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. Author manuscript; available in PMC: 2012 Apr 11.
Published in final edited form as: Science. 2012 Mar 30;335(6076):1638–1643. doi: 10.1126/science.1215135

Figure 2.

Figure 2

Disruption of mTORC2 in vivo after chronic rapamycin treatment. A, B) Effects of rapamycin on phosphorylation of PKCα, Akt, and the SGK substrate NDRG1 in liver in response to re-feeding (A) or insulin (B) after an overnight fast. C, D) Effects of rapamycin on phosphorylation of PKCα and Akt in response to re-feeding in white adipose tissue (C) and muscle (D). E-G) Effects of rapamycin on the integrity of mTORC1 and mTORC2. mTOR was immunoprecipitated from liver (E), skeletal muscle (F), and white adipose tissue (G), followed by immunoblotting for Raptor and Rictor (subunits of mTORC1 and mTORC2, respectively).