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. Author manuscript; available in PMC: 2014 Jun 30.
Published in final edited form as: Cell. 2013 Dec 19;155(7):1624–1638. doi: 10.1016/j.cell.2013.11.037

Figure 6. AMPK Activity Regulates Switch between PGC-1α-Dependent and -Independent Mechanisms of Mitochondrial Regulation by SIRT1.

Figure 6

(A) Immunoblot for p-AMPK (Thr172) and AMPK in SIRT1 flox/flox Cre-ERT2 primary myoblasts treated with vehicle (0 hr) or OHT to induce SIRT1 excision.

(B) Immunoblot for p-ACC (Ser79) and ACC in SIRT1 flox/flox Cre-ERT2 primary myoblasts treated with vehicle or OHT for 48 hr (SIRT1 iKO) and infected with AMPK-DN adenovirus.

(C) Expression of nuclear- and mitochondrially encoded genes as in SIRT1 flox/flox Cre-ERT2 primary myoblasts treated with vehicle or OHT (SIRT1 iKO) and infected with empty or AMPK-DN adenovirus for the same period of time (n = 4, *p < 0.05 versus vehicle; #p < 0.05 versus SIRT1 iKO).

(D) Immunoblot for p-AMPK (Thr172) and AMPK in SIRT1 flox/flox Cre-ERT2 primary myoblasts treated with vehicle or OHT for 24 or 48 hr, after which cells were infected with control or TFAM adenovirus.

(E) Immunoblot for p-AMPK (Thr172) and AMPK in gastrocnemius of WT and SIRT1 iKO mice under fed and fasted conditions.

(F) Representative immunoblot for p-AMPK (Thr172) and AMPK in gastrocnemius of 6- and 22-month-old mice. Nuclear- and mitochondrially encoded genes were ND1, Cytb, COX1, ATP6, and NDUFS8, SDHb, Uqcrc1, COX5b, and ATP5a1, respectively.

Values are expressed as mean ± SEM.