Figure 2
Figure 2. Pleckstrin-null platelets have a PKC-mediated aggregation defect. Washed murine platelets lacking pleckstrin were analyzed after agonist stimulation in a Lumi-Aggregometer. The y-axis shows the relative aggregation, and the x-axis shows time in minutes. Platelets lacking pleckstrin have nearly normal aggregation in response to high doses of a peptide agonist of PAR4 (the dominant murine thrombin receptor), collagen, and thrombin (bottom panels). In contrast, lower doses of these agonists show that pleckstrin-null platelets have a mild aggregation defect (top). Results are representative of 6 experiments.

Pleckstrin-null platelets have a PKC-mediated aggregation defect. Washed murine platelets lacking pleckstrin were analyzed after agonist stimulation in a Lumi-Aggregometer. The y-axis shows the relative aggregation, and the x-axis shows time in minutes. Platelets lacking pleckstrin have nearly normal aggregation in response to high doses of a peptide agonist of PAR4 (the dominant murine thrombin receptor), collagen, and thrombin (bottom panels). In contrast, lower doses of these agonists show that pleckstrin-null platelets have a mild aggregation defect (top). Results are representative of 6 experiments.

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