fig 1 (IMAGE)
Caption
PI3K signaling pathways. Upon activation by RTK, GPCR, Integrin, and Ras, p110 loses inhibition by p85 and converts PIP2 to PIP3. PIP3 recruits AKT to the cell membrane, where AKT is activated through phosphorylation by PDK1 at T308 and by mTORC2 at S473. Activated AKT phosphorylates TSC1/2 and relieves its inhibition function on mTORC1, promoting protein translation. AKT also phosphorylates and inhibits GSK3β, initiating glucose metabolism and glycogen synthesis. AKT regulates the cell cycle by phosphorylating FoxO1 and decreasing its transcription of CDK inhibitors p21 and p27. AKT, protein kinase B; CDK, cyclin dependent kinase; FoxO1, forkhead box O1; GPCR, G-protein coupled receptor; GSK3β, glycogen synthase kinase 3β; mTORC1/2, mammalian target of rapamycin complex 1/2; PDK1, phosphoinositide-dependent kinase 1; PI3K, phosphoinositide 3-kinase; PIP2, phosphatidylinositol (4,5)-bisphosphate; PIP3, phosphatidylinositol (3,4,5)-trisphosphate; RTK, receptor tyrosine kinase; TSC1/2, tuberous sclerosis complex 1/2.
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