ArticleInfection and immunity2004
Acid-responsive gene induction of ammonia-producing enzymes in Helicobacter pylori is mediated via a metal-responsive repressor cascade.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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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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.
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Who cites it
31 citing papers in PubMed, 81 citations in OpenAlex.
- Insights into the Orchestration of Gene Transcription Regulators inInternational journal of molecular sciences · 2022Review
- Biomarker Characterization and Prediction of Virulence and Antibiotic Resistance fromBiomolecules · 2022Review
- Delineation of the pH-Responsive Regulon Controlled by the Helicobacter pylori ArsRS Two-Component System.Infection and immunity · 2021Article
- Acid-responsive activity of theProceedings of the National Academy of Sciences of the United States of America · 2018Article
- Survival of Helicobacter pylori in gastric acidic territory.Helicobacter · 2017Review
- Gene Expression Profiling of Transcription Factors ofFrontiers in microbiology · 2017Article
- The allosteric behavior of Fur mediates oxidative stress signal transduction in Helicobacter pylori.Frontiers in microbiology · 2015Article
- Crosstalk between the HpArsRS two-component system and HpNikR is necessary for maximal activation of urease transcription.Frontiers in microbiology · 2015Article
- Helicobacter pylori RNA polymerase α-subunit C-terminal domain shows features unique to ɛ-proteobacteria and binds NikR/DNA complexes.Protein science : a publication of the Protein Society · 2014Article
- The ferric uptake regulator of Helicobacter pylori: a critical player in the battle for iron and colonization of the stomach.Future microbiology · 2013Review
- Integrative computational protocol for the discovery of inhibitors of the Helicobacter pylori nickel response regulator (NikR).Journal of molecular modeling · 2011Article
- Biochemical and mutational studies of the Bacillus cereus CECT 5050T formamidase support the existence of a C-E-E-K tetrad in several members of the nitrilase superfamily.Applied and environmental microbiology · 2011Article
- Holo-Ni(II)HpNikR is an asymmetric tetramer containing two different nickel-binding sites.Journal of the American Chemical Society · 2010Article
- Detailed in vivo analysis of the role of Helicobacter pylori Fur in colonization and disease.Infection and immunity · 2010Article
- Cytoplasmic histidine kinase (HP0244)-regulated assembly of urease with UreI, a channel for urea and its metabolites, CO2, NH3, and NH4(+), is necessary for acid survival of Helicobacter pylori.Journal of bacteriology · 2010Article
- Helicobacter pylori urease activity is influenced by ferric uptake regulator.Yonsei medical journal · 2010Article
- Expanding the Helicobacter pylori genetic toolbox: modification of an endogenous plasmid for use as a transcriptional reporter and complementation vector.Applied and environmental microbiology · 2007Article
- Metal-responsive gene regulation and metal transport in Helicobacter species.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2007Review
- The CrdRS (HP1365-HP1364) two-component system is not involved in ph-responsive gene regulation in the Helicobacter pylori Strains 26695 and G27.Current microbiology · 2007Article
- The HP0165-HP0166 two-component system (ArsRS) regulates acid-induced expression of HP1186 alpha-carbonic anhydrase in Helicobacter pylori by activating the pH-dependent promoter.Journal of bacteriology · 2007Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although the adaptive mechanisms allowing the gastric pathogen Helicobacter pylori to survive acid shocks have been well documented, the mechanisms allowing growth at mildly acidic conditions (pH approximately 5.5) are still poorly understood. Here we demonstrate that H. pylori strain 26695 increases the transcription and activity of its urease, amidase, and formamidase enzymes four- to ninefold in response to growth at pH 5.5. Supplementation of growth medium with NiCl2 resulted in a similar induction of urease activity (at low NiCl2 concentration) and amidase activity (at > or = 500 micro M NiCl2) but did not affect formamidase activity. Mutation of the fur gene, which encodes an iron-responsive repressor of both amidases, resulted in a constitutively high level of amidase and formamidase activity at either pH but did not affect urease activity at pH 7.0 or pH 5.5. In contrast, mutation of the nikR gene, encoding the nickel-responsive activator of urease expression, resulted in a significant reduction of acid-responsive induction of amidase and formamidase activity. Finally, acid-responsive repression of fur transcription was absent in the H. pylori nikR mutant, whereas transcription of the nikR gene itself was increased at pH 5.5 in wild-type H. pylori. We hypothesize that H. pylori uses a repressor cascade to respond to low pH, with NikR initiating the response directly via the urease operon and indirectly via the members of the Fur regulon.
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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.