Fig. 4: TAX1BP1 as an upstream regulator for the autophagic degradation of NDP52 and autophagic flux. | Cell Death & Disease

Fig. 4: TAX1BP1 as an upstream regulator for the autophagic degradation of NDP52 and autophagic flux.

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

Fig. 4

a Representative TAX1BP1 and NDP52 immunoblots from MDA-MB-231 cells treated with siRNA for TAX1BP1, NDP52, or both (double knockdown (DKD)) (two-way ANOVA, n = 3, *p < 0.05 according to Dunnett’s post-hoc test). b Immunoblots of TAX1BP1, NDP52, and LC3 from siCon-treated MDA-MB-231 cells in the presence and absence of Baf for 2 h. (two-way ANOVA, n = 3, *p < 0.05 as indicated by Tukey’s post-hoc test for changes in LC3-II within the treatment groups) (c) Immunoblot of TAX1BP1 and NDP52 using control siRNA (siCon)-treated MDA-MB-231 cells subjected to a DMSO, MitoQ (1 μM) and MitoApo (1 μM) for 24 h and Baf (5 nM) for 2 h prior to protein harvest (two-way ANOVA per graph, n = 3–5, *p < 0.05 as indicated by Tukey’s comparison test) d) Immunoblots of LC3 using cells treated with siTAX1BP1, siNDP52, or in combination with or without MTA exposure in the presence or absence of Baf for 2 h prior to harvest. (two-way ANOVA, n = 3, *p < 0.05 as indicated by Tukey’s post-hoc test for changes in LC3-II within the treatment groups) (e, f) Immunoblots of (e) NDP52 in siTAX1BP1-treated cells and (e) TAX1BP1 in siNDP52-treated cells in the presence and absence of MTA with and without Baf treatment for 2 h prior to harvest (two-way ANOVA per graph, n = 3–5, *p < 0.05 as indicated by Tukey’s comparison test) (Bars represent the mean and error bars are SEM).

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