1.5.99.14: 6-hydroxypseudooxynicotine dehydrogenase
This is an abbreviated version!
For detailed information about 6-hydroxypseudooxynicotine dehydrogenase, go to the full flat file.
Reaction
Synonyms
KdhA, KdhB, KdhC, KdhL, KdhM, KdhS, PNO
ECTree
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General Information
General Information on EC 1.5.99.14 - 6-hydroxypseudooxynicotine dehydrogenase
for references in articles please use BRENDA:EC1.5.99.14
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physiological function
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6-hydroxypseudooxynicotine dehydrogenase utilizes the electron transfer flavoprotein EtfAB as the physiological electron acceptor. The electrons are further transferred from the reduced EtfAB to coenzyme Q by the catalysis of electron transfer flavoprotein:ubiquinone oxidoreductase. Disruption of the EtfAB genes in the nicotine-degrading gene cluster decreases the growth rate of Agrobacter tumefaciens S33 on nicotine but not on 6-hydroxy-3-succinoylpyridine
physiological function
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Rid protein (participating in metabolite damage repair) encoded by a gene in the nicotine-degrading gene cluster enhances the reaction of 6-hydroxypseudooxynicotine dehydrogenase. Rid relieves the toxicity of the presumed imine intermediate produced in the 6-hydroxypseudooxynicotine dehydrogenase reaction and, in the presence of Rid, 6-hydroxypseudooxynicotine dehydrogenase maintains a high level of activity and the amount of the reaction product is increased by at least 5fold. Disruption of the Rid gene leads to slower growth on nicotine
physiological function
-
6-hydroxypseudooxynicotine dehydrogenase utilizes the electron transfer flavoprotein EtfAB as the physiological electron acceptor. The electrons are further transferred from the reduced EtfAB to coenzyme Q by the catalysis of electron transfer flavoprotein:ubiquinone oxidoreductase. Disruption of the EtfAB genes in the nicotine-degrading gene cluster decreases the growth rate of Agrobacter tumefaciens S33 on nicotine but not on 6-hydroxy-3-succinoylpyridine
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physiological function
-
Rid protein (participating in metabolite damage repair) encoded by a gene in the nicotine-degrading gene cluster enhances the reaction of 6-hydroxypseudooxynicotine dehydrogenase. Rid relieves the toxicity of the presumed imine intermediate produced in the 6-hydroxypseudooxynicotine dehydrogenase reaction and, in the presence of Rid, 6-hydroxypseudooxynicotine dehydrogenase maintains a high level of activity and the amount of the reaction product is increased by at least 5fold. Disruption of the Rid gene leads to slower growth on nicotine
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