Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery.
摘要：
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.
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关键词：
Animals Mice, Inbred BALB C Mice Neurons 3T3 Cells Serine Insulin-Like Growth Factor I Proto-Oncogene Proteins Signal Transduction Phosphorylation
DOI：
10.1016/S0092-8674(00)80405-5
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年份：
1997
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