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Suppression of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mice by transduced Tat-Annexin protein

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dc.contributor.authorLee, Sun Hwa-
dc.contributor.authorKim, Dae Won-
dc.contributor.authorEom, Seon Ae-
dc.contributor.authorJun, Se-Young-
dc.contributor.authorPark, Meeyoung-
dc.contributor.authorKim, Duk-Soo-
dc.contributor.authorKwon, Hyung Joo-
dc.contributor.authorKwon, Hyeok Yil-
dc.contributor.authorHan, Kyu Hyung-
dc.contributor.authorPark, Jinseu-
dc.contributor.authorHwang, Hyun Sook-
dc.contributor.authorEum, Won Sik-
dc.contributor.authorChoi, Soo Young-
dc.date.accessioned2021-08-12T02:48:41Z-
dc.date.available2021-08-12T02:48:41Z-
dc.date.issued2012-06-30-
dc.identifier.issn1976-6696-
dc.identifier.issn1976-670X-
dc.identifier.urihttps://scholarworks.bwise.kr/sch/handle/2021.sw.sch/15053-
dc.description.abstractWe examined that the protective effects of ANX1 on 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in animal models using a Tat-ANX1 protein. Topical application of the Tat-ANX1 protein markedly inhibited TPA-induced ear edema and expression levels of cyclooxygenase-2 (COX-2) as well as pro-inflammatory cytokines such as interleukin-1 beta (IL-1 beta), IL-6, and tumor necrosis factor-alpha (TNF-alpha). Also, application of Tat-ANX1 protein significantly inhibited nuclear translocation of nuclear factor-kappa B (NF-kappa B) and phosphorylation of p38 and extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase (MAPK) in TPA-treated mice ears. The results indicate that Tat-ANX1 protein inhibits the inflammatory response by blocking NF-kappa B and MAPK activation in TPA-induced mice ears. Therefore, the Tat-ANX1 protein may be useful as a therapeutic agent against inflammatory skin diseases. [BMB Reports 2012; 45(6): 354-359]-
dc.format.extent6-
dc.language영어-
dc.language.isoENG-
dc.publisher생화학분자생물학회-
dc.titleSuppression of 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced skin inflammation in mice by transduced Tat-Annexin protein-
dc.typeArticle-
dc.publisher.location대한민국-
dc.identifier.doi10.5483/BMBRep.2012.45.6.036-
dc.identifier.scopusid2-s2.0-84864385624-
dc.identifier.wosid000306036500006-
dc.identifier.bibliographicCitationBMB Reports, v.45, no.6, pp 354 - 359-
dc.citation.titleBMB Reports-
dc.citation.volume45-
dc.citation.number6-
dc.citation.startPage354-
dc.citation.endPage359-
dc.type.docTypeArticle-
dc.identifier.kciidART001668712-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.subject.keywordPlusLIPOPOLYSACCHARIDE-
dc.subject.keywordPlusINHIBITION-
dc.subject.keywordPlusINJURY-
dc.subject.keywordPlusALPHA-
dc.subject.keywordPlusLUNG-
dc.subject.keywordAuthorCytokine-
dc.subject.keywordAuthorInflammation-
dc.subject.keywordAuthorMAPK-
dc.subject.keywordAuthorTat-ANX1-
dc.subject.keywordAuthorTPA-
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