Figure 1.

Scheme of PI3K/AKT mediated antiapoptotic regulations at the mitochondria. AKT phosphorylated by PI3K activation. AKT phosphorylates and inhibits Bax and Bad (both are proapoptotic protein). AKT activates mTOR, which in turn phosphorylates and activates antiapoptotic protein MCL-1 (induced myeloid leukemia cell differentiation protein). AKT also activates NF-κB (nuclear factor kappa B), thus resulting in transcription of pro-survival gene Bcl-XL (B-cell lymphoma-extra large). AKT phosphorylates and inhibits proapoptotic protein Bax. NF-κB phosphorylates the X-linked inhibitor of apoptosis protein (XIAP), then binds to and inhibits caspases. Bim (Bcl-2 interacting mediator of cell death) and Noxa are the only proapoptotic BH-3 protein inhibited by FOXO3 protein (Forkhead box O3), phosphorylated by AKT in the PI3K signaling pathway.