Receptor for prostaglandin E2 (PGE2) (PubMed:1372606, PubMed:8381413, PubMed:8223569). Required for normal development of fever in response to pyrinogens, including IL1B, prostaglandin E2 and bacterial lipopolysaccharide (LPS) (PubMed:9751056). Required for normal potentiation of platelet aggregation by prostaglandin E2, and thus plays a role in the regulation of blood coagulation (PubMed:11535576). Required for increased HCO3(-) secretion in the duodenum in response to mucosal acidification, and thereby contributes to the protection of the mucosa against acid-induced ulceration (PubMed:10535876). Not required for normal kidney function, normal urine volume and osmolality (PubMed:9843913). Receptor for prostaglandin E2 (PGE2); ligand binding activates a signaling cascade via G(i) proteins that leads to inhibition of adenylate cyclase (PubMed:1372606, PubMed:8381413). Shows high agonist-independent constitutive inhibition of adenylate cyclase (PubMed:8223569). Receptor for prostaglandin E2 (PGE2); ligand binding activates a signaling cascade via G(i) proteins that leads to inhibition of adenylate cyclase. Requires much higher ligand concentrations than isoform Alpha for activation (PubMed:8381413). Does not display agonist-independent constitutive inhibition of adenylate cyclase (PubMed:8223569). Receptor for prostaglandin E2 (PGE2); ligand binding can activate several distinct signaling cascades, resulting in activation or inhibition of adenylate cyclase. Interacts (via C-terminus) with MKLN1. Additional isoforms seem to exist (Probable). Isoforms have identical ligand binding properties but different coupling properties with G proteins: isoform Alpha and isoform Beta couple to G(i) proteins, whereas isoform Gamma couples to multiple G proteins, G(i) and G(s) (PubMed:1372606, PubMed:8381413, PubMed:8223569). Detected in platelets (PubMed:11535576). Kidney, uterus, and mastocytoma cells, and in a lesser amount in brain, thymus, lung, heart, stomach and spleen (PubMed:1372606). Ligand binding is affected by cAMP-dependent phosphorylation in brain membranes. No visible phenotype. Mice are born at the expected Mendelian rate. Females have normal fertility. Mutant mice have normal renal function, urine volume and urine osmolality (PubMed:9843913). Mutant mice fail to develop fever in response to pyrinogens, including IL1B, prostaglandin E2 and bacterial lipopolysaccharide (LPS) (PubMed:9751056). Mutant mice lack the normal potentiation of platelet aggregation by prostaglandin E2 and display prolonged bleeding times and decreased susceptibility to thromboembolism (PubMed:11535576). Mutant mice have normal basal levels of HCO3(-) secretion in the duodenum, but fail to respond to mucosal acidification by increased HCO3(-) secretion. Unlike wild-type, they have a high incidence of ulcers in response to mucosal acidification (PubMed:10535876). Belongs to the G-protein coupled receptor 1 family.