Syk^{R41Afl/fl;PF4-Cre} Syk platelets have functional defects in response to GPVI and CLEC-2 agonists. (A) Platelets from Syk^{R41Afl/fl;PF4-Cre} (R41A) and WT mice (2 × 10⁸/mL) were stimulated with collagen (30 μg/mL), CRP (3 μg/mL), rhodocytin (300 nM), CLEC-2 mAb (10 μg/mL), Fc-Pdpn (10 μg/mL plus 10 μg/mL α-Fc to crosslink), or thrombin (0.1 U/mL). Adenosine triphosphate secretion was monitored with Chrono-lume (n = 3). (B) R41A platelets (2 × 10⁷/mL) were stimulated with either CRP (3 μg/ml) or CLEC-2 mAb (10 μg/mL) followed by staining with Alexa 488–labeled fibrinogen. Fibrinogen binding was measured by flow cytometry (n = 3, *P < .05). (C) R41A platelets (2 × 10⁷/mL) were allowed to spread on coverslips coated with either collagen (100 μg/mL) or CLEC-2 mAb (10 μg/mL) for 45 minutes (n = 3, **P < .01, ***P < .005).