Figure 2.

The activation of the mechanistic target of rapamycin (mTOR). Growth factor-mediated activation of the phosphatidylinositol 3-kinase (PI3K) pathway leads to the membrane recruitment and activation of phosphoinositide-dependent kinase 1 (PDK1) and Akt, which then phosphorylates and inactivates the tuberous sclerosis complex (TSC1/2), a negative regulator of ras homolog enriched in brain (Rheb), ultimately resulting in the activation of mTOR within complex 1. mTORC1 mediates its downstream effects primarily via the inhibition of eukaryotic translation initiation factor 4E (eIF4E)-binding protein 1 (4E-BP1) and the activation of S6 kinase (S6K).