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Purinergic receptor P2Y10, G-protein coupled (P2Y10), is an orphan G protein-coupled receptor classified as part of the purinergic receptor family based on sequence similarity[2][5]. Its endogenous ligand remains uncertain; candidates include lysophosphatidylserine (LysoPS) and ATP, but consensus is lacking and it is officially listed as an orphan receptor[2]. P2Y10 is expressed predominantly in CD4 and CD8 T cells, as well as in monocytes and dendritic cells, and has a role in facilitating chemokine-induced T cell migration, polarization, and RhoA activation—contributing to inflammation and neuroinflammatory conditions such as experimental autoimmune encephalomyelitis[2]. Signal transduction appears to involve coupling to G12/13 family G-proteins with autocrine/paracrine activation by LysoPS and ATP[2]. Despite confusion regarding endogenous ligand and family assignment, P2Y10 is not among the eight canonical human P2Y subtypes (P2Y1, 2, 4, 6, 11, 12, 13, 14)[2][6], but evidence suggests it mediates relevant ATP/ADP-dependent immune functions[2]. No known drugs specifically target P2Y10 to date, and its ligand pharmacology and intracellular signaling remain under investigation[2][5][6].
Drugs targeting P2Y10—mechanistically would modulate GPCR-mediated signal transduction, potentially affecting T cell migration and immune response
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