Enhancer ID: | E_01_0487 |
Species: | human |
Position : | chr7:152132016-152134016 |
Biosample name: | |
Experiment class : | High+Lowthroughput |
Enhancer type: | Enhancer |
Disease: | Mammary cancer |
Pubmed ID: | 29755131 |
Enhancer experiment: | CRISPR/Cas9,next-generation sequencing (IMPACT) assay,Proliferation assays,Immunoblotting,Lentiviral Infections,Quantitative RT-PCR,Chromatin Immunoprecipitation,Immunohistochemistry,Rapid immunoprecipitation mass spectrometry of endogenous proteins (RIME),Chromatin Immunoprecipitation followed by sequencing, |
Enhancer experiment description: | From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance. |
Target gene : | -- |
Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
Less strong evidence: | RNA-Seq |
Target gene experiment description: | From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance.;From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance. |
TF name : | KMT2CFOXA1(HNF3A,TCF3A) |
TF experiment: | CRISPR/Cas9,next-generation sequencing (IMPACT) assay,Proliferation assays,Immunoblotting,Lentiviral Infections,Quantitative RT-PCR,Chromatin Immunoprecipitation,Immunohistochemistry,Rapid immunoprecipitation mass spectrometry of endogenous proteins (RIME),Chromatin Immunoprecipitation followed by sequencing, |
TF experiment description: | From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance.;From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance. |
Enhancer function : | From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance. |
Enhancer function experiment: | Immunohistochemical staining |
Enhancer function experiment description: |
From a therapeutic standpoint, KMT2C-depleted cells that develop hormone-independence retain their dependence on ER?, displaying ongoing sensitivity to ER? antagonists. We conclude that KMT2C is a key regulator of ER? activity whose loss uncouples breast cancer proliferation from hormone abundance. |
SNP ID: | -- |
GeneName | Pathway Name | Source | Gene Number |
---|---|---|---|
KMT2C | Activation of anterior HOX genes in hindbrain development during early embryogenesis | reactome | 120 |
KMT2C | PKMTs methylate histone lysines | reactome | 64 |
FOXA1 | AndrogenReceptor | netpath | 167 |
FOXA1 | Direct p53 effectors | pid | 141 |
FOXA1 | FOXA1 transcription factor network | pid | 45 |
FOXA1 | FOXA2 and FOXA3 transcription factor networks | pid | 45 |
FOXA1 | Hs_Endoderm_Differentiation_WP2853_88152 | wikipathways | 62 |