Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mus musculus

ABSTRACT: Eed inactivation in Cdkn2a-null MLL-AF9 transformed cells

PROVIDER: PRJNA289896 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR2102380.fastq.gz	Fastqsanger.gz
	SRR2102381.fastq.gz	Fastqsanger.gz

Items per page:

1 - 2 of 2

Similar Datasets

PRC2 is required for acute myeloid leukemias initiated by MLL-AF9

Project description:The transcriptional activating and repressive functions performed by Trithorax and Polycomb group complexes, respectively, are critical for to maintain cellular fates in ontogeny and in cancer. Here we report that leukemias initiated by a Trithorax-related oncogene, MLL-AF9, depend upon the Polycomb Repressive Complex 2 (PRC2) to sustain a transformed cellular state. RNAi mediated suppression of PRC2 subunits is sufficient to inhibit proliferation of MLL-AF9 leukemias, with little impact on growth of non-transformed cells. This requirement is partly due to PRC2-mediated transcriptional repression of several anti-self-renewal regulators, including Cdkn2a. These results suggest that, unlike the classical antagonism generally observed between Polycomb and Trithorax group proteins during development, the activities of these two pathways can cooperate to promote myeloid neoplasia. In order to understand downstream targets of PRC2 complex in MLL-AF9 leukemia, we performed array in murine MLL-AF9/NrasG12D cell line under the condition that two subunits of PRC2(Eed and Suz12) were suppressed by using shRNAs.

2013-07-01 | E-GEOD-34183 | biostudies-arrayexpress

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

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

Eed inactivation in Cdkn2a-null MLL-AF9 transformed cells

Project description:We sequenced mRNA from MLL-AF9 transformed Cdkn2ako murine LSK-cells with and without a functional Eed locus

2015-07-15 | GSE70904 | GEO

Mus musculus

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

| PRJNA156135 | ENA

Expression data of MLL-AF9-transformed murine leukemia progenitor cells, following treatment with UNC1999, a dual Ezh1 and Ezh2 inhibitor, or knockdown of EED

Project description:Ezh2 and EZH1 are histone H3 lysine 27 specific methyltransferase. Their hyperactive mutations and overexpression were found in cancer including various hematological malignancies. UNC1999 is a highly selective inhibitor for both enzymes. It suppresses H3K27 tri- and di-methylation globally and inhibits growth of MLL-rearranged acute leukemia cell lines. UNC2400, a di-methylated derivative of UNC1999, is employed an inactive analog compound for assessment of off-target effects. EED knockdown was used to demonstrate gene targets of PRC2. Here we performed microarray analysis in MLL-AF9 transformed acute leukemia cells following treatment with DMSO, UNC2400 or UNC1999, or after induction of EED shRNA (Renilla shRNA as control). This study allows us to identify UNC1999-responsive gene signatures as well as their overlap with PRC2 targets in MLL-AF9-bearing leukemia cells. We analyzed 5 of DMSO-treated, 5 of UNC2400 (inactive analog of UN1999)-treated, and 6 of UNC1999-treated MLL-AF9 leukemia cell samples to identify UNC1999-responsive gene signatures. We also performed microarray in 3 of shRNA control lines (Renilla or Ren) and 3 of shEED lines to identify downstream targets of PRC2 complex in MLL-AF9 leukemia cells.

2014-10-10 | E-GEOD-62198 | biostudies-arrayexpress

Expression data of MLL-AF9-transformed murine leukemia progenitor cells, following treatment with UNC1999, a dual Ezh1 and Ezh2 inhibitor, or knockdown of EED

2014-10-10 | GSE62198 | GEO

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

2012-02-22 | GSE34959 | GEO

Maintenance of Leukemic Cell Identity by the Activity of the Polycomb Complex PRC1 (ChIP-seq)

Project description:These data include the genome wide occupancy of H2AUbq by ChIP sequencing in Cdkn2a-/- Lin- HSC cells non-transduced or transduced with MLL-AF9, HOXA9 and PML-RARa. Immuno-precipitation of formaldehyde cross-linked chromatin prepared from Cdkn2a-/- Lin- HSC cells non-transduced or transduced with MLL-AF9, HOXA9 and PML-RARa using H2AK119Ubq antibody.

2016-10-21 | E-GEOD-67498 | biostudies-arrayexpress

Maintenance of Leukemic Cell Identity by the Activity of the Polycomb Complex PRC1 (RNA-seq)

Project description:These data include RNA Seq data generated from Ring1b wild type and Ring1b KO Ring1a-/- Cdkn2a-/- Lin- HSC cells non-transduced or transduced with MLL-AF9, HOXA9 and PML-RARa. Total RNA extracted from Ring1b wild type and Ring1b KO Ring1a-/- Cdkn2a-/- Lin- HSC cells non-transduced or transduced with MLL-AF9, HOXA9 and PML-RARa.

2016-10-21 | E-GEOD-67517 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

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