EC Number   |
General Information |
Reference |
|---|
   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 | more |
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 |
