About Enhancer
| Enhancer ID: | E_01_0760 |
| Species: | human |
| Position : | chr11:67116871-67118871   |
| Biosample name: | |
| Experiment class : | High+Lowthroughput |
| Enhancer type: | Enhancer |
| Disease: | Mammary cancer |
| Pubmed ID: | 30118678 |
| Enhancer experiment: | RT-qPCR,GRO-seq,ChIP-seq,ChIP-qPCR ,weston blot,PRO-seq |
| Enhancer experiment description: | Surprisingly, these basally-active estrogen-repressed (BAER) enhancers are decommissioned by ER?-dependent recruitment of the histone demethylase, KDM2A, functioning independently of its demethylase activity. While indirectly bound ER? recruits coactivators to these enhancers in a ligand-dependent fashion, the repression events, unexpectedly, reflect the availability of the ER? 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. |
About Target gene
| Target gene : | KDM2A |
| Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
| Less strong evidence: | RNA-Seq |
| Target gene experiment description: | Surprisingly, these basally-active estrogen-repressed (BAER) enhancers are decommissioned by ER?-dependent recruitment of the histone demethylase, KDM2A, functioning independently of its demethylase activity. While indirectly bound ER? recruits coactivators to these enhancers in a ligand-dependent fashion, the repression events, unexpectedly, reflect the availability of the ER? 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. |
About TF
| TF name : | -- |
| TF experiment: | RT-qPCR,GRO-seq,ChIP-seq,ChIP-qPCR ,weston blot,PRO-seq |
| TF experiment description: | Surprisingly, these basally-active estrogen-repressed (BAER) enhancers are decommissioned by ER?-dependent recruitment of the histone demethylase, KDM2A, functioning independently of its demethylase activity. While indirectly bound ER? recruits coactivators to these enhancers in a ligand-dependent fashion, the repression events, unexpectedly, reflect the availability of the ER? 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. |
About Function
| Enhancer function : | Surprisingly, these basally-active estrogen-repressed (BAER) enhancers are decommissioned by ER?-dependent recruitment of the histone demethylase, KDM2A, functioning independently of its demethylase activity. While indirectly bound ER? recruits coactivators to these enhancers in a ligand-dependent fashion, the repression events, unexpectedly, reflect the availability of the ER? 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 function experiment: | Immunohistochemical staining |
| Enhancer function experiment description: |
Surprisingly, these basally-active estrogen-repressed (BAER) enhancers are decommissioned by ER?-dependent recruitment of the histone demethylase, KDM2A, functioning independently of its demethylase activity. While indirectly bound ER? recruits coactivators to these enhancers in a ligand-dependent fashion, the repression events, unexpectedly, reflect the availability of the ER? 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. |
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