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Fig. 3 | Journal of Biomedical Science

Fig. 3

From: Genetic and pharmacologic p32-inhibition rescue CHCHD2-linked Parkinson’s disease phenotypes in vivo and in cell models

Fig. 3

p32-knockdown reduces mutant CHCHD2 protein levels. A Representative Western blots of p32 and CHCHD2 expressions in Drosophila. Expression of wild type or mutant hCHCHD2 in Drosophila results in increased endogenous p32 level. Densitometric analysis of p32 expressions (shown as relative density, n = 3; One-way ANOVA with Bonferroni post hoc test) and CHCHD2 expressions (shown as fold change, n = 5; two-tailed Paired Samples t-test). Both the overexpressed human CHCHD2 (O-hCHCHD2) and the endogenous Drosophila CHCHD2 (E-dCHCHD2) expressions are shown. Negative control is of genotype Ddc-Gal4/ + . B Representative Western blots showing p32 and CHCHD2 expressions in the Hela cells. As in Drosophila, expression of wild type or mutant hCHCHD2 in Hela cells results in increased endogenous p32 level. Densitometric analysis of p32 (shown as relative density, n = 3; One-way ANOVA with Bonferroni post hoc test) and CHCHD2 expressions (shown as fold change, n = 4; two-tailed Paired Samples t-test). Both the over-expressed human CHCHD2 (O-hCHCHD2) and the endogenous human CHCHD2 (E-hCHCHD2) expressions are shown. Negative control is Hela cells expressing MYC alone. In both (A, B), the molecular weight markers are indicated in kDa. The p32 and the CHCHD2 expressions are detected using the anti-p32 and the anti-CHCHD2 antibodies. β-tubulin is used as the loading control. n = experimental repeats. Data are presented as mean ± SEM. *p < 0.05; **p < 0.01

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