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. Author manuscript; available in PMC: 2015 Dec 1.
Published in final edited form as: Semin Cell Dev Biol. 2014 Sep 19;0:79–90. doi: 10.1016/j.semcdb.2014.09.011

Figure 1. Regulation of the mTORC1 and mTORC2 signaling network by diverse upstream inputs.

Figure 1

Growth factors such as insulin or EGF activate mTORC1 through either the PI3K-Akt or the Ras-MAPK (ERK)-RSK axes, respectively. Growth factor-mediated activation of mTORC1 absolutely requires sufficient levels of amino acids, which are sensed through a variety of factors, as indicated. mTORC1 action also requires sufficient levels of energy (i.e. ATP) and/or oxygen, which are sensed by AMPK, REDD1, and TCA cycle metabolites (i.e. αKG). The TSC complex integrates diverse upstream signals to regulate mTORC1 action. TSC suppresses the conversion of Rheb-GDP to Rheb-GTP, a small GTPase that activates mTORC1. mTORC1 phosphorylates a limited known set of bona fide substrates to drive anabolic and suppress catabolic cellular processes and to mediate negative feedback toward PI3K. Growth factors (i.e. insulin) also activate mTORC2 through poorly defined signaling intermediates.