Fig. 6
From: Targeting Tyro3 ameliorates a model of PGRN-mutant FTLD-TDP via tau-mediated synaptic pathology
Vemurafenib rescues phosphorylation signals and phenotypes in PGRN-KI mice. a Experimental protocol for administration of B-Raf inhibitor (vemurafenib). The mice were fed vemurafenib (32 mg/kg of BW/day) or mock from 6 to 12 weeks of age. Behavioral tests and western blots were performed at 12 weeks. b In vivo effect of vemurafenib on B-Raf phosphorylation in cortical tissues of PGRN-KI mice. #p < 0.05; ##p<0.01 (N = 6, Tukey’s HSD test). Averages and s.e.m. are shown. c In vivo effect of vemurafenib on MEK phosphorylation in cortical tissues of PGRN-KI mice. #p < 0.05 (N = 6, Tukey’s HSD test). Averages and s.e.m. are shown. d In vivo effect of vemurafenib on ERK phosphorylation in cortical tissues of PGRN-KI mice. #p < 0.05 (N = 6, Tukey’s HSD test). Averages and s.e.m. are shown. e In vivo effect of vemurafenib on phosphorylation of tau in cortical tissues of PGRN-KI mice. Right panels show quantitation of western blot band intensities. ##p < 0.01 (N = 6, Tukey’s HSD test). Averages and s.e.m. are shown. f In vivo effect of vemurafenib on two parameters (% time spent at target region and number of target crosses) in the Morris water maze test. Numbers of mice are shown in the graph. **p < 0.01 (Student’s t-test). Averages and s.e.m. are shown. g Effect of vemurafenib on % total freezing time in the fear-conditioning test. Numbers of mice are shown in the graph. p-values were determined by Student’s t-test. Averages and s.e.m. are shown
