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. Author manuscript; available in PMC: 2013 Jan 1.
Published in final edited form as: Methods Mol Biol. 2012;821:349–359. doi: 10.1007/978-1-61779-430-8_22

Fig. 1.

Fig. 1

The allosteric mTORC1 inhibitor rapamycin induced p-Akt in glioma cells. PTEN mutant-type U87:MG and U373:MG cells were treated with rapamycin at doses shown and were assayed for total and phospho Akt and rpS6 by immunoblot. Rapamycin blocked p-rpS6 in both cell lines at a dose of 0.5 nM. Activation of Akt was dose-dependent, as indicated by increased levels of the p-Akt at Ser-473. β-tubulin is shown as loading control.