1 exon.

3.8 kb mRNA; 1140 bp open reading frame.

380 amino acids.

Blood vessels, hypothalamus, heart, stomach, colon, endocrine pancreas, bone, skeletic muscle, spleen.

Plasma membrane.

The apelin receptor APJ belongs to the family of G protein-coupled receptors (ODowd et al., 1993; Devic et al., 1996; Devic et al., 1999; Scott et al., 2007) and is coupled to a Gi/o protein (Masri et al., 2006). Its activation leads to the regulation of various intracellular effectors with the following consequences: adenylylcyclase inhibition (Masri et al., 2006; Habata et al., 1999), increase of intracellular calcium (Choe et al., 2000) and activation of extracellular signal-regulated kinases (ERKs), PI-3K, Akt or p70S6 kinase (S6K1) (Masri et al., 2006; Masri et al., 2004 ).
Expression of apelin receptors by the endothelial cell (Devic et al., 1996; Devic et al., 1999) is associated with two effects :
1) NO release leading to vessel vasodilatation (Tatemoto et al., 2001) and peripheral hypotension (Lee et al., 2000);
2) cell proliferation and migration (Masri et al., 2004; Kasai et al., 2004) linked to angiogenesis (Cox et al., 2006).
The expression in the central nervous system is high in hypothalamus (De Mota et al., 2000; OCarroll et al., 2000) where receptor activation leads to the decrease of vasopressin release (De Mota et al., 2004). Activation of apelin receptors expressed by cardiomyocytes results in a strong inotropic effect (Szokodi et al., 2002). In stomach, apelin receptors are expressed by enterochromaffin-like cells where their stimulation decreases gastrin-induced acid secretion (Lambrecht et al., 2006). Apelin receptors may regulate epithelial proliferation in the colon (Han et al., 2007). Expression of apelin receptors both in endocrine pancreas and skeletic muscle contributes to the regulation of insulin plasma levels and glucose uptake (Sorhede Winzell et al., 2005; Dray et al., 2008). Apelin signalling also increases osteoblast proliferation (Xie et al., 2007) and cytokine expression by T lymphocytes (Habata et al., 1999).

No mutation has been presently described.