Inhibition of gamma-thrombin-induced human platelet aggregation by histone H1subtypes and H1.3 fragments.

Human platelets are differentially activated by varying concentrations of alpha-thrombin or by beta- and gamma-thrombin via three thrombin receptors, PAR-1, PAR-4 and GPIbalpha.It is likely that the development of a normal or abnormal hemostatic event in humans is dictated, in part, by the selective activation of these receptors. The ability to differentially inhibit these thrombin receptors could, therefore, have clinical significance.