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Mitochondrial ATP synthase is a target for TNBS-induced protein carbonylation in XS-106 dendritic cells

DC Field Value Language
dc.contributor.author김동현-
dc.contributor.author김수찬-
dc.contributor.author이민걸-
dc.contributor.author이주희-
dc.contributor.author조영훈-
dc.date.accessioned2015-05-19T16:24:37Z-
dc.date.available2015-05-19T16:24:37Z-
dc.date.issued2008-
dc.identifier.issn1615-9853-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/106254-
dc.description.abstractROS are produced in dendritic cells (DCs) during antigen presentation in contact hypersensitivity (CHS). As a result, ROS cause a number of nonenzymatic protein modifications, including carbonylation, which is the most widely used marker of oxidative stress. 2,4,6-Trinitrobenzene sulfonic acid (TNBS) is a well-characterized contact allergen that results in the formation of ROS. However, proteins that are carbonylated in DCs in response to TNBS have not been identified. To study ROS-dependent protein carbonylation in response to TNBS, we used the well-established mouse DC line, XS-106. We focused on the effects of TNBS on oxidation by examining selected oxidative markers. We identified TNBS-induced ROS and myeloperoxidase (MPO) proteins and demonstrated that the increase in ROS resulted in IL-12 production. The increase in oxidation was further confirmed by an oxidation-dependent increase in protein modifications, such as carbonylation. In fact, TNBS strongly induced carbonylation of mitochondrial adenosine triphosphate (ATP) synthase in XS-106 DCs, as determined by MALDI-TOF analysis and 2-D Western blotting. ROS production and protein carbonylation were confirmed in human monocyte-derived DCs (Mo-DCs). Furthermore, glutathione (GSH) decreased ROS and protein carbonylation in Mo-DCs. Carbonylation of ATP synthase in DCs may contribute to the pathophysiology of CHS.-
dc.description.statementOfResponsibilityopen-
dc.format.extent2384~2393-
dc.relation.isPartOfPROTEOMICS-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHAnimals, Newborn-
dc.subject.MESHCell Culture Techniques-
dc.subject.MESHCell Line-
dc.subject.MESHCulture Media, Conditioned-
dc.subject.MESHDendritic Cells/drug effects*-
dc.subject.MESHDendritic Cells/metabolism-
dc.subject.MESHGranulocyte-Macrophage Colony-Stimulating Factor/pharmacology-
dc.subject.MESHHumans-
dc.subject.MESHMice-
dc.subject.MESHMitochondrial Proton-Translocating ATPases/metabolism*-
dc.subject.MESHMonocytes/cytology-
dc.subject.MESHPeroxidase/genetics-
dc.subject.MESHPeroxidase/metabolism-
dc.subject.MESHProtein Carbonylation/drug effects*-
dc.subject.MESHProteomics/methods-
dc.subject.MESHReactive Oxygen Species/metabolism-
dc.subject.MESHSkin/cytology-
dc.subject.MESHTrinitrobenzenesulfonic Acid/pharmacology*-
dc.titleMitochondrial ATP synthase is a target for TNBS-induced protein carbonylation in XS-106 dendritic cells-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Dermatology (피부과학)-
dc.contributor.googleauthorJeong Hwan Je-
dc.contributor.googleauthorTae Hyung Lee-
dc.contributor.googleauthorDong Hyun Kim-
dc.contributor.googleauthorYoung Hun Cho-
dc.contributor.googleauthorJu Hee Lee-
dc.contributor.googleauthorSoo Chan Kim-
dc.contributor.googleauthorSang-Kyou Lee-
dc.contributor.googleauthorJaewon Lee-
dc.contributor.googleauthorMin-Geol Lee-
dc.identifier.doi10.1002/pmic.200700962-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA02779-
dc.contributor.localIdA03171-
dc.contributor.localIdA03861-
dc.contributor.localIdA00637-
dc.contributor.localIdA00412-
dc.relation.journalcodeJ02566-
dc.identifier.eissn1615-9861-
dc.identifier.pmid18563732-
dc.identifier.urlhttp://onlinelibrary.wiley.com/doi/10.1002/pmic.200700962/abstract-
dc.subject.keywordATP synthase-
dc.subject.keywordProtein carbonylation-
dc.subject.keywordROS-
dc.subject.keywordTNBS-
dc.subject.keywordXS‐106-
dc.contributor.alternativeNameKim, Dong Hyun-
dc.contributor.alternativeNameKim, Soo Chan-
dc.contributor.alternativeNameLee, Min Geol-
dc.contributor.alternativeNameLee, Ju Hee-
dc.contributor.alternativeNameCho, Young Hun-
dc.contributor.affiliatedAuthorLee, Min Geol-
dc.contributor.affiliatedAuthorLee, Ju Hee-
dc.contributor.affiliatedAuthorCho, Young Hun-
dc.contributor.affiliatedAuthorKim, Soo Chan-
dc.contributor.affiliatedAuthorKim, Dong Hyun-
dc.rights.accessRightsnot free-
dc.citation.volume8-
dc.citation.number12-
dc.citation.startPage2384-
dc.citation.endPage2393-
dc.identifier.bibliographicCitationPROTEOMICS, Vol.8(12) : 2384-2393, 2008-
dc.identifier.rimsid56312-
dc.type.rimsART-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Dermatology (피부과학교실) > 1. Journal Papers

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