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MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [RNA-Seq human]

ABSTRACT: MEIS2 collaborates with AML1-ETO in inducing acute myeloid leukemia in a murine bone marrow transplantation model RNA-seq to evaluate consequence of MEIS2 Knock-down on the transcriptional profle of the t(8;21) positive Kasumi-1 cell line

ORGANISM(S): Homo sapiens

SUBMITTER: Medhanie Mulaw

PROVIDER: E-GEOD-81328 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [RNA-Seq mouse]

Project description:MEIS2 collaborates with AML1-ETO in inducing acute myeloid leukemia in a murine bone marrow transplantation model We employed RNA-seq to assess similarities/differences among murine leukemic bone marrow samples transduced with either AML1-ETO/Meis2, AML1-ETO9a/Meis2, or AML1-ETO9a

2016-07-04 | E-GEOD-81329 | biostudies-arrayexpress

MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [Affymetrix]

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MEIS2 is a novel oncogenic partner in AML1-ETO positive AML [Affymetrix]

Project description:MEIS2 collaborates with AML1-ETO in inducing acute myeloid leukemia in a murine bone marrow transplantation model We compared Gene expression profile (GEP) of murine bone marrow cells transduced with GFP, AML1-ETO, MEIS2, and AML1-ETO/MEIS2. Data from MEIS1 and AML1-ETO/MEIS1 is also included. Mouse bone marrow cells were kept in culture for 48hrs after retroviral transduction. GFP positive cells were then sorted and cells were kept for further 24 hours in culture before microarray analysis.

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MEIS2 is a novel oncogenic partner in AML1-ETO positive AML

Project description:MEIS2 is a novel oncogenic partner in AML1-ETO positive AML

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A Stable Transcription Factor Complex Nucleated by Dimeric AML1-ETO Controls Leukaemogenesis

Project description:AML1-ETO, a fusion protein generated by the t(8;21) translocation in acute myeloid leukemia, is a transcription factor implicated in both gene repression and activation. We now show that, in leukemic cells, AML1-ETO resides in and functions through a stable protein complex (AETFC) that contains several hematopoietic transcription factors and cofactors. In conjunction with biochemical and leukemia pathological studies, the ChIP-seq and RNA-seq analyses of the AETFC components in leukemic cells reveal that these components stabilize the complex through multivalent interactions, provide multiple DNA-binding domains for diverse target genes, colocalize genome-wide, cooperatively regulate gene expression, and contribute to leukemogenesis. RNA-seq analyses gene expression upon knockdown of each AETFC component, including AML1-ETO, HEB, E2A, LYL1, LDB1 and LMO2, and double-knockdown of HEB and E2A, in Kasumi-1 cells. ChIP-seq analyses of four AETFC components, namely AML1-ETO, HEB, E2A and LMO2, in Kasumi-1 cells.

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Stability of the neuronal fate determinant MEIS2 is controlled by calpain2

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Genome-wide co-occupancy of AML1-ETO and N-CoR defines the t(8;21) AML signature in leukemic cells

Project description:This study characterizes the genome-side occupancy of AML1, AML1-ETO and the cofactors N-CoR and p300 in leukemics cells (Kasumi-1) to discover novel regulatory mechanisms involving genes bound by the t(8:21) fusion protein AML1-ETO. A significant discovery of our study is the co-localization of AML1-ETO with the N-CoR co-repressor on genomic regions that are primarily distal to the transcriptional start sites (TSSs). These regions exhibit over-representation of the PU.1 motif: PU.1 is a key hematopoietic regulator and member of the ETS family of transcription factors. Functionally, genes co-occupied by AML1-ETO and N-CoR (e.g., TYROBP and LAPTM5) are associated with the leukemic phenotype, as determined by analyses of gene ontology and by the observation that these genes are predominantly up-regulated upon AML1-ETO depletion. To further probe the regulatory context of these leukemic cells, genome-wide enrichment of the transcriptional initiation-associated histone modification H3K4me3 was also measured. Genome-wide study of transcription factor-DNA binding for AML1 (RUNX1) and the t(8;21) fusion protien AML1-ETO (RUNX1T1) in the Kasumi-1 leukemia cell line. The genome-wide binding of the disease-related cofactors N-CoR and p300 was assayed, along with enrichments of the H3K4me3 and H3K27me3 histone modifications.

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