	MIF	" Mithramycin inhibited expression of MIF in
CEMC7A cells. This effect was specific to the intronic enhancer and was not
seen on the MIF promoter. "	human	kidney,lung	Low throughput	"Identification of a novel cell type-specific intronic enhancer of
macrophage migration inhibitory factor (MIF) and its regulation
by mithramycincei_4289 178..1"		--	Rheumatoid Arthritis	RA-FLS，A549，HEK293TTHP-1293T，SW982 cell	E_02_0978	Luciferase Reporter Assay,PCR,EMSA,DNaseI-seq	 DNase I hypersensitivity was used to identify potential hypersensitive sites (HS) across the MIF gene locus. Reporter gene assays were performed in different human cell lines with constructs containing the native or mutated HS element. Following phylogenetic and transcription factor binding profiling, electrophoretic mobility shift assay (EMSA) and RNA interference were performed and the effects of incubation with mithramycin, an antibiotic that binds GC boxes, were also studied. An HS centred on the first intron of MIF was identified. The HS acted as an enhancer in human T lymphoblasts (CEMC7A), human embryonic kidney cells (HEK293T) and human monocytic cells (THP-1), but not in a fibroblast-like synoviocyte (FLS) cell line (SW982) or cultured FLS derived from rheumatoid arthritis (RA) patients.	Enhancer	--	Luciferase Reporter Assay,PCR,EMSA,DNaseI-seq	 DNase I hypersensitivity was used to identify potential hypersensitive sites (HS) across the MIF gene locus. Reporter gene assays were performed in different human cell lines with constructs containing the native or mutated HS element. Following phylogenetic and transcription factor binding profiling, electrophoretic mobility shift assay (EMSA) and RNA interference were performed and the effects of incubation with mithramycin, an antibiotic that binds GC boxes, were also studied. An HS centred on the first intron of MIF was identified. The HS acted as an enhancer in human T lymphoblasts (CEMC7A), human embryonic kidney cells (HEK293T) and human monocytic cells (THP-1), but not in a fibroblast-like synoviocyte (FLS) cell line (SW982) or cultured FLS derived from rheumatoid arthritis (RA) patients.	GIF,GLIF,MMIF	--	--	--	SP1	SP1	Luciferase Reporter Assay,EMSA	In order to determine whether Sp1 is recruited to the MIF intron 1 Enhancer, EMSA was performed using CEMC7A nuclear extract and a radiolabelled DNA probe of the 5′region of the intronic sequence.We were able to demonstrate that Sp1 bound this sequence, as competition with excess cold Sp1 consensus sequence and addition of Sp1-specific antibody resulted in the abrogation of a shifted complex.	--	--	MIF
21056086	chr1	23881789	23881796	BMP2	Bone morphogenetic protein 2 (BMP2) stimulates expression of the inhibitors of DNA binding (Id) 1, 2, and 3 in a variety of cell types.	human		Low throughput	Mechanisms of bone morphogenetic protein 2 (BMP2) stimulated inhibitor of DNA binding 3 (Id3) transcription	否	--	--		E_02_0979	qRT-PCR,Luciferase Reporter Assay,ChIP	To determine if these base pairs also play a role in BMP2induction of the human ID3 promoter, we introduced mutations comparable to Mut4 and Mut5 in the murine Id3 promoter into the minimal hID3 promoter--reporter construct (?653/+402 ID3--luc) (Fig. 6(B)). 	Enhancer	--	ChIP	We identified the same sequence in the murine gene (?3283/?3276) (Fig. S8) and observed through ChIP analysis that BMP2 stimulated recruitment of SMAD1 to this region of the endogenous Id3 gene in L?T2 cells	HEIR-1,bHLHb25	A more distal Enhancer was shown to mediate BMP4-induction of the human ID3 gene in ovarian cancer cells.	ChIP	We identified the same sequence in the murine gene (?3283/?3276) and observed through ChIP analysis that BMP2 stimulated recruitment of SMAD1 to this region of the endogenous Id3 gene in LT2 cells. Mutation of the distal BRE in the longer murine Id3 reporter greatly reduced, but did not abolish, BMP2 induction.	BMP2	BDA2A, SSFSC, BMP2	ChIP	We identified the same sequence in the murine gene (?3283/?3276) (Fig. S8) and observed through ChIP analysis that BMP2 stimulated recruitment of SMAD1 to this region of the endogenous Id3 gene in LβT2 cells (Fig. S7A). Muta_x0002_tion of the distal BRE in the longer murine Id3 reporter greatly reduced, but did not abolish, BMP2 induction.	--	--	ID3
21056086	chr1	23881789	23881796	ID3	" a more distal enhancer
was shown to mediate BMP4-induction of the human ID3 gene in ovarian cancer cells."	human	gonad	Low throughput	"Mechanisms of bone morphogenetic protein 2 (BMP2) stimulated inhibitor of
DNA binding 3 (Id3) transcription"		--	--	LβT2 	E_02_0979	qRT-PCR,Luciferase Reporter Assay,ChIP	To determine if these base pairs also play a role in BMP2induction of the human ID3 promoter, we introduced mutations comparable to Mut4 and Mut5 in the murine Id3 promoter into the minimal hID3 promoter--reporter construct (?653/+402 ID3--luc) (Fig. 6(B)). 	Enhancer	--	ChIP	We identified the same sequence in the murine gene (?3283/?3276) (Fig. S8) and observed through ChIP analysis that BMP2 stimulated recruitment of SMAD1 to this region of the endogenous Id3 gene in L?T2 cells	HEIR-1,bHLHb25	A more distal Enhancer was shown to mediate BMP4-induction of the human ID3 gene in ovarian cancer cells.	ChIP	We identified the same sequence in the murine gene (?3283/?3276) and observed through ChIP analysis that BMP2 stimulated recruitment of SMAD1 to this region of the endogenous Id3 gene in LT2 cells. Mutation of the distal BRE in the longer murine Id3 reporter greatly reduced, but did not abolish, BMP2 induction.	BMP2	BDA2A, SSFSC, BMP2	ChIP	We identified the same sequence in the murine gene (?3283/?3276) (Fig. S8) and observed through ChIP analysis that BMP2 stimulated recruitment of SMAD1 to this region of the endogenous Id3 gene in LβT2 cells (Fig. S7A). Muta_x0002_tion of the distal BRE in the longer murine Id3 reporter greatly reduced, but did not abolish, BMP2 induction.	--	--	ID3
20942803	chr15	52315678	52316298	SLC30A8	The SLC30A8 gene encodes the zinc transporter ZnT-8, which provides zinc for insulin-hexamer formation.	mouse	lymphoid tissue	Low throughput	The pancreatic islet β-cell-enriched transcription factor Pdx-1 regulates Slc30a8 gene transcription through an intronic enhancer	否	--	--	insulin secreting cell	E_02_0980	Luciferase Reporter Assay,PCR	To address this hypothesis these regions, designated intronic enhancers A and B, respectively, were isolated using PCR and ligated 5′ of a heterologous thymidine kinase (TK)-luciferase fusion gene containing TK genomic sequence between ?105 and +51, relative to the transcription start site.Luciferase expression directed by these fusion genes was then analyzed by transient transfection of βTC-3 cells, an islet beta cell-derived line [31], αTC-6 cells, an islet alpha cell-derived line [32, 33] and HeLa cells, a cervix-derived cell line.	Enhancer	--	PCR,Luciferase Reporter Assay	Luciferase expression directed by these fusion genes was then analyzed by transient transfection of βTC-3 cells, an islet beta cell-derived line [31], αTC-6 cells, an islet alpha cell-derived line [32, 33] and HeLa cells, a cervix-derived cell line. Figure 2 shows that in βTC-3 cells, but not αTC-6 or HeLa cells, intronic enhancer A elevated reporter gene expression beyond that driven by the TK-luciferase fusion gene alone, indicating that this region is an islet beta cell-specific enhancer. In contrast, intronic enhancer B had no effect on fusion gene expression in any of the cell lines.	C820002P14Rik,ZnT-8,ZnT8	--	--	--	Pbx1	2310056B04Rik,D230003C07Rik,Pbx-1	ChIP,EMSA	Gel retardation and chromatin immunoprecipitation (ChIP) assays revealed that the islet-enriched transcription factor Pdx-1 binds Enhancer A in vitro and in situ, respectively.	--	--	Slc30a8
20878775	chr13	53463266	53463541	Dlx5	Here, we provide a molecular description of the cooperative effects of BMP and Wnt canonical pathway on the expression of the early osteogenic genes Dlx5, Msx2, and Runx2 in C2C12 cells, primary cultures of bone marrow-mesenchymal stem cells, and organotypic calvarial cultures. 	mouse		Low throughput	Conserved regulatory motifs in osteogenic gene promoters integrate cooperative effects of canonical Wnt and BMP pathways	否	--	--		E_02_0981	PCR,Luciferase Reporter Assay	The murine Dlx5 promoter from -1036 to +30 was obtained by polymerase chain reaction (PCR) and cloned in the pGL2basic vector. Murine Msx2 and Runx2 enhancers (from -3340 to -3615 for Msx2 and from -1170 to -1388 for Runx2) also were obtained by PCR and subcloned in the minimal promoter of c-fos promoter.	Enhancer	--	Luciferase Reporter Assay	The Msx2 gene shows a conserved region 3.5 kb upstream of the transcriptional start site, which also includes a combination of a TCF/LEF1 box and both GC-rich and CAGA SBEs. This region has been shown to be necessary and sufficient to confer BMP responsiveness in vitro and in vivo.Finally, a similar enhancer is located 1 kb upstream of the P1 osteoblast-specific promoter of the Runx2 gene (Supplemental Fig. S3). To test whether these regions have the ability to render responsiveness to Wnt3a and/or BMP-2, we generated the corresponding luciferase constructs and assayed them in C2C12 cells. 	BB122635,Hox-8,Hox8,Hox8.1	--	--	--	Msx2,Dlx3,Dlx5,Atf4,Runx2,Sp7	BB122635,Hox-8,Hox8,Hox8.1,AV237891,Dlx-3,AI385752,Atf-4,C/ATF,CREB2,TAXREB67,AML3,Cbf,Cbfa-1,Cbfa1,LS3,Osf2,PEBP2aA,Pebp2a1,Pebpa2a,6430578P22Rik,C22,Osx	qRT-PCR,Luciferase Reporter Assay,ChIP	To confirm that cooperative transcriptional interactions between canonical Wnt signaling and the Smad pathway on osteogenic genes occur in vivo, ChIP assays were performed in C2C12 cells.As shown in Fig.7D,TCF4,b-catenin,and Smad1 and Smad4 interacted with the responsive regions of Dlx5, Msx2, and Runx2 genes in vivo.	--	--	Msx2
20878775	chr13	53463266	53463541	Dlx6	Here, we provide a molecular description of the cooperative effects of BMP and Wnt canonical pathway on the expression of the early osteogenic genes Dlx5, Msx2, and Runx2 in C2C13 cells, primary cultures of bone marrow-mesenchymal stem cells, and organoty翼	mouse		Low throughput	Conserved regulatory motifs in osteogenic gene promoters integrate cooperative effects of canonical Wnt and BMP pathways	否	--	--		E_02_0981	PCR,Luciferase Reporter Assay	The murine Dlx5 promoter from -1036 to +30 was obtained by polymerase chain reaction (PCR) and cloned in the pGL2basic vector. Murine Msx2 and Runx2 enhancers (from -3340 to -3615 for Msx2 and from -1170 to -1388 for Runx2) also were obtained by PCR and subcloned in the minimal promoter of c-fos promoter.	Enhancer	--	Luciferase Reporter Assay	The Msx2 gene shows a conserved region 3.5 kb upstream of the transcriptional start site, which also includes a combination of a TCF/LEF1 box and both GC-rich and CAGA SBEs. This region has been shown to be necessary and sufficient to confer BMP responsiveness in vitro and in vivo.Finally, a similar enhancer is located 1 kb upstream of the P1 osteoblast-specific promoter of the Runx2 gene (Supplemental Fig. S3). To test whether these regions have the ability to render responsiveness to Wnt3a and/or BMP-2, we generated the corresponding luciferase constructs and assayed them in C2C12 cells. 	BB122635,Hox-8,Hox8,Hox8.1	--	--	--	Msx2,Dlx3,Dlx5,Atf4,Runx2,Sp7	BB122635,Hox-8,Hox8,Hox8.1,AV237891,Dlx-3,AI385752,Atf-4,C/ATF,CREB2,TAXREB67,AML3,Cbf,Cbfa-1,Cbfa1,LS3,Osf2,PEBP2aA,Pebp2a1,Pebpa2a,6430578P22Rik,C22,Osx	qRT-PCR,Luciferase Reporter Assay,ChIP	To confirm that cooperative transcriptional interactions between canonical Wnt signaling and the Smad pathway on osteogenic genes occur in vivo, ChIP assays were performed in C2C12 cells.As shown in Fig.7D,TCF4,b-catenin,and Smad1 and Smad4 interacted with the responsive regions of Dlx5, Msx2, and Runx2 genes in vivo.	--	--	Msx2
20093418	chr6	35574362	35576362	TULP1	However, the expression of C6orf81 or that of TULP1 showed no significant response to dex treatment in A549 cells	human	skin	Low throughput	Glucocorticoid receptor activates poised FKBP51 locus through long-distance interactions		--	--	A549 cell	E_02_0982	RT-qPCR,ChIP	"According to our quantitative ChIP and enhancer assays, there are at least three major distal gene regions that significantly bind GR
and also function as strong GR-regulated enhancers in isolation."	Enhancer	--	ChIP,Luciferase Reporter Assay	Our quantitative chromatin immunoprecipitation scans and enhancer activity analyses indicate that activation of the FKBP51 locus by glucocorticoids in vivo is triggered by the loading of GR to enhancers at about 34 kb 5 and about 87 kb 3 of the transcription start site. 	FKBP51,FKBP52,FKBP59,HBI,Hsp56,PPIase,p52	--	--	--	CTCF	MRD21	ChIP	We used the genome-wide CTCF-binding information from the CTCF-binding site database for choosing the regions to be ChIP scanned with anti-CTCF antibody.	--	--	FKBP4
19773398	chrx	30317939	30318739	NR0B1	". A reporter
construct lacking this enhancer element upstream of NR0B1 was unresponsive to SF-1 transcrip_x0002_tional activation"	human	blood	Low throughput	X-linked congenital adrenal hypoplasia with hypogonadotropic hypogonadism caused by an inversion disrupting a conserved noncoding element upstream of the NR0B1 (DAX1) gene		--	X-Linked Congenital Adrenal Hypoplasia	HEK-293 cells	E_02_0983	Luciferase Reporter Assay,PCR	Luciferase reporter gene activity in transiently transfected HEK293 cells. Relative luciferase activity refers to the activity of the firefly reporter gene normalized to Renilla luciferase internal control for transfection efficiency. Firefly reporter constructs contained the DAX1 conserved noncoding “enhancer” elements upstream of a minimal thymidine kinase promoter driving the firefly reporter.	Enhancer	--	Luciferase Reporter Assay,PCR	Our results therefore strongly suggest the existence of an SF-1 binding site 4kb upstream of NR0B1 that acts as an enhancer of DAX1 expression. 	AHC,AHCH,AHX,DAX-1,DAX1,DSS,GTD,HHG,NROB1,SRXY2	A reporter construct lacking this Enhancer element upstream of NR0B1 was unresponsive to SF-1 transcriptional activation.	Luciferase Reporter Assay	"SF-1 acted as an activator on the wild-type construct, whereas the mutant construct,lacking the SF-1 consensus binding site, showed no response to SF-1. 
"	NR5A1	AD4BP,ELP,FTZ1,FTZF1,POF7,SF-1,SF1,SPGF8,SRXX4,SRXY3,hSF-1	Luciferase Reporter Assay	Luciferase reporter gene activity in transiently transfected HEK293 cells. Relative luciferase activity refers to the activity of the firefly reporter gene normalized to Renilla luciferase internal control for transfection efficiency. The mutant CNE is unresponsive to the transcription enhancement seen in the presence of cotransfected SF-1.	--	--	NR0B1
19708858	chr3	48598405	48598558	Ucn2	"Site-directed mutagenesis
experiments demonstrated that HRE1 is required for HIF1α-
 dependent luciferase activation"	human	rhabdomyosarcoma	Low throughput	"The human urocortin 2 gene is regulated by hypoxia: identification of a
hypoxia-responsive element in the 3?-flanking region"		--	Myocardial Ischemia	TE-671	E_02_0984	Luciferase Reporter Assay,RT-PCR	"This activation was conserved in constructs with the 3' FLR fragment placed upstream of the luciferase gene, indicating an enhancer function for HRE1.To test their role as enhancers, we cloned several fragments of the 3 'FLR of the hUcn2 gene downstream of the firefly luciferase gene in (a) the pGL3 ?746 bp vector containing the functional hUcn2 promoter, and (b) the pGL3control vector containing an internal SV40 promoter (Figure 2A). 
"	Enhancer	--	Luciferase Reporter Assay,Transfection	To test their role as enhancers, we cloned several fragments of the 3 ' FLR of the hUcn2 gene downstream of the firefly luciferase gene in (a) the pGL3 ?746 bp vector containing the functional hUcn2 promoter, and (b) the pGL3control vector containing an internal SV40 promoter (Figure 2A). TE--671 cells were transfected with the different constructs and exposed to normoxia or hypoxia for 12 h. Hypoxia significantly increased luciferase expression, specifically in the constructs containing the fragment 3 'FLR3 (Figure 2A).	SRP,UCN-II,UCNI,UR,URP	Hypoxia induces hUcn2 expression via a specific HRE in the 3 FLR of the hUcn2 gene, which interacts with the transcription factor HIF1α.	Luciferase Reporter Assay	Similar to the results obtained with constructs that contained the 3' FLR3 variants downstream of the luciferase gene, the hypoxia- and CPX-induced luciferase activation was strongest in the 3' FLR3 containing both wild-type HRE1 and HRE2.	HIF1A	HIF-1-alpha,HIF-1A,HIF-1alpha,HIF1,HIF1-ALPHA,MOP1,PASD8,bHLHe78	ELISA	To prove that HIF1α binds to HRE1 and HRE2 in the 3_x0002_FLR of the hUcn2 gene, we performed HIF1α binding and competition ELISA assays. After 12 h of hypoxia, binding of HIF1α to the EPO HRE was stronger than under normoxic conditions.	--	--	UCN2
19285986	chr16	67519201	67519833	ATP6V0D1	"we show here that two adjacent
enhancers inside the first intron of the neighboring (1.4 kb downstream)
ATPase gene (ATP6V0D1) modulate the human AgRP promoter with
profound spatiotemporal variation despite their diminutive sizes (221 and
231 nt)"	human	kidney	Low throughput	"Control Elements in the Neighboring ATPase Gene
Influence Spatiotemporal Expression of the Human
Agouti-Related Protein"		--	--	H295R,N38	E_02_0985	Transgenic mice,Luciferase Reporter Assay	"Schematic representation of the genomic region encompassing the AgRP and the ATPase locus. Expression constructs for regions A, B, C, and D were directionally cloned into pGL3-basic luciferase vector.Regions C and D were evaluated in the same fashion. Region D (but not region C) contained
enhancer elements in both neuronal and somatic cell types (Fig. 1a). Region D was therefore
divided into three overlapping sub-regions: Di(-18/+312)(+2727/+3359), Dii(-18/+312)
(+3341/+3941), and Diii(-18/+312)(+3943/+4575). Sub-regions Di and Diii (but not Dii) had
enhancer properties for the AgRP basal promoter in both h295R and N38 cell lines (Fig. 1b).Fig. 1. In vitro determination of enhancer elements"	Enhancer	--	Transgenic mice,Luciferase Reporter Assay	Region D (but not C) increased activity of the human AgRP promoter, equally in the human adrenocortical NCI-h295R and the mouse clonal hypothalamic N38 cell lines. 	AGRT,ART,ASIP2	--	--	--	--	--	--	--	--	--	AGRP
19141476	chr5	147205131	147212149	Pdx1	 In addition, occupancy of the well-characterized proximal Pdx1 enhancer by Foxa1 and Foxa2 is developmental stage-dependent.	mouse	nonpancreatic tissues	Low+High throughput	Dynamic regulation of Pdx1 enhancers by Foxa1 and Foxa2 is essential for pancreas development	否	--	Pancreatic Hypoplasia	pancreatic A cell	E_02_0986	ChIP,ChIP-seq	Using chromatin immunoprecipitations (ChIP) and ChIP sequencing (ChIP-Seq) of fetal pancreas and islet chromatin, we demonstrate that Foxa1 and Foxa2 predominantly occupy a distal Enhancer at -6.4 kb relative to the transcriptional start site in the Pdx1 gene.	Enhancer	--	ChIP	We performed chromatin immunoprecipitation (ChIP) as_x0002_says with antibodies specific to either Foxa1 or Foxa2 on chromatin isolated from primary mouse islets. Both Foxa1 and Foxa2 bound to the Area I–II–III enhancer of Pdx1 in vivo.	IDX-1,IPF-1,Ipf1,Mody4,STF-1,pdx-1	--	--	--	Foxa2,Foxa1	HNF3-beta,HNF3beta,Hnf-3b,Hnf3b,Tcf-3b,Tcf3b,Hnf-3a,Hnf3a,Tcf-3a,Tcf3a	ChIP	We performed chromatin immunoprecipitation (ChIP) assays with antibodies specific to either Foxa1 or Foxa2 on chromatin isolated from primary mouse islets. Both Foxa1 and Foxa2 bound to the Area I–II–III Enhancer of Pdx1 in vivo .Notably, the binding of Foxa2 to Area IV or Area I–II–III is signifi-cantly enhanced in pancreatic islets compared with fetal pancreas.	--	--	Pdx1
19041414	chr15	97977739	97977942	Sox9	We have previously reported that TGF-β-regulated Smad3 induces chondrogenesis through the activation of Sox9-dependent transcription. 	mouse	Cancer tissues	Low throughput	Smad3 activates the Sox9-dependent transcription on chromatin	否	--	--	HeLa cell	E_02_0987	Luciferase Reporter Assay,EMSA	Transient transfections of Sox9, Smad3, and T_x0002_R-I(TD) did not increase luciferase activities of pGL3-B plasmids in SW1353 cells (pGL3-B). In pGL3-585E systems, Sox9 enhanced a relative luciferase activity to a level as high as 2.2-fold over the control. Cotransfection of Smad3 augmented a luciferase activity up to 2.3-fold higher level of Sox9-transfected cells. The additional transfection of constitutively active form of T_x0002_R-I(TD) induced an approximately 36% increase of the activity in Sox9- and Smad3-transfected SW1353 cells. Luciferase activities of pGL3-585E were not increased in the absence of Sox9. Note that Smad3 and T_x0002_R-I(TD) synergistically activated the native Col2a1 reporter-mediated transcription in a Sox9-dependent manner. 	Enhancer	--	Luciferase Reporter Assay,EMSA	Purified Sox9 associated with the Col2a1 enhancer probe in EMSA.	Col2,Col2a,Col2a-1,Del1,Dmm,Lpk,M100413,Rgsc413,Rgsc856	--	--	--	Sox9	2010306G03Rik,AV220920,mKIAA4243	EMSA	Purified Sox9 associated with the Col2a1 enhancer probe in EMSA. The unlabeled competitor decreased the signal of Sox9–DNA complex. Supershifted band was observed in the presence of anti-Sox9 antibody.	--	--	Col2a1
18552207	chr7	126406352	126406616	Cd19	 We identified a B cell-specific upstream enhancer and showed that the developmental regulation of Cd19 expression involves precisely coordinated alterations in transcription factor binding and chromatin remodeling at Cd19 cis-regulatory elements.	mouse	lymphoid tissue	Low throughput	Stem cell-specific epigenetic priming and B cell-specific transcriptional activation at the mouse Cd19 locus	否	--	--	B Cell,T Cell	E_02_0988	Luciferase Reporter Assay,ChIP	"Transient transfection assays in different mouse cell lines. A mouse Cd19 promoter reporter construct (_x005f_x005f_x005f_x005f_x005f_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x005f_x005F_x0007_7 to _x005F_x0007_200 bp; e) or a construct containing the _x0007_2 kb DHS (_x0007_1832 to _x0007_2096 bp) combined with the Cd19 promoter (f) was transiently transfected into various cell lines. The
relative activity was determined as the luciferase activity of each construct over control vector pXPG. Data represent the mean of 2 to 4 experiments performed in triplicate"	Enhancer	--	ChIP	As previously reported in human cells, the promoter was active in all analyzed cell types (Figure 1C white bars). In contrast, the _x005F_x0007_2 kb DHS had enhancer activity only in B cells (Figure 1C black bars), providing evidence that this enhancer is involved in the regulation of tissue specific expression of Cd19.	AW495831	Enhancer is involved in the regulation of tissue specific expression of Cd19	Transfection	As previously reported in human cells, the promoter was active in all analyzed cell types (Figure 1C white bars). In contrast, the -2 kb DHS had Enhancer activity only in B cells (Figure 1C black bars), providing evidence that this Enhancer is involved in the regulation of tissue specific expression of Cd19.	Tcf3,Ebf1,Pax5	A1,AA408400,ALF2,AW209082,E12,E12/E47,E2A,E47,KA1,ME2,Pan1,Pan2,TCF-3,Tcfe2a,VDIR,bHLHb21,Ebf,O/E-1,OE-1,Olf-1,Olf1,BSAP,EBB-1,KLP,Pax-5	ChIP,DMS Footprinting Assay	We performed an in vivo DMS footprinting assay to answer the question of which transcription factors bind to the Cd19 promoter and enhancer.The specific binding of these proteins was confirmed by ChIP analysis, demonstrating that EBF and PAX5 bound to the enhancer in B cells and that E2A bound in B and T cells.	--	--	Cd19
12861010	chr11	5293686	5294250	CTCF	We describe enhancer-blocking or boundary elements on either side of the locus that are bound in vivo by the transcription factor CTCF, but we found that they do not coincide with transitions in nuclease sensitivity flanking the locus or with patterns of histone modifications within it. 	human	adult erythroid tissue	Low throughput 	A Complex Chromatin Landscape Revealed by Patterns of Nuclease Sensitivity and Histone Modification within the Mouse 尾-Globin Locus	否	--	--	Pleen cell,MEL cell	E_02_0989	PCR,DNaseI-seq	We have also found DNase I HSs at kb -85.5 (HS-85.5) and -84.5 in mouse, but there is no corresponding se_x0002_quence or structure in human for these HSs.By comparison,neither the active _x0002_maj-globin gene promoter nor a region located ~1 kb from HS5 shows significant enrichment. HS-85.5 exhibits a modest (twofold) enrichment.	Enhancer	--	DNaseI-seq,Southern blot,PCR	"In ery_x0002_throid cells, the active _x0002_-globin locus contains several DNase I HSs, which have been shown to map to sequences with regu_x0002_latory functionIn addition, histone hyperacetylation anddimethylation of histone H3 K4 are not uniform features of the nuclease-sensitive mouse _x0001_-globin domain but rather define distinct subdomains within it. Our results reveal a complex chromatin landscape for the active
_x0001_-globin locus and illustrate the complexity of broad structural changes that accompany gene activation."	LOC110006319	--	--	--	CTCF	MRD21	ChIP	To determine whether CTCF binds to these sequences in vivo, we performed ChIP analysis using antibodies to CTCF.	--	--	LOC110006319