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M110005200v1
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Papers In Press, published online ahead of print November 27, 2001
J. Biol. Chem, 10.1074/jbc.M110005200
Submitted on October 16, 2001
Revised on November 21, 2001
Accepted on November 27, 2001

Activation of SHIP by NADPH oxidase stimulated Lyn leads to enhanced apoptosis in neutrophils

Shyra J. Gardai, Ben B. Whitlock, Cheryl Helgason, Dan Ambruso, Valerie Fadok, Donna Bratton, and Peter M. Henson

Department of Pediatrics, National Jewish Medical and Research Center, Denver, CO 80206

Corresponding Author: Shyra.Gardai{at}UCHSC.edu

Neutrophils undergo rapid spontaneous apoptosis. Multiple anti-apoptotic stimuli can inhibit this process via activation of the Akt pathway. However, despite no such effect singly, combined anti- and pro-apoptotic stimuli inhibit Akt activity, leaving the cells susceptible to accelerated apoptosis. The blockade of Akt activation depended on reduced PI(3,4,5)P3 levels, but not decreased PI-3K activity thus implicating the involvement of an inositolphosphatase. Evidence for SHIP involvement was provided by SHIP localization to membrane receptors and subsequent activation along with the observed inability of SHIP -/- neutrophils to exhibit enhanced apoptosis with the stimulus combination. Activation of SHIP was found to depend on Lyn activation and this, in turn, required NADPH oxidase. Neutrophils from CGD patients and Lyn -/- mice no longer responded to the combined stimuli. Thus, we propose a role for oxidants and Lyn in SHIP regulation and suggest a novel mechanism for regulating neutrophil apoptosis.


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