期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 104, 期 4, 页码 1260-1265出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0607894104
关键词
differentiation; transcriptional regulation; cell fate determination
资金
- NCI NIH HHS [R01 CA107429] Funding Source: Medline
- NIDDK NIH HHS [R01 DK52621, R01 DK52208, R01 DK052208, R01 DK052621] Funding Source: Medline
Appropriate hematopoietic stem cell (HSC) self-renewal reflects the tight regulation of cell cycle entry and lineage commitment. Here, we show that Id1, a dominant-negative regulator of E protein transcription factors, maintains HSC self-renewal by preserving the undifferentiated state. Id1-deficient HSCs show increased cell cycling, by BrdU incorporation in vivo, but fail to efficiently self-renew, leading to low steady-state HSC numbers and premature exhaustion in serial bone marrow transplant assays. The increased cycling reflects the perturbed differentiation process, because Id1 null HSCs more readily commit to myeloid differentiation, with inappropriate expression of myeloerythroid-specific genes. Thus, Id1 appears to regulate the fate of HSCs by acting as a true inhibitor of differentiation.
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