Platelet P2Y1 receptor (P2Y1)

The Platelet P2Y1 receptor is a purinergic G protein-coupled receptor predominantly expressed on platelets, as well as in other tissues such as the brain and vasculature[2][3][5]. It is selectively activated by ADP, resulting in Gαq-mediated calcium mobilization, platelet shape change, and the initiation of reversible platelet aggregation, which are crucial for normal hemostasis and thrombosis[1][2][3][5]. Pharmacological and genetic inhibition of P2Y1 abolishes ADP-induced platelet aggregation, highlighting its essential role[3]. Antagonists targeting P2Y1, such as MRS2500, offer antithrombotic potential with a lower risk of bleeding compared to P2Y12 receptor antagonists[1]. Various high-affinity antagonists and radiolabeled ligands are used to study its function and quantitation. The P2Y1 receptor is part of the larger purinergic GPCR family and exhibits rapid desensitization and internalization dynamics that continue to be areas of research interest. Genetic polymorphisms in the receptor may contribute to cardiovascular disease risk[2].

Other names

P2Y1 receptorPurinergic receptor P2Y1P2RY1

Agonists (e.g., ADP) bind and activate P2Y1, triggering Gαq protein coupling, intracellular calcium release, platelet shape change, and initial ADP-dependent aggregation[1][2][3]. Antagonists (e.g., MRS2500, BPTU, MRS2179) inhibit receptor activation, blocking ADP-induced platelet aggregation by stabilizing the inactive receptor conformation or occupying the ligand-binding site[1][2][5].