ArticleInfection and immunity2014
Genes required for assembly of pili associated with the Helicobacter pylori cag type IV secretion system.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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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Who cites it
53 citing papers in PubMed, 81 citations in OpenAlex.
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- Bacterial type IV secretion systems and spread of antimicrobial resistance: a study of potential inhibitors to T4SS-based resistance spread.Archives of microbiology · 2025Review
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- New strategies for Helicobacter pylori isolation and sequencing analysis for virulence genes contributing to its pathogenicity.Molecular biology reports · 2024Article
- Roles of the components of theFuture microbiology · 2024Review
- Essential role ofInfection and immunity · 2023Article
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- Conjugative Transfer of Acute Hepatopancreatic Necrosis Disease-Causing pVA1-Type Plasmid Is Mediated by a Novel Self-Encoded Type IV Secretion System.Microbiology spectrum · 2022Article
- Positive Selection of Mutations in the Helicobacter pyloriInfection and immunity · 2022Article
- Type IV secretion systems: Advances in structure, function, and activation.Molecular microbiology · 2021Review
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- The Helicobacter pylori Cag Type IV Secretion System.Trends in microbiology · 2020Review
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Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
Helicobacter pylori causes numerous alterations in gastric epithelial cells through processes that are dependent on activity of the cag type IV secretion system (T4SS). Filamentous structures termed "pili" have been visualized at the interface between H. pylori and gastric epithelial cells, and previous studies suggested that pilus formation is dependent on the presence of the cag pathogenicity island (PAI). Thus far, there has been relatively little effort to identify specific genes that are required for pilus formation, and the role of pili in T4SS function is unclear. In this study, we selected 7 genes in the cag PAI that are known to be required for T4SS function and investigated whether these genes were required for pilus formation. cagT, cagX, cagV, cagM, and cag3 mutants were defective in both T4SS function and pilus formation; complemented mutants regained T4SS function and the capacity for pilus formation. cagY and cagC mutants were defective in T4SS function but retained the capacity for pilus formation. These results define a set of cag PAI genes that are required for both pilus biogenesis and T4SS function and reveal that these processes can be uncoupled in specific mutant strains.
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Registered trials
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