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Fig. 4 | Molecular Neurodegeneration

Fig. 4

From: α-Synucleinopathy associated c-Abl activation causes p53-dependent autophagy impairment

Fig. 4

Constitutively active c-Abl causes p53-dependent autophagy deficit. a, b, c Human embryonic kidney cells, HEK-293 (a, c) or M17 human neuroblastoma cells (b) were transfected with empty vector (EV) or constitutively active c-Abl (c-Abl-PP) and, at 24 h post-transfection, the cells were treated with DMSO or Bafilomycin A1. Total lysates were immunoblotted for pY412c-Abl, c-Abl, and LC3. The quantitative analyses of the immunoblots show means ± SEM (n = 3). The results show that the expression of c-Abl-PP leads to suppression of autophagy (a, b). c, d HEK293 cells expressing c-Abl-PP were treated with a p53-inhibitor (pifithrin-α; PFT) (c) or p53 siRNA (Si) (d). In (d) scrambled siRNA (Sc Si) were used as a control and cells were further treated with DMSO or Bafilomycin A1. Analysis of pY412c-Abl, c-Abl, p53 and LC3 show that both pharmacological (PFT, c) or genetic (p53 Si, d) inhibition of p53 reverses the effects of c-Abl-PP. aa,bSignificantly different from c, p < 0.01, *p < 0.05, One-way ANOVA with Tukey’s multiple comparison posttest. b, c, d *p < 0.05; **p < 0.01, Student’s t test

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