Figure 2.
Figure 2. Platelet functions are defective in the absence of Ask1. (A-B) Representative Western blots of washed platelet lysates from WT and Ask1−/− mice blotted with antibodies specific to major platelet transmembrane proteins (A) and MAPK cascade proteins (B). (C) Quantitation of flow cytometric analysis of indicated surface protein expression from WT and Ask1−/− platelets. (D) Representative platelet aggregation tracings of platelet-rich plasma (PRP) from WT and Ask1−/− mice stimulated with 2 concentrations of agonists, as indicated. (E-F) Quantitation of flow cytometric analysis of PE-conjugated JON/A binding (E) and FITC-conjugated Fg binding (F) to WT and Ask1−/− mouse platelets stimulated with various concentrations of AYPGKF, as indicated. Data presented are from 3 independent experiments. CLEC2, C-type lectin-like receptor; MFI, mean fluorescence intensity; ns, not significant; WB, Western blot. *P < .05.

Platelet functions are defective in the absence of Ask1. (A-B) Representative Western blots of washed platelet lysates from WT and Ask1−/− mice blotted with antibodies specific to major platelet transmembrane proteins (A) and MAPK cascade proteins (B). (C) Quantitation of flow cytometric analysis of indicated surface protein expression from WT and Ask1−/− platelets. (D) Representative platelet aggregation tracings of platelet-rich plasma (PRP) from WT and Ask1−/− mice stimulated with 2 concentrations of agonists, as indicated. (E-F) Quantitation of flow cytometric analysis of PE-conjugated JON/A binding (E) and FITC-conjugated Fg binding (F) to WT and Ask1−/− mouse platelets stimulated with various concentrations of AYPGKF, as indicated. Data presented are from 3 independent experiments. CLEC2, C-type lectin-like receptor; MFI, mean fluorescence intensity; ns, not significant; WB, Western blot. *P < .05.

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