Figure 2.
Figure 2. The effect of an inhibitor of 14-3-3ζ-GPIb-IX interaction, MPαC, on ristocetin-induced platelet aggregation. (A) PRP was preincubated with DMSO as control or with increasing concentrations of the myristoylated 14-3-3ζ inhibitor peptide for 5 minutes, and stimulated with ristocetin to induce platelet aggregation. (B) Ristocetin-induced platelet aggregation in the presence of 100 μM myristoylated 14-3-3ζ inhibitor peptides; MPαC; control peptides MαC, MPαCsc, or MαCsc; or DMSO. (C) Ristocetin-induced platelet aggregation in the presence of nonmyristoylated peptide, PαC (phosphorylated) or αC (nonphosphorylated) with sequence identical to MPαC, or myristic anhydride (MA).

The effect of an inhibitor of 14-3-3ζ-GPIb-IX interaction, MPαC, on ristocetin-induced platelet aggregation. (A) PRP was preincubated with DMSO as control or with increasing concentrations of the myristoylated 14-3-3ζ inhibitor peptide for 5 minutes, and stimulated with ristocetin to induce platelet aggregation. (B) Ristocetin-induced platelet aggregation in the presence of 100 μM myristoylated 14-3-3ζ inhibitor peptides; MPαC; control peptides MαC, MPαCsc, or MαCsc; or DMSO. (C) Ristocetin-induced platelet aggregation in the presence of nonmyristoylated peptide, PαC (phosphorylated) or αC (nonphosphorylated) with sequence identical to MPαC, or myristic anhydride (MA).

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