Figure - PMC

Skip to main content

View full-text article in PMC

. Author manuscript; available in PMC: 2012 Jan 1.

Published in final edited form as: Mol Cancer Res. 2010 May 25;8(6):896–906. doi: 10.1158/1541-7786.MCR-09-0409

Characterization of the rictor Thr-1135 phosphorylation. A. The functional study of the rictor T1135 phosphorylation site. Reconstitution of the mTORC2 signaling in rictor null MEFs by expressing the wild type and phospho-rictor mutants (T1135A and T1135D). Following 48 hrs after transfection cells were lysed and cell extracts analyzed by immunoblotting for the indicated proteins and phosphorylation state of Akt on the Ser-473 site. B. The rapamycin-sensitive rictor phosphorylation does not require mTORC2. The wild type and Sin1 KO MEFs were serum starved overnight. As indicated the cells were stimulated by IGFI (50 ng/ml) for 20 min or treated with rapamycin (50 ng/ml) for 15 min prior stimulation of cells with the growth factor. The cells were lysed and analyzed as described in panel A.

Characterization of the rictor Thr-1135 phosphorylation. A. The functional study of the rictor T1135 phosphorylation site. Reconstitution of the mTORC2 signaling in rictor null MEFs by expressing the wild type and phospho-rictor mutants (T1135A and T1135D). Following 48 hrs after transfection cells were lysed and cell extracts analyzed by immunoblotting for the indicated proteins and phosphorylation state of Akt on the Ser-473 site. B. The rapamycin-sensitive rictor phosphorylation does not require mTORC2. The wild type and Sin1 KO MEFs were serum starved overnight. As indicated the cells were stimulated by IGFI (50 ng/ml) for 20 min or treated with rapamycin (50 ng/ml) for 15 min prior stimulation of cells with the growth factor. The cells were lysed and analyzed as described in panel A.