Phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathway becomes activated via stimulation of receptor tyrosine kinases (RTKs) and the assembly of receptor–PI3K complexes

The phosphatidylinositol 3-kinase-Akt (PI3K-Akt) pathway becomes activated via stimulation of receptor tyrosine kinases (RTKs) and the assembly of receptor–PI3K complexes. The complex then catalyses the conversion of PIP2 to PIP3. PIP3 then helps to activate AKT. Activated AKT then mediates the activation and inhibition of several targets, including GSK3β, glycogen synthase kinase-3β; mTOR, mammalian target of rapamycin; and NF-κB, nuclear factor of κB resulting in cellular growth, metabolism, and survival.Reprinted by permission from Macmillan Publishers Ltd: Vivanco I, Sawyers C. The phosphatidylinositol 3-Kinase AKT pathway in human cancer. Nat Rev Cancer 2002;2(7):489–501.

Publication

Signaling Mechanisms in Neuroendocrine Tumors as Targets for Therapy. () Barbara Zarebczan, et al. Endocrinol Metab Clin North Am. ;39(4):801-810. Figure: F1. All organisms Homo sapiens Mus musculus Drosophila melanogaster Danio rerio

Disease mentions