Journal
CANCER CELL
Volume 9, Issue 3, Pages 175-187Publisher
CELL PRESS
DOI: 10.1016/j.ccr.2006.02.017
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Funding
- NCI NIH HHS [KO1-CA099156] Funding Source: Medline
- NIDDK NIH HHS [R01 DK52208] Funding Source: Medline
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The transcriptional circuitry that regulates the quiescence of hematopoietic stem cells is largely unknown. We report that the transcription factor known as MEF (or ELF4), which is targeted by the t(X;21)(q26;q22) in acute myelogenous leukemia, regulates the proliferation of primitive hematopoietic progenitor cells at steady state, controlling their quiescence. Mef null HSCs display increased residence in Go with reduced 5-bromodeoxyuridine incorporation in vivo and impaired cytokine-driven proliferation in vitro. Due to their increased HSC quiescence, Mef null mice are relatively resistant to the myelosuppressive effects of chemotherapy and radiation. Thus, MEF plays an important role in the decision of stem/primitive progenitor cells to divide or remain quiescent by regulating their entry to the cell cycle.
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