| First Author | Liu Q | Year | 1999 |
| Journal | Genes Dev | Volume | 13 |
| Issue | 7 | Pages | 786-91 |
| PubMed ID | 10197978 | Mgi Jnum | J:77739 |
| Mgi Id | MGI:2182504 | Doi | 10.1101/gad.13.7.786 |
| Citation | Liu Q, et al. (1999) SHIP is a negative regulator of growth factor receptor-mediated PKB/Akt activation and myeloid cell survival. Genes Dev 13(7):786-91 |
| abstractText | SHIP is an inositol 5' phosphatase that hydrolyzes the PI3'K product PI(3,4,5)P3. We show that SHIP-deficient mice exhibit dramatic chronic hyperplasia of myeloid cells resulting in splenomegaly, lymphadenopathy, and myeloid infiltration of vital organs. Neutrophils and bone marrow-derived mast cells from SHIP-/- mice are less susceptible to programmed cell death induced by various apoptotic stimuli or by growth factor withdrawal. Engagement of IL3-R and GM-CSF-R in these cells leads to increased and prolonged PI3'K-dependent PI(3,4,5)P3 accumulation and PKB activation. These data indicate that SHIP is a negative regulator of growth factor-mediated PKB activation and myeloid cell survival. |
