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

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

Mus musculus

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

| PRJNA156135 | ENA

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data