SCUBA

GPR34 — G protein-coupled receptor 34

GPR34 belongs to a gene co-expression module in 6 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

GPR34's module in each cell type

Cell typeModuleShares the module with
CD4⁺ T cellsInflammatory activation
Immune regulation
ATF7IP2, ATP10D, B3GALT2, COMMD8, GBP3, GFI1, MAEA, MGAT1 +7 moreView in SCUBA
CD8⁺ T cellsTc17 program
Tc17 program
ABI3, ABRACL, CAPG, CCDC85B, FKBP11, IL17A, KLRB1, NFKBIA +4 moreView in SCUBA
Gamma-delta T cellsTissue Resident CD103+
Tissue residence
ADRB1, BCAS4, BLMH, CCNJL, CD160, CD96, CLIC5, CLNK +28 more
MacrophagesInnate Antiviral Sensing
Innate immunity
ADA2, ADPRH, ALDH9A1, APOBEC3C, BST2, C2, CAT, CD4 +26 moreView in SCUBA
MonocytesEfferocytosis Tissue Macrophage
Lysosomal & pahgocytosis
ADORA3, AKR1B1, CPM, FCHO2, MERTK, PDK4, SLC1A3, STARD13View in SCUBA
Natural Killer cellsTissue-Resident NK
Gut residency
ADRB1, CAMK4, GPR55, ITGAE, LRRC25, MYO1E, NCR2, S100A13 +2 moreView in SCUBA

About the gene

ChromosomeX: 41688973-41697275
Predicted locationMembrane
Essential geneNo
Protein classG-protein coupled receptors, Predicted membrane proteins
Molecular functionG-protein coupled receptor, Receptor, Transducer

Function

G-protein-coupled receptor of lysophosphatidylserine (LysoPS) that plays different roles in immune response. Acts a damage-sensing receptor that triggers tissue repair upon recognition of dying neutrophils (By similarity). Mechanistically, apoptotic neutrophils release lysophosphatydilserine that are recognized by type 3 innate lymphoid cells (ILC3s) via GPR34, which activates downstream PI3K-AKT and RAS-ERK signaling pathways leading to STAT3 activation and IL-22 production (By similarity). Plays an important role in microglial function, controlling morphology and phagocytosis (By similarity)

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.