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RNA-seq gene expression profiling of livers from wild-type male and female mice, and from mice with a Double Knockout (DKO) of Ezh1 and Ezh2.

ABSTRACT: RNA-seq gene expression profiling of livers from wild-type male and female mice, and from mice with a Double Knockout (DKO) of Ezh1 and Ezh2.

PROVIDER: PRJNA434735 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6754420.fastq.gz	Fastqsanger.gz
	SRR6754421.fastq.gz	Fastqsanger.gz
	SRR6754422.fastq.gz	Fastqsanger.gz
	SRR6754423.fastq.gz	Fastqsanger.gz
	SRR6754414.fastq.gz	Fastqsanger.gz

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Histone modifications in livers from wild-type male and female mice, and in livers from mice with a Double Knockout (DKO) of Ezh1 and Ezh2

Project description:Chromatin immunoprecipitation and sequencing for 3 histone marks (H3K27ac, H3K27me3 and H3K4me1) was performed on livers of male and female mice with a combined loss of Ezh1 and Ezh2. The DKO mouse model used in these analyses is a global deletion of Ezh1 and hepatocyte-specific deletion of Ezh2, and is described in Bae WK et al, FASEB J. 2015 May;29(5):1653-62. doi: 10.1096/fj.14-261537. PMID: 25477280.

2020-04-28 | GSE110887 | GEO

RNA-seq gene expression profiling of livers from wild-type male and female mice, and from mice with a Double Knockout (DKO) of Ezh1 and Ezh2.

Project description:PolyA-selected RNA isolated from livers of adult male and female mice with a combined loss of EZH1 and EZH2 in hepatocytes was analyzed by RNA-seq. The DKO mouse model used in these analyses is a global deletion of Ezh1 and hepatocyte-specific deletion of Ezh2, and is described in Bae WK, Kang K, Yu JH, Yoo KH, Factor VM, Kaji K, Matter M, Thorgeirsson S, Hennighausen L. FASEB J. 2015 May;29(5):1653-62. doi: 10.1096/fj.14-261537. PMID: 25477280

2020-04-28 | GSE110879 | GEO

Histone modifications in livers from wild-type male and female mice, and in livers from mice with a Double Knockout (DKO) of Ezh1 and Ezh2

Project description:Histone modifications in livers from wild-type male and female mice, and in livers from mice with a Double Knockout (DKO) of Ezh1 and Ezh2

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Expression data from LSK cells from mice with knock-out of Ezh1 versus LSK control

Project description:Ezh1 is a protein member of PRC2. Ezh1 has been described as a functional repressor gene, such as its homologous Ezh2. We are investigating the role of Ezh1 in hematopoietic stem cells, aging, self-renewal and differentiation. We used microarrays to detail the global program of gene expression in LSK cells from mice with knocked-down expression of Ezh1. LSK cells from EZH1 knockout and control mice were marked and isolated by fluorescence-activated cell sorting. 2 replicates each.

2012-03-06 | E-GEOD-36288 | biostudies-arrayexpress

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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

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mRNA-seq of ARID1B KO and ARID1A/1B DKO livers

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The Quantitative Analysis of Transcriptomes Derived From Ezh2- or Ezh1/2-Deleted Leukemia Stem Cells of Murine Acute Myloid Leukemia

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Expression data from LSK cells from mice with knock-out of Ezh1 versus LSK control

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Loss of EZH2 results in enhanced recruitment of EZH1, Pol II and Stat5 and precocious mammary gland development

Project description:Establishment and differentiation of mammary alveoli during pregnancy are controlled by prolactin through the transcription factor STAT5. As pregnancy progresses mammary signature genes are activated in a defined temporal order, which coincides with the recruitment of STAT5 to respective regulatory sequences. This study addressed the question whether the methyltransferase and transcriptional co-activator EZH2 controls the differentiation clock of mammary epithelium. Ablation of Ezh2 from mammary stem cells resulted in precocious differentiation of alveolar epithelium and accelerated activation of mammary signature genes. This coincided with enhanced occupancy by EZH1, Pol II and STAT5 to mammary-specific loci. Notably, loss of EZH2 did not result in overt changes in genome-wide and gene-specific H3K27me3 patterns, suggesting that enhanced EZH1 recruitment can compensate for the loss of EZH2. However, differentiated mammary epithelia failed to form in the combined absence of EZH1 and EZH2. Transplantation experiments failed to demonstrate a role for EZH2 in the biology of mammary stem and progenitor cells. In summary, while EZH1 and EZH2 serve redundant functions in the establishment of H3K27me3 and formation of mammary alveoli, the presence of EZH2 is required to obtain controlled temporal differentiation of mammary epithelium. ChIP-seq EZH1, EZH2, PolIII; WT and E2KO mammary cells

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