期刊
NATURE MEDICINE
卷 6, 期 11, 页码 1278-1281出版社
NATURE AMERICA INC
DOI: 10.1038/81390
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资金
- NCI NIH HHS [R01-CA82308-01] Funding Source: Medline
- NHLBI NIH HHS [P50 HL54881] Funding Source: Medline
- NIAID NIH HHS [R01-AI47833-01] Funding Source: Medline
Hematopoietic stem cells give rise to progeny that either self-renew in an undifferentiated state or lose self-renewal capabilities and commit to lymphoid or myeloid lineages. Here we evaluated whether hematopoietic stem cell self-renewal is affected by the Notch pathway. Notch signaling controls cell fate choices in both invertebrates and vertebrates(1-7) by inhibiting certain differentiation pathways, thereby permitting cells to either differentiate along an alternative pathway or to self-renew(1). Notch receptors are present in hematopoietic precursors and Notch signaling enhances the in vitro generation of human and mouse hematopoietic precursors(8-15), determines T- or B-cell lineage specification from a common lymphoid precursor(16,17) and promotes expansion of CD8(+) cells(18-20). Here, we demonstrate that constitutive Notch1 signaling in hematopoietic cells established immortalized, cytokine-dependent cell lines that generated progeny with either lymphoid or myeloid characteristics both in vitro and in vivo. These data support a role for Notch signaling in regulating hematopoietic stem cell self-renewal. Furthermore, the establishment of clonal, pluripotent cell lines provides the opportunity to assess mechanisms regulating stem cell commitment and demonstrates a general method for immortalizing stem cell populations for further analysis.
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