Figure 3.

Localized Akt activity in cells. Membrane binding helps restrict Akt substrate specificity. On early endosomes, phosphorylation and inactivation of Gsk3β by Akt stimulates dynamin1-dependent clathrin-mediated endocytosis (CME). On lysosomes, phosphorylation of Tsc2 by Akt results in its dissociation and activation of mTORC1. Phosphorylation of GFAP by Akt on lysosomes promotes its dissociation from LAMP-2, thereby inhibiting chaperone-mediated autophagy (CMA). At the mitochondrial level, phosphorylation of hexokinase-II (HK2) by Akt induces HK2 binding to mitochondrial membrane and promotes cell survival.