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. 2018 Feb 13;293(14):5281–5294. doi: 10.1074/jbc.RA117.000915

Figure 6.

Figure 6.

SIRT2 deacetylates NFATc2 and inhibits its activity. A, Western blot analysis of SIRT2 interaction with NFATc2. SIRT2 was immunoprecipitated from heart lysates and probed for its interaction with NFATc2. B, in vitro deacetylation assay where recombinant acetylated-NFATc2 was incubated with wildtype or SIRT2-H187Y in the presence of NAD+. NFATc2 acetylation was analyzed by Western blotting. C, representative confocal images showing control and SIRT2-KD cardiomyocytes stained for NFATc2. Scale bar = 5 μm. D, graph showing quantification of NFATc2 from Fig. 4C. Error bars, mean ± S.D.; *, p < 0.05. E, luciferase activity in vehicle- or AGK2-treated cells transfected with NFAT-Luc plasmid. n = 3–5; error bars, mean ± S.D.; *, p < 0.05. F, luciferase activity in control and SIRT2-KD cells treated with vehicle or PE (20 μm) for 48 h. n = 3; error bars, mean ± S.D.; *, p < 0.05. G, luciferase activity in control and SIRT2 overexpressing cardiomyocytes transfected with NFAT-Luc plasmid. Error bars, mean ± S.D.; n = 4; *, p < 0.05. H, luciferase activity in wildtype SIRT2 and SIRT2-H187Y overexpressing cells treated with vehicle or PE (20 μm) for 48 h. n = 3; error bars, mean ± S.D.; *, p < 0.05.