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. Author manuscript; available in PMC: 2012 Feb 1.
Published in final edited form as: Future Med Chem. 2011 Apr;3(5):549–565. doi: 10.4155/fmc.11.12

Figure 2. The phosphinositide-3-kinase/Akt signaling pathway.

Figure 2

RTKs, activated in response to growth factor signaling, initiate PI3K signaling. Activated PI3K phosphorylates PIP2 to generate PIP3. Akt and PDK1 then bind to PIP3 via their PH domains and are localized to the plasma membrane. Akt is activated by phosphorylation of Thr-308 by PDK1 and Ser-473 by mTORC2. Activated Akt controls cell death and survival, cell cycle regulation, regulation of protein synthesis, angiogenesis and cell metabolism through activation or inhibition phosphorylations of many downstream substrates. Signaling is terminated when enzymes, such as PTEN, dephosphorylate PIP3.

4EBP1: Eukaryotic initiation factor 4E binding protein 1; Casp9: Caspase 9; FOXO: Forkhead family of transcription factor;

GSK3: Glycogen synthase kinase 3; mTORC: Mammalian target of rapamycin (mTOR) complex; P: Phosphate;

PDK1: Phosphoinositide-dependent kinase 1; PI3K: Phosphinositide-3-kinase; PIP2: Phosphatidylinositol-4–5-P2;

PIP3: Phosphatidylinositol-3–4–5-P3; PTEN: Phosphatase and tensin homolog; Rheb: Ras homolog enriched in brain;

RTK: Receptor tyrosine kinase; S6K1: p70S6 kinase; TSC: Tuberous sclerosis complex.