EC Number   |
General Information |
Reference |
|---|
   3.4.24.61 | 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 |
754562 |
| 3.4.24.61 | malfunction |
enzyme-deficient mice show increased energy expenditure owing to enhanced brown adipose tissue thermogenesis and hyperactivity as well as hypothermia and cold intolerance |
734761 |
| 3.4.24.61 | malfunction |
knockdown of enzyme expression attenuates gastric cancer cell growth in vitro |
733727 |
| 3.4.24.61 | 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 |
753760 |
| 3.4.24.61 | 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 |
755470 |
| 3.4.24.61 | 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 |
753390 |
| 3.4.24.61 | 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 |
755470 |
| 3.4.24.61 | physiological function |
epithelial cell-specific overexpression of Nrdc significantly enhances tumor formation in ApcMin mice |
754562 |
| 3.4.24.61 | physiological function |
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 |
718147 |
| 3.4.24.61 | 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 |
753390 |
