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AKT, also referred to as PKB or Rac, plays a critical role in controlling survival and apoptosis. AKT is activated by phospholipid binding and activation loop phosphorylation at Thr308 by PDK1 and by phosphorylation within the carboxy terminus at Ser473.  AKT promotes cell survival by inhibiting apoptosis through phosphorylation and inactivation of several targets, including Bad, forkhead transcription factors, c-Raf, and caspase-9. Another essential AKT function is the regulation of glycogen synthesis through phosphorylation and inactivation of GSK-3α and β. AKT may also play a role in insulin stimulation of glucose transport. In addition to its role in survival and glycogen synthesis, AKT is involved in cell cycle regulation by preventing GSK-3β-mediated phosphorylation and degradation of cyclin D1 and by negatively regulating the cyclin dependent kinase inhibitors p27 Kip1 and p21 Waf1/Cip1.


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