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. 2005 Jul;25(14):5834–5845. doi: 10.1128/MCB.25.14.5834-5845.2005

FIG. 3.

FIG. 3.

REDD1 is not required for AKT or AMPK activation. (A) AMPK (T172) is phosphorylated following AICAR treatment in both wild-type and REDD1−/− MEFs (last two lanes). Primary MEFs of the indicated genotype were serum starved for 24 h (SS) and then treated as indicated (S, serum) for 90 min prior to Western blot analysis. (B) AMPK is functionally activated by ATP depletion in both wild-type and REDD1−/− MEFs. Primary MEFs were treated with 2DG (50 mM) for the indicated times, prior to Western blot analysis for phospho-AMPK (T172) or its substrate phospho-ACC (S79). (C) AMPK-dependent phosphorylation of TSC2 does not require REDD1. MEFs were serum starved as in panel A, pretreated with the AMPK inhibitor (AMPKI) compound C (10 μM) for 30 min where indicated, and then treated with AICAR (2.0 mM) for 30 min prior to Western blotting for endogenous TSC2. The phosphorylation-induced shift of TSC2 (upper versus lower arrowhead) is evident compared to the uniform migration of the nonspecific band (Non-Spec.). TSC2 phosphorylation correlates with AMPK activation, as evidenced by ACC (S79) phosphorylation.