About Enhancer

Enhancer ID: E_01_0426
Species: human
Position : chr12:7916539-7918539
Biosample name:
Experiment class : High+Lowthroughput
Enhancer type: Enhancer
Disease: Salmonella infection
Pubmed ID:  29880601
Enhancer experiment: transfection,RTqPCR,siRNA,Immunoblotting,FISH,immunocytochemistry,Northern blot
Enhancer experiment description: 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.

About Target gene

Target gene : SLC2A3(GLUT3)
Strong evidence: qRT-PCR,qPCR,ChIP,3C
Less strong evidence: RNA-Seq
Target gene experiment description: 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.

About TF

TF name : SOCS3
TF experiment: transfection,RTqPCR,siRNA,Immunoblotting,FISH,immunocytochemistry,Northern blot
TF experiment description: 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.

About Function

Enhancer function : 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 function experiment: Immunohistochemical staining
Enhancer function
experiment description:
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.

About SNP

SNP ID: --

Upstream Pathway Annotation of TF

GeneName Pathway Name Source Gene Number
SOCS3 Antigen processing: Ubiquitination & Proteasome degradation reactome 260
SOCS3 ATF-2 transcription factor network pid 59
SOCS3 Cytokine receptor degradation signaling ( JAK-STAT pathway and regulation pathway Diagram ) inoh 40
SOCS3 EGFR1 netpath 475
SOCS3 EPO signaling pathway pid 33
SOCS3 Gene expression of SOCS by STAT dimer ( JAK-STAT pathway and regulation pathway Diagram ) inoh 14
SOCS3 Gene expression of SOCS3 by STAT dimer ( JAK-STAT pathway and regulation pathway Diagram ) inoh 8
SOCS3 Growth hormone receptor signaling reactome 24
SOCS3 Growth hormone signaling pathway(JAK2 STAT5) ( Growth hormone signaling(JAK2 STAT5) ) inoh 9
SOCS3 IL2-mediated signaling events pid 54
SOCS3 IL2 netpath 81
SOCS3 IL23-mediated signaling events pid 37
SOCS3 IL3 netpath 84
SOCS3 IL4-mediated signaling events pid 66
SOCS3 IL4 netpath 75
SOCS3 IL6-mediated signaling events pid 48
SOCS3 IL6 netpath 85
SOCS3 Interferon-gamma signaling pathway panther 29
SOCS3 Interferon alpha/beta signaling reactome 67
SOCS3 Interferon gamma signaling reactome 88
SOCS3 Interleukin-6 signaling reactome 11
SOCS3 Leptin netpath 98
SOCS3 Prolactin netpath 105
SOCS3 Regulation of IFNA signaling reactome 26
SOCS3 Regulation of IFNG signaling reactome 14
SOCS3 Signaling by Leptin reactome 11
SOCS3 Signaling events mediated by PTP1B pid 53
SOCS3 TSH netpath 82
SOCS3 Jak-STAT signaling pathway kegg 149
SOCS3 Insulin signaling pathway kegg 134
SOCS3 Adipocytokine signaling pathway kegg 65
SOCS3 Type II diabetes mellitus kegg 44
SOCS3 Hepatitis C kegg 134
SOCS3 Hs_Apoptosis-related_network_due_to_altered_Notch3_in_ovarian_cancer_WP2864_79278 wikipathways 51
SOCS3 Hs_Oncostatin_M_Signaling_Pathway_WP2374_73668 wikipathways 44
SOCS3 Hs_IL-2_Signaling_Pathway_WP49_91243 wikipathways 33
SOCS3 Hs_Composition_of_Lipid_Particles_WP3601_89202 wikipathways 5
SOCS3 Hs_IL-6_signaling_pathway_WP364_89832 wikipathways 26
SOCS3 Hs_IL-4_Signaling_Pathway_WP395_89828 wikipathways 41

Enhancer associated network

The number on yellow line represents the distance between enhancer and target gene

Expression of target genes for the enhancer


Enhancer associated SNPs