ArticleThe Biochemical journal2013
Role of Helicobacter pylori methionine sulfoxide reductase in urease maturation.
Article in The Biochemical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Reactive oxygen species and reactive nitrogen species are double-edged swords in Salmonella infection.Archives of microbiology · 2025Review
- Methionine Redox Homeostasis in Protein Quality Control.Frontiers in molecular biosciences · 2021Review
- Identification of oxidant susceptible proteins in Salmonella Typhimurium.Molecular biology reports · 2020Article
- Noncatalytic Antioxidant Role for Helicobacter pylori Urease.Journal of bacteriology · 2018Article
- Oxidative and nitrosative stress defences of Helicobacter and Campylobacter species that counteract mammalian immunity.FEMS microbiology reviews · 2016Article
- Intrinsic disorder and metal binding in UreG proteins from Archae hyperthermophiles: GTPase enzymes involved in the activation of Ni(II) dependent urease.Journal of biological inorganic chemistry : JBIC : a publication of the Society of Biological Inorganic Chemistry · 2015Article
- Alkyl hydroperoxide reductase repair by Helicobacter pylori methionine sulfoxide reductase.Journal of bacteriology · 2013Article
- Improved identification and relative quantification of sites of peptide and protein oxidation for hydroxyl radical footprinting.Journal of the American Society for Mass Spectrometry · 2013Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The persistence of the gastric pathogen Helicobacter pylori is due in part to urease and Msr (methionine sulfoxide reductase). Upon exposure to relatively mild (21% partial pressure of O2) oxidative stress, a Δmsr mutant showed both decreased urease specific activity in cell-free extracts and decreased nickel associated with the partially purified urease fraction as compared with the parent strain, yet urease apoprotein levels were the same for the Δmsr and wild-type extracts. Urease activity of the Δmsr mutant was not significantly different from the wild-type upon non-stress microaerobic incubation of strains. Urease maturation occurs through nickel mobilization via a suite of known accessory proteins, one being the GTPase UreG. Treatment of UreG with H2O2 resulted in oxidation of MS-identified methionine residues and loss of up to 70% of its GTPase activity. Incubation of pure H2O2-treated UreG with Msr led to reductive repair of nine methionine residues and recovery of up to full enzyme activity. Binding of Msr to both oxidized and non-oxidized UreG was observed by cross-linking. Therefore we conclude Msr aids the survival of H. pylori in part by ensuring continual UreG-mediated urease maturation under stress conditions.
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Registered trials
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