Department of Medicine and Cardeza Foundation, Thomas Jefferson University, Philadelphia, PA, USA.
Platelets. 2010;21(4):239-43. doi: 10.3109/09537101003639931.
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.
在血管损伤部位血小板的快速激活是血栓形成和止血中的一个关键事件。在这里，我们综述了最近的发现，这些发现(a)在快速依赖 Ca(2+)的血小板激活的连接点鉴定了 CalDAG-GEFI（RasGRP2），(b)证明了 CalDAG-GEFI、蛋白激酶 C 和 Gi 偶联的 ADP 受体 P2Y12 提供的信号之间的复杂协同作用，以及(c)提示 CalDAG-GEFI 是一种新的抗血小板治疗靶点。
