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) .