PI3K-Akt pathway
On binding of ligand to receptor tyrosine kinases, the plasma-membrane-bound enzyme phosphoinositide 3-kinase (PI 3-kinase) is activated and converts phosphatidylinositol(3,4)-bis-phosphate (PIP2) to phosphatidylinositol(3,4,5)-trisphosphate (PIP3). PIP3 serves as a docking site for protein kinase B (PKB) (also called Akt). PKB is then phosphorylated and activated by mammalian target of rapamycin (mTOR) and the phosphoinositide-dependent kinase (PDK1). Activated PKB further brings about inhibition of apoptosis by phosphorylating Bad. PTEN, a phosphatase, acts as a negative regulator of the process, causing dephosphorylation of PIP3 to PIP2. Constitutive activation of PKB or inactivation of PTEN has been observed to be the cause for tumor generation in various cancers (Hemmings & Restuccia, 2012) .