ArticlePloS one2011
The Escherichia coli BtuE protein functions as a resistance determinant against reactive oxygen species.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 42 citations in OpenAlex.
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- Long-chain flavodoxin FldX1 improves Paraburkholderia xenovorans LB400 tolerance to oxidative stress caused by paraquat and H2O2.PloS one · 2019Article
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- Bacillithiol has a role in Fe-S cluster biogenesis in Staphylococcus aureus.Molecular microbiology · 2015Article
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- The molecular mechanisms and physiological consequences of oxidative stress: lessons from a model bacterium.Nature reviews. Microbiology · 2013Review
- Global gene expression changes in Candidatus Liberibacter asiaticus during the transmission in distinct hosts between plant and insect.Molecular plant pathology · 2013Article
- Why do bacteria use so many enzymes to scavenge hydrogen peroxide?Archives of biochemistry and biophysics · 2012Review
- A novel protein kinase-like domain in a selenoprotein, widespread in the tree of life.PloS one · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
This work shows that the recently described Escherichia coli BtuE peroxidase protects the bacterium against oxidative stress that is generated by tellurite and by other reactive oxygen species elicitors (ROS). Cells lacking btuE (ΔbtuE) displayed higher sensitivity to K(2)TeO(3) and other oxidative stress-generating agents than did the isogenic, parental, wild-type strain. They also exhibited increased levels of cytoplasmic reactive oxygen species, oxidized proteins, thiobarbituric acid reactive substances, and lipoperoxides. E. coli ΔbtuE that was exposed to tellurite or H(2)O(2) did not show growth changes relative to wild type cells either in aerobic or anaerobic conditions. Nevertheless, the elimination of btuE from cells deficient in catalases/peroxidases (Hpx(-)) resulted in impaired growth and resistance to these toxicants only in aerobic conditions, suggesting that BtuE is involved in the defense against oxidative damage. Genetic complementation of E. coli ΔbtuE restored toxicant resistance to levels exhibited by the wild type strain. As expected, btuE overexpression resulted in decreased amounts of oxidative damage products as well as in lower transcriptional levels of the oxidative stress-induced genes ibpA, soxS and katG.
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Registered trials
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