Fig. 9: K373 acetylation is required for refolding and mitochondrial enrichment of p53 mutants freed from PEPD.
From: Loss of peptidase D binding restores the tumor suppressor functions of oncogenic p53 mutants
a, b Cells were treated by siRNA (10 nM) for 48 h with or without C646 (8 μM). WCL was subjected to IP by PAb1620 or PAb240, followed by WB analysis of the precipitate for p53 mutants. c, d MDA-MD-231 (p53KO) cells were transfected with p53R175H/K373R, p53R248Q/K373R, p53R273H/K373R, or p53R280K/K373R and 24 h later treated with siRNA (10 nM) for 48 h. WCL was subjected to IP by PAb1620 or PAb240, followed by WB analysis of the precipitate by p53 mutants and PEPD. A p53-containing sample (WCL of untreated CAL-51 cells) was used as positive control during WB in c. e, f MDA-MD-231 (p53KO) cells were transfected with p53R175H/K373R or p53R280K/K373R and 24 h later treated with siRNA (10 nM) for 48 h. p53 mutants in subcellular fractions was analyzed by WB. Lamin B, α-tubulin and VDAC were measured as loading controls and for ruling out cross contamination.
