Figure 1.
Figure 1. Absence of GATA1 leads to a selective reduction in GPVI-mediated platelet aggregation at low concentrations of agonist. Washed murine platelets (1 × 108/mL) obtained from wild-type (WT; n = 3) and ΔneoΔHS (ΔneoΔHS; n = 8) mice were stimulated with thrombin (0.1 U/mL; left), collagen (2.0 μg/mL; middle), or CRP (1.0 μg/mL; right) and allowed to aggregate for 2.5 minutes, with stirring at 1200 rpm. Platelet aggregation was demonstrated by the change in light transmission. An arrow marks addition of agonist for thrombin 2 arrows are used, to assist in delineating between the WT and ΔneoΔHS tracings. Representative aggregation tracings are shown.

Absence of GATA1 leads to a selective reduction in GPVI-mediated platelet aggregation at low concentrations of agonist. Washed murine platelets (1 × 108/mL) obtained from wild-type (WT; n = 3) and ΔneoΔHS (ΔneoΔHS; n = 8) mice were stimulated with thrombin (0.1 U/mL; left), collagen (2.0 μg/mL; middle), or CRP (1.0 μg/mL; right) and allowed to aggregate for 2.5 minutes, with stirring at 1200 rpm. Platelet aggregation was demonstrated by the change in light transmission. An arrow marks addition of agonist for thrombin 2 arrows are used, to assist in delineating between the WT and ΔneoΔHS tracings. Representative aggregation tracings are shown.

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