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. Author manuscript; available in PMC: 2009 Apr 27.
Published in final edited form as: Mol Cell. 2008 Apr 25;30(2):214–226. doi: 10.1016/j.molcel.2008.03.003

Figure 7. Nutrients and Growth Factors control mTORC1 activity though common (TSC2) and unique (raptor, PRAS40) downstream targets.

Figure 7

Strikingly, both AMPK-mediated suppression of raptor and Akt-mediated suppression of PRAS40 involve the phosphorylation sites in each protein binding to 14-3-3, resulting in the inactivation of those targets. Inherited mutations in LKB1, TSC1. TSC2, and PTEN all result in hamartoma syndromes in humans indicating that hyperactivation of mTORC1 is a common biochemical mechanism underlying these genetic disorders.