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. Author manuscript; available in PMC: 2011 Apr 1.
Published in final edited form as: Curr Opin Cell Biol. 2009 Dec 16;22(2):157–168. doi: 10.1016/j.ceb.2009.11.005

Figure 1. Mechanisms of signaling redundancy in the TOR pathway.

Figure 1

Multiple inputs regulate activity of the TOR/Raptor/Lst8 complex (TORC1) through redundant upstream signaling pathways. Interactions leading to activation of a downstream component are indicated by arrows; those that inhibit are indicated by a bar. The canonical Tsc1/Tsc2-dependent TOR pathway is indicated by the blue lines. Recently described Tsc1/Tsc2-independent signals are shown in red. Decreases in cellular energy level (ATP/AMP ratio) cause phosphorylation of Raptor by the AMP-dependent protein kinase, leading to 14-3-3 mediated inhibition of TORC1 [20]. In response to insulin and other growth factors, Akt phosphorylates and inactivates PRAS40 (not shown), an inhibitor of TORC1 [21–24]. Decreases in cellular oxygen levels lead to increased expression of hypoxia-induced genes, including Bnip3, which binds and inhibits the small GTPase Rheb [27].