Fig. 5

SIRT3 diminishes the interaction between VDAC1, GRP75 and IP3R. a Lysine acetylation detected in a mitochondrial extract from SH-SY5Y cells by western blot using an anti-pan acetyl-lysine antibody. K-Ac, acetyl-lysine. COXIV and GAPDH were used as markers for mitochondria and cytoplasm, respectively. b, c VDAC1 acetylation status examined by immunoprecipitation with an anti-VDAC1 antibody followed by western blot analysis using an anti-acetylated-lysine antibody. The ratios of acetylated VDAC1/total VDAC1 were shown in c. K-Ac, acetyl-lysine. N = 3. d Co-immunoprecipitation (Co-IP) assay showing the interaction between SIRT3 and VDAC1. e Western blots of acetylated VDAC1 by immunoprecipitation in SH-SY5Y cells. K-Ac, acetyl-lysine. f–h Western blots of IP3R, GRP75, and VDAC1 in VDAC1 immunoprecipitation in SH-SY5Y cells (f); Quantification for the expression of IP3R and GRP75 normalised to VDAC1 (g, h); N = 4. i, j Western blots (i) and quantification analysis (j) of IP3R, GRP75, and VDAC1. GAPDH was used as the loading control, N = 4. k, m Western blot analysis of IP3R, GRP75, and VDAC1 expression in VDAC1 immunoprecipitate from hippocampal tissue. N = 4 mice per group. n, o Western blot analysis of IP3R, GRP75, and VDAC1 expression in the hippocampus. GAPDH was used as the loading control. Data were expressed as mean ± SD, N = 4.*p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001