Figure 6

Model depicting Akt anti-apoptotic activity through regulation of IP₃R type III-Ca²⁺ transfer to mitochondria. During basal condition, when Akt activation is physiological, a Ca²⁺-dependent apoptotic stimulus evokes Ca²⁺ release from the ER, especially through isoform III, with consequent mitochondrial Ca²⁺ accumulation, fragmentation of the network and apoptosis. In situations with enhanced Akt activity, a typical condition of many cancers, subtype III is inhibited, therefore decreasing the amount of Ca²⁺ accumulated by mitochondria. The mitochondrial network remains undamaged and apoptosis is blocked