SHIP is a negative regulator of growth factor receptor-mediated PKB/Akt activation and myeloid cell survival
Q Liu, T Sasaki, I Kozieradzki, A Wakeham… - Genes & …, 1999 - genesdev.cshlp.org
Q Liu, T Sasaki, I Kozieradzki, A Wakeham, A Itie, DJ Dumont, JM Penninger
Genes & development, 1999•genesdev.cshlp.orgSHIP 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 …
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 …
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.
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