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ATAC-seq analysis in bone marrow LSK cells in WT, G12D, Ezh2-KO and G12D with Ezh2-KO (G12D_Ezh2-KO) mice

ABSTRACT: ATAC-seq analysis in bone marrow LSK cells in WT, G12D, Ezh2-KO and G12D with Ezh2-KO (G12D_Ezh2-KO) mice

PROVIDER: PRJNA545887 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9180020.fastq.gz	Fastqsanger.gz
	SRR9180030.fastq.gz	Fastqsanger.gz
	SRR9180021.fastq.gz	Fastqsanger.gz
	SRR9180022.fastq.gz	Fastqsanger.gz
	SRR9180023.fastq.gz	Fastqsanger.gz

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Epigenomic and transcriptomic analysis of bone marrow LSK cells in WT, G12D, Ezh2-KO, and G12D with Ezh2-KO mice

Project description:Epigenomic and transcriptomic analysis of bone marrow LSK cells in WT, G12D, Ezh2-KO, and G12D with Ezh2-KO mice

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RNA-seq analysis of transcriptomic changes in bone marrow LSK cells in WT, G12D, Ezh2-KO and G12D with Ezh2-KO (G12D_Ezh2-KO) mice [RNA-seq]

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ChIP-seq analysis of H3K4me3,H3K27ac and H3K27me3 in bone marrow LSK cells in WT, G12D, Ezh2-KO and G12D with Ezh2-KO (G12D_Ezh2-KO) mice

Project description:ChIP-seq analysis of H3K4me3,H3K27ac and H3K27me3 in bone marrow LSK cells in WT, G12D, Ezh2-KO and G12D with Ezh2-KO (G12D_Ezh2-KO) mice

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ATAC-seq analysis in bone marrow LSK cells in WT, G12D, Ezh2-KO and G12D with Ezh2-KO (G12D_Ezh2-KO) mice

Project description:Epigenetic gene regulation and metabolism are highly intertwined, yet little is known whether and how altered epigenetics influences cellular metabolism in cancer progression. Here we show that EZH2 and NRasG12D mutations cooperatively induce progression of myeloproliferative neoplasms to fully penetrant, transplantable and lethal myeloid leukemias in mouse. EZH1, an EZH2 homolog, is indispensable for EZH2-deficient leukemia-initiating cells (LICs) and constitutes an epigenetic vulnerability. BCAT1, the first enzyme catalyzing transamination of branched-chain amino acids (BCAAs), is repressed by EZH2 in normal hematopoiesis and aberrantly activated in EZH2-deficient myeloid neoplasms in mouse and human. Enhanced BCAT1 promotes BCAA production in LICs ex vivo and in vivo, resulting in activated mTOR signaling. Genetic and pharmacological inhibition of BCAT1 selectively impairs EZH2-deficient LICs and constitutes a metabolic vulnerability. These findings establish an example how epigenetic alterations modify metabolic adaptation in myeloid transformation and provide a rationale for targeting the epigenetic and metabolic liabilities of cancer-initiating cells.

2019-06-17 | GSE132077 | GEO

RNA-seq analysis of transcriptomic changes in bone marrow LSK cells in WT, G12D, Ezh2-KO and G12D with Ezh2-KO (G12D_Ezh2-KO) mice [RNA-seq]

2019-06-17 | GSE132079 | GEO

ChIP-seq analysis of H3K4me3,H3K27ac and H3K27me3 in bone marrow LSK cells in WT, G12D, Ezh2-KO and G12D with Ezh2-KO (G12D_Ezh2-KO) mice

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Whole exome sequencing analysis of bone marrow c-Kit+ leukemia cells in Nras-G12D with Ezh2 KO (E2-KO) mice

Project description:Whole exome sequencing analysis of bone marrow c-Kit+ leukemia cells in Nras-G12D with Ezh2 KO (E2-KO) mice

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Expression data from LSK mice that overpexpress Ezh2 versus LSK Control

Project description:Ezh2 is a protein member of PRC2 and has described like a functional repressor gene. We are investigating the role of Ezh2 in hematopoietic stem cell, aging and leukemia. In the present study, we generated mouse models that allow gain-of-function of Ezh2 in the hematopoietic system. Activation of Ezh2 expression specifically in self-renewing HSCs alters gene expression programs and severely compromises hematopoietic function, leading to the development of myeloproliferative disease. We used microarrays to detail the global programme of gene expression in LSK that has relationship with the overexpression of Ezh2. LSK were marked and isolated by Fluorescence-activated cell sorting in Trizol.

2011-04-05 | E-GEOD-28369 | biostudies-arrayexpress

Epigenomic and transcriptomic analysis of bone marrow LSK cells in WT, G12D, Ezh2-KO, and G12D with Ezh2-KO mice

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-06-17 | GSE112995 | GEO

Expression data from diseased Ezh2 KO Lineage-c-Kit+Sca-1+ (LSK) bone marrow cells

Project description:Recent studies have shown that epigenetic regulator are mutated in myelodysplastic syndrome (MDS) patients. Ezh2 is frequently mutated in hematopoietic malignant patients, however, the pathophysiological role of Ezh2 mutations has not been elucidated yet. In this study, we examined the function of Ezh2 in murine hematopoietic disease. Ezh2 deleted mice with myeloid malignancies including MDS, Myelodysplasia/myeloneoplasm(MDS/MPN), Myelodysplasia/myeloneoplasm_thrombocytosis(MDS/MPN_TC)

2015-03-14 | GSE66897 | GEO

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