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. 2014 May 22;23(19):5227–5242. doi: 10.1093/hmg/ddu244

Figure 3.

Figure 3.

Knockdown of USP15 rescues the mitophagy defect of PARK2 mutant PD patient fibroblasts. (A) Fibroblasts from a PD patient with c.8_171del/c.535_871del PARK2 mutations (PARK2 mut.) and from age-matched healthy control 2 (Ctrl.) were analyzed by western blotting for Parkin expression. (B–E) Mutant and control 2 fibroblasts were treated for 48 h with DMSO, CCCP or valinomycin (Val.), as indicated, followed by anti-Hsp60 immunostaining (B and C) or western blotting (D and E). (C) Quantification of the percentage cells without detectable Hsp60 immunoreactivity (n = 3). * P < 0.001 compared with DMSO-treated control fibroblasts. (E) Quantification of the Hsp60/β-Actin ratio on western blot, normalized to this ratio in the DMSO condition (n = 3). * P < 0.01 compared with valinomycin-treated control fibroblasts. (F–I) PARK2 mutant fibroblasts were transfected with the indicated siRNAs and treated for 48 h with DMSO, CCCP or valinomycin, as indicated, followed by anti-Hsp60 immunostaining (F, G) or western blotting (H, I). (G) Quantification of the percentage cells without detectable Hsp60 immunoreactivity (n = 3). *P < 0.001 compared with the CCCP-treated control siRNA condition. (I) Quantification of the Hsp60/β-Actin ratio on western blot, normalized to this ratio in the DMSO condition (n = 8). *P < 0.001 compared with the valinomycin-treated control siRNA condition. Scale bars, 10 µm.