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American Journal of Medicine
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American Journal of Medicine
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Thrombin is also a very potent platelet agonist and Figure 4 depicts the major thrombin receptor on the platelet, called protease activated receptor 1 (PAR1).[1] This transmembrane receptor has an extracellular domain that binds thrombin; when thrombin binds to this extracellular domain it cleaves a portion of that domain to create a new amino terminus of the receptor, which, as shown on the right-hand side of the Figure, acts in a tethered ligand fashion to then fold over, contact the body of the receptor, and trigger signaling of the platelet. This signaling results in platelet activation and subsequent aggregation. So thrombin is really the bridge between coagulation because of its capacity to convert fibrinogen to fibrin and induce platelet activation and platelet aggregation because of its ability to serve as a very potent platelet agonist. Weitz JI. Am J Med 2013; published on-line at http://education.amjmed.com/00000.
[1] Coughlin SR. Thrombin signalling and protease-activated receptors. Nature. 2000;407:258-264.