Figure 7
Figure 7. Reduced TxA2 production is responsible for the defective aggregation of Pyk2-deficient platelets. Aggregation of platelets from WT and Pyk2-KO mice was monitored as an increase of light transmission up to 5 minutes on stimulation with thrombin, arachidonic acid, or U46619, as indicated in each panel. When indicated, platelets were preincubated with aspirin (ASA, 1mM, 30 minutes) or SB203580 (10μM, 10 minutes). Equivalent volumes of DMSO as vehicle were added to control samples. The arrows indicate the addition of the agonists. Traces in the figures are representative of at least 3 different experiments.

Reduced TxA2 production is responsible for the defective aggregation of Pyk2-deficient platelets. Aggregation of platelets from WT and Pyk2-KO mice was monitored as an increase of light transmission up to 5 minutes on stimulation with thrombin, arachidonic acid, or U46619, as indicated in each panel. When indicated, platelets were preincubated with aspirin (ASA, 1mM, 30 minutes) or SB203580 (10μM, 10 minutes). Equivalent volumes of DMSO as vehicle were added to control samples. The arrows indicate the addition of the agonists. Traces in the figures are representative of at least 3 different experiments.

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