Corin was first described as a trypsin-like serine proteinase in the heart which processed pro-atrial natriuretic peptide into the active form ANP. Corin cleaves pro-ANP at Arg98/Ser-99, and blocking Corin message inhibits pro-ANP processing. Null mutant mice lacking Corin develop hypertension, and a series of missense mutations have been identified in humans with high blood pressure and hypertension. Corin is a member of the type-II transmembrane serine proteinases, such as Hepsin, Epitheli