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Status |
Public on Jan 30, 2014 |
Title |
Genome wide maps of ZFX binding in human leukemia cell lines |
Organism |
Homo sapiens |
Experiment type |
Genome binding/occupancy profiling by high throughput sequencing
|
Summary |
Acute myeloid leukemia (AML) and acute T-lymphoblastic leukemia (T-ALL) maintain the undifferentiated phenotype and proliferative capacity of their respective cells of origin, hematopoietic stem/progenitor cells and immature thymocytes. The mechanisms that maintain these progenitor-like characteristics are poorly understood. We report that transcription factor Zfx is required for the development and propagation of experimental AML caused by MLL-AF9 fusion, and of T-ALL caused by Notch1 activation. In both leukemia types, Zfx activated progenitor-associated gene expression programs and prevented differentiation. Key Zfx target genes included mitochondrial enzymes Ptpmt1 and Idh2, whose overexpression partially rescued the propagation of Zfx-deficient AML. These studies identify a common mechanism that controls the cell-of-origin characteristics of acute leukemias derived from disparate lineages and transformation mechanisms.
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Overall design |
Analysis of genomic ZFX binding in the AML cell line NOMO-1 and the T-ALL cell line RPMI-8402
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Contributor(s) |
Weisberg SP, Reizis BV |
Citation(s) |
24485662 |
Submission date |
Dec 26, 2012 |
Last update date |
May 15, 2019 |
Contact name |
Stuart Weisberg |
E-mail(s) |
spw13@cumc.columbia.edu
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Organization name |
Columbia University
|
Department |
Pathology and Cell Biology
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Lab |
Weisberg
|
Street address |
650 W 168th Street
|
City |
New York |
State/province |
NY |
ZIP/Postal code |
10032 |
Country |
USA |
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Platforms (1) |
GPL11154 |
Illumina HiSeq 2000 (Homo sapiens) |
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Samples (4)
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This SubSeries is part of SuperSeries: |
GSE43022 |
ZFX controls the propagation and cell-of-origin characteristics of acute leukemia |
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Relations |
BioProject |
PRJNA184723 |
SRA |
SRP017686 |