ArticleCurrent microbiology2012
Characterization of CagI in the cag pathogenicity island of Helicobacter pylori.
Article in Current microbiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 11 citations in OpenAlex.
- The Helicobacter pylori Cag Pathogenicity Island Protein Cag1 is Associated with the Function of T4SS.Current microbiology · 2016Article
- The Helicobacter pylori protein CagM is located in the transmembrane channel that is required for CagA translocation.Current microbiology · 2013Article
- Predicting a novel pathogenicity island in Helicobacter pylori by genomic barcoding.World journal of gastroenterology · 2013Article
- Cag type IV secretion system: CagI independent bacterial surface localization of CagA.PloS one · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Helicobacter pylori is a highly successful human-specific gastric pathogen that infects up to 50% of the world's population. Virulent H. pylori isolates harbor the cytotoxin-associated genes pathogenicity island (cag-PAI), which encodes a type IV secretion system that translocates bacterial effector (e.g., CagA oncoprotein) molecules into host cells. Although some cag-PAI genes are shown to be required for CagA delivery or localization, the majority have no known function. In the current study, the authors performed a cell components fractionation assay and showed that CagI, one of the cag-PAI proteins located in the bacterial membrane, was not translocated into host cells. The homologous recombination method then was used to construct the isogenic mutant of H. pylori cagI, and the translocation assay was performed. The results showed that the isogenic mutant of H. pylori NCTC 11637 cagI could cause a reduction in the degree of CagA translocation. Overall, the results suggested that CagI might be an accessory component of the CagA secretion system not translocated into host cells and that it is located in the bacterial membrane.
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Registered trials
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