Role of PKC-θ in GPVI- and PAR-mediated platelet aggregation and dense granule secretion. Aspirin-treated washed human platelets in the presence or absence of PKC-θ antagonistic RACK peptide and isolated mouse platelets (as indicated) from PKC-θ^−/− mice and WT littermates were stimulated with GPVI agonists (A) CRP (10 and 20 μg/mL) and collagen (10 and 20 μg/mL); and (B) PAR4 agonist AYPGKF (100 and 200 μM), PAR1 and PAR4 agonist thrombin (0.1 and 0.2 U/mL), and PAR1 agonist SFLLRN (5 and 10 μM) for 3.5 minutes at 37°C in stirring condition and their aggregation and simultaneous dense granule secretion were measured and compared. Dense-granule secretion is expressed as ATP released (nmol/10⁸ platelets). The tracings are representative of results from at least 3 different donors.