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Fig. 4 | Alzheimer's Research & Therapy

Fig. 4

From: Selective suppression of the α isoform of p38 MAPK rescues late-stage tau pathology

Fig. 4

MK2-deficient mice are resistant to LPS-induced tau phosphorylation and show reduced p38α MAPK. a Quantitative real-time PCR analysis for MK2 in the brains of 2-month-old nontransgenic vs. MK2–/– mice confirms a significant knockdown of MK2 in these mice (n = 4 for non-Tg and n = 3 for MK2–/– mice; ***p < 0.0001; unpaired t test; mean ± SEM). b Western blots of detergent soluble hippocampal lysates from 2-month-old nontransgenic and MK2–/– mice treated with either vehicle (VEH) or LPS (10 mg/kg b.w.; intraperitoneal; single dose for 24 h). Note the LPS-induced AT8 and AT180 site tau phosphorylation in LPS-treated nontransgenic mice, which is reduced in MK2–/– mice. No significant difference is seen in PHF1-antibody specific tau phosphorylation and phosphorylated p38α MAPK (pT180/pY182) levels. However, the total p38α MAPK levels are reduced in MK2–/– mice. c–e Quantifications of the western blots in b show a statistically (n = 3 mice per group; mean ± SEM of IDV ratios of AT8/Tau5 and AT180/Tau5; **p < 0.01; two-way ANOVA with Bonferroni’s multiple comparison test) significant increase in IDV ratios for AT8/Tau5 and AT180/Tau5 in LPS-treated non-Tg, but not in LPS-treated MK2–/– mice. f Quantifications of the total-p38α MAPK levels show statistically significant reduction in the levels of total-p38α MAPK/GAPDH IDV ratio (n = 3 per group; mean ± SEM; **p < 0.01; unpaired t test) in MK2–/– mice compared with nontransgenic mice. Tg transgenic

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