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Fig. 8 | Molecular Neurodegeneration

Fig. 8

From: Pim1 inhibition as a novel therapeutic strategy for Alzheimer’s disease

Fig. 8

Pim 1i increases proteasome function. a Representative western blots of protein extracted from treated and untreated 3xTg-AD and NonTg mice. Blots were probed with the indicated antibodies. b Quantitative analyses of the p62 blots show that p62 levels are reduced in both 3xTg-AD groups compared to the NonTg groups, as indicated by a significant main effect of Genotype (F(1, 15) = 7.238, p < 0.05). These p62 changes were independent of Pim1 inhibition. c. Quantitative analyses of the ATG3 blots show that the ATG3 levels are reduced in both 3xTg-AD groups compared to the NonTg groups, as indicated by a significant main effect of Genotype (F(1, 15) = 10.851, p < 0.01). d, e Quantitative analyses of the ATG5 and ATG12 blots indicate no significant difference among the four groups. f-h Proteasome analyses of proteins extracted from the brains of the four groups of mice revealed significant main effects of treatment for chymotrypsin-like (F(1, 20) = 10.127, p < 0.05), trypsin-like (F(1, 20) = 16.18, p < 0.001), and caspase-like (F(1, 20) = 19.804, p < 0.001) activities. Quantitative analyses of the blots were obtained by normalizing the levels of the protein of interest to β-Actin, used as a loading control. Error bars represent mean ± SEM

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