Figure 3. The Phosphatidylinsoitol-3 kinase (PI3K)-Akt Signaling Pathway.

PI3K is activated by binding of growth factors (GF) to a receptor tyrosine kinase (RTK) through direct interaction or adapter molecules. PIP₂ is then phosphorylated by PI3K to form PIP₃, which then engages Akt and PDK1 resulting in phosphorylation of Akt (either directly or by PDK1). Activated Akt then stimulates pathways involved in cell growth and protein synthesis (mTOR), activates pro-survival molecules (NF-κB), and inhibits pro-apoptotic molecules (FOXO, Bad, p53) thereby promoting cell survival and proliferation. PTEN negatively regulates PI3K-Akt signaling.