CORIN
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Lua error in Module:Infobox_gene at line 33: attempt to index field 'wikibase' (a nil value). Corin, also called atrial natriuretic peptide-converting enzyme, is a protein that in humans is encoded by the CORIN gene.[1][2]
Protein
The CORIN gene encodes a member of the type II transmembrane serine protease class of the trypsin superfamily. Members of this family are composed of multiple structurally distinct domains.
Human corin, a polypeptide of 1042 amino acids, consists of an N-terminal cytoplasmic domain, a transmembrane domain and an extracellular region with two frizzled-like domains, eight LDL receptor-like domains, a scavenger receptor-like domain and a C-terminal trypsin-like serine protease domain.[1][3] Corin is synthesized as a zymogen that is activated by PCSK6.[4]
Corin exhibits a trypsin-like catalytic activity favoring basic residues at the P1 position.[5]
Human corin contains 19 N-glycosylation sites.[1] N-glycans promote corin expression on the cell surface and protect corin from metalloproteinase-mediated shedding.[6][7][8]
Function
Corin converts the atrial natriuretic peptide (ANP) precursor, pro-ANP, to mature ANP, a cardiac hormone that regulates salt-water balance and blood pressure.[9] In mice, corin deficiency prevents pro-ANP processing and causes salt-sensitive hypertension.[10][11]
Corin may also function as a pro-brain-type natriuretic peptide convertase.[9][12][13]
Corin-mediated ANP production in the pregnant uterus promotes spiral artery remodeling and trophoblast invasion.[14] CORIN mutations have been reported in patients with preeclampsia.[14][15]
In mice, corin functions in the dermal papilla to regulate coat color in an Agouti-dependent pathway.[16]
Variants and mutations
Variants encoded by alternative exons were reported in human and mouse corin.[17] A variant allele (T555I/Q568P) was found in African Americans with hypertension and cardiac hypertrophy.[18][19] The amino acid substitutions impaired corin activity.[20][21] An insertion variant in exon 1 alters the cytoplasmic tail.[22] This variant appeared more frequently in hypertensive patients. CORIN mutations were found in patients with hypertension.[14][15][23]
References
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Further reading
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