Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Genome-wide maps of H3K27me3 in endpoint Ezh2+/+ or Ezh2-/- Tet ON PyVmT mouse mammary gland tumours

ABSTRACT: Genome-wide maps of H3K27me3 in endpoint Ezh2+/+ or Ezh2-/- Tet ON PyVmT mouse mammary gland tumours

PROVIDER: PRJNA429046 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR6451010.fastq.gz	Fastqsanger.gz
	SRR6451001.fastq.gz	Fastqsanger.gz
	SRR6451011.fastq.gz	Fastqsanger.gz
	SRR6451002.fastq.gz	Fastqsanger.gz
	SRR6451012.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 18

Similar Datasets

Genome-wide maps of H3K27me3 in endpoint Ezh2+/+ or Ezh2-/- Tet ON PyVmT mouse mammary gland tumours

Project description:We report the application of single-molecule-based sequencing technology for high-throughput profiling of histone modifications in endpoint tumours from Ezh2+/+ or Ezh2-/- Tet ON PyVmT mammary gland tumours. In order to understand the H3K27me3 targets in the context of mouse mamamry gland tumorigenesis, data were generated by deep sequencing a pool of 5 tumours per genoype, in duplicate using Illumina HiSeq2500. Using an optimized data analysis workflow, we mapped about 30 million sequence reads per sample to the mouse genome (build mm10). Raw reads were trimmed for length (n>=32), quality (phred score >= 30) and adaptor sequence using fastx v0.0.13.1.Trimmed reads were (pools of 5 different tumors per genotype) then aligned to the mouse reference genome mm10 using BWA v0.5.9 Broad peaks were called using MACS v1.4.1 software (mfold=10,30; bandwith=300; pvalue cutoff=1E-5) using sequenced libraries of input DNA as control. Peak list intersections were done using BEDTools v2.12.0. Binding peaks were considered overlapping if at least 1 base of the peaks overlapped. Our study demonstrated the first mapping of H3K27me3 in the endpint tumours of tetracycline ducible PyVmT mouse mamary tumours.

2018-03-01 | GSE108899 | GEO

Expression data from endpoint mammary gland tumours from Ezh2 +/+ or Ezh2 -/- Tet ON PyVmT mice

Project description:Expression data from endpoint mammary gland tumours from Ezh2 +/+ or Ezh2 -/- Tet ON PyVmT mice

| PRJNA428969 | ENA

Expression data from endpoint mammary gland tumours from Ezh2 +/+ or Ezh2 -/- Tet ON PyVmT mice

Project description:In this dataset we include expression profiles of whole endpoint tumours snap frozen in liquid nitrogen that have been crushed and processed with the Qiagen RNeAsy mRNA extraction kit

2018-02-26 | GSE108861 | 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

Genome-wide analysis of H3K27me3 in Ezh2-conditional iMEFs

Project description:We analyzed the genomic distribution of H3K27me3 in a clone of c-Myc iMEFs (clone C2) either i) wild-type for Ezh2, ii) in the presence of overexpressed exogenous Ezh2, iii) Ezh2-mutant, and iv) Ezh1/Ezh2 pre-deletion (Ezh1/Ezh2 introduced before deletion of endogenous Ezh2) and Ezh2 post-deletion rescue (Ezh2 re-introduced in Ezh2-mutant cells).

2015-10-01 | GSE59293 | 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

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

scRNA-Seq of MC38 CD45+ Cells treated with EZH2 inhibitor PF-06821497

Project description:The purpose of this study was to determine the effect of EZH2 inhibitor (EZH2i) PF-06821497 on CD45+ cells isolated from MC38 tumors at day 17 post implantation. Mice were either treated for 7 days prior to endpoint or 16 days prior to endpoint with the EZH2i or with vehicle control. CD45+ cells were isolated and scRNA-Seq was performed on cells

2021-11-10 | GSE188473 | GEO

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

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