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.

Keywords

BiologyRegulatorMyeloidGrowth factorProtein kinase BCancer researchCell biologyNegative regulatorCell growthInternal medicineEndocrinologyReceptorSignal transductionBiochemistryMedicine

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Publication Info

Year
1999
Type
article
Volume
13
Issue
7
Pages
786-791
Citations
344
Access
Closed

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Qiang Liu, Takehiko Sasaki, I. Kozieradzki et al. (1999). SHIP is a negative regulator of growth factor receptor-mediated PKB/Akt activation and myeloid cell survival. Genes & Development , 13 (7) , 786-791. https://doi.org/10.1101/gad.13.7.786

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DOI
10.1101/gad.13.7.786