Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Characterization of EZH2-deficient human embryonic stem cells [ChIP-seq and bulk RNA-seq]

ABSTRACT: Here we analyze histone modifications and transcriptome profiles of EZH2-deficient human embroynic stem cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE76626 | GEO | 2016/12/06

SECONDARY ACCESSION(S): PRJNA308197

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Characterisation of EZH2-deficient human embryonic stem cells [single cell RNA-seq]

Project description:Here we analyse single cell transcriptome profiles of EZH2-deficient human embroynic stem cells

2016-12-06 | GSE81673 | GEO

Characterisation of EZH2-deficient human embryonic stem cells

Project description:Characterisation of EZH2-deficient human embryonic stem cells

| PRJNA322289 | ENA

Ezh2 deficient T-cell

Project description:Lymph node T cells isolated from Ezh2fl/fl or Ezh2 deficient mice Keywords: repeat sample

2005-09-01 | GSE1566 | GEO

RNA-sequencing analysis of differentiating wildtype and Ezh2 deficient immature mouse chondrocytes

Project description:Objective: To evalute the role of Ezh2 in chondrocyte differentiation. Method: Ezh2 was inactivated in chondrocytes using the Col2a1-Cre driver in vivo. Immature mouse chondrocytes (IMC) were isolated from wildtype and Ezh2 deficient mice, and plated in micromass culture. Chondrocytes were differentiated and RNA was isolated at days 3, 7, and 14 of culture. Isolated RNA was subjected to RNA sequencing analysis. Results: Ezh2 deficient chondrocytes exhibit enhanced expression of osteogenic genes compared to wildtype cells.

2017-03-29 | GSE97118 | GEO

Affinify Purification of EZH2 and phosphodeficient EZH2 identifies phosphorylation dependent interactions of EZH2

Project description:Overexpression of EZH2 in estrogen receptor negative (ER-) breast cancer promotes metastasis. EZH2 has been mainly studied as the catalytic component of the Polycomb Repressive Complex 2 (PRC2) that mediates gene repression by trimethylating histone H3 at lysine 27 (H3K27me3). However, how EZH2 drives metastasis despite the low H3K27me3 levels observed in ER- breast cancer is unknown. We have shown that in human invasive carcinomas and distant metastases, cytoplasmic EZH2 phosphorylated at T367 is significantly associated with ER- disease and low H3K27me3 levels. Here, we explore the interactome of EZH2 and of a phosphodeficient mutant EZH2_T367A. We identified novel interactors of EZH2, and identified interactions that are dependent on the phosphorylation and cellular localization of EZH2 that may play a role in EZH2 dependent metastatic progression.

2018-07-03 | PXD010073 | Pride

Gene expression profile of right ventricles from adult wild type and Ezh2-deficient hearts

Project description:Adult-onset diseases can be associated with in utero events, but mechanisms for this remain unknown. The polycomb histone methyltransferase, Ezh2, stabilizes transcription by depositing repressive marks during development that persist into adulthood, but its function in postnatal organ homeostasis is unknown. We show that Ezh2 stabilizes cardiac gene expression and prevents cardiac pathology by repressing the homeodomain transcription factor Six1, which functions in cardiac progenitors but is stably silenced upon cardiac differentiation. Ezh2 deletion in cardiac progenitors caused postnatal myocardial pathology and destabilized cardiac gene expression with activation of Six1-dependent skeletal muscle genes. Six1 induced cardiomyocyte hypertrophy and skeletal muscle gene expression. Furthermore, genetically reducing Six1 levels rescued the pathology of Ezh2-deficient hearts. Thus, Ezh2-mediated repression of Six1 in differentiating cardiac progenitors is essential for stable postnatal heart gene expression and homeostasis. Our results suggest that epigenetic dysregulation in embryonic progenitor cells predisposes to adult disease and dysregulated stress responses. Four samples were analyzed. RNA was obtained from ventricles from two wild type and two Ezh2-deficient hearts.

2011-12-09 | E-GEOD-34274 | biostudies-arrayexpress

EZH2 deficient T-cell acute lymphoblastic leukemia is sensitized to CHK1 inhibition through enhanced replication stress

Project description:Loss-of-function mutations of EZH2, the enzymatic component of PRC2, are recurrently found in T-cell acute lymphoblastic leukemia (T-ALL) and have been associated with chemotherapy resistance and poor outcome. Using isogenic T-ALL cells, with and without CRISPR-induced EZH2-inactivating mutations, we performed a cell-based synthetic lethal drug screen. EZH2 deficient cells exhibited increased sensitivity to structurally diverse CHK1 inhibitors, an interaction that could be validated genetically. Notably, EZH2 deficient cells acquired a gene expression signature of immature T-ALL cells, with significant enrichment of MYC target genes. Mechanistically, EZH2 deficiency was associated with marked transcriptional upregulation of MYCN, increased replication stress, and enhanced dependency on CHK1 for cell survival. Furthermore, small molecule inhibition of CHK1 had efficacy in delaying tumor progression in isogenic EZH2 deficient, but not EZH2 wild-type T-ALL cells in vivo, suggesting there is an exploitable therapeutic window for CHK1 inhibitors in high risk EZH2 mutated T-ALL.

2020-08-28 | GSE127261 | GEO

Overactivation of wound healing-associated TGF-beta responses in EZH2-deficient decidual stromal cells.

Project description:Our objective was to identify genes upregulated by TGF-beta in control and Ezh2 cKO decidual stromal cells (DSCs), and to compare this set of genes with a previously identified gene set of H3K27me3-marked decidual genes that are putatively silenced by EZH2/PRC2 (Nancy et al. JCI. 2018). We also wanted to assess baseline (BL) gene expression in control and Ezh2 cKO DSCs, and compare it to an RNA-seq analysis of differential gene expression in whole tissue Ezh2 cKO and control decidua. RNA was isolated from untreated and TGF-beta treated decidual stromal cells from control and Ezh2 cKO mice. Sequencing provided was 706 million total reads with an average of 82.2% of these reads aligning uniquely to the mouse genome. Reads uniquely mapped to known mRNAs were used to identify gene expression changes between housing conditions using DESeq2. TGF-beta induced 638 protein-coding genes in EZH2-deficient DSCs versus 480 in control DSCs (with a 295 gene overlap), demonstrating that EZH2-deficient DSCs are transcriptionally more responsive to TGF- (P=0.0025, Fisher’s exact test). Within the 638 genes, activated fibroblast signature genes were highly over-represented. TGF-target genes were 2.7-fold over-represented within the set of genes with higher expression in EZH2-deficient DSCs at baseline (BL; i.e., when neither EZH2-deficient nor control DSCs were treated with TGF-beta; P<1x10-20) . 741 genes were overexpressed in Ezh2 cKO DSCs compared to control DSCs, and 904 genes were underexpressed. Moreover, by comparing to our laboratory's previous CHIP-Seq analysis (Nancy et al. JCI 2018), we noted that genes overexpressed in cKO mice were enriched in previously identified H3K27me3-marked genes (P<1x10-26).

2022-01-11 | GSE171724 | GEO

Transcription profiling of lymph node T cells isolated from Ezh2fl/fl or Ezh2 deficient mice to study the role of ezh2 on actin polymerization and cell signaling

Project description:Lymph node T cells isolated from Ezh2fl/fl or Ezh2 deficient mice

2007-11-22 | E-GEOD-1566 | biostudies-arrayexpress

Ezh2 promotes mammary tumor initiation through epigenetic regulation of the Wnt and mTORC1 signaling pathways (ChIP-Seq)

Project description:The regulation of gene expression through histone post-translational modifications plays a crucial role in breast cancer progression. However, the molecular mechanisms underlying the contribution of histone modification to tumor initiation remain unclear. To gain a deeper understanding of the role of the histone modifier Enhancer of Zeste homology 2 (Ezh2) in the early stages of mammary tumor progression, we employed an inducible mammary organoid system bearing conditional Ezh2 alleles that faithfully recapitulates key events of Luminal B breast cancer initiation. We showed that the loss of Ezh2 severely impairs oncogene-induced organoid growth, with Ezh2-deficient organoids maintaining a polarized epithelial phenotype. Transcriptomic profiling showed that Ezh2-deficient mammary epithelial cells upregulated the expression of negative regulators of Wnt signaling and downregulated genes involved in mTORC1 (mechanistic target of rapamycin complex 1) signaling. We identified Sfrp1, a Wnt signaling suppressor, as an Ezh2 target gene that is de-repressed and expressed in Ezh2-deficient epithelium. Furthermore, an analysis of breast cancer data revealed that Sfrp1 expression was associated with favorable clinical outcomes in Luminal B breast cancer patients. Finally, we confirmed that targeting Ezh2 impairs mTORC1 activity through an indirect mechanism that upregulates the expression of the tumour suppressor Pten. These findings indicate that Ezh2 integrates the mTORC1 and Wnt signaling pathways during early mammary tumor progression, arguing that inhibiting Ezh2 or therapeutically targeting Ezh2-dependent programs could be beneficial for the treatment of early-stage Luminal B breast cancer.

2023-07-15 | GSE235144 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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