The PI3K/Akt/mTOR signaling pathway is a key regulator in growth, survival, cell cycle proliferation, protein synthesis and glucose metabolism. Growth factors, hormones, and cytokines can activate this pathway by binding their cognate receptor tyrosine kinase (RTK), cytokine receptor, or GPCR, resulting in the activation of lipid kinase PI3K which produces PIP3 at the plasma membrane.
The binding of PIP3 translocates Akt to cell membranes, enables Akt activation through phosphorylation at Thr308 mediated by phosphoinositide dependent kinase 1 (PDK1). In addition, Akt is phosphorylated at Ser473 by the mTOR-rictor complex, mTORC2. PTEN is a negative regulator of Akt signaling that reverses the function of PI3K by removing 3’-phosphate groups. Akt activity is also negatively regulated by the phosphatases PP2A and PHLPP. Akt propagates its signal to affect DNA transcription, cell cycle and apoptosis. Akt can activate mTOR directly by phosphorylation or indirectly, by phosphorylation and inactivation of mTOR inhibitor TSC2 and PRAS40. Together these mechanisms stimulate cell growth and G1 cell cycle progression through signaling via p70 S6 Kinase and inhibition of 4E-BP1. Defects in PI3K/AKT/mTOR signaling are implicated in cancer, diabetes and cardiovascular disease etc.
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- B5246 740 Y-P5 CitationTarget: PI3KSummary: PI 3-kinase activator,cell permeable
- B4660 PI-3065Target: PI3KSummary: P110δkinase inhibitor
- B1374 WZ4003Target: NUAK1|NUAK2Summary: NUAK1/2 inhibitor, potent and selective
- C5867 Akt Inhibitor IV
- A8764 Rapalink-1Target: mTORSummary: third-generation mTOR inhibitor
- B7826 GDC-0084Summary: PI3K and mTOR inhibitor, brain-permeable
- C5645 3-Guanidinopropionic AcidSummary: AMPK stimulator
- C5216 NG,NG-dimethyl-L-Arginine (hydrochloride)1 CitationSummary: endogenous nitric oxide synthase inhibitor
- B7875 Adenosine 5-monophosphateSummary: 5'-AMP-activated protein kinase
- C5053 KP372-1Summary: specific Akt inhibitor