3.4.24.61: nardilysin
This is an abbreviated version!
For detailed information about nardilysin, go to the full flat file.
Word Map on EC 3.4.24.61
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3.4.24.61
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metalloendopeptidase
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ectodomain
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heparin-binding
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pitrilysins
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adam17
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hb-egf
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insulysin
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insulinase
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hxxeh
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dynorphins
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medicine
- 3.4.24.61
- metalloendopeptidase
- ectodomain
-
heparin-binding
- pitrilysins
- adam17
- hb-egf
- insulysin
- insulinase
-
hxxeh
- dynorphins
- medicine
Reaction
hydrolysis of polypeptides, preferably at -Xaa-/-Arg-Lys-, and less commonly at -Arg-/-Arg-Xaa-, in which Xaa is not Arg or Lys =
Synonyms
hNRDc1, MGE, miniglucagon-generating endopeptidase, More, N-arginine dibasic (NRD) convertase, N-Arginine dibasic convertase, nardilysin, nardilysin (V8), nardilysin convertase, NRD convertase, NRD-convertase, Nrd1, Nrd1 and NRDc, NRDc
ECTree
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General Information on EC 3.4.24.61 - nardilysin
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GENERAL INFORMATION 
ORGANISM
UNIPROT
COMMENTARY 
LITERATURE
malfunction
metabolism
the enzyme regulates inflammation, metaplasia, and tumors in murine stomach. It promotes ectodomain shedding of the precursor forms of various growth factors and cytokines by enhancing the protease activities of a disintegrin and metalloproteinase (ADAM) proteins. The enzyme crucially regulates gastric inflammation caused by Helicobacter felis infection or forced expression of prostaglandin E2 in K19-C2mE mice
physiological function
malfunction
enzyme-deficient mice show increased energy expenditure owing to enhanced brown adipose tissue thermogenesis and hyperactivity as well as hypothermia and cold intolerance
malfunction
knockdown of enzyme expression attenuates gastric cancer cell growth in vitro
malfunction
deletion of the Nrdc gene in ApcMin mice crucially suppresses intestinal tumor development. In ApcMin mice, epithelial cell-specific deletion of Nrdc recapitulates the tumor suppression observed in Nrdc-null mice
malfunction
metaplastic changes following gastric inflammation are suppressed by the deletion of Nrdc. The deletion of Nrdc significantly suppresses N-methyl-N-nitrosourea (MNU)-induced gastric tumorigenesis in the murine stomach
malfunction
metaplastic changes following gastric inflammation were suppressed by the deletion of Nrdc. The deletion of Nrdc significantly suppresses N-methyl-N-nitrosourea (MNU)-induced gastric tumorigenesis in the murine stomac
malfunction
Nrd1-/- mice show glucose intolerance and severely decreased glucose-stimulated insulin secretion (GSIS). Islets isolated from Nrd1-/- mice exhibit reduced insulin content and impaired GSIS in vitro. Moreover, beta-cell-specific NRDc-deficient (Nrd1delbeta) mice show a diabetic phenotype with markedly reduced GSIS. MafA is specifically downregulated in islets from Nrd1delbeta mice
physiological function
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nardilysin is essential for regulation of axonal maturation and myelination in the central and peripheral nervous system. Nardilysin is a metalloendopeptidase enhancer of protein ectodomain shedding, is a critical regulator of these processes for establishing an efficient neuronal signaling network. The level of neuronal enzyme regulates myelin thickness
physiological function
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nardilysin is involved in degradation of neuropeptides and limited intracellular proteolysis. It might play a role in human brain pathology of in Alzheimer's disease and in Down syndrome that nardilysin enhances the activity of alpha-secretases ADAM10 and ADAM17. Alzheimer's disease and in Down syndrome brains show decreased cellular expression of all three antigens, and a reduction in the number of those neurons that co-express nardilysin with ADAM10 or with ADAM17
physiological function
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nardilysin and thimet oligopeptidase (TOP) are required, either together or alone, for the generation of a tumor-specific CTL epitope from PRAME, an immunodominant CTL epitope from Epstein-Barr virus protein EBNA3C, and a clinically important epitope from the melanoma protein MART-1
physiological function
NRDc is physically associated with and recruits the NCoR complex to some of the repressed genes and this association correlates with binding of H3K4me2
physiological function
nardilysin promotes gastric cancer cell growth by activating intrinsic cytokine signalling via enhanced ectodomain shedding of tumor necrosis factor-alpha
physiological function
the activity of alpha-secretase in the mouse brain is enhanced by the overexpression of the enzyme. The enzyme controls amyloid beta formation through the regulation of alpha-secretase
physiological function
the enzyme is a critical regulator of body temperature homoeostasis
physiological function
the interaction between the enzyme and centaurin-1alpha contribute to brain structural damage observed in Alzheimer's disease
physiological function
epithelial cell-specific overexpression of Nrdc significantly enhances tumor formation in ApcMin mice
physiological function
nardilysin controls beta-cell function via regulation of the Islet-1-MafA pathway. Overexpression of NRDc upregulates MafA and insulin expression in INS832/13 cells
physiological function
strong and specific accumulation of nardilysin in the manchette and axoneme suggests that the enzyme probably contributes either to the establishment of these specific microtubular structures and/or to their functional properties
physiological function
the enzyme controls intestinal tumorigenesis through HDAC1/p53-dependent transcriptional regulation
physiological function
the enzyme inhibits pancreatitis and suppresses pancreatic ductal adenocarcinoma initiation. Crucially regulates gastric inflammation caused by Helicobacter felis infection or forced expression of prostaglandin E2 in K19-C2mE mice. Metaplastic changes following gastric inflammation are suppressed by the deletion of Nrdc
