About Enhancer

Enhancer ID: E_02_0338
Species: human
Position : chr20:22578409-22580409
Biosample name:
Experiment class : High+Lowthroughput
Enhancer type: Enhancer
Disease: Nothing
Pubmed ID:  29648668
Enhancer experiment: 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,
Enhancer experiment description: Conditional uterine deletion of ER?, 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 ER? 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 ER? 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 ER?-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ER? binding sites near estrogen-regulated genes.

About Target gene

Target gene : FOXA2,FOXO1
Strong evidence: qRT-PCR,qPCR,ChIP,3C
Less strong evidence: RNA-Seq
Target gene experiment description: Conditional uterine deletion of ER?, 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 ER? 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 ER? 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 ER?-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ER? binding sites near estrogen-regulated genes.;Conditional uterine deletion of ER?, 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 ER? 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 ER? 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 ER?-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ER? binding sites near estrogen-regulated genes.

About TF

TF name : --
TF experiment: 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,
TF experiment description: Conditional uterine deletion of ER?, 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 ER? 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 ER? 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 ER?-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ER? binding sites near estrogen-regulated genes.;Conditional uterine deletion of ER?, 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 ER? 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 ER? 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 ER?-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ER? binding sites near estrogen-regulated genes.

About Function

Enhancer function : Conditional uterine deletion of ER?, 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 ER? 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 ER? 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 ER?-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ER? binding sites near estrogen-regulated genes.
Enhancer function experiment: Immunohistochemical staining
Enhancer function
experiment description:
Conditional uterine deletion of ER?, 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 ER? 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 ER? 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 ER?-dependent. These data suggest that DES alters uterine development and consequently adult reproductive function by modifying the enhancer landscape at ER? binding sites near estrogen-regulated genes.

About SNP

SNP ID: --

Upstream Pathway Annotation of TF

GeneName Pathway Name Source Gene Number

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