Fig. (1).

Signalling through the phosphatidylinositol 3-kinase (PI3K) affects cell growth, apoptosis and cell cycle regulation. The PI3K/Akt related pathways have a key role in initiating intracellular signalling cascades subsequent to the activation of membrane tyrosine kinases. The PI3K phosphorylates phosphatidylinositol-biphosphates (PIP₂), generating phosphatidylinositol-triphosphates (PIP₃). PIP₃ act as docking sites for Akt and PDK at the plasma membrane. Upon phosphorylation by PDK, AKT becomes activated and phosphorylates in turn several downstream proteins, regulating cell growth, survival, apoptosis and cell cycle. PTEN, phosphatase and tensin homolog deleted on chromosome 10; PDK, phosphoinositide-dependent kinases; GSK3, glycogen synthase kinase-3; MDM2, murine double minute; FKHR, forkhead; NF-κB, nuclear factor κB; Rheb, Ras homologue enriched in the brain; TSC1, TSC2, tuberous sclerosis complex 1 and 2; mTOR, mammalian target of rapamycin; 4EBP1, eukaryotic translation initiation factor 4E binding protein; S6K, S6 kinase.