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Gene expression profile and DNA binding pattern of AML1/ETO in U937 cells

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE10537 | GEO | 2008/11/28

SECONDARY ACCESSION(S): PRJNA107891

REPOSITORIES: GEO

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Gene expression profile and DNA binding pattern of AML1/ETO in U937 cells

Project description:This SuperSeries is composed of the following subset Series: GSE10520: Genes regulated by AML1/ETO in U937 cells GSE10537: Gene expression profiling of AML1/ETO regulated genes and binding pattern on human promoters in U937 cells GSE10578: AML1/ETO, AML1, and HEB binding patterns on chromosme 19 GSE10579: Analysis of expression levels of genes on chromosome 19 in U937 cells expressing AML1/ETO Keywords: SuperSeries Refer to individual Series

2010-06-24 | E-GEOD-10537 | biostudies-arrayexpress

AML1-ETO induction and knockdown

Project description:This SuperSeries is composed of the SubSeries listed below.

2009-05-01 | GSE15648 | GEO

AML1/ETO binding pattern on human promoters

2008-12-22 | GSE10531 | GEO

U937 AML1-ETO inducible samples

Project description:U937 AML cells that express an inducible AML1-ETO construct under the control of the tetracycline promoter. Microarrays used to discover an AML1-ETO signature for a GE-HTS screen to identify AML1-ETO modulators.

2009-05-01 | GSE15647 | GEO

AML1/ETO binding pattern on human promoters

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 microarrays to identify human promoters bound by AML1/ETO in U937 cells. 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. Cells were treated for 8h with 100uM ZnSO4 to induce transgene expression, and ChIP was performed using an anti-HA antibody. ChIP products were then PCR amplified, labeled with Cy3/Cy5 fluorescent dyes and hybridized to the NimbleGen HG17 Human Promoter 2 Array set, which explores 4 kb upstream and 1 kb downstream the transcription start site (TSS) of 24,434 annotated genes. Two biological replicates were prepared and hybridized to independent array sets. U937-Mt cells, which carry the empty vector, served as control for non-specific binding of the anti-HA antibody.

2008-12-21 | E-GEOD-10531 | biostudies-arrayexpress

RUNX1/AML1 DNA-binding domain and ETO/MTG8 NHR2-dimerization domain are critical to AML1-ETO9a leukemogenesis.

Project description:The 8;21 translocation, which involves the gene encoding the RUNX family DNA-binding transcription factor AML1 (RUNX1) on chromosome 21 and the ETO (MTG8) gene on chromosome 8, generates AML1-ETO fusion proteins. Previous analyses have demonstrated that full-length AML1-ETO blocks AML1 function and requires additional mutagenic events to promote leukemia. More recently, we have identified an alternatively spliced form of AML1-ETO, AML1-ETO9a, from t(8;21) acute myeloid leukemia (AML) patient samples. AML1-ETO9a lacks the C-terminal NHR3 and NHR4 domains of AML1-ETO and is highly leukemogenic in the mouse model. Here, we report that the AML1 DNA-binding domain and the ETO NHR2-dimerization domain, but not the ETO NHR1 domain, are critical for the induction of AML by AML1-ETO9a. A region between NHR1 and NHR2 affects latency of leukemogenesis. These results provide valuable insight into further analysis of the molecular mechanism of t(8;21) in leukemogenesis.

| S-EPMC2630273 | biostudies-literature

AML1-ETO induces leukemia via C/D box snoRNA/RNPs.

Project description:This SuperSeries is composed of the SubSeries listed below.

2017-06-20 | GSE80602 | GEO

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

Project description:This SuperSeries is composed of the SubSeries listed below.

2016-07-04 | GSE81330 | GEO

Definition of a Small Core Transcriptional Circuit Regulated by AML1-ETO

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-12-31 | GSE153281 | GEO

AML1/ETO oncoprotein is directed to AML1 binding regions and co-localizes with AML1 and HEB on its targets.

Project description:A reciprocal translocation involving chromosomes 8 and 21 generates the AML1/ETO oncogenic transcription factor that initiates acute myeloid leukemia by recruiting co-repressor complexes to DNA. AML1/ETO interferes with the function of its wild-type counterpart, AML1, by directly targeting AML1 binding sites. However, transcriptional regulation determined by AML1/ETO probably relies on a more complex network, since the fusion protein has been shown to interact with a number of other transcription factors, in particular E-proteins, and may therefore target other sites on DNA. Genome-wide chromatin immunoprecipitation and expression profiling were exploited to identify AML1/ETO-dependent transcriptional regulation. AML1/ETO was found to co-localize with AML1, demonstrating that the fusion protein follows the binding pattern of the wild-type protein but does not function primarily by displacing it. The DNA binding profile of the E-protein HEB was grossly rearranged upon expression of AML1/ETO, and the fusion protein was found to co-localize with both AML1 and HEB on many of its regulated targets. Furthermore, the level of HEB protein was increased in both primary cells and cell lines expressing AML1/ETO. Our results suggest a major role for the functional interaction of AML1/ETO with AML1 and HEB in transcriptional regulation determined by the fusion protein.

| S-EPMC2577924 | biostudies-literature

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