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. Author manuscript; available in PMC: 2011 Jun 25.
Published in final edited form as: Immunity. 2010 Jun 25;32(6):743–753. doi: 10.1016/j.immuni.2010.06.002

Figure 2.

Figure 2

Impaired Akt phosphorylation and activity in rictor-deficient T cells. (A) T cell numbers from lymphoid organs of 6–8 week-old mice. Shown are mean (±SEM) numbers of cells of the indicated types (spleen and pooled lymph nodes of 8 WT and 8 cKO mice; *p < 0.05) (B) Previously activated CD4+ T cells were stimulated (40 min) with αCD3, αCD28, or both and analyzed by immunoblotting (as in Fig. 1A). Akt S473 and S6K1 T389 phosphorylation were normalized to amounts of unphosphorylated protein in the same sample, and then to amounts in WT CD4+ cells (bar graphs from one experiment representative of two complete replicates, with additional replicates of αCD3 + αCD28 vs control). (C, D) Decreased Akt enzymatic activity in T cells deficient for mTORC2. (C)) Akt activation loop (T308) phosphorylation in T cells lacking rictor (one result representative of two replicates with similar results). (D) A representative result assaying Akt kinase in extracts of WT and cKO CD4+ T cells. Cells were activated and restimulated as in (B); numbers represent quantified signals, normalized to the amounts of Akt in each sample and expressed as arbitrary light units with resting WT cells set as 1. Samples are as in (C). Additional information is in supplemental Fig. S1.