EC Number   |
Natural Substrates |
|---|
   1.10.5.1 | 1-(beta-D-ribofuranosyl)-1,4-dihydronicotinamide + a quinone |
- |
| 1.10.5.1 | 1-(beta-D-ribofuranosyl)-1,4-dihydronicotinamide + co-enzyme Q |
natural substrate nicotinamide riboside, NRH |
| 1.10.5.1 | 1-(beta-D-ribofuranosyl)-1,4-dihydronicotinamide + menadione |
- |
| 1.10.5.1 | 1-(beta-D-ribofuranosyl)-1,4-dihydronicotinamide + menadione |
natural substrate nicotinamide riboside, NRH |
| 1.10.5.1 | more |
by deleting QR2 it seems that mice become increasingly susceptible to polycyclic aromatic hydrocarbon-induced skin carcinogenesis |
| 1.10.5.1 | more |
enzyme exhibits melatonin-binding activity |
| 1.10.5.1 | more |
high QR2 activity might make individuals more susceptible to Parkinsons disease. By inhibiting QR2, it seems that anti-malarial compounds such as quinacrine favour the red blood cell oxidative stress leading to the death of the parasite |
| 1.10.5.1 | more |
knockdown K562 cells exhibit increased antioxidant and detoxification enzyme expression and reduced proliferation rates |
| 1.10.5.1 | more |
organs of mice deleted for NQO2 are depleted of MT3 binding sites. NQO2 is part of the melatonin receptor MT3 binding sites |
| 1.10.5.1 | more |
the expression of the NQO2 gene is induced in response to 2,3,7,8-tetrachlorodibenzo-p-dioxin |
