The function of ENSG00000187474 (FPR3, formyl peptide receptor 3) is as follows. May function as a pattern recognition G protein-coupled receptor (PRR/GPCR) involved in innate recognition of peptides derived from a specific set of bacterial pathogens or host mitochondria as pathogen- and damage-associated molecular patterns (PAMPs and DAMPs) (PubMed:24108355, PubMed:25605714). Low affinity receptor for a restricted repertoire of bacterial N-formylated peptides including fMKKIML from L. monocytogenes and fMPKLNR from V. cholerae. Contrary to FPR1 and FPR2 does not act as a receptor for fMLF peptide (PubMed:15187149, PubMed:25605714). High affinity receptor for N- acetylated F2L peptide derived from the cleavage of heme-binding protein HEBP1. F2L peptide binding may trigger chemotaxis of monocytes and dendritic cells to facilitate tissue repair (PubMed:15623572). Low affinity receptor for N-acetylated Ac2-26 peptide derived from ANXA1, an anti-inflammatory and pro-resolving agonist. Ac2-26 peptide binding can direct myeloid cell chemotaxis within the inflammatory site where ANXA1 is at high concentrations, but it can also lead to receptor desensitization to limit the inflammatory response (PubMed:15187149). Receptor for MT-RNR2/humanin, a mitochondrial-derived peptide that has an anti-inflammatory role in resolution of inflammation (PubMed:15465011). Peptide binding leads to conformational changes coupled to heterotrimeric G(i) protein signaling. Upon GDP to GTP conversion, G(i)-alpha subunit dissociates from G-beta and G-gamma subunits. Free G(i)-alpha subunit inhibits cyclic adenylate cyclase and cAMP synthesis whereas the G-beta and G-gamma dimer activates downstream phospholipase C-beta and phosphoinositide 3-kinase signaling cascades leading to Ca(2+) influx (PubMed:15187149, PubMed:15465011, PubMed:15623572, PubMed:25605714). {ECO:0000269|PubMed:15187149, ECO:0000269|PubMed:15465011, ECO:0000269|PubMed:15623572, ECO:0000269|PubMed:24108355, ECO:0000269|PubMed:25605714}.