Figure 1.

Activation of PI3K-AKT pathway by external signals via G-protein coupled receptors (GPCR) or receptor tyrosine kinases (RTK) leads to dissociation of the p85 regulatory subunit from the active p110 PI3K subunit. The active subunit catalyses the conversion of PIP2 to PIP3 at the plasma membrane, leading to the recruitment and activation of the AKT kinase. Via multiple downstream effector pathways, cellular states of growth, proliferation, heightened metabolic activity and survival are promoted. For more details, see text.