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Analysis of the 3 ' variable region of the cagA gene of Helicobacter pylori isolated in Koreans

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dc.contributor.authorChoi, Kee Don-
dc.contributor.authorKim, Nayoung-
dc.contributor.authorLee, Dong Ho-
dc.contributor.authorKim, Jung Mogg-
dc.contributor.authorKim, Joo Sung-
dc.contributor.authorJung, Hyun Chae-
dc.contributor.authorSong, In Sung-
dc.date.accessioned2022-12-21T08:49:29Z-
dc.date.available2022-12-21T08:49:29Z-
dc.date.created2022-08-26-
dc.date.issued2007-04-
dc.identifier.issn0163-2116-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/180280-
dc.description.abstractCagA protein of Helicobacter pylori is injected into epithelial cells, and it undergoes tyrosine phosphorylation, resulting in inducing cytoskeletal rearrangements. A few studies have suggested that the number of CagA tyrosine phosphorylation motifs (EPIYA) and subtypes of CagA were associated with gastric cancer. This study was performed to characterize the 3' variable regions of the cagA gene of H. pylori and to investigate whether or not there is any relationship between the diversities of cagA and the disease outcome in Korea. Seventy-nine patients (chronic gastritis, 15; duodenal ulcer, 27; benign gastric ulcer, 18; gastric cancer, 19) were enrolled. Biopsy specimens were taken from the antrum for H. pylori culture, and genomic DNA was extracted. PCR and DNA sequence analysis was carried out for the 3' variable region of the cagA gene. Seventy-eight strains (98.8%) contained three EPIYA motifs and one strain (1.2%) isolated from a patient with duodenal ulcer contained four EPIYA motifs. Seventy-six strains (96.2%) were the East Asian type. In conclusion, there was no significant difference between the number of EPIYA motifs or CagA subtypes and various gastroduodenal diseases in Korea.-
dc.language영어-
dc.language.isoen-
dc.publisherSPRINGER-
dc.titleAnalysis of the 3 ' variable region of the cagA gene of Helicobacter pylori isolated in Koreans-
dc.typeArticle-
dc.contributor.affiliatedAuthorKim, Jung Mogg-
dc.identifier.doi10.1007/s10620-005-9030-z-
dc.identifier.scopusid2-s2.0-33947609115-
dc.identifier.wosid000245131900015-
dc.identifier.bibliographicCitationDIGESTIVE DISEASES AND SCIENCES, v.52, no.4, pp.960 - 966-
dc.relation.isPartOfDIGESTIVE DISEASES AND SCIENCES-
dc.citation.titleDIGESTIVE DISEASES AND SCIENCES-
dc.citation.volume52-
dc.citation.number4-
dc.citation.startPage960-
dc.citation.endPage966-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaGastroenterology & Hepatology-
dc.relation.journalWebOfScienceCategoryGastroenterology & Hepatology-
dc.subject.keywordPlusGASTRIC EPITHELIAL-CELLS-
dc.subject.keywordPlusVIRULENCE FACTORS-
dc.subject.keywordPlusTYROSINE PHOSPHORYLATION-
dc.subject.keywordPlusPATHOGENICITY ISLAND-
dc.subject.keywordPlusINCREASED RISK-
dc.subject.keywordPlusPROTEIN-
dc.subject.keywordPlusINFECTION-
dc.subject.keywordPlusCANCER-
dc.subject.keywordPlusADENOCARCINOMA-
dc.subject.keywordPlusPHOSPHATASE-
dc.subject.keywordAuthorCagA-
dc.subject.keywordAuthorEPIYA-
dc.subject.keywordAuthorHelicobacter pylori-
dc.subject.keywordAuthortyrosine phosphorylation-
dc.identifier.urlhttps://link.springer.com/article/10.1007/s10620-005-9030-z-
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