Figure 6.
MPαC rescues the functional defects of 10aa−/− platelets. (A-C) The effect of (A) low-dose MPαC- (6.25 μM) on PAR4-AP– (40 μM) induced washed WT and 10aa−/− platelet aggregation (n = 5 independent experiments), (B) JON/A binding (n = 3 independent experiments), and (C) P-selectin exposure (n = 3 independent experiments). (D) High-dose MPαC only–induced washed WT and 10aa−/− platelet JON/A binding (n = 4 independent experiments), (E) P-selectin exposure (n = 4 independent experiments), (F) PKC substrate (pleckstrin) phosphorylation (n = 3 independent experiments). Two-way ANOVA followed by Bonferroni post hoc test in panels A-F. Data are shown as mean ± SEM for panels A-F. ∗P < .05 and ∗∗∗P < .001; NS, not significant.

MPαC rescues the functional defects of 10aa−/− platelets. (A-C) The effect of (A) low-dose MPαC- (6.25 μM) on PAR4-AP– (40 μM) induced washed WT and 10aa−/− platelet aggregation (n = 5 independent experiments), (B) JON/A binding (n = 3 independent experiments), and (C) P-selectin exposure (n = 3 independent experiments). (D) High-dose MPαC only–induced washed WT and 10aa−/− platelet JON/A binding (n = 4 independent experiments), (E) P-selectin exposure (n = 4 independent experiments), (F) PKC substrate (pleckstrin) phosphorylation (n = 3 independent experiments). Two-way ANOVA followed by Bonferroni post hoc test in panels A-F. Data are shown as mean ± SEM for panels A-F. ∗P < .05 and ∗∗∗P < .001; NS, not significant.

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