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Vol. 13, No. 7, pp. 786-791, April 1, 1999
1 Amgen Institute, Toronto, Ontario, Canada M5G 2C1;
Departments of 2 Immunology, and 3 Department of Medical
Biophysics, University of Toronto, Toronto, Ontario, Canada
M5G 2C1; 4 Sunnybrook Hospital and Women's College Health
Science Center, Toronto, Canada, M4N 3M5
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.
[Key Words: SHIP; inositol phosphatase; PKB/Akt; cell survival; myeloid cells]
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