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Fig. 3 | Molecular Neurodegeneration

Fig. 3

From: Alzheimer risk gene product Pyk2 suppresses tau phosphorylation and phenotypic effects of tauopathy

Fig. 3

Pyk2 expression suppresses Tau phosphorylation in a PS190/+ animal model of tauopathy. A–L, TBS-insoluble, SDS-soluble hippocampal (A–F) and cortical (G–L) lysates from 9.5–10.5-month-old WT, Pyk2−/−, PS190/+ and PS190/+;Pyk2−/− animals were separated by SDS-PAGE and immunoblotted with antibodies against multiple pathophysiologically-relevant phospho-Tau residues as well as total Tau. A, Representative immunoblot images of TBS-insoluble, SDS-soluble hippocampal Tau. B–F, Quantification of protein levels by densitometric analysis reveals significantly greater phosphorylation of hippocampal Tau in lysates from PS190/+;Pyk2−/− animals at pTau S396/S404 (PHF-1) (B), pTau S262 (C) and pTau S199/S202 (E) compared to lysates from PS190/+ animals. All data are normalized total (HT7) levels of hippocampal Tau. Data are graphed as mean ± SEM, unpaired two-tailed t-test, *p < 0.05, n = 4–8 mice. G, Representative immunoblot images of TBS-insoluble, SDS-soluble cortical Tau. H–L, Quantification of protein levels by densitometric analysis reveals significantly greater phosphorylation of cortical Tau in lysates from PS190/+;Pyk2−/− animals at pTau S262 (L) compared to those from PS190/+ animals. All data are normalized to total (HT7) levels cortical Tau. Data are graphed as mean ± SEM, unpaired two-tailed t-test, *p < 0.05, n = 4–8 mice

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