ArticleJournal of bacteriology2014
Ammonium metabolism enzymes aid Helicobacter pylori acid resistance.
Article in Journal of bacteriology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 55 citations in OpenAlex.
- Alkaloids Mediate Multi-Level Modulation of Gastric Carcinogenesis: From Antibacterial and Anti-Inflammatory Actions to Antitumor Effects.International journal of molecular sciences · 2026Review
- The dual role of gastric microbiota dysbiosis in gastric cancer progression and therapy.International journal of clinical oncology · 2026Review
- FFoods (Basel, Switzerland) · 2026Article
- Molecular Insights intoCancers · 2026Review
- Characterization ofFrontiers in microbiology · 2026Article
- Article
- Helicobacter pylori, microbiota and gastric cancer - principles of microorganism-driven carcinogenesis.Nature reviews. Gastroenterology & hepatology · 2025Review
- TargetingNutrients · 2025Review
- Association betweenFrontiers in medicine · 2025Article
- Transcriptomic Analysis Reveals the Effect of Urea on Metabolism ofLife (Basel, Switzerland) · 2024Article
- A transcriptomic atlas of acute stress response to low pH in multipleMicrobiology spectrum · 2024Article
- Unraveling the Role of Metals and Organic Acids in Bacterial Antimicrobial Resistance in the Food Chain.Antibiotics (Basel, Switzerland) · 2023Review
- Helicobacter pylori in the post-antibiotics era: from virulence factors to new drug targets and therapeutic agents.Archives of microbiology · 2023Review
- Antigenic Determinant ofPathogens (Basel, Switzerland) · 2022Article
- Article
- Intrinsic specificity of plain ammonium citrate carbon dots forMaterials today. Bio · 2022Article
- Helicobacter pylori: an up-to-date overview on the virulence and pathogenesis mechanisms.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2022Review
- RNA atlas of human bacterial pathogens uncovers stress dynamics linked to infection.Nature communications · 2021Article
- Draft genome of a novel methanotrophic Methylobacter sp. from the volcanic soils of Pantelleria Island.Antonie van Leeuwenhoek · 2021Article
- Development of the PANI/MWCNT Nanocomposite-Based Fluorescent Sensor for Selective Detection of Aqueous Ammonia.ACS omega · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The gastric pathogen Helicobacter pylori possesses a highly active urease to support acid tolerance. Urea hydrolysis occurs inside the cytoplasm, resulting in the production of NH3 that is immediately protonated to form NH4 (+). This ammonium must be metabolized or effluxed because its presence within the cell is counterproductive to the goal of raising pH while maintaining a viable proton motive force (PMF). Two compatible hypotheses for mitigating intracellular ammonium toxicity include (i) the exit of protonated ammonium outward via the UreI permease, which was shown to facilitate diffusion of both urea and ammonium, and/or (ii) the assimilation of this ammonium, which is supported by evidence that H. pylori assimilates urea nitrogen into its amino acid pools. We investigated the second hypothesis by constructing strains with altered expression of the ammonium-assimilating enzymes glutamine synthetase (GS) and glutamate dehydrogenase (GDH) and the ammonium-evolving periplasmic enzymes glutaminase (Ggt) and asparaginase (AsnB). H. pylori strains expressing elevated levels of either GS or GDH are more acid tolerant than the wild type, exhibit enhanced ammonium production, and are able to alkalize the medium faster than the wild type. Strains lacking the genes for either Ggt or AsnB are acid sensitive, have 8-fold-lower urea-dependent ammonium production, and are more acid sensitive than the parent. Additionally, we found that purified H. pylori GS produces glutamine in the presence of Mg(2+) at a rate similar to that of unadenylated Escherichia coli GS. These data reveal that all four enzymes contribute to whole-cell acid resistance in H. pylori and are likely important for assimilation and/or efflux of urea-derived ammonium.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.