Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mus musculus

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

OTHER RELATED OMICS DATASETS IN: E-GEOD-34961E-GEOD-34959

PROVIDER: PRJNA156137 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Similar Datasets

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

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

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

Mus musculus

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

| PRJNA156135 | ENA

E-GEOD-34959

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

2015-09-22 | E-GEOD-34959 | ExpressionAtlas

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

2012-02-22 | GSE34961 | GEO

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. 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.

2012-02-22 | E-GEOD-34962 | 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

Hes1 is responsible for Notch signaling-mediated suppression of acute myeloid leukemia development

Project description:In leukemogenesis Notch signaling can be up- and down-regulated in a context-dependent manner. Here we report that deletion of hairy and enhancer of split-1 (Hes1) promotes acute myeloid leukemia (AML) development induced by the MLL-AF9 fusion protein. Subsequently, the FMS-like tyrosine kinase 3 (FLT3) was up-regulated in mouse cells of a Hes1- or RBP-J-null background. MLL-AF9-expressing Hes1-null AML cells showed enhanced proliferation and ERK phosphorylation following FLT3 ligand stimulation. FLT3 inhibition efficiently abrogated proliferation of MLL-AF9-induced Hes1-null AML cells. Furthermore, an agonistic anti-Notch2 antibody induced apoptosis of MLL-AF9-induced AML cells in a Hes1-wild type but not a Hes1-null background. These observations demonstrate that Hes1 mediates tumor suppressive roles of Notch signaling in AML development by down-regulating FLT3 expression. 4 samples are analyzed, two pairs of MLL-AF9/Hes1-/- and MLL-AF9/Hes1+/+ leukemic bone marrows.

2017-05-02 | E-GEOD-50234 | biostudies-arrayexpress

Hes1 is responsible for Notch signaling-mediated suppression of acute myeloid leukemia development

2017-05-02 | GSE50234 | GEO