Orphan receptor. Could be involved in modulating differentiation and maintaining homeostasis of epithelial cells. This retinoic acid-inducible GPCR provide evidence for a possible interaction between retinoid and G-protein signaling pathways. Functions as a negative modulator of EGFR signaling (By similarity). May act as a lung tumor suppressor (PubMed:18000218). Interacts (via its transmembrane domain) with EGFR. Localized in perinuclear vesicles, probably Golgi-associated vesicles. Expressed at high level in fetal and adult lung tissues but repressed in most human lung cancers (PubMed:9857033, PubMed:18000218). Constitutively expressed in fetal kidney and adult placenta, kidney, prostate, testis, ovary, small intestine, colon, stomach, and spinal cord at low to moderate levels. Not detectable in fetal heart, brain, and liver and adult heart, brain, liver, skeletal muscle, pancreas, spleen, thymus, and peripheral leukocytes. According to PubMed:10783259, expressed at low but detectable level in pancreas and heart. By all-trans retinoic acid (ATRA). Phosphorylated in two conserved double-tyrosine motifs, TYR-317/TYR-320 and TYR-347/TYR-350, by EGFR; leading to inactivation of the tumor suppressive function of GPRC5A in lung cancer cells. TYR-317 and TYR-320 are the preferred residues responsible for EGFR-mediated GPRC5A phosphorylation. Belongs to the G-protein coupled receptor 3 family.