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Homo sapiens

ABSTRACT: ChIP-seq analysis of EZH1, H3K4me3 and H3K27me3 in 5F cells

OTHER RELATED OMICS DATASETS IN: GSE89416GSE89415GSE89418

PROVIDER: PRJNA352136 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5285060.fastq.gz	Fastqsanger.gz
	SRR5284501.fastq.gz	Fastqsanger.gz
	SRR5285061.fastq.gz	Fastqsanger.gz
	SRR5284502.fastq.gz	Fastqsanger.gz
	SRR5285062.fastq.gz	Fastqsanger.gz

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EZH2 controls mammary differentiation independently of its methyltransferase activity through controlling genomic STAT5 access

Project description:Mammary development is characterized by the proliferation and progressive differentiation of alveolar epithelium during pregnancy, culminating in lactation. These processes are largely controlled by hormones through transcription factors. We now explore the contributions of histone methyltransferases, which establish H3K27me3 marks, in the temporally-regulated differentiation of mammary epithelium. Loss of EZH2, but not EZH1, resulted in precocious mammary differentiation, which was facilitated by STAT5 binding to specific target genes and their activation. Mammary stem cells were not compromised in the absence of EZH2. Genome-wide H3K27me3 patterns remained intact in the absence of EZH2. Mammary-specific loci were devoid of H3K27me3 marks in mammary progenitor and mature cells, suggesting no regulatory role for this repressive mark. Lastly, the combined absence of EZH1 and EZH2 inhibited the formation of alveoli. Taken together, EZH2 controls temporally-restricted differentiation of mammary epithelium through H3K27me3-independent mechanisms. mRNA-seq and ChIP-seq in MMTV-Cre (Control), E1-/- (E1KO), E1+/-;E2f/f;control (E1+/-E2KO) and Ezh2f/f;control (E2KO) mammary gland tissues or MECs (purified mammary epithelial cells). H3K27me3 and STAT5 ChIP-seqs in mammary tissues at p13; H3K4me3 ChIP-seq in MECs (mammary epithelial cells) at p13; RNA-seqs at mature virgin (with/without prolactin injection), p13 and p18 mammary tissues.

2013-12-31 | E-GEOD-52016 | biostudies-arrayexpress

Homo sapiens

Project description:ChIP-seq analyses of H3K27me3 and H3K4me3 in JMJD3c-hESCs

| PRJNA317931 | ENA

Homo sapiens

Project description:Whole genome ChIP/chip tiling of human ES cells for H3K4me3 and H3K27me3

| PRJNA101545 | ENA

ATAC-seq analysis in 5F cells and AGM cells with EZH1 depletion

Project description:ATAC-seq analysis in 5F cells and AGM cells with EZH1 depletion

| PRJNA352134 | ENA

An Ezh2 and Ezh1 dual inhibitor, UNC1999, re-shapes the landscape of H3K27me3 versus H3K27ac in MLL-AF9-transformed murine leukemia

Project description:Ezh2 and EZH1 are histone H3 lysine 27 (H3K27)-specific methyltransferases. Their hyperactive mutations and overexpression were found in cancer including various hematological malignancies. UNC1999 is a highly selective inhibitor for both enzymes. It suppresses H3K27 tri- and di-methylation globally and inhibits growth of MLL-rearranged acute leukemia. Here we performed ChIP-Seq to profile how UNC1999 affects distribution of H3K27me3 and its antagonizing H3K27ac in MLL-AF9-immortalized leukemia cells. We also performed ChIP-seq of SUZ12, an essential common cofactor of EZH2 and EZH1 following compound treatments. We treated MLL-AF9 transformed murine leukemia cells with DMSO, UNC1999 or UNC2400 (an inactive analog compound of UNC1999). Cells were then collected and used for ChIP-Sequencing of Input, H3K27me3, SUZ12, and H3K27ac.

2014-10-30 | E-GEOD-62437 | biostudies-arrayexpress

Divergent mechanisms of EZH1 regulation of heart development and regeneration [RNA-Seq]

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

Divergent mechanisms of EZH1 regulation of heart development and regeneration [ChIP-Seq]

Project description:Through EZH1, H3K27me3 and H3K27ac ChIP-seq and RNA-seq data in 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.

2017-07-26 | GSE97731 | GEO

Disruption of H3K27me3 through loss of EZH1 and EZH2 accelerates progression of hepatosteatosis to fatal liver fibrosis

Project description:Although epigenetic mechanisms, such as specific histone modifications, control common and cell-specific genetic programs, a role for histone modifying enzymes in liver metabolism and disease has not been investigated. This report demonstrates that the combined loss of the histone methyltransferases EZH1 and EZH2 in mouse hepatocytes led to the disruption of H3K27me3 homeostasis by age three months, simple fatty liver by age six months and fatal fibrosis by age 15 months. Global and gene-specific reduction of H3K27me3 marks paralleled a concomitant increase of H3K4me3 marks at genes associated with chronic liver disease. Advanced disease was accompanied by widespread infiltration of immune cells, an increase of activated hepatic stellate cells and collagen deposition. Expression of genes from the cytochrome P450 family that control drug metabolism was already deregulated by age two months and mice were fatally hypersensitive to carbon tetrachloride (CCl4). These genetic experiments, for the first time, illustrate that the simple loss of EZH1/EZH2, which results in the disruption of epigenetic modifications, is sufficient for the progression of fatal liver disease. RNA-seq and ChIP-seq were performed in liver tissues.

2013-12-24 | E-GEOD-53627 | biostudies-arrayexpress

Homo sapiens

Project description:ChIP-chip of lymphocytes using H3K9Ac, H3K4me3, H3K9me3, H3K27me3 and H4K16Ac antibodies

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Homo sapiens

Project description:ChIP-chip and MeDIP-chip from glioblastoma BTSCs (brain tumor stem cells) with H3K4me3, H3K27me3, H3K9me3, methylated DNA

| PRJNA259603 | ENA