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Transduced Tat-Annexin protein suppresses inflammation-associated gene expression in lipopolysaccharide (LPS)-stimulated Raw 264.7 cells

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dc.contributor.authorLee, Sun Hwa-
dc.contributor.authorKim, Dae Won-
dc.contributor.authorBack, Su Sun-
dc.contributor.authorHwang, Hyun Sook-
dc.contributor.authorPark, Eun Young-
dc.contributor.authorKang, Tae-Cheon-
dc.contributor.authorKwon, Oh-Shin-
dc.contributor.authorPark, Jong Hoon-
dc.contributor.authorCho, Sung-Woo-
dc.contributor.authorHan, Kyu Hyung-
dc.contributor.authorPark, Jinseu-
dc.contributor.authorEum, Won Sik-
dc.contributor.authorChoi, Soo Young-
dc.date.available2021-02-22T13:16:51Z-
dc.date.created2020-09-03-
dc.date.issued2011-07-
dc.identifier.issn1976-6696-
dc.identifier.urihttps://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/12532-
dc.description.abstractAnnexin-1 (ANX1) is an anti-inflammatory protein as well as an important modulator in inflammation. However, the precise action of ANX1 remains unclear. To elucidate the protective effects of ANX1 on lipopolysaccharide (LPS)-induced murine macrophage Raw 264.7 cells, we constructed a cell-permeable Tat-ANX1 protein. The transduced Tat-ANX1 protein markedly inhibited the expression of cyclooxygenase-2, production of prostaglandin E-2, and generation of pro-inflammatory cytokines in the cells. Furthermore, transduced Tat-ANX1 protein caused a significant reduction in the activation of nuclear factor-kappa B (NF-kappa B) and mitogen-activated protein kinase (MAPK). The results indicate that Tat-ANX1 inhibits the production of inflammatory response cytokines and enzymes by blocking NF-kappa B and MAPK. Therefore, Tat-ANX1 protein may be useful as a therapeutic agent against various inflammatory diseases. [BMB reports 2011; 44(7): 484-489]-
dc.language영어-
dc.language.isoen-
dc.publisherKOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY-
dc.titleTransduced Tat-Annexin protein suppresses inflammation-associated gene expression in lipopolysaccharide (LPS)-stimulated Raw 264.7 cells-
dc.typeArticle-
dc.contributor.affiliatedAuthorPark, Jong Hoon-
dc.identifier.doi10.5483/BMBRep.2011.44.7.484-
dc.identifier.scopusid2-s2.0-79961035071-
dc.identifier.wosid000293358300010-
dc.identifier.bibliographicCitationBMB REPORTS, v.44, no.7, pp.484 - 489-
dc.relation.isPartOfBMB REPORTS-
dc.citation.titleBMB REPORTS-
dc.citation.volume44-
dc.citation.number7-
dc.citation.startPage484-
dc.citation.endPage489-
dc.type.rimsART-
dc.type.docTypeArticle-
dc.identifier.kciidART001572949-
dc.description.journalClass1-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.description.journalRegisteredClasskci-
dc.relation.journalResearchAreaBiochemistry & Molecular Biology-
dc.relation.journalWebOfScienceCategoryBiochemistry & Molecular Biology-
dc.subject.keywordPlusNF-KAPPA-B-
dc.subject.keywordPlusCU,ZN-SUPEROXIDE DISMUTASE-
dc.subject.keywordPlusEFFICIENTLY PROTECTS-
dc.subject.keywordPlusTRANSCRIPTION FACTOR-
dc.subject.keywordPlusTNF-ALPHA-
dc.subject.keywordPlusINHIBITION-
dc.subject.keywordPlusPEPTIDE-
dc.subject.keywordPlusDISEASE-
dc.subject.keywordPlusMACROPHAGES-
dc.subject.keywordPlusINVOLVEMENT-
dc.subject.keywordAuthorCytokine-
dc.subject.keywordAuthorInflammation-
dc.subject.keywordAuthorMAPK-
dc.subject.keywordAuthorProtein therapy-
dc.subject.keywordAuthorTat-ANX1-
dc.identifier.urlhttp://koreascience.or.kr/article/JAKO201123163432857.page-
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