| 23796 | Q9WV08 | APJ_MOUSE | Apelin receptor (Angiotensin receptor-like 1) (G-protein coupled receptor APJ) (MSR) | DISRUPTION PHENOTYPE | Mice lacking APLNR are not represented at Mendelian ratios. Mutant embryos exhibit incomplete penetrance of embryonic lethality (PubMed:28854362, PubMed:28663440). Mutant embryos display improper establishment of the fetal-maternal circulation, such as underdeveloped yolk sac vasculature, embryonic vascular malformations and impaired cardiac tube looping at 10.5 dpc (PubMed:28854362, PubMed:28663440). Mice heart of embryos show reduced coronary vessel growth at 13.5 dpc (PubMed:28890073). The heart of mutant adult mice induced by pressure overload display no improvement in cardiac dysfunction, hypertrophy and fibrosis in response to peptide hormone APELA treatment (PubMed:28371822). Conditional knockout in heart endothelial cells leads to delayed progression of vessel growth onto the heart and reduced branching of the developing coronary plexus in both the subepicardial and intramyocardial layers at 13.5 and 15.5 dpc (PubMed:28890073). Conditional endothelial-specific knockout adult mice, despite severe embryonic coronary vessel defects recover normal cardiac functions; endocardial-derived coronary vessels expand to rescue defective sinus venosus development in a APELA-APLNR-independent manner (PubMed:28890073). Double knockout mice of APLNR and APELA genes exhibited the same penetrance and embryonic lethality as single APELA knockout mice (PubMed:28854362). {ECO:0000269|PubMed:28371822, ECO:0000269|PubMed:28663440, ECO:0000269|PubMed:28854362, ECO:0000269|PubMed:28890073}. |