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No association between interleukin 23 receptor gene polymorphisms and systemic lupus erythematosus

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dc.contributor.authorKim, Hee-Sun-
dc.contributor.authorKim, Il-
dc.contributor.authorKim, Ji On-
dc.contributor.authorBae, Joon Seol-
dc.contributor.authorShin, Hyoung Doo-
dc.contributor.authorBae, Sang-Cheol-
dc.date.accessioned2022-12-20T20:13:27Z-
dc.date.available2022-12-20T20:13:27Z-
dc.date.created2022-08-26-
dc.date.issued2009-11-
dc.identifier.issn0172-8172-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/175909-
dc.description.abstractThe objective of this study was to elucidate whether polymorphisms of the interleukin 23 receptor gene (IL23R) are associated with susceptibility to systemic lupus erythematosus (SLE) in a Korean population. We recruited 602 SLE patients and 991 healthy controls. Seven single nucleotide polymorphisms (rs1004819, rs7517847, rs10489629, rs2201841, rs1343151, rs11209032, and rs1495965) were selected for genotyping among previously reported variants used in a genome-wide association study of inflammatory bowel disease. Polymorphic sites were genotyped using the TaqMan assay. The genotype distributions of IL23R polymorphisms and haplotypes were compared between the SLE patients and healthy controls using multiple logistic regression models. None of the IL23R genetic variants differed significantly between SLE patients and healthy controls, which suggests that IL23R polymorphisms play no role in the susceptibility to SLE in the Korean population.-
dc.language영어-
dc.language.isoen-
dc.publisherSPRINGER HEIDELBERG-
dc.titleNo association between interleukin 23 receptor gene polymorphisms and systemic lupus erythematosus-
dc.typeArticle-
dc.contributor.affiliatedAuthorBae, Sang-Cheol-
dc.identifier.doi10.1007/s00296-009-0893-8-
dc.identifier.scopusid2-s2.0-71349084584-
dc.identifier.wosid000271989400004-
dc.identifier.bibliographicCitationRHEUMATOLOGY INTERNATIONAL, v.30, no.1, pp.33 - 38-
dc.relation.isPartOfRHEUMATOLOGY INTERNATIONAL-
dc.citation.titleRHEUMATOLOGY INTERNATIONAL-
dc.citation.volume30-
dc.citation.number1-
dc.citation.startPage33-
dc.citation.endPage38-
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.keywordPlusIL-23-
dc.subject.keywordPlusIL23R-
dc.subject.keywordPlusDISEASE-
dc.subject.keywordPlusIL-12-
dc.subject.keywordPlusDISEQUILIBRIUM-
dc.subject.keywordPlusSUSCEPTIBILITY-
dc.subject.keywordPlusINFLAMMATION-
dc.subject.keywordPlusREGULATORS-
dc.subject.keywordPlusINNATE-
dc.subject.keywordPlusROLES-
dc.subject.keywordAuthorInterleukin 23 receptor gene (IL23R gene)-
dc.subject.keywordAuthorPolymorphisms-
dc.subject.keywordAuthorSystemic lupus erythematosus (SLE)-
dc.subject.keywordAuthorSusceptibility-
dc.identifier.urlhttps://link.springer.com/article/10.1007/s00296-009-0893-8-
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