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. Author manuscript; available in PMC: 2014 Nov 4.
Published in final edited form as: J Clin Exp Pathol. 2012 May 17;Suppl 4:7327. doi: 10.4172/2161-0681.S4-002

Figure 2. Rapamycin.

Figure 2

Acute treatment with rapamycin directly inhibits mTORC1, blocking the phosphorylation of S6K1 and 4E-BP1. mTORC1 signaling causes feedback at the level of the insulin receptor, mediated in part by S6K through phosphorylation of IRS1/2 [163] and in part by Grb10 [164]and relieving this inhibition enhances insulin signaling to mTORC2. Chronic treatment with rapamycin inhibits mTORC2 indirectly, most likely by interfering with its the assembly [116] resulting in the decreased signaling to the mTORC2 substrates Akt, PKCα and SGK.