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Figure 10 | Molecular Brain

Figure 10

From: Neurological characterization of mice deficient in GSK3α highlight pleiotropic physiological functions in cognition and pathological activity as Tau kinase

Figure 10

Biochemical analysis of protein Tau in GSK3α deficient mice. A. Biochemical analysis by western blotting of total protein extracts from forebrain of AAC and AA- mice aged 3, 6 and 18 months (n=5/age). Tau protein levels are normalized to actin and expressed relative to control AA- mice at age 3 months. Data (mean±SEM) are statistically analyzed by two-way Anova (Bonferroni post hoc test), genotype: F(1,24)=3.40, p=0.5093; age: F(2,24)=37.60, p=0.0027; interaction: F(2,24)=0.20, p=0.7759. Lower panels show representative western blots. B. Biochemical analysis by western blotting for phospho-epitopes pS396/404, pS199 and pT231 of endogenous mouse Tau in total protein extracts from hippocampus and forebrain of AAC and control AA- mice. C. Biochemical analysis by western blotting for phospho-epitopes pS396/404, pS199 and pT231 of endogenous mouse Tau in total protein extracts from hippocampus and cortex of GSK3α.KO and FVB wild-type mice. D. Biochemical analysis by western blotting for phospho-epitopes pS396/404, pS199 and pT231 of human Tau.P301L in total protein extracts from hippocampus and cortex of GSK3α.KOxTau.P301L mice and the parental Tau.P301L mice. In panels B-D, all data are normalized for total Tau and reported relative to the respective control mice. Data (mean±SEM) are statistically analyzed by unpaired Student’s t-test (two-tailed), n=6 or 7 per genotype; * p<0.05.

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