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dc.contributor.authorSeo, Ji-Eun-
dc.contributor.authorHasan, Mahbub-
dc.contributor.authorHan, Joon-Seung-
dc.contributor.authorKim, Nak-Kyoon-
dc.contributor.authorLee, Ji Eun-
dc.contributor.authorLee, Kang Mi-
dc.contributor.authorPark, Ju-Hyung-
dc.contributor.authorKim, Ho Jun-
dc.contributor.authorSon, Junghyun-
dc.contributor.authorLee, Jaeick-
dc.contributor.authorKwon, Oh-Seung-
dc.date.accessioned2024-01-20T04:32:52Z-
dc.date.available2024-01-20T04:32:52Z-
dc.date.created2021-09-04-
dc.date.issued2016-04-
dc.identifier.issn0364-3190-
dc.identifier.urihttps://pubs.kist.re.kr/handle/201004/124239-
dc.description.abstractExperimental autoimmune encephalomyelitis (EAE) is commonly induced with myelin oligodendrocyte glycoprotein (MOG)(35-55); occasionally, EAE is not well induced despite MOG(35-55) immunization. To confirm that EAE induction varies with difference in MOG(35-55) properties, we compared three MOG(35-55) from different commercial sources, which are MOG-A, MOG-B, and MOG-C. The peptides induced EAE disease with 100, 40, and 20 % incidence, respectively. Compared with others, MOG-A showed higher peptide purity (99.2 %) and content (92.2 %) and presented a sheet shape with additional sodium and chloride chemical elements. In MOG-A-treated group, MMP-9 activity and IL-6 levels were considerably higher than the other groups in CNS tissues, and significantly increased VCAM-1, IFN-gamma, and decreased IL-4 were also shown compared to MOG-B- and/or MOG-C-treated group. In conclusion, the immunological and toxicological changes by the difference in MOG(35-55) properties modulate EAE induction, and MOG(35-55) which affects MMP-9 activity and IL-6 levels may be the most effective EAE-inducing antigen. This study can be potentially applied by researchers using MOG(35-55) peptide and manufacturers for MOG(35-55) synthesis.-
dc.languageEnglish-
dc.publisherSPRINGER/PLENUM PUBLISHERS-
dc.titleDependency of Experimental Autoimmune Encephalomyelitis Induction on MOG(35-55) Properties Modulating Matrix Metalloproteinase-9 and Interleukin-6-
dc.typeArticle-
dc.identifier.doi10.1007/s11064-015-1732-9-
dc.description.journalClass1-
dc.identifier.bibliographicCitationNEUROCHEMICAL RESEARCH, v.41, no.4, pp.666 - 676-
dc.citation.titleNEUROCHEMICAL RESEARCH-
dc.citation.volume41-
dc.citation.number4-
dc.citation.startPage666-
dc.citation.endPage676-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.identifier.wosid000373860300005-
dc.identifier.scopusid2-s2.0-84944691148-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalResearchAreaNeurosciences & Neurology-
dc.type.docTypeArticle-
dc.subject.keywordPlusBLOOD-BRAIN-BARRIER-
dc.subject.keywordPlusMYELIN OLIGODENDROCYTE GLYCOPROTEIN-
dc.subject.keywordPlusT-CELL RESPONSES-
dc.subject.keywordPlusMULTIPLE-SCLEROSIS-
dc.subject.keywordPlusANIMAL-MODELS-
dc.subject.keywordPlusMICE-
dc.subject.keywordPlusEAE-
dc.subject.keywordPlusAUTOANTIGEN-
dc.subject.keywordPlusEXPRESSION-
dc.subject.keywordPlusMIGRATION-
dc.subject.keywordAuthorMOG(35-55)-
dc.subject.keywordAuthorEAE-
dc.subject.keywordAuthorMMP-9-
dc.subject.keywordAuthorIL-6-
dc.subject.keywordAuthorProperty-
dc.subject.keywordAuthorInduction-
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