Serine-type endopeptidase involved in atrial natriuretic peptide (NPPA) processing (PubMed:11884416, PubMed:15637153). Converts through proteolytic cleavage the non-functional propeptide NPPA into the active hormone, thereby regulating blood pressure in heart and promoting natriuresis, diuresis and vasodilation (PubMed:11884416, PubMed:15637153, PubMed:22418978). Proteolytic cleavage of pro-NPPA also plays a role in female pregnancy by promoting trophoblast invasion and spiral artery remodeling in uterus (PubMed:22437503). Also acts as a regulator of sodium reabsorption in kidney (PubMed:20613715, PubMed:22418978). May also process pro-NPPB the B-type natriuretic peptide (By similarity). Soluble form produced following cleavage by ADAM10. Highly expressed in heart. Also expressed in pregnant uterus. N-glycosylated; required for processing and activation. Activated through proteolytic processing by a trypsin-like protease; cleaved into a N-terminal propeptide and an activated corin protease fragment. Atrial natriuretic peptide-converting enzyme, 180 kDa soluble fragment is produced by cleavage by ADAM10. Cleavage by ADAM10 to produce soluble 180 kDa soluble fragment takes place after the transmembrane region and before FZ 1 (By similarity). A disulfide bond links the activated corin protease fragment and the N-terminal propeptide. The disulfide bond also links the activated corin protease fragment with Atrial natriuretic peptide-converting enzyme, 180 kDa soluble fragment (By similarity). Mice develop normally, are viable and fertile but develop hypertension. They display increased body weight associated with impaired maturation of pro-NPPA which can be restored by injection of Corin. Spontaneous and salt-sensitive hypertension exacerbated during pregnancy is also noticed. A cardiac hypertrophy is also detected together with a decline in cardiac function later in life (PubMed:15637153). Blood pressure on a high-salt diet is significantly increased: knockout mice show an impairment of urinary sodium excretion and an increase in body weight, but no elevation of plasma renin or serum aldosterone levels (PubMed:22418978). Conditional knockout mice which express Corin in heart only do not display any visible phenotype in non-pregnant mice. In contrast, pregnant conditional knockout mice develop high blood pressure and proteinuria, characteristics of pre-eclampsia. In these mice, trophoblast invasion and uterine spiral artery remodeling are markedly impaired (PubMed:22437503). Corin is disrupted in C57BL/6-Kit(W-sh/W-sh) mice, a genetic inversion used as mast cell-deficient model. Phenotypes in C57BL/6-Kit(W-sh/W-sh) mice are mainly due to the absence of Kit, a receptor for mast cell development. The absence of Corin probably leads to immediate significant cardiac hypertrophy and contractile dysfunction in response to pressure overload (PubMed:21903139). Belongs to the peptidase S1 family.