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. 2012 Jan 20;287(11):8001–8012. doi: 10.1074/jbc.M111.315812

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© 2012 by The American Society for Biochemistry and Molecular Biology, Inc.

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FIGURE 5. — Increased acetylation and decreased degradation of p53 in Ampkα1^−/− MEFs due to defective SIRT1 activation. A, increased acetylation of p53 (Ace-p53) and total p53 levels in Ampkα1^−/− MEFs compared with wild-type MEFs. B, inhibition of AMPK by compound C (CmpC) increased the doxorubicin (Dox)-induced acetylation of p53 in wild-type MEFs. C, intracellular NAD⁺ content (**, p < 0.01; n = 6 in each group). D, NADH levels in MEFs. E, calculated NAD⁺/NADH ratio (**, p < 0.01; n = 6 in each group). F, p53 protein levels after resveratrol treatment in Ampkα1-deficient MEFs for 16 h at the indicated dose. G, p53 protein levels after resveratrol treatment in Ampkα1^−/− MEFs at 100 μm for indicated time points. H, MG132 blocks the effect of resveratrol in decreasing p53 levels in Ampkα1^−/− MEFs. Ctrl, control; p-ACC, phospho-acetyl-CoA carboxylase; AICAR, 5-aminoimidazole-4-carboxamide ribonucleoside.