| First Author | Birnbaum RA | Year | 2000 |
| Journal | Mol Cell | Volume | 5 |
| Issue | 1 | Pages | 189-95 |
| PubMed ID | 10678181 | Mgi Jnum | J:60155 |
| Mgi Id | MGI:1352920 | Doi | 10.1016/s1097-2765(00)80415-3 |
| Citation | Birnbaum RA, et al. (2000) Nf1 and Gmcsf interact in myeloid leukemogenesis. Mol Cell 5(1):189-95 |
| abstractText | The NF1 tumor suppressor gene encodes neurofibromin, a GTPase-activating protein (GAP) for p21ras (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 play a central role in establishing and maintaining the MPD and that recipients engrafted with Nf1-/- Gmcsf-/- hematopoietic cells are hypersensitive to exogenous GM-CSF. |
