R&D Systems supports platelet research with a full line of recombinant proteins, antibodies, and assays. Our immunoassay selection includes Quantikine® and DuoSet® ELISA kits, ELISpot kits, Luminex® Assays, Proteome Profiler™ Antibody Arrays, and Simple Plex™ automated assays. Our sister brand Tocris Bioscience supplies a wide range of small molecule agonists, antagonists and enzyme inhibitors for the study of platelets and coagulation. We also provide stem cell and cell culture products to support your research. Learn More.
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Recombinant Proteins
Quantikine® and DuoSet® ELISA Kits
Plasminogen Activators and Inhibitors
Small Molecule Agonists and Antagonists
u-Plasminogen Activator/Urokinase Inhibitors
Platelet Literature and Resources
Brochures and Product Guides
Cardiovascular Research Product Guide
Products for Glycobiology Research
Products for Angiogenesis Research
Posters
References and Troubleshooting Guides
Blood Coagulation Signaling Pathways
Atherosclerosis Disease Progression Cell Markers
Protocols/Troubleshooting Guides From Novus Biologicals
Protocols/Troubleshooting Guides From R&D Systems®
Background
Blood coagulation (clot formation or thrombosis) relies on a proteolytic cascade that results in the formation of an insoluble mass of proteins and platelets. It is critical for hemostasis during vascular damage. The intrinsic (contact factor) pathway is triggered by consecutive activation of Coagulation Factors XII, XI, and IX. The extrinsic (tissue factor) pathway is triggered when circulating Factor VII crosses damaged vascular endothelium to interact with Factor III/Tissue Factor. Both the intrinsic and extrinsic pathways lead to activation of Factor II/Thrombin and the crosslinking of Fibrin. Clot dissolution is carried out by Plasmin which is activated by the Plasminogen Activators tPA and uPA. Many cascade and regulatory factors circulate in the blood, while others are supplied by activated platelets.
Blood coagulation is tightly regulated to limit bleeding but avoid pathological initiation. Activation at multiple steps is restricted by serine protease inhibitors including alpha 2-Macroglobulin, Kininogen, Serpin A1/alpha 1-Antitrypsin, Serpin A5/Protein C Inhibitor, Serpin C1/Antithrombin-III, Serpin E1/PAI-1, and TFPI. Hypocoagulability, such as in hemophilia and von Willebrand disease, can result from deficiencies in Vitamin K, von Willebrand Factor, Factors V, VIII, IX, X, or XII or from thrombocytopenia (low platelet count). In contrast, life threatening clot formation occurs in atherosclerosis, stroke, and deep vein thrombosis. High coagulation risk or emergency treatment of dangerous clotting can be addressed with anticoagulants/blood thinners (e.g. warfarin) or thrombolytic/clot buster drugs (e.g. tPA).