Thrombin-induced platelet activation is attenuated in sGC β₁ deficient platelets, and expression of receptors and signaling molecules is not affected by sGC deficiency. (A) Washed platelets from wild-type (sGC^+/+) or sGC β₁ deficient mice (sGC^–/–) were stimulated with increasing concentrations of thrombin in a lumi-aggregometer at 37°C. Real-time ATP secretion and platelet aggregation were recorded simultaneously. Data shown are representative of 4 independent experiments. (B) Washed platelets from wild type (sGC^+/+) or sGC β₁ deficient mice (sGC^–/–) were solubilized in 2 × SDS sample buffer. GPVI, Akt, ERK, and β-actin were detected by Western blot. (C) Expression integrin β₃ on platelets from wild-type (sGC^+/+) or sGC β₁ deficient mice (sGC^–/–) was analyzed by flow cytometry with a FITC-labeled anti–mouse β₃ monoclonal antibody. Data shown in panels B and C are representative of 2 independent experiments