3.4.17.3	malfunction	among mice genetically deficient in either carboxypeptidase B2 (Cpb2) or carboxypeptidase N (Cpn), in a model of hemolytic-uremic syndrome, Cpb2-/- mice have the worst disease, followed by Cpn-/- mice, with wild-type mice being the most protected. This model is driven by complement component C5a, and shows that carboxypeptidase B2 is important in inactivating complement component C5a. Cpn-/- mice are generated by disruption of complement component Cpn1. When mice are challenged acutely with cobra venom factor, the reverse phenotype is observed. Cpn-/- mice have markedly worse disease than Cpb2-/- mice, and wild-type mice are resistant	754517	
3.4.17.3	malfunction	the knockdown of cpn1 by morpholino injection impairs the growth of intersegmental vessels and caudal vein plexus. Loss of cpn1 affects the expression of the vascular markers flt4, mrc1, flk, stabilin, and ephrinb2	755462	
3.4.17.3	additional information	the enzyme is constitutively active	754517	
3.4.17.3	physiological function	carboxypeptidase N is responsible for systemic inactivation of complement component C3a and C5a	754517	
3.4.17.3	physiological function	cpn1 is involved in vascular development of zebrafish	755462	
3.4.17.3	physiological function	the enzyme removes C-terminal basic amino acids from bioactive peptides and proteins, thereby inactivating them	754517