期刊
MOLECULAR CELL
卷 5, 期 1, 页码 189-195出版社
CELL PRESS
DOI: 10.1016/S1097-2765(00)80415-3
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资金
- NCI NIH HHS [CA74886, CA72614] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA072614, R01CA074886, R37CA072614] Funding Source: NIH RePORTER
The NF1 tumor suppressor gene encodes neurofibromin, a GTPase-activating protein (GAP) for p21(ras) (Ras). Children with NF1 are predisposed to juvenile myelomonocytic leukemia (JMML). Some heterozygous Nf1 mutant mice develop a similar myeloproliferative disorder (MPD), and adoptive transfer of Nf1-deficient fetal liver cells consistently induces this MPD. Human JMML and murine Nf1-deficient cells are hypersensitive to granulocyte-macrophage colony-stimulating factor (GM-CSF) in methylcellulose cultures. We generated hematopoietic cells deficient in both Nf1 and Gmcsf to test whether GM-CSF is required to drive excessive proliferation of Nf1(-/-) cells in vivo. Here we show that GM-CSF plays a central role in establishing and maintaining the MPD and that recipients engrafted with Nf1(-/-) Gmcsf(-/-) hematopoietic cells are hypersensitive to exogenous GM-CSF.
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