Abstract:
: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.
journal_name
Celljournal_title
Cellauthors
Datta SR,Dudek H,Tao X,Masters S,Fu H,Gotoh Y,Greenberg MEdoi
10.1016/s0092-8674(00)80405-5subject
Has Abstractpub_date
1997-10-17 00:00:00pages
231-41issue
2eissn
0092-8674issn
1097-4172pii
S0092-8674(00)80405-5journal_volume
91pub_type
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