Snaclecs (Snake C-Type Lectins) that activate platelets

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Abstract

One of the major targets for snake venom proteins is haemostasis. This weakens the prey and helps with swallowing and digestion. The venom proteins act either on coagulation factor or on platelets. Snake venom proteins mainly adapt physiological mechanisms to inhibit or activate platelets. The most efficient way for snake venom to reduce platelet function is not by inhibiting the function of individual or several receptors but rather by activating platelets so that they are removed from the circulation producing thrombocytopenia. Platelets can be activated efficiently by an agonist using low molecule numbers in two main ways already used physiologically. One of these is by proteases acting on proteolytically activated receptors. The other major route is by clustering receptors mimicking physiological ligands such as von Willebrand factor and collagen. The snaclecs described in this chapter fall into this latter category. Their targets are those of the physiological ligands and include GPIb, GPVI, α2β1 and the recently discovered CLEC2.

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Clemetson, K. J. (2011). Snaclecs (Snake C-Type Lectins) that activate platelets. In Toxins and Hemostasis: From Bench to Bedside (pp. 621–636). Springer Netherlands. https://doi.org/10.1007/978-90-481-9295-3_35

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