Fig. 3: TAX1BP1 and NDP52 are selectively degraded by the lysosome following MTA treatment, but only NDP52 delivers aggregated protein to the lysosome. | Cell Death & Disease

Fig. 3: TAX1BP1 and NDP52 are selectively degraded by the lysosome following MTA treatment, but only NDP52 delivers aggregated protein to the lysosome.

From: Mitochondrial dysfunction generates aggregates that resist lysosomal degradation in human breast cancer cells

Fig. 3

a Representative immunoblots of the OPTN, TAX1BP1, p62, and NDP52 from MDA-MB-231 cells exposed to MitoQ (1 μM) or MitoApo (1 μM) in the presence or absence of Bortezomib (Bort) (5 nM) or Baf (5 nM) at the indicated times (ANOVA at 24 h per protein, n = 3–5, *p < 0.05 as according to Tukey’s post-hoc test between treatments, while #p < 0.05 compared to all treatments.) b Representative immunoblots of TAX1BP1 and NDP52 in MDA-MB-231, MCF-12A, MCF-7, and SKBR3 cells exposed to MitoQ (1 μM) or MitoApo (1 μM) in the presence or absence of Baf (5 nM) for 24 h (two-way ANOVA per cell line for MTA dependency on Baf effects, n = 3–5, *p < 0.05 as according to Tukey’s post-hoc test at 24-h. two-way ANOVA for cell type dependency on treatment effects, #p < 0.05 indicates difference between cell types per treatment) (c) TAX1BP1 and (d) NDP52 immuno-labeled mt-GFP expressing MDA-MB-231 cells stained with Proteostat. Cells were treated with DMSO (Control), CCCP (30 μM), MitoQ (1 μM) or MitoApo (1 μM) for 24 h. Scale bar is 5 μm. Whole cells were used to establish the Pearson’s correlation coefficient (R values shown) between mt-GFP, autophagic receptor, and Proteostat (ANOVA per comparison, n = 3–8 fields (5 × 5 tiles per field), *p < 0.05 according to Tukey’s post-hoc test identified significant differences between the control and indicated treatment.). For all graphs, the dots represent mean and error bars are SEM.

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