AKT2
AKT2 is the second of the three AKT isoforms, distinguished by its dominant role in insulin-stimulated glucose metabolism.
Function
AKT2 shares the activation mechanism of AKT1 — membrane recruitment by PI3K-generated PIP3, phosphorylation by PDK1 and mTORC2 — and much of its substrate set, but its tissue distribution and knockout phenotype mark it as the insulin-response isoform. AKT2 knockout mice are insulin-resistant and diabetic, while AKT1 knockouts show growth defects; the two isoforms phosphorylate overlapping substrates with different efficiencies, and AKT2 dominates the GLUT4 trafficking route that moves glucose transporters to the muscle and fat cell membrane after a meal.
In cancer
AKT2 is amplified in a
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