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EZH2-mediated H3K27me3 targets transcriptional circuits of neuronal differentiation ChIP-seq

ABSTRACT: EZH2-mediated H3K27me3 targets transcriptional circuits of neuronal differentiation ChIP-seq

PROVIDER: PRJEB50421 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR8135060.fastq.gz	Fastqsanger.gz
	ERR8135070.fastq.gz	Fastqsanger.gz
	ERR8135080.fastq.gz	Fastqsanger.gz
	ERR8135090.fastq.gz	Fastqsanger.gz
	ERR8135100.fastq.gz	Fastqsanger.gz

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EZH2-mediated H3K27me3 targets transcriptional circuits of neuronal differentiation

Project description:EZH2-mediated H3K27me3 targets transcriptional circuits of neuronal differentiation

| PRJEB52197 | ENA

EZH2-mediated H3K27me3 targets transcriptional circuits of neuronal differentiation

Project description:Our work describes novel roles for EZH2 in the specification of cortical neurons. Previous reports established the current model of EZH2-mediated control of neuronal progenitors differentiation through the regulation of their proliferation and developmental transitions. We built on these findings and studied the role of EZH2 in post-mitotic glutamatergic neurons differentiated from embryonic stem cells, a particularly relevant cell type where the impact of its regulation has thus far remained elusive. Briefly, our key results can be summarized as follows: 1. The conditional deletion of EZH2 at the moment of cell cycle exit in neural progenitors allowed us to study the role of EZH2 selectively in post-mitotic glutamatergic neurons. 2. Time course transcriptomic and epigenomic analyses of H3K27me3 in absence of EZH2 revealed a significant dysregulation of transcriptional networks affecting synaptic plasticity, in particular long term depression. 3. These analyses also revealed potential novel roles of EZH2 in controlling the regulation between the glutamatergic signature and the GABAergic one, suggesting a mechanism entailing failure of Prdm13 repression, a histone methyltransferase with a known role in determining GABAergic neurons specification.

2022-04-18 | E-MTAB-11387 | biostudies-arrayexpress

EZH2-mediated H3K27me3 targets transcriptional circuits of neuronal differentiation ChIP-seq

2022-03-28 | E-MTAB-11363 | biostudies-arrayexpress

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

Genome-wide maps of H3K27me3 and H3K27ac in cells treated with HDAC inhibition, EZH2 inhibition, or combined HDAC/EZH2 inhibition

Project description:Investigation of the mechanism by which combined EZH2 and HDAC inhibition kills PC3 prostate cancer cells. Next-generation sequencing was used to identify changes in genome localization of HDAC targets (H3K27ac) and EZH2 targets (H3K27me3) upon treatment with each inhibitor alone or in combination.

2020-05-12 | GSE150336 | GEO

Chip-chip from HepG2 cells with EZH2, SUZ12 and H3K27me3

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

EZH2-H3K27me3 mediated KRT14 upregulation promotes TNBC peritoneal metastasis

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

Ezh2 and H3K27me3 in cardiomyocytes

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

Targeting EZH2 in MYCN-amplified Neuroblastoma [ChIP-seq]

Project description:Purpose: Identify new targets in MYCN-amplified Neuroblastoma Methods: ChIP-Seq experiments were performed on Kelly and LAN-1 neuroblastoma cells by using the following antibodies: anti-EZH2 (Cell Signaling 5246S); anti-H3K27me3 (Millipore 07-449); anti-H3K4me3 (Abcam ab8580). We evaluated the global EZH2 PRC2-dependence by identifiying direct genome-wide target genes for EZH2, H3K27me3 and H3K4me3. Results: We found that EZH2 serves a PRC2-dependent function in neuroblastoma, repressing neuronal differentiation. Moreover, EZH2-regulated genes were strongly repressed in MYCN-amplified and high-risk primary tumors. Conclusion: Our study supports testing EZH2 inhibitors in patients with MYCN-amplified neuroblastoma.

2017-12-02 | GSE85430 | GEO

CUT&Tag analysis on H3K27me3 in mouse embryonic medial ganglionic eminence (MGE) under deletion of Ezh2 gene

Project description:Enhancer of zeste homolog 2 (Ezh2) is the methyltransferase component of the Polycomb Repressive Complex 2 (PRC2), which is critical for trimethylation of histone 3 at lysine 27 (H3K27me3) and results in gene repression. Mutations in EZH2 and dysregulation of H3K27me3 can lead to neurodevelopmental abnormalities such as Weaver Syndrome and ataxia-telangiectasia. During cortical neurogenesis, H3K27me3 is a critical epigenetic modification that regulates cellular maturation rate, and in turn, determines when precursor cells exit the cell cycle. Loss of function studies reveal that Ezh2 plays a critical role in epigenetic regulation of neuronal fate and maturation in some brain regions, but a role for Ezh2 in forebrain GABAergic interneurons has not been explored. Here, we removed Ezh2 from the medial ganglionic eminence (MGE) to study its role in interneuron development.

2023-11-15 | GSE233190 | GEO

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