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Lack of association between promoter polymorphisms of HLA-G gene and rheumatoid arthritis in Korean population

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dc.contributor.authorKim, S. K.-
dc.contributor.authorChung, J. H.-
dc.contributor.authorKim, D. H.-
dc.contributor.authorYun, D. H.-
dc.contributor.authorHong, S. J.-
dc.contributor.authorLee, K. H.-
dc.date.accessioned2022-07-16T16:48:54Z-
dc.date.available2022-07-16T16:48:54Z-
dc.date.created2021-05-12-
dc.date.issued2012-02-
dc.identifier.issn0172-8172-
dc.identifier.urihttps://scholarworks.bwise.kr/hanyang/handle/2021.sw.hanyang/166351-
dc.description.abstractThe aim of this study was to determine whether the HLA-G gene was associated with susceptibility to rheumatoid arthritis (RA). Major histocompatibility complex, class I, G (HLA-G) is involved in immunoregulatory processes and particularly in pathogenesis of inflammatory disorders. To investigate possible association between HLA-G and RA, 296 RA patients and 468 healthy controls were enrolled in this study. Two-promoter single-nucleotide polymorphisms (SNPs) (rs1736936, -1202T/C and rs2735022, -586C/T) in HLA-G gene were analyzed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). For analysis of data, Helixtree software, SNPAnalyzer, SNPStats, and Haploview version 4.2 were used. Multiple logistic regression models (codominant, dominant, and recessive) were performed for odds ratio (OR), 95% confidence interval (CI), and P value. There were no significant differences in distributions of genotypes and haplotypes between RA patients and control subjects. In clinical features of RA, we found differences between C-reactive protein levels (a parts per thousand yen0.5 or < 0.5 mg/dL) and two-promoter SNPs. Rs1736936 was significant in codominant (P = 0.028, OR = 0.66, 95% CI = 0.45-0.96) and dominant (P = 0.046, OR = 0.58, 95% CI = 0.34-0.99) models. Also, rs2735022 was significant in codominant (P = 0.038, OR = 0.67, 95% CI = 0.46-0.98) and dominant (P = 0.03, OR = 0.55, 95% CI = 0.33-0.94) models. However, these significant associations disappear after Bonferroni correction. Our results suggest that HLA-G promoter polymorphisms may be not associated with the development of RA in Korean population.-
dc.language영어-
dc.language.isoen-
dc.publisherSPRINGER HEIDELBERG-
dc.titleLack of association between promoter polymorphisms of HLA-G gene and rheumatoid arthritis in Korean population-
dc.typeArticle-
dc.contributor.affiliatedAuthorLee, K. H.-
dc.identifier.doi10.1007/s00296-010-1735-4-
dc.identifier.scopusid2-s2.0-84857047557-
dc.identifier.wosid000299507900041-
dc.identifier.bibliographicCitationRHEUMATOLOGY INTERNATIONAL, v.32, no.2, pp.509 - 512-
dc.relation.isPartOfRHEUMATOLOGY INTERNATIONAL-
dc.citation.titleRHEUMATOLOGY INTERNATIONAL-
dc.citation.volume32-
dc.citation.number2-
dc.citation.startPage509-
dc.citation.endPage512-
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.keywordPlusC reactive protein-
dc.subject.keywordPlusHLA G antigen-
dc.subject.keywordPlusadult-
dc.subject.keywordPlusallele-
dc.subject.keywordPlusarticle-
dc.subject.keywordPlusclinical feature-
dc.subject.keywordPluscomputer program-
dc.subject.keywordPluscontrolled study-
dc.subject.keywordPlusdisease predisposition-
dc.subject.keywordPlusDNA polymorphism-
dc.subject.keywordPlusfemale-
dc.subject.keywordPlusgene linkage disequilibrium-
dc.subject.keywordPlusgenotype-
dc.subject.keywordPlushaplotype-
dc.subject.keywordPlushuman-
dc.subject.keywordPlusimmunoregulation-
dc.subject.keywordPlusKorea-
dc.subject.keywordPlusmajor clinical study-
dc.subject.keywordPlusmale-
dc.subject.keywordPluspathogenesis-
dc.subject.keywordPluspolymerase chain reaction-
dc.subject.keywordPluspopulation research-
dc.subject.keywordPluspriority journal-
dc.subject.keywordPlusrestriction fragment length polymorphism-
dc.subject.keywordPlusrheumatoid arthritis-
dc.subject.keywordPlussingle nucleotide polymorphism-
dc.subject.keywordAuthorAssociation study-
dc.subject.keywordAuthorHLA-G-
dc.subject.keywordAuthorSingle-nucleotide polymorphism-
dc.subject.keywordAuthorRheumatoid arthritis-
dc.identifier.urlhttps://link.springer.com/article/10.1007/s00296-010-1735-4-
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