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Purinergic receptor P2Y10, G-protein coupled (P2Y10)

Target
P2Y10
Molecular classification
G protein-coupled receptor (GPCR), Receptor, Purinergic receptor
01

Overview

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].

Other names
Putative P2Y purinoceptor 10P2Y10P2RY10LPS2P2Y-like receptorLysophosphatidylserine receptor 2 (LYPSR2)G-protein coupled purinergic receptor P2Y10
02

Mechanism of action

Drugs targeting P2Y10—mechanistically would modulate GPCR-mediated signal transduction, potentially affecting T cell migration and immune response

03

Biological functions

Signal transductionImmune response (modulation of T cell migration)Regulation of chemokine-induced migration, polarization, RhoA activation in T cells
04

Disease associations

Inflammation (contributory role in autoimmune and hypersensitivity models)Neuroinflammatory disease (upregulated in murine neuroinflammation, e.g. experimental autoimmune encephalomyelitis)Other (potential general immune and inflammatory regulation mediated by T cell migration)
05

Safety considerations

Modulation could affect immune cell migration and immune response (theoretical risk of immunosuppression or exacerbation of immune-mediated disease)Unknown off-target effects due to orphan status and unclear endogenous ligands

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