EC Number |
Natural Substrates |
---|
3.4.24.61 | alpha-neoendorphin + H2O |
- |
3.4.24.61 | amyloid precursor protein + H2O |
the enzyme enhances alpha-cleavage of amyloid precursor protein, which results in the decreased generation of amyloid beta in vitro |
3.4.24.61 | dynorphin A + H2O |
- |
3.4.24.61 | Glucagon + H2O |
- |
3.4.24.61 | heparin-binding epidermal growth factor-like growth factor + H2O |
substrate is synthesized as a transmembrane protein. Enzyme enhances ectodomain shedding of substrate in coperation with tumor necrosis factor-alpha-converting enzyme. Metalloendopeptidase activity of enzyme is not required for enhancement of shedding |
3.4.24.61 | malate dehydrogenase + H2O |
- |
3.4.24.61 | more |
physiological substrates of nardilysin have yet to be identified |
3.4.24.61 | more |
enhancement of alpha-secretase cleavage of amyloid precursor protein by a metalloendopeptidase nardilysin, resulting in down-regulation of beta-amyloid protein, overview, the enzyme also enhances ectodomain shedding of heparin-binding epidermal growth factor-like growth factor through activation of ADAM17, NRDc is regulatorally involved in the metabolism |
3.4.24.61 | more |
expression of nardilysin synergistically enhances TNF-alpha-converting enzyme-induced TNF-alpha ectodomain-shedding via activation of ADAM proteases ADAM9 and ADAM10, activation is independent of protein kinase C, overview |
3.4.24.61 | more |
the enzyme interacts with the brain-specific protein p42IP4/centaurin-alpha1, the interactionis regulated by phosphatidylinositol 3,4,5-triphosphate and inositol-1,3,4,5-tetrakisphophate, nardilysin might play a role in brain development, overview |