Akt inhibitor

Akt antagonizes apoptotic signals by directly modifying or altering several key modulators involved in apoptosis signaling pathways. Phosphorylation activates CREB, which increases the transcription of anti-apoptotic genes Bcl-2, Mcl-2, and Akt itself. Phosphorylation of BAD induces interaction of BAD with 14-3-3 proteins, which are multifunctional phosphoserine binding molecules that are effectors of prosurvival signaling. This interaction prevents binding to Bcl-XL on the mitochondrial membrane and thereby suppresses apoptosis. Phosphorylation of IkB kinase-a increases its activity, resulting in phosphorylation of IκB , and targets it for degradation. This leads to nuclear translocation of transcription factor NF-κB , inducing transcription of pro-survival genes Bcl-XL, caspase inhibitors, and c-Myb as well as the expression of anti-apoptotic proteins such as cIAPl and cIAP2. Akt has also been reported to phosphorylate and stabilize a ubiquitously expressed cytosolic antiapoptotic protein PED/PEA-15.

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