Fig. 4: Involvement of the ubiquitin-proteasome pathway in α-Syn-induced TOM40 loss. | Cell Death & Disease

Fig. 4: Involvement of the ubiquitin-proteasome pathway in α-Syn-induced TOM40 loss.

From: Mitochondria-targeted oligomeric α-synuclein induces TOM40 degradation and mitochondrial dysfunction in Parkinson’s disease and parkinsonism-dementia of Guam

Fig. 4

A Schematic diagram depicting the different inhibitors used to test potential mitochondrial quality control pathways involved in TOM40 loss. Inhibitors: MG132, Bafilomycin A1 (BafA1), Pespstatin (PepsA), E64d, Mdivi. Scheme created with BioRender.com. B Representative immunoblot of WT α-Syn cells pre-treated for 24 h with different inhibitors followed by 48 h of Dox-induced α-Syn expression. C Densitometry analysis showing high TOM40 level (Ln 3, red arrow) in MG132 treated WT α-Syn cell. D Densitometry analysis shows high LC3B level in MG132 (Ln 3) and bafilomycin A1 (Ln 4) treated WT α-Syn cells. E Representative immunoblot of endogenous TOM40 co-IP with ubiquitin from WT α-Syn cells pre-treated with MG132 for 24 h and induced with Dox for 48 h. F Densitometry analysis of ubiquitinylated protein levels in TOM40 co-IP. Data are presented as mean ± s.e.m. from three independent experiments. Statistical analysis was performed using one-way ANOVA.

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