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Hemostatic plug formation at sites of vascular injury is strongly dependent on rapid platelet activation and aggregation. However, to prevent thrombotic complications, platelet aggregate formation is regulated, in part, by the desensitization of the platelet P2Y1 receptor. Here, we analyzed a novel knock-in mouse strain expressing a P2Y1 receptor variant that cannot be desensitized. The study, led by David S. Paul and Tasha Blatt, demonstrates that loss of P2Y1 receptor desensitization in platelets leads to increased P2Y1 receptor signaling in vitro, with little impact on in vivo platelet adhesion/aggregation at sites of vascular injury, likely due to rapid ADP degradation or being swept away in the bloodstream. The project was a collaborative effort supported by senior authors, Wolfgang Bergmeier of the UNC BRC and Dept. of Biochemistry and Biophysics and Robert Nicholas of the UNC Dept. of Pharmacology. Other contributing BRC members include: Wyatt Schug, Emily Clark, Katie Poe, Jean Marie Mwiza, Tomohiro Kawano and Nigel Mackman.


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