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. 2020 Sep 2;40(36):6991–7007. doi: 10.1523/JNEUROSCI.0455-20.2020

Figure 4.

Figure 4.

CMKLR1 deficiency attenuates hyperphosphorylation of tau in the brain of APP/PS1 mice and ICV-STZ mice. A, Representative Western blots showing tau phosphorylation at Ser199, Thr205, Ser396, and Ser404 in the hippocampus of WT, APP/PS1, CMKLR1−/−, and APP/PS1-CMKLR1−/− mice at the age of 9 months. The levels of nonphosphorylated tau (Tau1) and total tau (Tau5) were also measured. Quantification of the immunoreactivity of the blots, normalized against total tau (B) and β-actin (C). Data are mean ± SEM, with 6 mice in each group. *p < 0.05 compared with WT mice. $p < 0.05 compared with APP/PS1 mice. D, Representative Western blots showing tau phosphorylation in the brain of WT and CMKLR1−/− mice receiving ICV injection of STZ or saline. Quantification of the immunoreactivity of the blots, normalized against total tau (E) and β-actin (F). Data are mean ± SEM, with 6 mice in each group. *p < 0.05; **p < 0.01; ***p < 0.001; compared with WT ICV-saline mice. $p < 0.05; $$p < 0.01; compared with WT ICV-STZ mice.