PKC activity is decreased in 10aa^−/− platelets, and GPIbα cytoplasmic tail regulates PKC activity by sequestering 14-3-3. (A) Representative blots of ADP-, U46619-, PAR4-AP-, collagen- and botrocetin/VWF-induced phosphorylation of PKC substrate (pleckstrin) in WT and 10aa^−/− platelets (n = 3 independent experiments). (B) Representative blot of PKC substrate (pleckstrin) phosphorylation in resting WT and 10aa^−/− platelets and quantification of densitometry in the blots (n = 6 mice per genotype). (C) Representative blots and quantification of immunoprecipitation of PKCα with 14-3-3ζ in human platelets treated with MPαC and MPαCsc (n = 4 independent experiments). (D) Representative blots and quantification of immunoprecipitation of PKCα with 14-3-3ζ in resting WT and 10aa^−/− platelets (n = 4 independent experiments). (E) Representative blot and quantification of PKC substrate (pleckstrin) phosphorylation in 1b9 and Δ605 cells (n = 5 independent experiments). (F) Representative blots and quantification of immunoprecipitation of PKCα with 14-3-3ζ in 1b9 and Δ605 cells (n = 4 independent experiments). Two-tailed Student t test in panels B-F. Data are shown as mean ± SEM for panels B-F. ∗P < .05, ∗∗P < .01, and ∗∗∗P < .001.