2.1.1.222: 2-polyprenyl-6-hydroxyphenol methylase
This is an abbreviated version!
For detailed information about 2-polyprenyl-6-hydroxyphenol methylase, go to the full flat file.
Reaction
Synonyms
2-polyprenyl-6-hydroxyphenyl methylase, 3-demethyl ubiquinone-9 3-methyltransferase, UbiG, UbiG methyltransferase, ubiquinone biosynthesis O-methyltransferase
ECTree
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Engineering
Engineering on EC 2.1.1.222 - 2-polyprenyl-6-hydroxyphenol methylase
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H186A
the mutation completely destroys the interaction of the enzyme with liposomes
I177A
the mutation sharply reduces the interaction of the enzyme with liposomes
K183A
the mutation nearly completely destroys the interaction of the enzyme with liposomes
L132Q
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the mutation results in ubiquinone deficiency in Escherichia coli leading to a high sensitivity to thiols and a failure to grow on succinate
L178A
the mutation nearly completely destroys the interaction of the enzyme with liposomes
L178E
the mutation nearly completely destroys the interaction of the enzyme with liposomes
R179A
the mutation sharply reduces the interaction of the enzyme with liposomes
V181A
the mutation nearly completely destroys the interaction of the enzyme with liposomes
V181A/P182A/K183A/G184A/T185A/H186A
the mutations nearly completely destroy the interaction of the enzyme with liposomes
additional information
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a mutant deleted for ubiG exhibits longer lifespan, as well as enhanced resistance to thermal and oxidative stress (paraquat) compared to wild type at extracellular pH 9.0. The hypoxia-inducible transcription factor ArcA is required for the fully extended lifespan of the mutant
additional information
for mutant UbiGDELTA 165-187 lacking the sequence insertion that covers the methyl donor binding pocket, the binding affinity to SAH is approximately 58fold higher than that of wild-type
additional information
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a mutant deleted for ubiG exhibits longer lifespan, as well as enhanced resistance to thermal and oxidative stress (paraquat) compared to wild type at extracellular pH 9.0. The hypoxia-inducible transcription factor ArcA is required for the fully extended lifespan of the mutant
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