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AML1-ETO target genes

ABSTRACT: human CD34 cells isolated from cord blood or peripheral blood transduced with AML1-ETO or Empty vector (MIGR1) Keywords = AML1-ETO Leukemia Keywords: repeat sample

ORGANISM(S): Homo sapiens

PROVIDER: GSE2049 | GEO | 2005/03/01

SECONDARY ACCESSION(S): PRJNA91705

REPOSITORIES: GEO

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Gene expression data from human CD34+ cord blood cells infected with MIGR1, MIGR1-AML1-ETO or MIGR1-AML1-ETO∆NHR1

2011-07-19 | GSE28317 | GEO

Transcription profiling of human CD34 cells isolated from cord blood or peripheral blood transduced with AML1-ETO or empty vector (MIGR1)

Project description:Human CD34 cells isolated from cord blood or peripheral blood transduced with AML1-ETO or empty vector (MIGR1).

2007-08-30 | E-GEOD-2049 | biostudies-arrayexpress

Gene expression data from human CD34+ cord blood cells infected with MIGR1, MIGR1-AML1-ETO or MIGR1-AML1-ETO∆NHR1

Project description:Compare the gene expression profile among human CD34+ cord blood cells infected with MIGR1, MIGR1-AML1-ETO or MIGR1-AML1-ETO∆NHR1 AML1-ETO promotes the self-renewal of human hematopoietic stem/progenitor cells (HSPCs). We found deletion of NHR1 domain abrogates AML1-ETO induced expasion of HSPCs. GFP+CD34+ human cord blood cells were sorted by FACS 72 hours after the infection for RNA extraction and hybridyzation for Affymetrix microarrays.

2011-07-18 | E-GEOD-28317 | biostudies-arrayexpress

Transcription profiling of mouse bone marrow LSK cells transduced with wild type AML1/ETO or AML1/ETO harboring the W692A substitution in the MYND domain reveals a structural basis for recognition of SMRT/N-CoR by the MYND domain and its contribution to AML1/ETO activity

Project description:To examine the effects of disrupting the AML1/ETO MYND-SMRT interaction with the W692A substitution on AML1/ETO function, the global gene expression profile of mouse bone marrow LSK cells transduced with GFP was compared to that of cells transduced with either wild-type AML1/ETO or AML1/ETO harboring the W692A substitution in the MYND domain. Three independent biological replicates were assessed for both the control (GFP/MigR1) and AML1/ETO (intact MYND-SMRT interaction) conditions, whereas four independent biological replicates were assessed for the W692A (disrupted MYND-SMRT interaction) condition. The three GFP replicates were used to establish a baseline signal for comparison to both the AML1/ETO and W692A samples. Experiment Overall Design: Global gene expression profiles of FACS-sorted Lin-Sca1+cKit+ mouse bone marrow cells transduced with empty vector (GFP-MigR1), AML1/ETO, or AML1/ETO with the W692A substitution (W692A).

2008-06-15 | E-GEOD-7324 | biostudies-arrayexpress

FOXO1 is an oncogenic mediator in AML1-ETO leukemia

Project description:Transcriptome analysis by RNAseq of human CD34+ hematopoietic stem and progenitor cells transduced with empty vector control(MIT), AML1-ETO (AE), wildtype FOXO1 (F WT) or FOXO1 DNA binding deficient mutant (F DB). We find wildtype FOXO1 partially recapitulates gene signature of AML1-ETO

2017-12-15 | GSE81084 | GEO

Structural basis for recognition of SMRT/N-CoR by the MYND domain and its contribution to AML1/ETO's activity

2007-03-21 | GSE7324 | GEO

AML1-ETO transduced human cord blood cells, CD34 selected, compared to normal cord blood cells, CD34 selected

Project description:AML1-ETO expression in normal human umbilical cord blood CD34+ cells leads to long-term proliferation of an early self-renewing primitive progenitor cell with multilineage potential and stem cell ability, but these cells do not induce leukemia in immunodeficient mice. This comparative microarray study was initiated to determine the differences in the transcriptome of AML-ETO-expressing CD34+ cells after extended culture in vitro, using normal cord blood cells expanded for 6-8 weeks in vitro and subsequently purified for the CD34+ population as the control comparison. Keywords: Disease state analysis; comparison of changes in transcriptome due to long-term AML1-ETO expression in normal human hematopoietic CD34+ progenitor cells

2007-12-20 | GSE8023 | GEO

Binding pattern and chromatin modifications induced by AML1/ETO in human hematopoietic stem/progenitor cells

Project description:The AML1/ETO fusion protein, which is present in 10% to 15% of cases of acute myeloid leukemia, is known to repress myeloid differentiation genes through DNA binding and recruitment of chromatin-modifying proteins and transcription factors in target genes. ChIP-chip analysis of human hematopoietic stem/progenitor cells transduced with the AML1/ETO fusion gene enabled us to identify 1168 AML1/ETO target genes, 103 of which were co-occupied by HDAC1 and had lost the hyperacetylation at histone H4 marks and 264 of which showed a K9 trimethylation at histone H3. Enrichment of genes involved in hematopoietic differentiation and in specific signaling pathways was observed in the presence of these epigenetic modifications associated with an inactive chromatin status. Furthermore, AML1/ETO target genes had a significant correlation between the chromatin marks studied and transcriptional silencing. ChIP-chip comparison of human hematopoietic stem/progenitor cells (HSPCs) retrovirally transduced with the AML1/ETO fusion protein with HSPCs transduced with an empty vector (Mulloy et al., Blood, 2002) using antibodies tagging the AML1/ETO fusion protein, the HDAC1 protein, as well as H4Ac and H3K9m3 chromatin modifications.

2012-01-18 | E-GEOD-27663 | biostudies-arrayexpress

AML1/ETO, AML1, and HEB binding patterns on chromosme 19

Project description:Approximately 20% of Acute Myelogenous Leukemia (AML) cases carry the t(8;21) translocation, which involves the AML1 and ETO genes, and express the resulting AML1/ETO fusion protein that functions as a transcriptional repressor by recruiting NCoR/SMRT/HDAC complexes to DNA. We used ChIP-chip to identify the determinants of AML1/ETO binding on a contiguous DNA region (chromosome 19). AML1/ETO binding regions are characterized by a specific sequence signature that includes the presence of the consensus binding sites for the AML1 and HEB transcription factors. We therefore assessed the binding patterns of AML1 and HEB on chromosome 19. A specific chromatin modification (tri-methylation of lysine 4 on histone 3 = 3MetK4) was also studied in U937 cells expressing AML1/ETO in order to correlate the identified binding profiles with active transcription sites. Keywords: ChIP-chip A U937 cell line that conditionally expresses HA-tagged AML1/ETO under the control of the mouse metallothionine promoter (U937-A1E) (Alcalay et al., J.Clin.Invest, 2003,112, 1751-1761) was used. Cell lines were treated for 8h with 100uM ZnSO4 to induce transgene expression in U937-A1E. We performed ChIP using anti-HA, anti-ETO, anti-AML1/RUNX1, anti-HEBor anti-3MetK4 antibodies. ChIP products were then PCR amplified, labeled with Cy3/Cy5 fluorescent dyes and hybridized to the NimbleGen custom made NGS_HG17_Chr.19Array. U937-Mt cells, which carry the empty vector, served as control (C) for non-specific antibody binding. Each sample identifier indicates Antibody_Cell line (example: HA_A1E = ChIP using anti HA antibody in U937-A1E cells; HA_C = ChIP using anti HA antibody in U937-Mt control cells)

2008-11-27 | E-GEOD-10578 | biostudies-arrayexpress

AML1/ETO, AML1, and HEB binding patterns on chromosme 19

2008-11-28 | GSE10578 | GEO

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