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Cited 35 time in webofscience Cited 40 time in scopus
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Disease-specific proteins from rheumatoid arthritis patients

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dc.contributor.authorKim, Choong Won-
dc.contributor.authorCho, Eun Hye-
dc.contributor.authorLee, Yun Jong-
dc.contributor.authorKim, Yoon Hee-
dc.contributor.authorHah, Young-Sool-
dc.contributor.authorKim, Deok Ryong-
dc.date.accessioned2025-04-01T07:00:45Z-
dc.date.available2025-04-01T07:00:45Z-
dc.date.issued2006-06-
dc.identifier.issn1011-8934-
dc.identifier.issn1598-6357-
dc.identifier.urihttps://scholarworks.gnu.ac.kr/handle/sw.gnu/77640-
dc.description.abstractRheumatoid arthritis (RA) is a chronic inflammatiory disease that mainly destroys cartilages or bones at the joints. This inflammatory disorder is initiated by self-attack using own immune system, but the detail of pathological mechanism is unclear. Features of autoantigens leading to autoimmune disease are also under veil although several candidates including type II collagen have been suggested to play a role in pathogenesis. In this report, we tried to identify proteins responding to antibodies purified from RA patients and screen proteins up-regulated or down-regulated in RA using proteomic approach. Fibronectin, semaphorin 7A precursor, growth factor binding protein 7 (GRB7), and immunoglobulin mu chain were specifically associated with antibodies isolated from RA synovial fluids. In addition, some metabolic proteins such as adipocyte fatty acid binding protein, galectin-1 and apolipoprotein A1 precursor were overexpressed in RA synovium. Also, expression of peroxiredoxin 2 was up-regulated in RA. On the contrary, expression of vimentin was severely suppressed in RA synoviocytes. Such findings might give some insights into understanding of pathological mechanism in RA.-
dc.format.extent7-
dc.language영어-
dc.language.isoENG-
dc.publisher대한의학회-
dc.titleDisease-specific proteins from rheumatoid arthritis patients-
dc.typeArticle-
dc.publisher.location대한민국-
dc.identifier.doi10.3346/jkms.2006.21.3.478-
dc.identifier.scopusid2-s2.0-33745239254-
dc.identifier.wosid000238870800018-
dc.identifier.bibliographicCitationJournal of Korean Medical Science, v.21, no.3, pp 478 - 484-
dc.citation.titleJournal of Korean Medical Science-
dc.citation.volume21-
dc.citation.number3-
dc.citation.startPage478-
dc.citation.endPage484-
dc.type.docTypeArticle-
dc.identifier.kciidART001116255-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaGeneral & Internal Medicine-
dc.relation.journalWebOfScienceCategoryMedicine, General & Internal-
dc.subject.keywordPlusSYNOVIAL-FLUID-
dc.subject.keywordPlusB-CELL-
dc.subject.keywordPlusFIBRONECTIN-
dc.subject.keywordPlusAUTOANTIBODIES-
dc.subject.keywordPlusIDENTIFICATION-
dc.subject.keywordPlusANTIBODIES-
dc.subject.keywordPlusFILAMENTS-
dc.subject.keywordPlusEPITOPES-
dc.subject.keywordPlusCOLLAGEN-
dc.subject.keywordPlusALPHA-
dc.subject.keywordAuthorarthritis, rheumatoid-
dc.subject.keywordAuthorautoantigens-
dc.subject.keywordAuthorfibronectins-
dc.subject.keywordAuthorproteomics-
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