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. 2011 Dec 19;287(10):6969–6973. doi: 10.1074/jbc.C111.298596

FIGURE 3.

FIGURE 3.

GSK3β Thr-330 is critical for Pin1 to promote non-amyloidogenic APP processing. A and B, mutation of the Pin1-binding site (T330A) reduced αAPPs production. totAPP, total APP. C and D, when Pin1 was knocked down (Pin1 KD), there was no difference between GSK3β WT and T330A on the level of αAPPs production. E and F, the Thr-668 phosphorylation level was reduced in the presence of Pin1 when cells were transfected with GSK3β WT, but not GSK3β T330A. G–I, higher and lower endogenous APP levels were found in Pin1-KO and Pin1-Tg mouse brain lysates, respectively, when compared with Pin1-WT controls. *, p < 0.05; **, p < 0.005; n.s., p > 0.05 (not significant). Error bars in panels B, D, F, H, and I indicate S.D.