About Enhancer

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.

About Target gene

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.

About TF

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.

About Function

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.

About SNP

SNP ID: --

Upstream Pathway Annotation of TF

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

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