Skip to main content
. Author manuscript; available in PMC: 2020 Jun 4.
Published in final edited form as: Cell Metab. 2019 Mar 28;29(6):1274–1290.e9. doi: 10.1016/j.cmet.2019.03.001

Fig. 2. P53 regulates sirtuins in telomere dysfunctional mice.

Fig. 2

(a) RT-qPCR analysis of sirtuin transcripts in WT, p53−/−, G4/p53 +/+ and G4/p53 −/− liver tissue demonstrates that mitochondrial sirtuins (Sirt3, 4 & 5) are repressed in G4/p53 +/+ mice and p53 deficiency in G4 mice rescues their expression (9 mice per group analyzed); (b) Western blot analysis using total liver tissue or isolated liver mitochondria shows elevated sirtuin protein expression in G4/p53 −/− mice compared to G4/p53 +/+ mice (9 mice per group were analyzed); (c) Combined IP-western blot analysis of liver tissues derived from WT, p53 −/−, G4/p53 +/+ and G4/p53 −/− mice demonstrates decreased acetylation levels of PGC-1α, FOXO1, SOD2, CPS1 in G4/p53 −/− compared to G4/p53 +/+ mice (6 mice per group were analyzed); (d) Analysis of acetylation levels of mitochondrial proteins from WT, p53 −/−, G4/p53 +/+, and G4/p53 −/− mice shows that G4/p53 −/− have decreased acetylation compared to G4/p53 +/+ mice (6 mice per group were analyzed). Results are quantified by densitometry and expressed as mean ± s.e.m.; t-test was used to determine statistical significance with p <0.05 considered as significant, as indicated by (*).