1.10.5.1: ribosyldihydronicotinamide dehydrogenase (quinone)
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For detailed information about ribosyldihydronicotinamide dehydrogenase (quinone), go to the full flat file.
Word Map on EC 1.10.5.1
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1.10.5.1
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nadph:quinone
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resveratrol
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two-electron
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isoalloxazine
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medicine
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bnah
- 1.10.5.1
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nadph:quinone
- resveratrol
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two-electron
- isoalloxazine
- medicine
- bnah
Reaction
Synonyms
bQR2, dihydronicotinamide riboside:quinone oxidoreductase, dihydronicotinamide riboside:quinone oxidoreductase 2, dihydronicotinamide riboside:quinone reductase 2, EC 1.10.99.2, melatonin-binding site MT3, MT3, MT3/NQO2, N-ribosyldihydronicotinamide dehydrogenase (quinone), N-ribosyldihydronicotinamide:quinone oxidoreductase 2, NQO2, NRH-oxidizing enzyme, NRH:QR2, NRH:quinone oxidoreductase, NRH:quinone oxidoreductase 2, NRH:quinone oxireductase 2, NRH:quinone reductase 2, QR2, quinone oxidoreductase 2, quinone reductase 2, quinone reductase type 2
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General Information
General Information on EC 1.10.5.1 - ribosyldihydronicotinamide dehydrogenase (quinone)
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malfunction
physiological function
additional information
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adult QR2 knock-out mice demonstrate enhanced learning abilities in various tasks, including Morris water maze, object recognition, and rotarod performance test, while other behaviors related to anxiety (elevated plus maze), depression (forced swim), and schizophrenia (prepulse inhibition) are not affected in QR2-deficient mice. QR2 inhibition protects hippocampal cells against menadione-induced toxicity and serum deprivation and can reverse cognitive deficits
malfunction
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specific inhibitors of QR2, tested in vivo, show outstanding properties impairing memory loss
physiological function
quinone reductase 2 is an FAD-linked enzyme and the only known human target of two antimalarial drugs, primaquine and chloroquine, a functional role for NQO2 as a flavin redox switch
physiological function
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ribosyldihydronicotinamide dehydrogenase is a detoxification oxidoreductase, it is a flavoprotein that catalyzes the 2-electron reduction of various quinones, redox dyes, and the vitamin K menadione. NQO2 predominantly uses dihydronicotinamide riboside as the electron donor
physiological function
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the enzyme functions in metabolic reduction and detoxification processes. Evidence exists linking QR2 to the metabolic activation of quinones, which can lead to cell toxicity. Inhibition of the enzymme by resveratrol may protect cells against reactive intermediates and eventually cancer
physiological function
cells overexpressing NQO2 show a significant increase in the ROS production due to the fast reduction of quinone into quinol that can re-oxidize to form superoxide radicals. NQO2 inhibition decreases the amount of superoxide cells overexpressing NQ2 by decreasing the amount of quinol formed, and it increases the toxicity of menadione in the cells co-expressing NQO2 with the conjugation enzyme UDPglucuronosyltransferase (UGT1A6, E.C. 2.4.1.17). For the cells coexpressing NQO2 and UGT1A6, the homeostasis dysregulation is lower in presence of menadione than for its counterpart expressing only NQO2
physiological function
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in NQ2 knockout cells, cell growth is slower. In a mouse model with xenografts formed by NQO2 knockout cells, the NQO2 knockout group exhibited significant smaller tumor volume and tumor weight than the control. Deletion of NQO2 suppresses cancer proliferation in vivo
physiological function
knockdown of NQO2 enhances the albumin secretion of primary hepatocytes
physiological function
NQO2 catalyzes the reduction of quinone-like metabolites derived from acetaminophen, clozapine, 4'-hydroxydiclofenac, mefenamic acid, amodiaquine, and carbamazepine. NQO2 may be a genetic risk factor for clozapine-induced agranulocytosis
physiological function
silencing of NQO2 strongly reduces flavone-induced autophagic flux, although it increases basal LC3-II levels in HepG2 cells. Flavones apigenin and luteolin induce AMP kinase (AMPK) activation, while its reduction by AMPK beta (PRKAB1) silencing inhibits flavone-induced autophagy. The depletion of NQO2 levels by siRNA increases the basal AMPK phosphorylation but abrogates its further increase by apigenin
additional information
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QR2 does not share many features with QR1. Particularly, it does not seem to have a similar detoxifying function in cells. QR2 is overexpressed in neurodegenerative diseases