Figure 2.
HAG abolishes P2Y12-dependent signaling but only partially inhibits CalDAG GEFI-dependent signaling in mouse platelets. Washed mouse platelets lacking CalDAG GEFI (A) or P2Y12 (B) were pretreated with 10 μM HAG or DMSO for 30 minutes at room temperature and stimulated with 1.25 μg/mL convulxin. Aggregation was observed for 3 minutes (panel A, **P < .007 for HAG vs DMSO; panel B, *P < .05 for HAG vs DMSO, n = 4 for each group).

HAG abolishes P2Y12-dependent signaling but only partially inhibits CalDAG GEFI-dependent signaling in mouse platelets. Washed mouse platelets lacking CalDAG GEFI (A) or P2Y12 (B) were pretreated with 10 μM HAG or DMSO for 30 minutes at room temperature and stimulated with 1.25 μg/mL convulxin. Aggregation was observed for 3 minutes (panel A, **P < .007 for HAG vs DMSO; panel B, *P < .05 for HAG vs DMSO, n = 4 for each group).

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