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• W2023552723 abstract "After vessel wall injury, platelets adhere to the exposed subendothelium, are activated, and release mediators such as thromboxane A2 (TXA2) and nucleotides stored at very high concentration in the so-called dense granules. Among other soluble agents, released nucleotides act in a positive feedback mechanism to cause further platelet activation and amplify platelet responses induced by agents such as thrombin or collagen. Adenine nucleotides act on platelets through three distinct P2 receptors: two are G protein-coupled adenosine diphosphate (ADP) receptors, namely the P2Y1 and P2Y12 receptor subtypes; the P2X1 receptor ligand-gated cation channel is activated by adenosine triphosphate (ATP). The P2Y1 receptor initiates platelet aggregation but is not sufficient for a full platelet aggregation in response to ADP, whereas the P2Y12 receptor is responsible for completion of the aggregation to ADP. This receptor, the molecular target of the antithrombotic drug clopidogrel, is responsible for most of the potentiating effects of ADP when platelets are stimulated by agents such as thrombin, collagen, or immune complexes. The P2X1 receptor is involved in platelet shape change and in activation by collagen under shear conditions. Each of these receptors is coupled to specific signal transduction pathways in response to ADP or ATP and is differentially involved in all of the sequential events involved in platelet function and hemostasis. As such, they represent potential targets for antithrombotic drugs." @default.
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• W2023552723 date "2005-04-01" @default.
• W2023552723 modified "2023-10-03" @default.
• W2023552723 title "The P2 Receptors in Platelet Function" @default.
• W2023552723 doi "https://doi.org/10.1055/s-2005-869520" @default.
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