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. Author manuscript; available in PMC: 2012 Aug 31.
Published in final edited form as: Cell. 2012 Feb 3;148(3):421–433. doi: 10.1016/j.cell.2012.01.017

Figure 1. Resveratrol Activates AMPK in an Epac1-Dependent Manner.

Figure 1

(A) Cyclic AMP levels in C2C12 myotubes 30 min after treatment with 0–100 μM resveratrol (Resv).

(B) Cyclic AMP levels in C2C12 myotubes after treatment with resveratrol (50 μM) for the indicated times.

(C) Phosphorylation of AMPK (T172) and AMPK substrate ACC (S79) after treatment with resveratrol (50 μM) in the presence of the AC inhibitor MDL-12,330A in C2C12 myotubes and HeLa cells.

(D) The effect of PKA catalytic subunit α (PKAc) siRNA on resveratrol-induced phosphorylation of ACC and AMPK.

(E) The effect of Epac1 siRNA on resveratrol-induced phosphorylation of ACC and AMPK.

(F) GTP-bound Rap1 was pulled down using the immobilized ras-binding domain (RBD) of RalGDS (left). Quantification of binding is shown on the right (n = 3).

(G) Phosphorylation of ACC and AMPK induced by the Epac agonist 007 (10 μM).

See also Figure S1.

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