Fig. 2: Overexpressed and endogenous p53 repress PINK1 transcription.
From: Nuclear p53-mediated repression of autophagy involves PINK1 transcriptional down-regulation
SH-SY5Y cells transiently transfected with an empty vector (EV, white bars) or wild-type p53 cDNA (p53, black bars) were assessed for PINK1 protein (a, N = 8), promoter activation (b, N = 6) and mRNA levels (c, N = 12). PINK1 protein levels in basal (−, white bars) and CCCP ( + , black bars, 10 µM/6 h) stress conditions were analyzed in control (p53+/+, black bars) or p53-deficient (p53−/−, white bars) HCT116 cells (d, N = 12). PINK1 promoter transactivation (e, N = 6) and mRNA levels (f, N = 12) were analyzed in control (p53+/+, black bars) or p53-deficient (p53−/−, white bars) HCT116 cells in basal conditions as described in the Methods section. p53 and actin protein levels are provided in a and d as transfection and protein charge controls. HCT116 p53-deficient (p53−/−) cells transiently transfected with an empty vector (EV, white bars) or wild-type p53 cDNA (p53, black bars) were assessed for p53 expression (g, left panel) PINK1 promoter transactivation (g, N = 8) and mRNA levels (h, N = 6). Bars represent the means ± SEM of 3 independent experiments performed in duplicates (a,b,e,g,h) or quadruplicates (c,d,f) and are expressed as percentage of control EV (a-c, g,h) or p53+/+ cells (d-f). Statistical analyses were performed with GraphPad Prism software by using unpaired student’s t-test. Significant differences are: *p < 0.05,**p < 0.01, and ****p < 0.0001.
