ChIP-seq of Ezh2 and H3K27me3 in E12.5 heart apex
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE29994 | GEO | 2012/03/15
SECONDARY ACCESSION(S): PRJNA155343
REPOSITORIES: GEO
Similar Datasets
Project description:Ezh2 and H3K27me3 binding sites in E12.5 heart apex PRC2 binding sites in wild type cardiomyocytes
2012-03-15 | E-GEOD-29994 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series: GSE29992: Genome-wide profiling of E12.5 cardiomyocytes RNA expression in both hetozygeous control and mutant GSE29994: ChIP-seq of Ezh2 and H3K27me3 in E12.5 heart apex Refer to individual Series
2012-03-15 | E-GEOD-29997 | biostudies-arrayexpress
Project description:Congenital heart disease is among the most frequent major birth defects. Epigenetic marks are crucial for organogenesis, but their role in heart development is poorly understood. Polycomb Repressive Complex 2 (PRC2) trimethylates histone H3 at lysine 27, establishing H3K27me3 repressive epigenetic marks that promote tissue-specific differentiation by silencing ectopic gene programs. We studied the function of the catalytic subunit of PRC2, EZH2, in murine heart development. Early EZH2 inactivation by Nkx2-5Cre caused lethal congenital heart malformations, but slightly later EZH2 inactivation by cTNT-Cre did not. To study how the cardiomyocytes gene expression program is properly established in the early heart development, we combined the technologies of RNA sequencing and chromatin immunoprecipitation sequencing to identify the functional target genes directly repressed by EZH2. Intriguingly, these were enriched for transcriptional regulators of non-cardiac expression programs, such as transcription factors that regulate neuronal (Pax6) and cardiac progenitor genes (Isl1 and Six1). EZH2 was also required to maintain spatiotemporal regulation of cardiac gene expression, as Hcn4, Mlc2a, and Bmp10 were inappropriately upregulated in ventricular RNA. Furthermore, EZH2 was required for normal cardiomyocyte proliferation, establishing H3K27me3 epigenetic marks at cell cycle inhibitors Ink4a/b and repressing their expression. Our study reveals a previously undescribed role of EZH2 in regulating heart formation and shows that perturbation of the epigenetic landscape early cardiogenesis has sustained disruptive effects at later developmental stages. 8 E12.5 heart apex were used for RNA preparation each group.
2012-03-15 | E-GEOD-29992 | biostudies-arrayexpress
Project description:ChIP-seq of Ezh2 and H3K27me3 in E12.5 heart apex
| PRJNA155343 | ENA
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
Project description:RNA-seq for DKO, E1KO, E2KO and WT E12.5 heart revealed that EZH1 and EZH2 play a partially redundant role to trimethylate histone H3 at Lys 27 (H3K27me3). Through EZH1, H3K27me3 and H3K27ac ChIP-seq and RNA-seq for P13 EZH1 and GFP overexpressing heart (AAVEzh1 and AAVGFP respectively) suffered MI at P10, we surprisingly found that EZH1 can active the expression of regenerating relevant genes by directly binding to the promoter of targeted genes and through a mechanism independent of H3K27me3 deposition. Together, we unravel a requirement but divergent mechanisms of EZH1 in heart development and regeneration
2017-07-26 | GSE97732 | GEO
Project description:Expression data from neonatal heart after apex resection
| PRJNA645066 | ENA
Project description:Polycomb group (PcG) proteins including EZH2, SUZ12 and so on, which specifically catalyze trimethylation of histone 3 lysine 27 (H3K27me3), and methylated H3K27 can be recognized by other specific binding proteins to compress chromatin structure, leading to the transcriptional repression of the target genes. To completely understand the epigenetic profile and molecular network of PcG in HCC, we performed ChIP-on-chip screens with EZH2, SUZ12 and H3K27me3 antibodies in HepG2 cells. Comparison of ChIP-on-chip results from EZH2, SUZ12 and H3K27me3.
2013-11-13 | E-GEOD-52300 | biostudies-arrayexpress
Project description:Triple-Negative Breast Cancer (TNBC) has a poor prognosis and adverse clinical outcomes among all breast cancer subtypes as there is no available targeted therapy. Overexpression of Enhancer of zeste homolog 2 (EZH2) has been shown to correlate with TNBC's poor prognosis, but the contribution of EZH2 catalytic (H3K27me3) versus non-catalytic EZH2 (NC-EZH2) function in TNBC progression remains elusive. We reveal that selective hyper-activation of functional EZH2 (H3K27me3) over NC-EZH2 alters TNBC metastatic landscape and fosters its peritoneal metastasis, particularly splenic. Instead of H3K27me3-mediated repression of gene expression; here, it promotes KRT14 transcription by attenuating binding of repressor Sp1 to its promoter. Further, KRT14 loss significantly reduces TNBC migration, invasion, and peritoneal metastasis. Consistently, human TNBC metastasis displays positive correlation between H3K27me3 and KRT14 levels. Finally, EZH2 knockdown or H3K27me3 inhibition by EPZ6438 reduces TNBC peritoneal metastasis. Altogether, our preclinical findings suggest a rationale for targeting TNBC with EZH2 inhibitors.
2022-11-10 | GSE217474 | GEO
Project description:We prepared RNA from mouse embryonic hearts and performed mRNA micro-array analysis to compare gene expression profiles between control and Rhau-deletion mice (E12.5), in order to understand how RHAU regulates heart development.
2015-10-10 | GSE73544 | GEO