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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

SUBMITTER: Myriam Alcalay

PROVIDER: E-GEOD-10537 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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

Gardini Alessandro A Cesaroni Matteo M Luzi Lucilla L Okumura Akiko J AJ Biggs Joseph R JR Minardi Simone P SP Venturini Elisa E Zhang Dong-Er DE Pelicci Pier Giuseppe PG Alcalay Myriam M

PLoS genetics 20081128 11

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 transcriptio ...[more]

PMID: 19043539

Similar Datasets

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 binding pattern on human promoters

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

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.

2015-05-26 | E-GEOD-62847 | biostudies-arrayexpress

U937 AML1-ETO inducible samples

2009-05-01 | GSE15647 | GEO

Genes regulated by AML1/ETO in U937 cells

2008-11-28 | GSE10520 | GEO

Transcription profiling of human U937 expressing an inducible AML1-ETO construct - time series

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. Experiment Overall Design: U937 AML cells that express an inducible AML1-ETO construct under the control of the tetracycline promoter at 0, 12, 24, 48, and 72 hours and corresponding controls (2 replicates each).

2009-05-14 | E-GEOD-15647 | biostudies-arrayexpress

Transcription profiling of human U937 cells expressing AML1/ETO compared to vector transfected U937 cells to identify genes regulated by AML1/ETO

2009-01-13 | E-GEOD-10520 | biostudies-arrayexpress

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.

2013-06-20 | E-GEOD-43834 | biostudies-arrayexpress

AML1/ETO binding pattern on human promoters

2008-12-22 | GSE10531 | GEO

Analysis of expression levels of genes on chromosome 19 in U937 cells expressing AML1/ETO

2010-06-24 | E-GEOD-10579 | biostudies-arrayexpress