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Cyclooxygenase-2 polymorphisms and risk of systemic lupus erythematosus in Koreans

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dc.contributor.authorHer, Min-Young-
dc.contributor.authorEl-Sohemy, Ahmed-
dc.contributor.authorCornelis, Marilyn C.-
dc.contributor.authorKim, Tae-Hwan-
dc.contributor.authorBae, Sang-Cheol-
dc.date.accessioned2022-12-21T09:54:00Z-
dc.date.available2022-12-21T09:54:00Z-
dc.date.created2022-09-16-
dc.date.issued2006-11-
dc.identifier.issn0172-8172-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/180769-
dc.description.abstractCyclooxygenase-2 (COX-2) is a key regulatory enzyme in the synthesis of prostanoids associated with trauma and inflammation. Upregulation of COX-2 in human lupus T cells resists anergy and apotosis. We investigated the COX-2 gene for functional variants that may influence susceptibility, clinical outcomes and severity of systemic lupus erythematosus (SLE) in a Korean population. The study included 345 patients with SLE and 400 unrelated healthy controls. Genotyping for the -765G -> C polymorphism of COX-2 was performed by PCR - RFLP analysis. No difference in the distribution of the genotype frequencies between patients and controls was found. COX-2 genotypes were not associated with clinical features except hematologic abnormalities and anti-RNP antibody. We did not detect any association between COX-2 genotype and disease severity in SLE patients. These results suggest that the -765G -> C polymorphism of COX-2 does not play a significant role in the development of SLE in a Korean population. A possible protective effect of the low activity C allele against the production of anti-RNP antibodies merits further investigation.-
dc.language영어-
dc.language.isoen-
dc.publisherSPRINGER-
dc.titleCyclooxygenase-2 polymorphisms and risk of systemic lupus erythematosus in Koreans-
dc.typeArticle-
dc.contributor.affiliatedAuthorKim, Tae-Hwan-
dc.contributor.affiliatedAuthorBae, Sang-Cheol-
dc.identifier.doi10.1007/s00296-006-0162-z-
dc.identifier.scopusid2-s2.0-33750485335-
dc.identifier.wosid000241580800001-
dc.identifier.bibliographicCitationRHEUMATOLOGY INTERNATIONAL, v.27, no.1, pp.1 - 5-
dc.relation.isPartOfRHEUMATOLOGY INTERNATIONAL-
dc.citation.titleRHEUMATOLOGY INTERNATIONAL-
dc.citation.volume27-
dc.citation.number1-
dc.citation.startPage1-
dc.citation.endPage5-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaRheumatology-
dc.relation.journalWebOfScienceCategoryRheumatology-
dc.subject.keywordPlusT-CELLS-
dc.subject.keywordPlusGENE-
dc.subject.keywordPlusNEPHRITIS-
dc.subject.keywordPlusDEATH-
dc.subject.keywordAuthorcyclooxygenase-2-
dc.subject.keywordAuthorsystemic lupus erythematosus-
dc.subject.keywordAuthorpolymorphism-
dc.identifier.urlhttps://link.springer.com/article/10.1007/s00296-006-0162-z-
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