Fig. 3: Mitophagy defects caused by PrP106-126 can be alleviated by NMN, UA, and overexpression of Parkin. | Cell Death & Disease

Fig. 3: Mitophagy defects caused by PrP106-126 can be alleviated by NMN, UA, and overexpression of Parkin.

From: PINK1-parkin-mediated neuronal mitophagy deficiency in prion disease

Fig. 3

A, B Western blots of LC3-I and LC3-II levels in N2a cells from Figure S6A–D, with and without PrP106-126, nicotinamide mononucleotide (NMN), and urolithin A (UA) treatments. C Immunofluorescence images of mitophagy events indicated by the colocalization of autophagosome protein LC3-II and the mitochondria (labeled with DsRed-Mito). Scale bar: 10 µm. D Comparison of the localization of LC3-II and DsRed-Mito in cells from C. E, F Mitophagy was characterized by the COX8-mKeima fluorescence ratio change in Figure S7A, B. Data were mean (SD). ns not significant; *P < 0.05; **P < 0.01; ***P < 0.001. All experiments were repeated at least three times.

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