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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

SUBMITTER: Jeffrey Zhao

PROVIDER: E-GEOD-28317 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The leukemogenicity of AML1-ETO is dependent on site-specific lysine acetylation.

Wang Lan L Gural Alexander A Sun Xiao-Jian XJ Zhao Xinyang X Perna Fabiana F Huang Gang G Hatlen Megan A MA Vu Ly L Liu Fan F Xu Haiming H Asai Takashi T Xu Hao H Deblasio Tony T Menendez Silvia S Voza Francesca F Jiang Yanwen Y Cole Philip A PA Zhang Jinsong J Melnick Ari A Roeder Robert G RG Nimer Stephen D SD

Science (New York, N.Y.) 20110714 6043

The chromosomal translocations found in acute myelogenous leukemia (AML) generate oncogenic fusion transcription factors with aberrant transcriptional regulatory properties. Although therapeutic targeting of most leukemia fusion proteins remains elusive, the posttranslational modifications that control their function could be targetable. We found that AML1-ETO, the fusion protein generated by the t(8;21) translocation, is acetylated by the transcriptional coactivator p300 in leukemia cells isola ...[more]

PMID: 21764752

Similar Datasets

Genome-wide studies identify a novel interplay between AML1 and AML1/ETO in t(8;21) acute myeloid leukemia

Project description:The AML1/ETO fusion protein is essential to the development of acute myeloid leukemia (AML), and is well recognized for its dominant-negative effect on the co-existing wild-type protein AML1. However, the involvement of wild-type AML1 in AML1/ETO-driven leukemogenesis remains elusive. Through chromatin immunoprecipitation sequencing, computational analysis plus a series of experimental validations, we report here that AML1 is able to orchestrate the expression of AML1/ETO targets regardless of being activated or repressed, via forming a complex with AML1/ETO and via recruiting the cofactor. 4 ChIP-seq assays were used to identify the high confidence binding regions of AML1-ETO and AML1 in t(8;21) AML Kasumi-1 cell lines. The anti-AML1 (N20) antibody targets the N-terminus of AML1 and recognizes both AML1 and AML1/ETO; the anti-AML1 (C19) antibody targets the C-terminus of AML1 and recognizes AML1 but not AML1/ETO; the anti-ETO (C20) antibody targets the C-terminus of ETO and specifically recognizes AML1/ETO. 2 ChIP-seq assays were used to identify the binding regions of AML1 in human macrophage U937 cell lines. And the total input was used as control.

2015-11-04 | E-GEOD-65427 | biostudies-arrayexpress

AML1-ETO target genes

Project description: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

2005-03-01 | GSE2049 | GEO

AML1-ETO induced leukemia stem cell self-renewal depends on Plcg1

Project description:High-resolution proteomic analysis of acute myeloid leukemia (AML) stem cells identified phospholipase C- and Ca++-signaling pathways to be differentially regulated in AML1-ETO (AE) driven leukemia. Phospholipase C gamma 1 (Plcg1) could be identified as a direct target of the AE fusion. Genetic Plcg1 inactivation abrogated disease initiation by AE, reduced intracellular Ca++-release and inhibited AE-driven self-renewal programs. In AE-induced leukemia, Plcg1 deletion significantly reduced disease penetrance, number of leukemia stem cells and abrogated leukemia development in secondary recipient hosts. In human AE-positive leukemic cells inactivation of Plcg1 reduced colony formation and AML development in vivo. In contrast, Plcg1 was dispensable for maintenance of murine and human hematopoietic stem- and progenitor cells (HSPCs). Pharmacologic inhibition of Ca++-signaling downstream of Plcg1 resulted in impaired proliferation and self-renewal capacity in AE-driven AML. Thus, the Plcg1 pathway represents a novel specific vulnerability of AE-driven leukemia and poses an important new therapeutic target.

2022-01-12 | PXD011251 | Pride

RNAi profiling of human Kasumi-1 AML1-ETO knockdown samples

Project description:Kasumi-1 AML cells that were transfected in triplicate with AML1-ETO or luciferase siRNA constructs by either Amaxa nucleofection or Biorad siLentFect and incubated for 96 hours. Microarrays used to discover an AML1-ETO signature for a GE-HTS screen to identify AML1-ETO modulators. Experiment Overall Design: Kasumi-1 AML cells incubated for 96 hours after they were transfected in triplicate with AML1-ETO or luciferase siRNA constructs by either Amaxa nucleofection or Biorad siLentFect along with three control samples not transfected with a construct.

2009-05-11 | E-GEOD-15646 | biostudies-arrayexpress

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 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

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

Transcription profiling and RNAi of human Kasumi-1 AML cell line and U937 cell lines - AML1-ETO induction and knockdown

Project description:This SuperSeries is composed of the following subset Series:; GSE15646: Kasumi-1 AML1-ETO knockdown samples; GSE15647: U937 AML1-ETO inducible samples Experiment Overall Design: Refer to individual Series

2009-05-08 | E-GEOD-15648 | 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

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

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