| Literature DB >> 10197978 |
Q Liu1, T Sasaki, I Kozieradzki, A Wakeham, A Itie, D J Dumont, J M Penninger.
Abstract
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.Entities:
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Year: 1999 PMID： 10197978 PMCID： PMC316591 DOI： 10.1101/gad.13.7.786
Source DB: PubMed Journal: Genes Dev ISSN： 0890-9369 Impact factor: 11.361