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Mus musculus

ABSTRACT: ChIP-seq of H3K27me3 in Asxl1 or Asxl2 KO mice

PROVIDER: PRJNA360172 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5145760.fastq.gz	Fastqsanger.gz
	SRR5145761.fastq.gz	Fastqsanger.gz
	SRR5145762.fastq.gz	Fastqsanger.gz

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ChIP-seq of H3K27me3 in Asxl1 or Asxl2 KO mice

Project description:The goals of this study are to identify H3K27me3 changes in Asxl1 or Asxl2 KO mice

2017-06-26 | GSE93165 | GEO

Genome-wide maps of chromatin modifications in wild-type or mutant HAP1 cells

Project description:Using ChIP-seq, we profiled several histone marks associated with active transcription (H3K4me3) or with Polycomb-mediated silencing (H2AK119ub1 and H3K27me3) in wild-type HAP1 cells and in cells mutated in BAP1, ASXL1, ASXL2, EZH2 and RING1B.

2018-11-21 | GSE110133 | GEO

Differential expression in wild type and mutant HAP1 cells [RNA-seq I]

Project description:using RNA-seq we characterized gene expression changes occuring upon knockout of BAP1, ASXL1, ASXL2, ASXL1/2 or Polycomb genes RING1B and EZH2. We also investigated the response to retinoic acid treatment in wild-type and BAP1 KO cells.

2018-11-21 | GSE110142 | GEO

Mus musculus

Project description:RNA-seq of Asxl2 KO LSK cells

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Mus musculus

Project description:Loss of Asxl2 leads to myeloid malignancies in mice. [ChIP-Seq]

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Cancer-associated ASXL1 mutations may act as gain-of-function mutations of the ASXL1-BAP1 complex

Project description:ASXL1 is the obligate regulatory subunit of a deubiquitinase complex whose catalytic subunit is BAP1. Heterozygous mutations of ASXL1 that result in premature truncations are frequent in myeloid leukemias and Bohring-Opitz syndrome. Here, we demonstrate that truncated ASXL1 proteins confer enhanced activity on the ASXL1-BAP1 complex. Stable expression of truncated, hyperactive ASXL1-BAP1 complexes in a hematopoietic precursor cell line resulted in global erasure of H2AK119Ub, striking depletion of H3K27me3, selective upregulation of a subset of genes whose promoters bore both H2AK119Ub and H3K4me3, and spontaneous differentiation to the mast cell lineage. These outcomes required the catalytic activity of BAP1, indicating these events were downstream consequences of H2AK119Ub erasure. In bone marrow precursors, truncated ASXL1-BAP1 expression cooperated with TET2 loss-of-function to increase differentiation to the myeloid lineage in vivo. We propose that pathological ASXL1 mutations confer gain-of-function on the ASXL-BAP1 complex. ChIP-Seq for H2AK119Ub, H3K4me3, H3K27me3 on EML cells. RNA-Seq on EML cells expressing ASXL1(1-479)+BAP1 and control.

2015-03-11 | E-GEOD-65555 | biostudies-arrayexpress

ASXL1 Mutations Promote Myeloid Transformation Through Loss of PRC2-Mediated Gene Repression

Project description:Recurrent somatic ASXL1 mutations occur in patients with myelodysplasia (MDS), myeloproliferative neoplasms (MPN), and acute myeloid leukemia (AML), and are associated with adverse outcome. Despite the genetic and clinical data implicating ASXL1 mutations in myeloid malignancies, the mechanisms of transformation by ASXL1 mutations are not understood. Here we identify that ASXL1 mutations result in loss of PRC2-mediated histone H3 lysine 27 (H3K27) tri-methylation. Through integration of microarray data with genome-wide histone modification ChIP-Seq data we identify targets of ASXL1 repression including the posterior HOXA cluster that is known to contribute to myeloid transformation. We demonstrate that ASXL1 associates with the Polycomb repressive complex 2 (PRC2), and that loss of ASXL1 in vivo collaborates with NRASG12D to promote myeloid leukemogenesis. To assess the genome-wide effects of ASXL1 loss on chromatin state we performed chromatin immunoprecipitation followed by next generation sequencing (CHIP-seq) for histone modifications known to be associated with PcG (histone H3 lysine 27 trimethylation (H3K27me3)) or TxG activity (histone H3 lysine 4 trimethylation (H3K4me3)) in UKE1 cells expressing empty vector (EV) or 2 independent validated shRNAs for ASXL1. This Series represents the ChIP-Seq data (not the microarray data referenced in the summary above). The related micorarray data are available in GEO as GSE38692.

2012-08-21 | E-GEOD-38861 | biostudies-arrayexpress

Genome Wide Chromatin Mapping of H3K27me3 and H3K4me3 histone modifications in wild type and ASXL1-/- Osteoclast

Project description:We report a novel role of ASXL1 protein in altering epigentic profile of osteoclast. ASXL1 is an ETP protein that bind to polycomb repressive complex. We asked if ASXL1 regulates osteoclast differentiation by maintaining balance between positive and negative epigenetic regulators. To address this question, we performed ChIP-seq using H3K27me3 and H3K4me3 antbody in day2 osteoclast. Our data reveals that there was a global loss of H3K27me3 in ASXl1-/- osteoclast which includes loss of this repressive methylation of NFATc1 promoter, which is a master regulator of osteoclastogenesis.

2019-03-14 | GSE111852 | GEO

ATAC-seq profiling of Nfat5 KO and WT in Mus musculus macrophages

Project description:ATAC-seq profiling of Nfat5 KO and wild type macrophages derived from bone marrow (primary cells), treated or not with Lipopolysaccharide (LPS).

2021-06-09 | GSE111476 | GEO

RNA-seq of Asxl2 KO LSK cells

Project description:The goals of this study are to compare transcriptome profiling (RNA-seq) of Asxl2 KO LSK cells to that of Asxl2 wild-type cells. We found substantial number of genes are differentially expressed in Asxl2 KO cells.

2017-06-26 | GSE84357 | GEO

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