Rapid activation of platelets at sites of vascular injury is a critical event in thrombosis and hemostasis. Here, we review recent findings, which (a) identified CalDAG-GEFI (RasGRP2) at the nexus of the rapid Ca(2+)-dependent platelet activation, (b) demonstrated a complex synergy between signaling provided by CalDAG-GEFI, protein kinase C and the Gi-coupled receptor for ADP, P2Y12, and (c) suggested CalDAG-GEFI as a novel target for anti-platelet therapy.
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Stefanini et al. (2010) studied this question.
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