Class IA PI3K isoforms lead to differential signalling downstream of PKB/Akt

Abstract

The catalytic subunits of Class IA PI3K, p110α, p110β, and p110δ, phosphorylates phosphatidylinositol 4,5-bisphosphate (PIP2) into phosphatidylinositol 3,4,5-trisphosphate (PIP3) on the plasma membrane. In cancer, these catalytic subunits are usually found to be altered or amplified. Because pan-PI3K inhibition results in systemic toxicities, finding specific targets for the ubiquitous PI3K isoforms offers considerable potential for enhancing the effectiveness of PI3K-targeted therapy.

Keywords

• phosphoinositide 3-kinase
• protein kinase b
• mammalian target of rapamycin (mtor)
• cell cycle
• cytotoxicity