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. |
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. |
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. |
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. |
SNP ID: | -- |
GeneName | Pathway Name | Source | Gene Number |
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