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血小板聚集所必需的糖蛋白Ibα-凝血酶复合物的晶体结构。

Crystal structure of the GpIbalpha-thrombin complex essential for platelet aggregation.

作者信息

Dumas John J, Kumar Ravindra, Seehra Jasbir, Somers William S, Mosyak Lidia

机构信息

Department of Chemical and Screening Sciences, Wyeth, 200 Cambridge Park Drive, Cambridge, MA 02140, USA.

出版信息

Science. 2003 Jul 11;301(5630):222-6. doi: 10.1126/science.1083917.

Abstract

Direct interaction between platelet receptor glycoprotein Ibalpha (GpIbalpha) and thrombin is required for platelet aggregation and activation at sites of vascular injury. Abnormal GpIbalpha-thrombin binding is associated with many pathological conditions,including occlusive arterial thrombosis and bleeding disorders. The crystal structure of the GpIbalpha-thrombin complex at 2.6 angstrom resolution reveals simultaneous interactions of GpIbalpha with exosite I of one thrombin molecule,and with exosite II of a second thrombin molecule. In the crystal lattice,the periodic arrangement of GpIbalpha-thrombin complexes mirrors a scaffold that could serve as a driving force for tight platelet adhesion. The details of these interactions reconcile GpIbalpha-thrombin binding modes that are presently controversial,highlighting two distinct interfaces that are potential targets for development of novel antithrombotic drugs.

摘要

血小板聚集和血管损伤部位的激活需要血小板受体糖蛋白Ibalpha(GpIbalpha)与凝血酶之间的直接相互作用。GpIbalpha-凝血酶结合异常与许多病理状况相关,包括闭塞性动脉血栓形成和出血性疾病。GpIbalpha-凝血酶复合物在2.6埃分辨率下的晶体结构揭示了GpIbalpha与一个凝血酶分子的外位点I以及第二个凝血酶分子的外位点II同时发生相互作用。在晶格中,GpIbalpha-凝血酶复合物的周期性排列反映了一个支架结构,该支架结构可能是血小板紧密黏附的驱动力。这些相互作用的细节协调了目前存在争议的GpIbalpha-凝血酶结合模式,突出了两个不同的界面,它们是新型抗血栓药物开发的潜在靶点。

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