Target intelligence / Profile preview

NADH-dependent oxidoreductase

Molecular classification
Enzyme, Oxidoreductase, Flavoprotein oxidoreductase
01

Overview

NADH-dependent oxidoreductases are a broad class of enzymes that catalyze the transfer of electrons from NADH to various electron acceptors, such as flavins (FMN, FAD), quinones, or ferredoxins, playing a central role in cellular redox metabolism and energy production[1][2][3][4][5]. These enzymes often contain flavin cofactors and share conserved structural motifs but can differ in substrate specificity and physiological roles depending on the organism and context[3][4]. Important representatives include NADH:FMN oxidoreductase, NADH:quinone oxidoreductase (NDH-2), and ferredoxin:NADP+ oxidoreductase (Nfn), among others[2][4]. Their physiological functions extend across oxidative phosphorylation in mitochondria, metabolic fermentation in bacteria, and redox homeostasis in various cell types. They are considered potential therapeutic targets in cancer and infection due to their involvement in mitochondrial and bacterial electron transport, but selectivity and safety remain significant challenges[4].

Other names
NADH:FMN oxidoreductaseNADH:quinone oxidoreductaseNADH oxidaseNADH dehydrogenaseFerredoxin:NADP+ oxidoreductase (for some enzyme classes)Flavoprotein oxidoreductase
02

Mechanism of action

Competitive or noncompetitive inhibition of electron transfer from NADH to acceptors (such as FMN, quinone, or ferredoxin)[1][2][4][5] Modulation of mitochondrial or bacterial electron transport chain

03

Biological functions

Electron transferCellular respirationOxidative phosphorylationMetabolic energy productionRedox homeostasis
04

Disease associations

Mitochondrial disease (dysfunction)Cancer (mitochondrial dysfunction)Infection (antibiotic target, particularly in bacteria)Other (neurological disorders, rare diseases)
05

Safety considerations

Off-target effects on mammalian (mitochondrial) vs. bacterial oxidoreductases due to structural similarities[4]Disruption of cellular energy metabolism can cause toxicity
06

Interacting drugs

None are specifically named in the current context, but drugs modulating mitochondrial respiration and antibiotics targeting NDH-2-like proteins are under investigation[4].
07

Biomarkers

Altered NADH/NAD+ ratio (redox status)Expression or activity levels of specific oxidoreductase isoforms in disease

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