Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Promoter context-specific positive and negative transcriptional regulation of Glucocorticoid Receptor target genes by coregulator G9a

ABSTRACT: A549 lung cancer cells were not infected (NI), transfected by plasmids containing shG9a (sequence targeting G9a gene) or shNS (non-specific sequence). These cells were treated with dex to identify subsets of genes regulated by dex (hormone) and G9a (EHMT2)

ORGANISM(S): Homo sapiens

PROVIDER: GSE35962 | GEO | 2012/11/02

SECONDARY ACCESSION(S): PRJNA152057

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Promoter context-specific positive and negative transcriptional regulation of Glucocorticoid Receptor target genes by coregulator G9a

Project description:A549 lung cancer cells were not infected (NI), transfected by plasmids containing shG9a (sequence targeting G9a gene) or shNS (non-specific sequence). These cells were treated with dex to identify subsets of genes regulated by dex (hormone) and G9a (EHMT2) Cells (NI/shNS/shG9a) were treated with 100nM dex for 24h and total RNA was extracted to identify differentially expressed genes

2012-11-02 | E-GEOD-35962 | biostudies-arrayexpress

Promoter context-specific positive and negative transcriptional regulation of Glucocorticoid Receptor target genes by coregulator GLP.

Project description:A549 lung cancer cells were not infected (NI), transfected by plasmids containing shGLP (sequence targeting GLP gene) or shNS (non-specific sequence). These cells were treated with dex to identify subsets of genes regulated by dex (hormone) and GLP (EHMT1). NI and shNS data were submitted on the GSE35962.

2017-06-13 | GSE94646 | GEO

Identification of proteins stably associated with G9a/GLP (EHMT2/EHMT1) complex of histone methyltransferases

Project description:G9a (EHMT2) and the G9a-like protein GLP (EHMT1) form a stable G9a/GLP heterodimer in embryonic stem cells and function cooperatively to establish and maintain the abundant repressive H3K9me2 modification, in addition to modifying several non-histone proteins. The G9a-dependent H3K9me2 is implicated in lineage-specific gene silencing and covers large chromosomal domains. While the mechanism of H3K9me2maintenance by G9a/GLP is known, how new patterns of this modification are established is not well understood. With this in mind, we used FLAG affinity purification of G9a under two different stringency conditions (150 and 300 mM NaCl) coupled with mass spectrometry to identify proteins stably associated with G9a/GLP, which could serve as potential recruiters of the complex to unmodified chromatin.

2016-03-16 | PXD003466 | Pride

Global transcriptional profiling changes upon knockdown of G9a in human non-small cell lung cancer cells

Project description:The experiment was designed to display differential gene expression profiling changes in two human Non-small cell lung cancer cells upon knockdown of G9a/EHMT2, by using RNAseq technology.

2018-10-21 | GSE113493 | GEO

Gene expression profiling of cardiomyocyte-enriched populations isolated from G9a-KO and Cre mice

Project description:The role of the histone mehyltrasferase G9a (also known as Ehmt2) in heart has not been extensively studied. To identify the genes regulated by G9a in the normal heart, we first generated a conditional, cardiac-specific KO mouse for this gene using the Cre-Lox approach, crossing G9a flox/flox mice with αMHC-MerCreMer mice (Cre mice were used as controls). Then, we sequenced total RNA (Total-RNA-seq) from cardiomyocyte-enriched populations isolated from G9a-KO and Cre mice, and compared the two expression profiles.

2017-08-30 | GSE93753 | GEO

The genomic distribution of G9a, H3K9me2, H3K27me3 and Mef2c in cardiomyocyte-enriched populations isolated from G9a-KO and Cre mice

Project description:The role of the histone methyltrasferase G9a (also known as Ehmt2) in the normal heart has not been studied extensively. To identify the genomic regions bound to G9a in cardiomyocytes (CMs),we first generated a conditional, cardiac-specific KO mouse for this gene using the Cre-Lox approach, crossing G9a flox/flox mice with αMHC-MerCreMer mice (Cre mice were used as controls). Then we performed ChIP-seq for G9a and H3K9me2 – the main histone methylation catalysed by the HMT – on isolated G9a-KO and Cre CMs, and considered the best G9a-bound genomic regions as those that had a loss or decrease of G9a binding as well as a lower level of H3K9me2 in G9a-KO CMs. Since G9a contributes to trimethylation of H3K27 at a set of developmental genes through its interaction with PRC2, we also evaluated whether the loss of G9a had an effect on the distribution of this histone mark. To this end, we performed ChIP-seq for H3K27me3 in Cre CMs and G9a-KO CMs. Finally co-immunoprecipitation assays revealed that G9a interacts with Mef2c, thus to elucidate the function of the G9a–Mef2c interaction in adult cardiomyocytes, we used ChIP-seq to define the genomic distribution of Mef2c in Cre CMs and G9a-KO CMs.

2017-08-30 | GSE93690 | GEO

The genomic distribution of G9a, H3K9me2 and H3K27me3 in cardiac hypertrophy.

Project description:The role of the histone methyltrasferase G9a (also known as Ehmt2) in the normal heart has not been studied extensively. To identify which genes were direct targets of G9a in hypertrophic cardiomyocytes, we performed ChIP-seq for G9a and H3K9me2 – the main histone methylation catalysed by the HMT – on cardiomyocytes isolated from normal mice (sham) and mice subject to transverse aortic constriction (TAC) for 1 wk, a surgical procedure that causes cardiac hypertrophy following the induction of pressure overload. We considered the best G9a-bound genomic regions as those in which G9a and H3K9me2 peaks overlapped. Since G9a contributes to trimethylation of H3K27 at a set of developmental genes through its interaction with PRC2, we also evaluated whether G9a had an effect on the distribution of this histone mark in hypertrophic cardiomyocytes. To this end, we performed ChIP-seq for H3K27me3 in CMs isolated from sham and TAC mice.

2017-08-30 | GSE93752 | GEO

Gene expression data of cancer cell lines treated with inhibitors of G9a and EZH2

Project description:Epigenetic modifications modulate gene expression and, when deregulated, contribute to the development and progression of cancer. G9a (EHMT2) and EZH2 are two histone methyltransferases commonly upregulated in several cancer types, leading to the silencing of tumor suppressor genes. We performed high throughput sequencing of a breast cancer cell line (MDA-MB-231), an ovarian cancer cell line (CAOV3) and a melanoma cell line (D14) treated with a G9a inhibitor (UNC0642), EZH2 inhibitor (GSK126) and their combination.

2022-02-20 | GSE168763 | GEO

GLP is critical for oogenesis exhibiting a G9A-independent role in transcriptional repression

Project description:GLP (EHMT1) functions as an H3K9me1 and H3K9me2 methyltransferase through its reportedly obligatory dimerization with G9A (EHMT2). Here, we investigated the role of GLP in oocyte and embryo development in comparison to G9A using oocyte-specific conditional knockout mouse models (G9a cKO, Glp cKO, G9a-Glp cDKO). Loss of GLP in oogenesis severely impairs oocyte maturation, fertilization and embryo development, resulting in lethality before embryonic day E12.5. In contrast, loss of G9A has a milder effect with a proportion of embryos producing viable offspring. The Glp cKO also showed loss of G9A protein and, hence, was phenotypically very similar to the G9a-Glp cDKO. H3K9me2 was equally depleted in all cKO genotypes, whereas H3K9me1 was decreased only in Glp cKO and G9a-Glp cDKO oocytes. Furthermore, the transcriptome, DNA methylome and proteome were markedly more affected in G9a-Glp cDKO than G9a cKO oocytes, demonstrating that in the absence of GLP there are widespread epigenetic and gene expression changes in the oocyte independent of H3K9me2. Gene dysregulation with coupled changes in DNA methylation suggest localised loss of chromatin repression, resulting in upregulated protein expression. Together, our findings demonstrate that GLP can function independently of G9A in the oocyte and is required for oocyte developmental competence.

2022-12-02 | GSE191026 | GEO

G9a-Mediated Methylation of ERα Links the PHF20/MOF Histone Acetyltransferase Complex to Hormonal Gene Expression

Project description:The euchromatin histone methyltransferase 2 (EHMT2, aka G9a) methylates histone H3K9 to repress gene expression, but it also acts as a coactivator for some nuclear receptors. The molecular mechanisms underlying this activation remain elusive. Here we show that G9a functions as a bona fide coactivator of the endogenous estrogen receptor α (ERα) in breast cancer cells in a histone methylation-independent manner. G9a dimethylates ERα protein at lysine 235 both in vitro and in cells. Dimethylation of ERαK235 (ERαK235me2) is recognized by the Tudor domain of PHF20, which in turn recruits the MOF histone acetyltransferase (HAT) complex to ERα target gene promoters to deposit histone H4K16 acetylation promoting active transcription. Together, our in vitro and in vivo data establish the molecular mechanism by which G9a functions as an ERα coactivator. Along with the PHF20/MOF complex, G9a links the crosstalk between ERα methylation and histone acetylation governing the epigenetic regulation of hormonal gene expression.

2016-04-07 | GSE76507 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data