Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery

Experiment was conducted to examine the hypothesis that the Pl3'K/Akt pathway may result in BAD phosphorylation and may, thus, suppress cell death and promote cell survival. Growth factors can promote cell survival by activating the phosphatidylinositide-3'-OH kinase and its downstream target, the serine-threonine kinase Akt but the mechanism by which Akt functions need to be examined. Akt phosphorylates BAD in vitro and in vivo, and blocks the BAD-induced death of primary neurons. Results suggest a mechanism by which growth factors inactivate a vital component of cell-death machinery.