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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Epigenetic profiling of WT and Ezh2-null MLL-AF9 murine leukemic cells

ABSTRACT: Chromatin immunoprecipitation (ChIP) for H3K27me3 followed by Solexa sequencing in WT and Ezh2-null leukemic cells from primary and secondary recipients. Leukemic cells from primary and secondary recipients of MLL-AF9-transduced WT and Ezh2-null cells were sorted for GFP and YFP expression and analyzed by Chip-Seq.

ORGANISM(S): Mus musculus

SUBMITTER: Amit Sinha

PROVIDER: E-GEOD-34962 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The Polycomb Repressive Complex 2 Is Required For MLL-AF9 Leukemia

Project description:This SuperSeries is composed of the following subset Series: GSE34959: Expression profiling of primary wild type (WT), Ezh2-null and Eed-null murine MLL-AF9 AML GSE34961: Expression profiling of secondary wild type (WT) and Ezh2-null murine MLL-AF9 AML GSE34962: Epigenetic profiling of WT and Ezh2-null MLL-AF9 murine leukemic cells Refer to individual Series

2012-02-22 | E-GEOD-34963 | biostudies-arrayexpress

Epigenetic profiling of WT and Ezh2-null MLL-AF9 murine leukemic cells

Project description:Chromatin immunoprecipitation (ChIP) for H3K27me3 followed by Solexa sequencing in WT and Ezh2-null leukemic cells from primary and secondary recipients.

2012-02-22 | GSE34962 | GEO

Expression profiling of secondary wild type (WT) and Ezh2-null murine MLL-AF9 AML

Project description:We evaluated gene expression changes in secondary recipient murine leukemia caused by retroviral overexpression of MLL-AF9. We compared wild-type (WT) leukemia cells with mutant leukemia cells after cre-mediated inactivation of a homozygous conditional allele for Ezh2, a component of the Polycomb Repressive Complex2. For WT cells, 4 biological replicates were hybridized. For Ezh2-null cells, 5 biological replicates were hybridized.

2012-02-22 | E-GEOD-34961 | biostudies-arrayexpress

Expression profiling of primary wild type (WT), Ezh2-null and Eed-null murine MLL-AF9 AML

Project description:We evaluated gene expression changes in murine leukemia caused by retroviral overexpression of MLL-AF9. We compared wild-type (WT) leukemia cells with mutant leukemia cells after cre-mediated inactivation of homozygous conditional alleles for Ezh2 or Eed, both of which are components of the Polycomb Repressive Complex2. For WT cells, 3 biological replicates were hybridized. For Ezh2-null cells, 4 biological replicates were hybridized. For Eed-cells, 3 biological replicates were hybridized.

2012-02-22 | E-GEOD-34959 | biostudies-arrayexpress

Expression profiling of secondary wild type (WT) and Ezh2-null murine MLL-AF9 AML

2012-02-22 | GSE34961 | GEO

Mus musculus

Project description:Epigenetic profiling of WT and Ezh2-null MLL-AF9 murine leukemic cells

| PRJNA156139 | ENA

Mus musculus

Project description:Expression data from Ezh2-null leukemic cells

| PRJNA148129 | ENA

E-GEOD-34961

Project description:Expression profiling of secondary wild type (WT) and Ezh2-null murine MLL-AF9 AML

2015-09-22 | E-GEOD-34961 | ExpressionAtlas

ChipSeq of MLL1 in mouse leukemic blast cells

Project description:We performed a chip-seq to determine the binding of MLL1 in mouse leukemic blast cells transduces with MLL-AF9 fusion MLL1 chip-seq in mouse leukemic blast cells

2012-02-22 | E-GEOD-34261 | biostudies-arrayexpress

RNA-seq analysis of Men1-/- versus Men1wt MN1-driven AML

Project description:Purpose: To characterize transcriptional changes associated with homozygous inactivation of Men1 in MN1 driven AML Methods: In vivo MN1 transformed cells were transduced with Cre-vector to inactivate Men1 and injected into sublethially irradiated syngeneic recipients. Men1-/- and Men1wt MN1-driven leukemic cells were isolated from moribund recipients and plated in methylcellulose for 7 days before RNA was extracted. Results: Men1-/- MN1-driven leukemic cells failed to propagate leukemia in most secondary recipients, in comparison with Men1wt MN1-driven. In vitro, cells had lost their colony forming activity. Gene expression analysis revealed a downregulation of the MN1 leukemic expression program. Conclusions: Men1 regulates long term maintenance of MN1-driven leukemia.

2020-05-09 | GSE150151 | GEO

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