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Growth factors can promote cell survival by activating the phosphatidylinositide-3'-OH
kinase and its downstream target, the serine-threonine kinase Akt. However, the mechanism
by which Akt functions to promote survival is not understood. We show that growth
factor activation of the PI3'K/Akt signaling pathway culminates in the phosphorylation
of the BCL-2 family member BAD, thereby suppressing apoptosis and promoting cell survival.
Akt phosphorylates BAD in vitro and in vivo, and blocks the BAD-induced death of primary
neurons in a site-specific manner. These findings define a mechanism by which growth
factors directly inactivate a critical component of the cell-intrinsic death machinery.