About Enhancer

Enhancer ID: E_01_0537
Species: human
Position : chr8:7052292-7054292
Biosample name:
Experiment class : High+Lowthroughput
Enhancer type: Enhancer
Disease: Inflammatory bowel disease (ibd)
Pubmed ID:  29695774
Enhancer experiment: CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,
Enhancer experiment description: 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.

About Target gene

Target gene : DEFA5,DEFA6,REG1A,REG1B,REG3A,CLDN2,CLDN10,CLDN14,CLDN18,ST6GAL1,PF4V1,CXCL1,PF4,PPBP,CXCL5,PPBPP2,CXCL2(CINC-2a,GROb,Gro2,MIP-2,MIP-2a,Mgsa-b,Mip2,Scyb,Scyb2)
Strong evidence: qRT-PCR,qPCR,ChIP,3C
Less strong evidence: RNA-Seq
Target gene experiment description: 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.;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.;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.;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.;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.;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.;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.;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.;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.;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.;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.

About TF

TF name : CLDN1CXCL8CXCL6CXCL3
TF experiment: CAGE assay,real-time quantitative reverse transcription polymerase chain reaction (qPCR),TSS-enhancer linkage,ChIP,RNA-seq,ChIPseq,FAIRE-seq,motif-seq,
TF experiment description: 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.;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.;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.;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.;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.;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.;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.;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.;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.;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.;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.

About Function

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

About SNP

SNP ID: rs11676348

Upstream Pathway Annotation of TF

GeneName Pathway Name Source Gene Number
CLDN1 Nectin adhesion pathway pid 30
CLDN1 Tight junction interactions reactome 30
CLDN1 Cell adhesion molecules (CAMs) kegg 133
CLDN1 Tight junction kegg 131
CLDN1 Leukocyte transendothelial migration kegg 116
CLDN1 Hepatitis C kegg 134
CXCL8 AP-1 transcription factor network pid 71
CXCL8 ATF-2 transcription factor network pid 59
CXCL8 ATF4 activates genes reactome 25
CXCL8 Calcineurin-regulated NFAT-dependent transcription in lymphocytes pid 50
CXCL8 Chemokine receptors bind chemokines reactome 57
CXCL8 G alpha (i) signalling events reactome 241
CXCL8 Glucocorticoid receptor regulatory network pid 85
CXCL8 Heterotrimeric GPCR signaling pathway (through G alpha i and pertussis toxin) ( GPCR signaling (pertussis toxin) ) inoh 228
CXCL8 Heterotrimeric GPCR signaling pathway (through G alpha q, PLC beta and ERK cascade) ( GPCR signaling (G alpha q) ) inoh 239
CXCL8 Heterotrimeric GPCR signaling pathway (through G alpha s ACs Epac BRaf and ERKcascade) ( GPCR signaling (G alpha s, Epac and ERK) ) inoh 237
CXCL8 Heterotrimeric GPCR signaling pathway (through_G alpha s_ACs_PKA_BRaf_and_ERKcascade)(canonical) ( GPCR signaling (G alpha s, PKA and ERK) ) inoh 227
CXCL8 Heterotrimeric GTP-binding protein coupled receptor signaling pathway (through G alpha i, adenylate cyclase and cAMP) ( GPCR signaling (G alpha i) ) inoh 228
CXCL8 Heterotrimeric GTP-binding protein coupled receptor signaling pathway (through_G_alpha_s,_cholera_toxin,_adenylate_cyclase_and_cAMP) ( GPCR signaling (cholera toxin) ) inoh 227
CXCL8 IL8- and CXCR1-mediated signaling events pid 29
CXCL8 IL8- and CXCR2-mediated signaling events pid 35
CXCL8 Inflammation mediated by chemokine and cytokine signaling pathway panther 189
CXCL8 Interleukin signaling pathway panther 86
CXCL8 JAK-STAT pathway and regulation pathway ( JAK-STAT pathway and regulation pathway Diagram ) inoh 97
CXCL8 LPA receptor mediated events pid 65
CXCL8 Peptide ligand-binding receptors reactome 103
CXCL8 Regulation of nuclear beta catenin signaling and target gene transcription pid 80
CXCL8 Senescence-Associated Secretory Phenotype (SASP) reactome 108
CXCL8 Syndecan-2-mediated signaling events pid 38
CXCL8 Syndecan-3-mediated signaling events pid 23
CXCL8 Validated transcriptional targets of AP1 family members Fra1 and Fra2 pid 37
CXCL8 Hs_Hepatitis_C_and_Hepatocellular_Carcinoma_WP3646_88640 wikipathways 36
CXCL8 Hs_Senescence_and_Autophagy_in_Cancer_WP615_81193 wikipathways 62
CXCL6 Chemokine receptors bind chemokines reactome 57
CXCL6 G alpha (i) signalling events reactome 241
CXCL6 Chemokine signaling pathway kegg 187
CXCL3 Chemokine receptors bind chemokines reactome 57
CXCL3 G alpha (i) signalling events reactome 241
CXCL3 Chemokine signaling pathway kegg 187

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