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Fig. 1 | Molecular Neurodegeneration

Fig. 1

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

Fig. 1

Activation of c-Abl, p53 and Mdm2 with α-synucleinopathy in TgA53T mice. a, b Levels of phospho-Tyr245 c-Abl (pY245c-Abl) (a) and phospho-Ser15P53 (pS15p53) (b) in the cortex (CTX) and brainstem (BST) of mice at various disease states: Non-transgenic (nTg), aged asymptomatic TgA53T mice (Asymp), and early stage/end stage (Early/End) symptomatic TgA53T mice. Quantitative analysis graphs for corresponding protein levels in BST and CTX are shown on the right side of each figure. Levels of phosphorylated c-Abl (a) or p53 (b) were not changed in the cortex, but significantly increased in BST region of symptomatic (Early and End) animals. All values are mean ± SEM, n = 3–4 animal per group. ***p < 0.001, **p < 0.01, *p < 0.05 compared with the nTg littermate mice, one-way ANOVA followed by Dunnett’s multiple comparison test. c, d Activation of Mdm2 in A53TαSyn Tg mice. c Levels of Mdm2 in cortex (CTX), brainstem (BST) and spinal cord (SPC) of non-transgenic (nTg), and end stage transgenic (Tg) mice. d Tyrosine phosphorylated Mdm2 was evaluated by Mdm2 immunoprecipitation followed by immunoblotting using an anti-phospho-Tyr antibody. Despite the reduced levels of Mdm2 in the SPC (c), Increased pTyr-Mdm2 is seen with SPC of TgA53T compared to the nTg mice. Bar graph for corresponding protein levels were shown next to each figure. All values are mean ± SEM, n = 3–4 animals. **p < 0.01 and *p < 0.05 compared with the nTg littermate by Student’s t test

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